Does prednisone cause dizziness: Page not found – Drugwatch.com
Side Effects of Prednisone (Prednisone Tablets, USP), Warnings, Uses
round, white, imprinted with 54 899
round, white, imprinted with 54 760
round, white, imprinted with 54 343
round, white, imprinted with 54 612
round, white, imprinted with 54 092
round, white, imprinted with 54 339
round, white, imprinted with 54 612
round, white, imprinted with 54 339
round, orange, imprinted with West-ward 477
round, white, imprinted with WEST-WARD 473
round, white, imprinted with West-ward 475
round, white, imprinted with 5052, DAN DAN
round, white, imprinted with 5442, DAN DAN
round, peach, imprinted with 5443, DAN DAN
round, white, imprinted with 5084, V
round, white, imprinted with 5085, V
round, white, imprinted with 5094, V
round, white, imprinted with 50 93, V
round, orange, imprinted with 5092, V
round, white, imprinted with TL 171
round, white, imprinted with TL 172
round, white, imprinted with TL173
round, pink, imprinted with TL175
Deltasone 10 mg
round, white, imprinted with DELTASONE 10
Deltasone 5 mg
round, white, imprinted with DELTASONE 5
Prednisone 1 mg-ROX
round, white, imprinted with 54 092
Prednisone 10 mg-IVA
round, white, imprinted with WESTWARD, 473
Prednisone 10 mg-IVA
round, white, imprinted with WEST-WARD, 473
Prednisone 10 mg-URL
round, white, imprinted with MP 52
Prednisone 10 mg-WAT
round, white, imprinted with 5442, DAN DAN
Prednisone 20 mg-IVA
round, orange, imprinted with WESTWARD 477
Prednisone 20 mg-IVA
round, peach, imprinted with WESTWARD 477
Prednisone 20 mg-URL
round, peach, imprinted with MP 53
Prednisone 5 mg-IVA
round, white, imprinted with WESTWARD 475
Prednisone 5 mg-ROX
round, white, imprinted with 54 612
Prednisone 5 mg-URL
round, white, imprinted with MP 51
Prednisone 50 mg-ROX
round, white, imprinted with 54 343
Prednisone: MedlinePlus Drug Information
Prednisone comes as a tablet, delayed-release tablet, as a solution (liquid), and as a concentrated solution to take by mouth. Prednisone is usually taken with food one to four times a day or once every other day. Your doctor will probably tell you to take your dose(s) of prednisone at certain time(s) of day every day. Your personal dosing schedule will depend on your condition and on how you respond to treatment. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take prednisone exactly as directed. Do not take more or less of it or take it more often or for a longer period of time than prescribed by your doctor.
If you are taking the concentrated solution, use the specially marked dropper that comes with the medication to measure your dose. You may mix the concentrated solution with juice, other flavored liquids, or soft foods such as applesauce.
Swallow the delayed-release tablet whole; do not chew or crush it.
Your doctor may change your dose of prednisone often during your treatment to be sure that you are always taking the lowest dose that works for you. Your doctor may also need to change your dose if you experience unusual stress on your body such as surgery, illness, infection, or a severe asthma attack. Tell your doctor if your symptoms improve or get worse or if you get sick or have any changes in your health during your treatment.
If you are taking prednisone to treat a long-lasting disease, the medication may help control your condition but will not cure it. Continue to take prednisone even if you feel well. Do not stop taking prednisone without talking to your doctor. If you suddenly stop taking prednisone, your body may not have enough natural steroids to function normally. This may cause symptoms such as extreme tiredness, weakness, slowed movements, upset stomach, weight loss, changes in skin color, sores in the mouth, and craving for salt. Call your doctor if you experience these or other unusual symptoms while you are taking decreasing doses of prednisone or after you stop taking the medication.
Dizziness Can Be a Fatal Side Effect of Many Medications
Dizziness—a deficit in spatial perception that leaves people feeling lightheaded, unbalanced or disoriented—is one of the most common side effects of prescription drugs. Some of the most popular medications, including those that control high blood pressure or alter the neurochemistry of the brain, can intensify or cause dizziness in up to 30 percent of patients who take them, experts estimate.
“As we age, we are already dealing with changes to our physiology and our brain that make us more prone to dizziness,” says Ann Tucker Gleason, director of the Vestibular and Balance Center at the University of Virginia. “To add to this, many of us also take drugs that significantly exacerbate dizziness and make us more likely to injure ourselves falling.” According to the U.S. Centers for Disease Control and Prevention, falls are the leading cause of accidental injury and death in people older than 65.
Still, many people remain uninformed of the dangers of dizziness or unaware that one or more of their prescription drugs may leave them off-balance. Experts estimate that dizziness affects up to 30 percent of the general population, most frequently caused by disorders of the inner ear or vestibular system but also caused by conditions or medications that af-fect our vision, brain function or nervous system.
“Dizziness, especially lightheadedness, is not only a global problem but also a near epidemic in the geriatric population, making it a serious health concern,” says Christopher Zalewski, a researcher at the U.S. National Institute on Deafness and Other Communication Disorders. Below are the most common drugs that can cause dizziness and advice about how to treat it.
If you experience dizziness, the best thing you can do is consult your doctor. If a medication is to blame, your doctor may be able to lower the dose or switch you to a different drug. If the problem has a different origin or your medication cannot be altered, many other treatment options exist:
Exercise. Experts have developed several exercise regimens that can restore balance for some people. So-called vestibular rehabilitation encompasses exercises for the eye and head that help to retrain the brain to cope with the skewed signals coming from the inner ear. Canalith repositioning procedure, which also involves performing a sequence of head movements, shifts the contents of the inner ear to ease some instances of vertigo. Consult a doctor before attempting these exercises. Maintaining general fitness and doing exercises that strengthen balance, such as tai chi, may improve dizziness. Although the evidence is limited, playing Wii Fit on a Nintendo Wii could be a fun way to enhance your balance.
Change surroundings. Determine where around your home or workplace you may be most prone to falls and make adjustments. For instance, wear secure footwear to prevent falling on wet or slippery surfaces, improve lighting, and put carpet or additional railings on stairs.
Modify your diet. Eating less sodium may reduce dizziness, as may cutting back on alcohol, caffeine and nicotine.
Try an antidizziness drug. If all else fails, your doctor may prescribe medication such as an antiemetic that suppresses mixed signals from the inner ear and reduces motion sickness. Yet many drugs used to combat dizziness come with problems of their own, such as unpleasant side effects. Ironically, some of them can even increase dizziness.
Prednisone | UPMC Hillman Cancer Center
About This Drug
Prednisone is a steroid that may be used to treat cancer. It is given orally (by mouth).
Possible Side Effects
- Abnormal heart beat
- High blood pressure
- Increased sweating
- Blurred vision or other changes in eyesight
- Tiredness and weakness
- Changes in mood, which may include depression or a feeling of extreme well-being
- Trouble sleeping
- Feeling restless (unable to relax)
- Skin changes such as rash, dryness redness
- Increased appetite (increased hunger)
- Weight gain
- Electrolyte changes
- Increased risk of infections
- Aggravation of stomach ulcers
- Pain in your abdomen
- Blood sugar levels may change
- Swelling of your legs, ankles and/or feet
- Muscle loss and/or weakness (lack of muscle strength)
- Increased risk of developing osteoporosis – your bones may become weak and brittle
- Increased risk for cataracts, glaucoma or infections of the eye
- Changes in your liver function
Note: Not all possible side effects are included above.
Warnings and Precautions
- High blood pressure and changes in electrolytes, which can cause fluid build-up around your heart, lungs or elsewhere.
- Severe infections, which can be life-threatening.
- Allergic reactions, including anaphylaxis are rare but may happen in some patients. Signs of allergic reaction to this drug may be swelling of the face, feeling like your tongue or throat are swelling, trouble breathing, rash, itching, fever, chills, feeling dizzy, and/or feeling that your heart is beating in a fast or not normal way. If this happens, do not take another dose of this drug. You should get urgent medical treatment.
- Increased risk of developing a hole in your stomach, small, and/or large intestine if you have ulcers in the lining of your stomach and/or intestine, or have diverticulitis, ulcerative colitis and/or other diseases that affect the gastrointestinal tract.
- Blurred vision or other changes in eyesight.
- Severe depression and other psychiatric disorders such as mood changes.
- Effects on the endocrine glands including pituitary, adrenals and thyroid during or after use of this medication.
Note: Some of the side effects above are very rare. If you have concerns and/or questions, please discuss them with your medical team.
- Talk to your doctor or your nurse before stopping this medication, it should be stopped gradually. Depending on the dose and length of treatment, you could experience serious side effects if stopped abruptly (suddenly).
- Talk to your doctor before receiving any vaccinations during your treatment. Some vaccinations are not recommended while receiving prednisone.
How to Take Your Medication
- For oral (by mouth): You can take the medicine with or without food, but it is preferable to be taken with food, especially If you have nausea or upset stomach.
- Missed dose: If you miss or vomit a dose, contact your physician. Do not take 2 doses at the same time and do not double up on the next dose.
- Handling: Wash your hands after handling your medicine, your caretakers should not handle your medicine with bare hands and should wear latex gloves.
- Storage: Store this medicine in the original container at room temperature, protect from moisture. Discuss with your nurse or your doctor how to dispose of unused medicine.
Treating Side Effects
- Drink plenty of fluids (a minimum of eight glasses per day is recommended).
- To help with nausea and vomiting, eat small, frequent meals instead of three large meals a day. Choose foods and drinks that are at room temperature. Ask your nurse or doctor about other helpful tips and medicine that is available to help stop or lessen these symptoms.
- If you throw up, you should drink more fluids so that you do not become dehydrated (lack of water in the body from losing too much fluid).
- Manage tiredness by pacing your activities for the day. Be sure to include periods of rest between energy-draining activities.
- To help with muscle weakness, get regular exercise. If you feel too tired to exercise vigorously, try taking a short walk.
- If you are having trouble sleeping, talk to your nurse or doctor on tips to help you sleep better.
- If you are feeling depressed, talk to your nurse or doctor about it.
- Keeping your pain under control is important to your well-being. Please tell your doctor or nurse if you are experiencing pain.
- If you have diabetes, keep good control of your blood sugar level. Tell your nurse or your doctor if your glucose levels are higher or lower than normal.
- To decrease the risk of infection, wash your hands regularly.
- Avoid close contact with people who have a cold, the flu, or other infections.
- Take your temperature as your doctor or nurse tells you, and whenever you feel like you may have a fever.
- If you get a rash do not put anything on it unless your doctor or nurse says you may. Keep the area around the rash clean and dry. Ask your doctor for medicine if your rash bothers you.
- Moisturize your skin several times a day.
- Avoid sun exposure and apply sunscreen routinely when outdoors.
Food and Drug Interactions
- This drug may interact with grapefruit and grapefruit juice. Talk to your doctor as this could make side effects worse.
- Check with your doctor or pharmacist about all other prescription medicines and over-the-counter medicines and dietary supplements (vitamins, minerals, herbs and others) you are taking before starting this medicine as there are known drug interactions with prednisone. Also, check with your doctor or pharmacist before starting any new prescription or over-the-counter medicines, or dietary supplements to make sure that there are no interactions.
- There are known interactions of prednisone with other medicines and products like aspirin, and other nonsteroidal anti-inflammatory agents. Ask your doctor what over-the-counter (OTC) medicines you can take.
- There are known interactions of prednisone with blood thinning medicine such as warfarin. Ask your doctor what precautions you should take.
- Avoid the use of St. John’s Wort while taking prednisone as this may lower the levels of the drug in your body, which can make it less effective.
When to Call the Doctor
Call your doctor or nurse if you have any of these symptoms and/or any new or unusual symptoms:
- Fever of 100.4° F (38° C) or higher
- A headache that does not go away
- Blurry vision or other changes in eyesight
- Feel irritable, nervous or restless
- Trouble sleeping
- Tiredness or weakness that interferes with your daily activities
- Trouble breathing
- Feeling that your heart is beating in a fast or not normal way (palpitations)
- Chest pain or symptoms of a heart attack. Most heart attacks involve pain in the center of the chest that lasts more than a few minutes. The pain may go away and come back or it can be constant. It can feel like pressure, squeezing, fullness, or pain. Sometimes pain is felt in one or both arms, the back, neck, jaw, or stomach. If any of these symptoms last 2 minutes, call 911.
- Nausea that stops you from eating or drinking and/or is not relieved by prescribed medicines
- Throwing up more than 3 times a day
- Severe abdominal pain that does not go away
- Heartburn or indigestion
- Abnormal blood sugar
- Severe mood changes such as depression or unusual thoughts and/or behaviors
- Thoughts of hurting yourself or others, and suicide
- Feeling hopeless on most days
- Unusual thirst, passing urine often, headache, sweating, shakiness, irritability
- Swelling of legs, ankles, or feet
- Weight gain of 5 pounds in one week (fluid retention)
- A new rash or a rash that is not relieved by prescribed medicines
- Signs of possible liver problems: dark urine, pale bowel movements, bad stomach pain, feeling very tired and weak, unusual itching, or yellowing of the eyes or skin
- Signs of allergic reaction: swelling of the face, feeling like your tongue or throat are swelling, trouble breathing, rash, itching, fever, chills, feeling dizzy, and/or feeling that your heart is beating in a fast or not normal way. If this happens, call 911 for emergency care.
- If you think you may be pregnant
- Pregnancy warning: It is not known if this drug may harm an unborn child. For this reason, be sure to talk with your doctor if you are pregnant or planning to become pregnant while receiving this drug. Let your doctor know right away if you think you may be pregnant.
- Breastfeeding warning: It is not known if this drug passes into breast milk. For this reason, women should talk to their doctor about the risks and benefits of breastfeeding during treatment with this drug because this drug may enter the breast milk and cause harm to a breastfeeding baby.
- Fertility warning: Human fertility studies have not been done with this drug. Talk with your doctor or nurse if you plan to have children. Ask for information on sperm or egg banking.
Revised August 2019
This patient information was developed by Via Oncology, LLC © 2019. This information is not intended to be used as a substitute for professional medical advice, diagnosis, or treatment. You should not rely entirely on this information for your health care needs. Ask your own doctor or health care provider any specific medical questions that you have.
CLIENT acknowledges that the Via Pathways and Via Portal are information management tools only, and that Via Oncology, LLC has not represented the Via Pathways or Via Portal as having the ability to diagnose disease, prescribe treatment, or perform any other tasks that constitute the practice of medicine. The clinical information contained in the Via Pathways and Via Portal are intended as a supplement to, and not a substitute for, the knowledge, expertise, skill, and judgment of physicians, pharmacists and other healthcare professionals involved with patient care at CLIENT facilities.
What is Prednisone? Uses, side effects, dosage
What is prednisone?
Prednisone is a prescription drug. This means your healthcare provider has given it to you as part of a treatment plan. Prednisone is part of a group of drugs called corticosteroids (often called “steroids”). Other steroid drugs include prednisolone, hydrocortisone, and methylprednisolone. Prednisone can be given in different ways, including pill, injection, and inhaled. It is usually given as a pill when used after a kidney transplant, or for certain kidney disorders.
How does it work?
Steroid drugs, such as prednisone, work by lowering the activity of the immune system. The immune system is your body’s defense system. Steroids work by slowing your body’s response to disease or injury. Prednisone can help lower certain immune-related symptoms, including inflammation and swelling.
What is prednisone used for?
Prednisone is used to treat many different diseases like:
- Certain types of arthritis
Prednisone can also help avoid organ rejection after a kidney transplant, because of its ability to lower your immune system’s response to the new kidney. The body recognizes a transplanted organ as a foreign mass. This triggers a response by the body’s immune system to attack it.
Prednisone can also be used to manage other kidney disorders, including:
These conditions can lead to nephrotic syndrome. As a result, large amounts of protein leaks into the urine. This in turn reduces the amount of protein in your blood, known as proteinuria. Prednisone is used to help lower proteinuria in these disorders.
What are the side effects of prednisone?
However, prednisone also has possible side effects. These may include:
- Changes in mood
- Slowed healing of cuts and bruises
- Changes in appetite
- Weight gain
- Swelling (face, arms, hands, lower legs, or feet)
Can prednisone worsen other health conditions?
People taking prednisone can also experience higher blood sugar, which is a special concern for those with diabetes. Because prednisone suppresses the body’s immune system, it can also increase the risk of infection. Therefore, some precautions need to be taken.
Before taking prednisone, talk to your healthcare provider about the following:
- If you have a history of allergies to prednisone or other steroid drugs
- Other medications you are currently taking
- If you have diabetes
- Whether you have high blood pressure
- If you are pregnant or planning to get pregnant
What can I do to stay healthy while taking prednisone?
Your healthcare provider will weigh the possible benefits and side effects when giving this and other medications. Many people have benefitted from prednisone without serious side effects. Talking to your healthcare provider, using your medication as instructed, and taking the necessary precautions, can help you benefit from prednisone while managing side effects. Here are some things you can do to keep yourself healthy:
- Take your medication as prescribed.
- Avoid double dosing. Find out from your healthcare provider what to do if you miss a dose.
- Do not stop taking the medication without your healthcare provider’s consent. Usually your dose of prednisone is tapered (or slowly reduced), to help avoid the effects of withdrawal. A sudden stoppage of using prednisone can lead to withdrawal symptoms including:
- Dramatic changes in mood
- Reduce the amount salt and sugar in your diet.
- Monitor your weight.
- Contact your healthcare provider if you experience any sudden or unusual symptoms, including dizziness, vision problems, shortness of breath, and/or irregular heartbeat.
Prednisone Withdrawal & Detox: What to Expect
Prednisone is a synthetic steroid hormone prescribed for a variety of conditions including asthma, autoimmune disorders, and organ transplants. Prednisone is not an addictive substance but taking it for longer than a few days can cause withdrawal symptoms.
If it sounds strange that a non-addictive drug can cause withdrawal, consider how hormones work. Near the kidneys are two small glands called adrenal glands. The adrenal glands release hormones that tell different parts of the body what they should do. Hormones are like switches in the body. When enough of a hormone enters the bloodstream, the body interprets the message and acts accordingly.
Hormones are signal molecules, but what is a steroid and how are they related? Not all steroids are hormones, and not all hormones are steroids, but prednisone is both. The drug is molecularly shaped like a steroid and sends signals to distant parts of the body like a hormone.
Prednisone withdrawal occurs when people take the drug for too long. Understanding how the drug interacts with natural hormones helps clarify how the drug can cause withdrawal symptoms. Prednisone mimics the natural steroid hormone cortisol. When stressed, the body releases cortisol. The released cortisol has the following functions:
- Breaks down fats, proteins, and carbohydrates: Cortisol regulates hunger and helps increase the metabolism of the food that we eat. During stressful situations, the body anticipates it will need more fuel to react to danger. So, cortisol causes hunger and can lead to weight gain over long periods.
- Increases blood sugar: The body stores sugar as the molecule glucose and then links glucose molecules together as glycogen. Cortisol signals the body to break down glycogen stores into smaller glucose molecules. Glucose enters the bloodstream and causes a spike in blood sugar.
- Suppresses the immune system: The immune system takes a lot of energy for the body to maintain. During a stress response, the body reduces its ability to fight off an infection. Since cortisol is telling the body it is under a direct threat, cortisol shifts the energy usage from long-term defense (the immune system) to short-term defense (fight or flight).
When someone starts taking prescription prednisone, their body recognizes the extra steroid hormone and starts making less cortisol. The adrenaline glands are efficient at adjusting to extra steroid hormones because too much would be harmful. Once the adrenal glands adjust, people taking prednisone become dependent on prednisone to provide the natural baseline level of cortisol. This process takes several days.
Once the body becomes dependent on prednisone, if a person suddenly stops taking prednisone, their adrenal glands will continue making less-than-normal levels of cortisol. The body takes several days to adjust to the lack of prednisone. Until the body can produce more cortisol, this person will experience prednisone withdrawal.
For prednisone withdrawal, remedies at home are generally not helpful. In this case, withdrawal happens because the body is not producing enough cortisol.
Prednisone Withdrawal Symptoms
If prednisone use is halted after a period where the body developed a dependency, withdrawal symptoms may develop. While experiencing prednisone withdrawal, a person may experience:
- Body aches and pains
- Fatigue or tiredness
- Joint pains
- Low appetite
- Nausea and vomiting
- Unintentional weight loss
Prednisone withdrawal symptoms will generally resolve on their own or with the help of a taper.
Topical steroids can produce symptoms similar to prednisone withdrawal. A rash is a common difference between oral prednisone and topical steroids.
How Long Prednisone Withdrawal Lasts
Prednisone and other steroids must be tapered slowly to allow the adrenal glands to readjust to how much cortisol they produce. A typical tapering regimen can last anywhere from days to weeks depending on the dose of prednisone a person used and how long they used it. Most prednisone regimens longer than five days will need a taper.
Prednisone Withdrawal Medications
The treatment for steroid withdrawal syndrome (SWS) is to slow down the steroid taper or increase the dose being used. A doctor should either extend the length of the “step” their patient was on or increase the dose of that step.
For example, if a person took 20 mg for five days and decreased to 10 mg and experienced withdrawal, the doctor could:
- Return the dose to 20 mg for a few days
- Increase the dose to 15 mg before moving down to 10 mg
Prednisone Withdrawal Deaths
Prednisone withdrawal is not deadly, just uncomfortable. Such uncomfortable symptoms include fatigue, vomiting, and lightheadedness. Those types of symptoms can cause dangerous situations (e.g., driving a car while fatigued), but prednisone withdrawal itself is not deadly. For safety, it’s best to plan a taper schedule with a doctor.
Prednisone Withdrawal Cold Turkey
Stopping prednisone “cold turkey” is not recommended. Ideally, a doctor would taper the patient by prescribing a dose that slowly reduces the amount of prednisone consumed to give the adrenal glands time to adjust production of cortisol. This process helps to avoid withdrawal symptoms. If a person took prednisone for more than five days, they should consider speaking with their doctor about tapering.
Prednisone Withdrawal Tips
Keep the following tips in mind when attempting to withdraw from prednisone:
- Speak to a doctor about symptoms to gauge withdrawal risks
- Get a healthy amount of sleep
- Eat healthy meals
- Exercise normally
- Understand that the withdrawal symptoms will pass
Prednisone leaves the body in about a day, however, the effects of steroids last several days. A person should never need a prednisone detox as long as they communicate their needs with their doctor.
Forgetting to take prednisone for a day or two will not trigger withdrawal symptoms, but if a person waits any longer they might cause withdrawal symptoms to develop.
Prednisone Detox at Home
In the hospital, prednisone withdrawal is closely monitored and patients should not experience any withdrawal symptoms. However, if a person is tapering at home, they should make sure to follow the directions on their prescription carefully. The taper is designed to prevent any withdrawal symptoms, so patients should follow it closely. If a person follows the taper and still experiences withdrawal, they should call their doctor for an adjustment to be made.
Helping Someone Withdrawing or Detoxing from Prednisone
To help someone as they stop taking prednisone, make sure they follow the directions on their taper prescription. Using a pill-box with labeled days might be helpful. Other options include writing the daily dose on a calendar or using a calendar app on a smartphone to make sure they do not forget to take their dose.
Finding a Prednisone Withdrawal and Detox Center
Prednisone withdrawal is not treated in an addiction or rehab center since it is not an addictive medication. Prednisone can cause physical dependence and withdrawal symptoms if used longer than five days. If someone experiences symptoms of prednisone withdrawal, call a doctor or go to an urgent care clinic.
If a person forgets to pick up their medication or takes tapering medication incorrectly, they might experience uncomfortable withdrawal symptoms. A prescriber can help correct that with an appropriate additional prednisone prescription.
Most medications that cause withdrawal are addictive, but prednisone is not. If you or a loved one have an issue with an addictive medication, contact The Recovery Village to speak with a representative about how addiction treatment can help you achieve the healthier future you deserve.
Bhattacharyya, A; Kaushal, K; Tymms, DJ; Davis, JR. “Steroid Withdrawal Syndrome after Successful Treatment of Cushing’s Syndrome: A Reminder.” European Journal of Endocrinology, 2005. Accessed June 19, 2019.
Dhossche, Julie; Simpson, Eric; Hajar, Tamar. “Topical Corticosteroid Withdrawal in a Pediatric Patient.” 2017. Accessed June 19, 2019.
Chang-Miller, April. “Do You Know What Problems Can Occur with a Sudden Stop of Prednisone?” Mayo Clinic, 2017. Accessed June 19, 2019.
How to Stop Steroid Medicines Safely
Steroids are a type of medicine with strong anti-inflammatory effects. They help to reduce redness, swelling, and soreness. They come in pill form, as inhalers or nasal sprays, and as creams and ointments. Steroid pills help treat inflammation and pain in conditions such as arthritis and lupus. Inhalers and nasal sprays help treat asthma and allergies. Creams and ointments can help some skin conditions, such as eczema and contact dermatitis.
Path to improved safety
Steroids are effective and lifesaving medicines. However, they also can cause side effects. These include thin skin, dry mouth, abnormal menstrual cycles, and weakened bones. They can increase your blood sugar level or blood pressure. Because of these side effects, steroids often are prescribed for short-term use.
Your body naturally makes steroids by itself. When your body is under stress, such as infection or surgery, it makes extra steroids. When you use steroid pills, sprays, or creams, your body may stop making its own steroids. If you take steroids for a long time, your body may not make enough steroids during times of stress. If this happens, you may have to take more steroid medicine.
The amount of steroids you take should reduce a little at a time. Your doctor will give you a schedule to follow for taking the medicine. It is important that you follow this schedule with care. Once the amount reduces enough, the doctor will have you stop taking steroids. Do not cut back or stop the medicine without your doctor’s approval.
After you stop taking steroids, your body may be slow in making the extra steroids that you need. Your doctor may want to do a simple blood test to see how your body is doing. If needed, they will have you continue or restart your steroid medicine.
Things to consider
It may take your body a few weeks or months to make more steroids on its own. During this time, you may have steroid withdrawal symptoms. These include feeling dizzy, lightheaded, or tired. You may have stomach pain and body aches. Contact your doctor if you have these or other abnormal symptoms.
There are a few ways you can stop steroid medicines safely. These things also can help prevent steroid withdrawal symptoms.
- Do not stop taking your steroid medicine unless your doctor tells you to.
- Do not take other medicines at the same time as steroids without asking your doctor first. This includes over-the-counter drugs and prescriptions.
- If you feel sick while your steroid medicine is being reduced, tell your doctor right away.
- Consider buying a bracelet with your medical information on it. If you become unconscious, this bracelet will tell health workers that you take steroids. Always tell health care workers if you are taking steroid medicine.
Questions for your doctor
- What type of steroid medicine do I need to take?
- How long do I have to take it?
- What will happen once you start to reduce the amount?
- What should I do if I have steroid withdrawal symptoms?
- How will I know if my body is making enough steroids naturally?
- If I have a bad reaction to steroids should I stop taking them?
U.S. National Library of Medicine, MedlinePlus: Steroids
Copyright © American Academy of Family Physicians
This information provides a general overview and may not apply to everyone. Talk to your family doctor to find out if this information applies to you and to get more information on this subject.
Prednisolone-Ferein solution for intravenous and intramuscular injection. 30 mg / ml in amp. 1 ml in unit No. 5×2 – Planet of Health
Main active ingredient
solution for intravenous and intramuscular administration
1 ml of the drug in glass ampoules or glass ampoules with a break ring. 3, 5 or 10 ampoules of the drug, together with instructions for medical use and a ceramic cutting disc for opening the ampoules, are placed in a pack of cardboard box with partitions or a corrugated insert, or with a polymer insert made of polyvinyl chloride film for placing and fixing the ampoules.1 ml of the drug in glass ampoules with a break ring with a volume of 1 ml. 5 ampoules of the drug are put into a blister made of polyvinyl chloride film, which is covered
a pack of box cardboard (chrome-ersatz).
30 mg / 1 ml 1 ml
Has anti-inflammatory, anti-allergic, immunosuppressive, anti-shock and antitoxic effects.
In relatively large doses, it inhibits the activity of fibroblasts, the synthesis of collagen, reticuloendothelium and connective tissue (inhibition of the proliferative phase of inflammation), delays synthesis and accelerates protein catabolism in muscle tissue, but increases its synthesis in the liver.Antiallergic and immunosuppressive properties of the drug are due to inhibition of the development of lymphoid tissue with its involution with prolonged use, a decrease in the number of circulating T- and B-lymphocytes, inhibition of mast cell degranulation, suppression of antibody production.
The anti-shock effect of the drug is due to an increase in the reaction of blood vessels to endo- and exogenous vasoconstrictor substances, with the restoration of the sensitivity of vascular receptors to catecholamines and an increase in their hypertensive effect, as well as a delay in the excretion of sodium and water from the body.The antitoxic effect of the drug is associated with the stimulation of protein synthesis processes in the liver and the acceleration of the inactivation of endogenous toxic metabolites and xenobiotics in it, as well as an increase in the stability of cell membranes, incl. hepatocytes. It enhances the storage of glycogen in the liver and the synthesis of glucose from the products of protein metabolism. An increase in blood glucose levels stimulates the release of insulin. It inhibits the uptake of glucose by fat cells, which leads to the activation of lipolysis. However, due to the increase in insulin secretion, lipogenesis is stimulated, which contributes to the accumulation of fat.Reduces absorption of calcium in the intestine, increases its leaching from the bones and excretion by the kidneys. Suppresses the release of adrenocorticotropic hormone and β-lipotropin by the pituitary gland, and therefore, with prolonged use, the drug can contribute to the development of functional insufficiency of the adrenal cortex.
The main factors limiting long-term therapy with prednisone are osteoporosis and Itsenko-Cushing’s syndrome. Prednisolone inhibits the secretion of thyroid-stimulating and follicle-stimulating hormones.In high doses, it can increase the excitability of brain tissue and help lower the seizure threshold.
Stimulates excessive secretion of hydrochloric acid and pepsin in the stomach, and therefore may contribute to the development of peptic ulcers.
When administered intramuscularly, it is absorbed into the blood quickly, however, compared to reaching the maximum level in the blood, the pharmacological effect of the drug is significantly delayed and develops 2-8 hours. In blood plasma, most of prednisolone binds to transcortin (cortisol-binding globulin), and when the process is saturated, to albumin.With a decrease in protein synthesis, a decrease in the binding capacity of albumin is observed, which can cause an increase in the free fraction of prednisolone and, as a consequence, the manifestation of its toxic effect when using conventional therapeutic doses. The half-life in adults is 2-4 hours, in children it is shorter. Biotransformed by oxidation mainly in the liver, as well as in the kidneys, small intestine, bronchi. The oxidized forms are glucuronized or sulfated and are excreted by the kidneys in the form of conjugates.About 20% of prednisolone is excreted from the body by the kidneys unchanged; a small part is excreted in the bile.
In liver diseases, the metabolism of prednisolone slows down and the degree of its binding to blood plasma proteins decreases, which leads to an increase in the half-life of the drug.
Indications for use
Intramuscular, intravenous administration: systemic connective tissue diseases: systemic lupus erythematosus, dermatomyositis, scleroderma, periarteritis nodosa, ankylosing spondylitis;
hematological diseases: acute hemolytic anemia, lymphogranulomatosis, granulocytopenia, thrombocytopenic purpura, agranulocytosis, various forms of leukemia;
skin diseases: common eczema, exudative erythema multiforme, common pemphigus, erythroderma, exfoliative dermatitis, seborrheic dermatitis, psoriasis, alopecia, adrenogenital syndrome;
replacement therapy: Addison’s crisis;
emergency conditions: severe forms of ulcerative colitis and Crohn’s disease, shock (burn, traumatic, surgical, anaphylactic, toxic, transfusion), status asthma, acute adrenal insufficiency, hepatic coma, severe allergic and anaphylactic reactions, hypoglycemic reactions;
Intra-articular administration: chronic polyarthritis, osteoarthritis of large joints, rheumatoid arthritis, post-traumatic arthritis, arthrosis;
In infectious diseases and latent forms of tuberculosis, the drug should be prescribed only in combination with antibiotics and anti-tuberculosis drugs.If it is necessary to use prednisolone while taking oral hypoglycemic drugs or anticoagulants, it is necessary to adjust the dosage regimen of the latter. In patients with thrombocytopenic purpura, the drug should be used only intravenously.
After discontinuation of treatment, withdrawal syndrome, adrenal insufficiency, as well as exacerbation of the disease, in connection with which prednisolone was prescribed, may occur. If, after the end of treatment with prednisolone, functional adrenal insufficiency is observed, the use of the drug should be resumed immediately, and the dose reduction should be carried out very slowly and with caution (for example, the daily dose should be reduced by 2-3 mg over 7-10 days).Because of the danger of developing hypercortisolism, a new course of cortisone treatment, after a previous long-term treatment with prednisolone for several months, should always start with low initial doses (except for acute conditions that are life-threatening).
The electrolyte balance should be especially carefully monitored with the combined use of prednisolone with diuretics. With long-term treatment with prednisolone in order to prevent hypokalemia, it is necessary to prescribe potassium preparations and an appropriate diet in connection with a possible increase in intraocular pressure and the risk of developing subcapsular cataracts.During treatment, especially long-term, it is necessary to observe an ophthalmologist. With indications of a history of psoriasis, high-dose prednisone should be used with extreme caution.
If there is a history of psychosis, convulsions, prednisone should be used only in the minimum effective doses.
With extreme caution, the drug should be prescribed for migraine headaches, a history of data on certain parasitic diseases (especially amebiasis).
Prescribe prednisolone to children with extreme caution.
Prescribe with particular caution in case of immunodeficiency conditions (including AIDS or HIV infection).Also prescribe with caution after a recent myocardial infarction (in patients with acute, subacute myocardial infarction, it is possible to expand the focus of necrosis, slow down the formation of scar tissue, rupture of the heart muscle).
With particular caution, it is prescribed for liver failure, conditions that cause the occurrence of hypoalbuminemia, obesity of III-IV degree.
Women during menopause should undergo research regarding the possible occurrence of osteoporosis.
With the liver, glucocorticoids for a long time are recommended to regularly monitor blood pressure, determine the level of glucose in urine and blood, perform fecal occult blood tests, blood clotting tests, and X-ray monitoring of the spine.Before starting treatment with glucocorticoids, it is necessary to conduct a thorough examination of the gastrointestinal tract to exclude gastric ulcer and duodenal ulcer.
Method of administration and doses
The dose of the drug and the duration of treatment are set by the doctor individually, depending on the indications and severity of the disease.
Prednisolone is administered intravenously (drip or jet) or intramuscularly. Intravenous drug is usually administered first by jet, then by drip.In acute adrenal insufficiency, a single dose of the drug is 100-200 mg, the daily dose is 300-400 mg.
In case of severe allergic reactions, Prednisolone is administered in a daily dose of 100-200 mg for 3-16 days.
In bronchial asthma, the drug is administered, depending on the severity of the disease and the effectiveness of complex treatment, from 75 mg to 675 mg for a course of treatment from 3 to 16 days; in severe cases, the dose can be increased to 1400 mg per course of treatment or more with a gradual dose reduction.In status asthmaticus, Prednisolone is administered at a dose of 500-1200 mg per day, followed by a decrease to 300 mg per day and a transition to maintenance doses.
In case of a thyrotoxic crisis, 100 mg of the drug is administered in a daily dose of 200-300 mg; if necessary, the daily dose can be increased to 1000 mg. The duration of administration depends on the therapeutic effect, usually up to 6 days.
In shock resistant to standard therapy, Prednisolone is usually administered in a stream at the beginning of therapy, after which they switch to drip.If the blood pressure does not rise within 10-20 minutes, repeat the jet injection of the drug. After withdrawal from the shock state, drip administration is continued until the blood pressure stabilizes. A single dose is 50-150 mg (in severe cases – up to 400 mg). The drug is re-administered after 3-4 hours. The daily dose may be 300-1200 mg (with subsequent dose reduction).
In acute hepatic renal failure (in acute poisoning, in the postoperative and postpartum periods, etc.) Prednisolone is administered at 25-75 mg / day; if indicated, the daily dose can be increased to 300-1500 mg / day and above.
In rheumatoid arthritis and systemic lupus erythematosus, Prednisolone is administered in addition to the systemic intake of the drug at a dose of 75-125 mg per day for no more than 7-10 days.
In acute hepatitis, Prednisolone is administered but 75-100 mg / day for 7-10 days.
In case of poisoning with cauterizing liquids with burns of the digestive tract and upper respiratory tract, Prednisolone is prescribed at a dose of 75-400 mg / day for 3-18 days.If intravenous administration is impossible, Prednisolone is administered intramuscularly in the same doses. After the relief of the acute condition, Prednisolone is administered orally in tablets, followed by a gradual decrease in the dose.
With prolonged use of the drug, the daily dose should be reduced gradually.
Long-term therapy should not be stopped suddenly!
Use in children over 6 years of age only as directed and under the supervision of a physician. The doctor determines the dose and duration of therapy individually, depending on the age and severity of the disease.With prolonged use in children, growth retardation is possible, therefore, it is necessary to limit the use of minimum doses for certain indications for the shortest time. The benefits of treatment should outweigh the potential for adverse reactions.
Application during pregnancy and lactation
Do not use the drug during pregnancy.
If it is necessary to use the drug during lactation, it is recommended to stop breastfeeding.
Ability to influence the reaction rate when driving motor transport or other mechanisms
Patients who are treated with prednisone should refrain from potentially hazardous activities that require increased attention to the speed of mental and motor reactions.Special patient groups
With prolonged therapy, muscle atrophy, muscle pain or weakness, delayed wound healing, atrophy of the protein matrix of the bone leading to osteoporosis, compression fractures of the vertebrae, aseptic necrosis of the femoral head or shoulder head, pathological fractures of the long bones can be observed. Especially serious complications can be observed in elderly and debilitated patients.
Before starting glucocorticoid therapy in postmenopausal women, it should be borne in mind that such patients are especially prone to osteoporosis.Use with caution in patients with osteoporosis.
In patients with cirrhosis, an increase in the effect of glucocorticoids is observed.
Use with caution.
Interaction with other drugs
Anticoagulants: when used simultaneously with glucocorticoids, the effect of anticoagulants may increase or decrease. Parenteral administration of prednisolone causes a thrombolytic effect of vitamin K antagonists (fluindione, acenocoumarol).Salicylates and other non-steroidal anti-inflammatory drugs: Concomitant use of salicylates, indomethacin and other non-steroidal anti-inflammatory drugs may increase the likelihood of gastric ulceration. Prednisolone reduces the level of salicylates in the blood serum, increasing their renal clearance. Caution is needed when reducing the dose of prednisolone with prolonged concomitant use.
Hypoglycemic drugs: Prednisolone partially inhibits the hypoglycemic effect of oral hypoglycemic drugs and insulin.Liver enzyme inducers such as barbiturates, phenytoin, pyramidone, carbamazepine and rimfampicin increase the systemic clearance of prednisolone, thus reducing the effect of prednisolone by almost 2 times.
CYP3A4 inhibitors such as erythromycin, clarithromycin, ketoconazole, diltiazem, aprepitant, itraconazole, and oleandomycin increase the elimination and plasma levels of prednisolone, which increases the therapeutic and side effects of prednisolone.
Estrogen can potentiate the effect of prednisone by slowing down its metabolism.It is not recommended to adjust the dosage of prednisolone for women using oral contraceptives, which contribute not only to an increase in the half-life, but also to the development of an atypical immunosuppressive effect of prednisolone.
Fluoroquinolones: Simultaneous use may damage tendons. Amphotericin, diuretics and laxatives: Prednisolone can increase the excretion of potassium from the body in patients who receive these drugs at the same time. Immunosuppressants: Prednisolone has active immunosuppressive properties, which can cause an increase in therapeutic effects or the risk of developing various adverse reactions when used simultaneously with other immunosuppressants.Only some of them can be explained by pharmacokinetic interactions. Glucocorticoids increase the antiemetic efficacy of antiemetic drugs, which are used in parallel with therapy with anticancer drugs that induce vomiting.
Corticosteroids can increase the concentration of tacrolimus in the blood plasma when they are used simultaneously; when they are canceled, the concentration of tacrolimus in the blood plasma decreases.
Immunization: Glucorticoids can reduce the effectiveness of immunizations and increase the risk of neurological complications.The use of therapeutic (immunosuppressive) doses of glucocorticoids with live viral vaccines may increase the risk of developing viral diseases. During therapy with the drug, emergency vaccines can be used.
Anticholinesterase drugs: in patients with myasthenia gravis, the use of glucocorticoids and anticholinesterase drugs can cause muscle weakness, especially in patients with myasthenia gravis.
Cardiac glycosides: the risk of developing glycosidic intoxication increases.
Others: Two serious cases of acute myopathy were reported in elderly patients who took high doses of doxocarium chloride and prednisolone.With prolonged therapy, glucocorticoids can reduce the effect of growth hormone.
Cases of acute myopathy with the use of corticosteroids in patients who simultaneously receive treatment with blockers of neuromuscular transmission (for example, pancuronium) have been described.
With the simultaneous use of prednisolone and cyclosporine, there have been cases of seizures. Since the simultaneous administration of these drugs causes a mutual inhibition of metabolism, it is likely that seizures and other side effects associated with the use of each with these drugs as monotherapy may occur more often with their simultaneous use.Concomitant use can cause an increase in the concentration of other drugs in the blood plasma.
Antihistamines reduce the effect of prednisone.
With the simultaneous use of prednisolone with antihypertensive drugs, the effectiveness of the latter may decrease.
Prednisolone should not be mixed and used concurrently with other drugs in the same infusion set or syringe.
When mixing a solution of prednisolone with heparin, a precipitate is formed.
Incompatible with aerosols of sympathomimetic agents for the treatment of bronchial asthma in children (risk of respiratory paralysis).
Hypersensitivity to drug components; peptic ulcer and duodenal ulcer, osteoporosis, Itsenko-Cushing’s disease, tendency to thromboembolism, renal failure, arterial hypertension, viral infections (including viral lesions of the eyes and skin), decompensated diabetes mellitus, vaccination period (at least 14 days before and after preventive immunization), lymphadenitis after BCG vaccination, active tuberculosis, glaucoma, cataracts, productive symptoms in mental illness, psychosis, depression; systemic mycosis, herpetic diseases, syphilis, severe myopathy (excluding myasthenia gravis), poliomyelitis (excluding bulbar-encephalitic form), pregnancy and lactation.For intra-articular injections – infections at the injection site.
active ingredient: 1 ml of solution contains prednisotkg for prednisolone – 30 mg;
excipients: sodium hydrogen phosphate anhydrous, sodium dihydrogen phosphate dihydrate, propylene glycol, water for injection.
Basic physical and chemical properties: transparent colorless or almost colorless solution.
In case of overdose, nausea, vomiting, bradycardia, arrhythmia, increased heart failure, cardiac arrest are possible; hypokalemia, increased blood pressure, muscle cramps, hyperglycemia, thromboembolism, acute psychosis, dizziness, headache, symptoms of hypercortisolism may develop: weight gain, development of edema, arterial hypertension, glucosuria, hypokalemia.In children with an overdose, it is possible to suppress the hypothalamic-pituitary-adrenal system, Itsenko-Cushing’s syndrome, a decrease in the excretion of growth hormone, an increase in intracranial pressure.
There is no specific antidote.
Treatment: discontinuation of the drug, symptomatic therapy, if necessary, correction of the electrolyte balance.
The development of severe adverse reactions depends on the dose and on the duration of treatment. Adverse reactions usually develop with prolonged treatment with the drug.Over a short period, the risk of their occurrence is unlikely.
Infections and invasions: hypersensitivity to bacterial, viral, fungal infections, their severity with masking symptoms, opportunistic infections.
On the part of the blood and lymphatic system: an increase in the total number of leukocytes with a decrease in the number of eosinophils, monocytes and lymphocytes. The mass of lymphoid tissue decreases. Blood clotting may increase, which leads to thrombosis, thromboembolism.
From the endocrine system and metabolism: suppression of the hypothalamic-pituitary-adrenal system, growth retardation in children and adolescents, menstrual irregularities, impaired secretion of sex hormones (amenorrhea), postmenopausal bleeding, cushingoid face, hirsutism, weight gain, decreased carbohydrate tolerance , increased need for insulin and oral sugar-reducing drugs, hyperlipidemia, negative balance of nitrogen and calcium, increased appetite, impaired mineral metabolism and electrolyte balance, hypokalemic alkalosis, hypokalemia, possible fluid and sodium retention in the body.Mental disorders: irritability, euphobia, depression, suicidal tendencies, insomnia, labile mood, increased concentration, psychological dependence, mania, hallucinations, exacerbation of schizophrenia, dementia, psychosis, anxiety, sleep disturbances, epileptic seizures, cognitive dysfunction (including amnesia and impairment consciousness), increased intracranial pressure, which is accompanied by nausea and edema of the optic nerve disc in children.
From the nervous system: increased intracranial pressure, epileptic seizures, peripheral neuropathies, paresthesias, dizziness, headache, autonomic disorders.From the side of the organs of vision: increased intraocular pressure, glaucoma, puffiness of the optic nerve, cataracts, thinning of the cornea and sclera, exacerbation of viral and fungal ocular infections, exophthalmos.
From the side of the cardiovascular system: myocardial rupture due to myocardial infarction, arterial hypo- or hypertension, bradycardia, combined ventricular arrhythmia, asystole (due to rapid drug administration), atherosclerosis, thrombosis, vasculitis, heart failure, peripheral edema.In patients with acute myocardial infarction – the spread of the focus of necrosis, the slowing down of scar formation.
From the immune system: allergic reactions that cause fatal anaphylactic shock, angioedema, allergic dermatitis, changes in the reaction to skin tests, relapse of tuberculosis, immunosuppression, hypersensitivity reactions, including rash, itching of the skin.
From the gastrointestinal tract: nausea, bloating, an unpleasant taste in the mouth, dyspepsia, peptic ulcers with perforation and bleeding, esophageal ulcer, esophageal candidiasis, pancreatitis, gallbladder perforation, gastric bleeding, local ileitis and ulcerative colitis.During the use of the drug, an increase in ALT, AST and alkaline phosphatase can be observed, which is usually not significant and reversible after discontinuation of the drug.
From the side of the skin: slowing down of regeneration, atrophy of the skin, the formation of hematomas and atrophic stripes of the skin (striae), telangiectasia, acne, acne, hirsutism, microbleeds, ecchymosis, purpura, hypo- or hyperpigmentation, post-steroidal panniculitis, which is characterized by the appearance of subcutaneous erythematosis, thickening for 2 weeks after discontinuation of the drug, Kaposi’s sarcoma.From the musculoskeletal system: proximal myopathy, osteoporosis, tendon rupture, muscle weakness, atrophy, myopathy, fractures of the spine and long bones, aseptic osteonecrosis.
From the urinary system: an increased risk of urolith formation and the content of leukocytes and erythrocytes in the urine without obvious kidney damage.
General: malaise, persistent hiccups when using the drug in high doses, adrenal insufficiency, which leads to arterial hypotension, hypoglycemia and death in stressful situations, such as surgery, trauma or infection, if the dose of prednisolone is not increased.With a sharp withdrawal of the drug, a withdrawal syndrome is possible, the severity of symptoms depends on the degree of adrenal atrophy, headache, nausea, abdominal pain, dizziness, anorexia, weakness, mood changes, lethargy, fever, myalgia, arthralgia, rhinitis, conjunctivitis, painful skin syndrome, weight loss. In more severe cases, severe mental disorders and increased intracranial pressure, steroid pseudo-rheumatism in patients with rheumatism, death.Reactions at the injection site: pain, burning, changes in pigmentation (depigmentation, leucoderma), skin atrophy, sterile abscesses, rarely lipoatrophy.
Store in original packaging to protect from light at a temperature not exceeding 25 ° C. Keep out of the reach of children.
Drug dossier: 60 years of experience with methylprednisolone
Corticosteroid hormones are synthesized by the adrenal cortex.All corticosteroids can be divided into mineral and glucocorticoids (GC). The former regulate water-electrolyte metabolism by influencing the transport of sodium and potassium ions, and the latter got their name due to their influence on maintaining a stable blood glucose level. In addition, HA are involved in the control of fat and protein metabolism, increase gastric secretion, etc. The property of HA to suppress the inflammatory and immune response is especially important for practical medicine (Cronstein B. N., 1995).
The effectiveness of the steroid hormones cortisone, hydrocortisone, prednisone and prednisolone in the treatment of bronchial asthma (BA), other diseases of allergic origin, rheumatoid arthritis, inflammatory bowel diseases and autoimmune pathology is beyond doubt.At the same time, the use of these HA is limited due to their ability to cause such adverse effects as mineral imbalance, activation of inflammatory lesions (tuberculosis, peptic ulcer), hyperglycemia, muscle spasms, hirsutism, formation of a moon-like face, excessive appetite (Feinberg S. M. et al., 1957; Barnes P. J., 1998).
Creation of methylprednisolone and its modern preparations
The aforementioned side effects necessitated the search for anti-inflammatory HA, characterized by a better safety and tolerability profile.As a result, methylprednisolone (MP) was synthesized, which differs from prednisolone in the replacement of a hydrogen atom with a methyl group at position 6α (Feinberg S. M. et al., 1957).
MP was synthesized in the USA in the Upjohn laboratory founded in 1886, which was later acquired by Pfizer (USA). This laboratory from the middle of the twentieth century. specialized in the industrial production of steroids using bacterial fermentation and oxidation (Hogg J. A., 1992). The idea of creating a MP was prompted by scientists from Upjohn’s laboratory that hydrocortisone is metabolically deactivated by oxidation in the liver to form 6-hydroxy derivatives.Based on this fact, the researchers blocked the metabolism of prednisolone by placing a methyl group in a vulnerable 6-position in order to protect the steroid from oxidative enzymes. The MP thus obtained turned out to be more powerful than prednisolone (Sneader W., 2005). In 1955, MP was approved for medical use (Fischer J., Robin G. C., 2006), and in 1957 it was introduced to the pharmaceutical market as Medrol. Nowadays, MP is included in the Model List of Essential Medicines of the World Health Organization, that is, it is an extremely important drug for modern medicine (WHO Model List of Essential Medicines, 2015).
Synthetic HA are presented in the form of forms for oral and parenteral administration. Their field of application includes the control of inflammation in many diseases (AD, rheumatoid arthritis), as well as suppression of unwanted immune responses (for example, in transplant rejection) (Cronstein B. N., 1995). At the moment, a line of high-quality MP drugs manufactured by Pfizer is presented on the Ukrainian pharmaceutical market, which includes:
- Medrol is a tablet preparation containing 4, 16 or 32 mg MP in 1 tablet;
- Solu-Medrol – powder containing methylprednisolone sodium succinate (MPNS) 40, 125, 500 or 100 mg, as well as a solvent (benzyl alcohol 9 mg / ml, water for injection) for preparing a solution for injection;
- Depo-Medrol is a suspension for injection containing 40 mg of MP acetate (MPA) in 1 ml.
The anti-inflammatory effect of MPNS (Solu-Medrol) is approximately 20% higher than that of prednisolone (Szefler S. J. et al., 1986). Since MPNS is highly soluble in water, it can be administered in a small volume of solvent, which is especially convenient for intravenous administration when it is necessary to achieve high MP concentration in the blood as quickly as possible (Physicians’ Desk Reference, 1994).
The use of oral GC can reduce mortality in patients with systemic lupus erythematosus (Weissmann G., 1993). High-dose intravenous MP therapy (1 g MP for 30 min 1 r / day 3 days) in patients with lupus nephritis led to an improvement in renal function by 20%. In 60% of those who responded to steroid therapy, the improvement achieved with the help of MP persisted for 6 months (Kimberly R. P. et al., 1981).
For many patients with osteoarthritis, the only way to maintain daily activity and ability to work is intra-articular injections of HA, which can effectively eliminate pain and eliminate synovitis.The mode of application of HA in each case is determined individually, while 3-4 times administration of the drug into the affected joint during the year is optimal. The minimum allowable interval between injection for short-acting HAs is 5-7 days, for HAs with an average duration of action – 1 month, for HAs with prolonged action – 2 months.
Today, Depo-HA MP (Depo-Medrol) is well studied and widely used in clinical practice, which is characterized by a lower risk of side effects compared to other HA prescribed for osteoarthritis.Depo-Medrol has a pronounced and long-term anti-inflammatory effect (up to 8 weeks), which allows it to be used for intra-articular administration with an optimal frequency (1 time in 2 months) while maintaining high response rates to therapy (Protsenko G.A., 2016).
A. Silvinato and W. M.Bernardo (2017) conducted a generalized analysis of studies of intra-articular administration of various GCs (MPA, triamcinolone acetonide (TA) and trimacinolone hexacetonide – TG) in inflammatory arthritis or osteoarthritis of the knee joint.It was found that MPA and TA are equally effective in improving joint function in the period up to 12 weeks after administration, however, MPA reduces pain more pronouncedly than TA, in the period up to 6 weeks. Although the analgesic effect of TG develops faster, 2-24 weeks after administration, there is no difference between MPA and TG in terms of the severity of pain relief. When assessing the functional state of the joint in the period up to 6 weeks after administration in rheumatoid arthritis and up to 24 weeks after administration in osteoarthritis, no differences were found between MPA and TG.
An open clinical study by V.V. Palamarchuk and K.A. Bulavin (2010) included patients (n = 73) aged 34-84 years with osteoarthritis of the knee and hip joints (n = 24), as well as with osteochondrosis of the lumbar and cervical parts of the spine, accompanied by disc protrusions and various radicular symptoms (n = 49). All patients underwent complex treatment (vasotropic therapy, non-steroidal anti-inflammatory drugs, physiotherapeutic measures, physiotherapy exercises).Patients of the main group were additionally prescribed the drug Solu-Medrol (daily single administration of 125 mg intravenously for 5 days). During or after administration of Solu-Medrol in 9 (12.3%) cases, arterial hypertension occurred (mainly in elderly / senile patients). There were no other side effects. Already after 1-2 days of therapy, the participants of the main group noted a positive trend in the form of a decrease in the intensity of the pain syndrome. After a 5-day course of Solu-Medrol, most patients showed no joint / radicular pain or a marked decrease in their intensity.After 10 days of using the drug in patients with osteochondrosis of the MP group, a significant improvement was recorded, which was confirmed by a decrease in the subjective assessment of pain according to the visual analogue scale (VAS) both at rest and during movement (by 38.6 and 41.7%, respectively; p <0.05 in both cases). At the same time, in the control group, the dynamics of indicators was less pronounced (a decrease in pain by 17.5 and 21.2%, respectively). In 89.8% of patients, there was a decrease in the severity of pain in the lumbar spine and a complete absence of radicular pain; in the remaining 10.2%, the intensity of the pain syndrome decreased.In patients with osteoarthritis, pain according to VAS at rest and while walking decreased by 32.7 and 39.1%, respectively (for both indicators, p <0.05) in the Solu-Medrol group and only by 15.6 and 19.4%, respectively. (p <0.05) in the control group. Thus, Solu-Medrol is an effective drug, the addition of which to the complex therapy regimen for patients with osteochondrosis and osteoarthritis significantly improves the result of treatment. At the same time, Solu-Medrol showed a good tolerance profile.
In the STIVEA study, patients with early inflammatory polyarthritis (n = 222) were randomized to 3x weekly intramuscular injection of MPA or placebo.The results were assessed 6 and 12 months after the first injection. It turned out that patients in the placebo group were more likely to need disease-modifying antirheumatic drugs (DMARDs) than those in the MP group (76% versus 61%). After 12 months, resolution of arthritis without BMARP was achieved in 9.9% (11/111) of the placebo group and 19.8% (22/111) of the MPA group. Thus, in the case of early inflammatory polyarthritis, MP treatment can delay the appointment of BMARP and prevent the progression of the disease to rheumatoid arthritis in every 10 patient (Verstappen S.M. et al., 2009).
It has also been shown that preoperative administration of 125 mg MP to patients undergoing total knee arthroplasty is accompanied by a decrease in markers of endothelial damage (syndecan 1, soluble plasma thrombomodulin, sE-selectin) and a decrease in the systemic inflammatory response (according to the level of C-reactive protein) compared to with the corresponding indicators in the placebo group (Lindberg-Larsen V. et al., 2017).
MP is indicated for the treatment of severe or disabling allergic conditions not responding to standard therapy, including anaphylactic shock and status asthmaticus (Cronstein B.N., 1995). Although adrenaline is the drug of choice for anaphylactic shock, high doses of injectable GCs, such as MPNS, reduce inflammation and reduce excessive vascular permeability as adjunctive therapy, preventing deterioration of the patient’s condition (Holgate S. T., 1993). Positive results were also obtained when prescribing MP for allergic dermatitis, bullous pemphigoid (Cronstein B. N., 1995).
HA are an integral component of AD treatment, since they inhibit airway inflammation – the central component of the pathogenesis of this disease.The anti-inflammatory effect of HA is mediated by the suppression of the genetic transcription of inflammatory cytokines and the activation of the transcription of some other mediators. Non-genomic mechanisms of the anti-inflammatory effect of HA are their binding to non-classical membrane-bound receptors and potentiation of α 1 -adrenergic action in bronchial smooth muscles. Non-genomic mechanisms act faster, but less long-term than genomic ones (Alangari A. A., 2010).
In a study involving children aged 8 months – 15 years with exacerbations of asthma S.Press and R. S. Lipkin (1991) found that intravenous use of MP and aminophylline in the emergency department significantly reduced the number of hospitalizations. These drugs were prescribed as second-line therapy for children with acute bronchospasm who did not respond to inhaled albuterol sulfate or metaproterenol therapy. In a study by T.Oxaki et al. (1990) 28 patients with BA exacerbations were prescribed intravenous MP for 3 days. The performed determination of the lung function showed that the intake of MPNS was accompanied by a tendency to an increase in the forced expiratory volume in 1 second (FEV 1 ) and the partial pressure of oxygen.Overall clinical improvement was rated as good / excellent in 85% of patients. In a double-blind, randomized study, S. M. Schneider et al. (1988), the use of 30 mg / kg MPNS in patients with acute bronchospasm also resulted in a pronounced decrease in the frequency of hospitalizations: 19% of participants in the MPNS group and 44% of those in the placebo group required inpatient treatment.
Multiple sclerosis (MS) is an inflammatory demyelinating disease in which the myelin sheath of neurons in the central nervous system is destroyed.MP plays an important role in the treatment of MS due to inhibition of the inflammatory cytokine cascade and activation of T cells, and a decrease in the extravasation of immune cells in the central nervous system. In addition, MP promotes apoptosis of activated immunocytes, reduces the cytotoxic effect of nitric oxide and tumor necrosis factor (Sloka J. S., Stefanelli M., 2005).
S. Liu et al. (2017) conducted a meta-analysis of randomized controlled trials of the use of oral and intravenous MP in the treatment of MS.It was found that both forms of MP are equally effective. With regard to side effects, only one difference was observed: with oral MP, insomnia was more common than with the introduction of an intravenous drug. The authors explain this by the prolonged bioavailability of the oral form and, in order to avoid sleep disturbances, recommend taking the drug in the morning.
In the trial of D. H. Miller et al. (1992) patients with MS underwent magnetic resonance imaging of the brain before and after a 3-day course of high-dose intravenous MP therapy.It was shown that in 36% of cases such treatment had a stable and rapid effect in terms of reducing the severity of violations of the blood-brain barrier. Rapid correction of these impairments accelerates recovery from acute episodes of MS. When determining the MP content in breast milk in lactating women to whom this drug was prescribed for the treatment of postpartum exacerbation of MS, it turned out that the level of MP intake in breast milk is very low. Since MP therapy is usually short-term, the infant’s contact with the drug is extremely low, that is, if indicated, MP can be used in women during lactation (Boz C.et al., 2017).
In a study by T. C. Spoor et al. (1986) in patients with optic neuritis, the administration of MPNS 1 g / day for 2-5 days led to a rapid resolution of the process and restoration of visual function, while in patients who did not receive such treatment, irreversible vision loss developed. The team of authors recommends a short course of megadoses of intravenous GC to patients aged 21-45 years with optic neuropathies of autoimmune or unknown origin.
Patients with acute spinal cord injury (SPI) are at risk of developing permanent neurological damage. One of the main ways of realizing such damage – lipid peroxidation – can be inhibited by prescribing MPNS. Intravenous administration of this HA should be started within 8 hours after injury, since the damage mediated by lipid peroxidation is irreversible (Hall E. D., 1991). The National Acute Spinal Cord Injury Study 2 confirmed the benefits of prescribing MPNS in patients with APS.In a randomized controlled study by W. Young and M. B. Bracken (1992), patients who received intravenous MP within 8 hours after injury showed a more pronounced improvement than patients who received placebo, with control both after 6 weeks and and 6 months after OPSM. Improvement was noted when assessing motor functions (p = 0.05 after 6 weeks; p = 0.03 after 6 months), pain sensitivity to needle pricks (p = 0.06 after 6 weeks; p = 0.02 after 6 months). ), tactile sensitivity (p = 0.03 for both measurements).High-dose MP therapy significantly increased recovery rates even in severe PPSI with complete loss of sensitivity below the lesion level. The MPNS prescription regimen included a bolus dose of 30 mg / kg followed by a maintenance infusion of 5.4 mg / kg / h over the next 23 hours. The beneficial effect of MP occurred when treatment was started within 8 hours after injury, which emphasizes the importance of early intervention. with the appointment of the maximum recommended doses. In the course of further observation of the participants in the National Acute Spinal Cord Injury Study, it was found that after 1 year, patients receiving MPSS had better indicators of sensitivity and motor function than in the control group (BrackenM.B. et al., 1992).
Diseases of the respiratory system
A meta-analysis of 9 randomized controlled (n = 1667) and 6 cohort (n = 4095) studies found that in almost all trials, GC reduced the length of hospital stay, in particular in the intensive care unit; reduced the duration of intravenous antibiotic therapy; accelerated the stabilization of the clinical state. Since the existing evidence indicates that the benefit of prescribing GC for community-acquired pneumonia can only be obtained with the maintenance of sufficient serum concentrations throughout the day, it is advisable in these patients to use GC with a long half-life (for example, MP) and drugs with prolonged action (MP in the form of a depot ) (WanY.D. et al., 2016).
In Pneumocystis pneumonia, which is the most common life-threatening condition in patients with acquired immunodeficiency syndrome, adjuvant GC therapy is also recommended (Cronstein B. N., 1995). In this group, HA should be used when the partial pressure of oxygen decreases to a level of <70 mm Hg. Art. In patients with Pneumocystis pneumonia, HA therapy reduces mortality, the likelihood of developing respiratory failure, and the severity of a decrease in oxygenation.In pneumonia caused by Pneumocystis carinii , MPNS should be administered at a dose of 30 mg 2 r / day on days 1-5, 30 mg 1 r / day on days 6-10 and 15 mg 1 r / day – on the 11-21st day of therapy (The National Institutes of Health-University of California Expert Panel, 1990).
A. Tamura et al. (2008) studied the effect of MP pulse therapy in children with pneumonia caused by Mycoplasma pneumoniae refractory to antibiotic therapy (no clinical and radiographic improvement after 7 days of antibacterial drug use).Intravenous administration of MP at a dose of 30 mg / kg for 10.2 ± 2.8 days with a further gradual dose reduction was accompanied by a decrease in fever as early as 4-14 hours after initiation of steroid therapy. In parallel, a rapid decrease in the severity of radiological disorders (infiltrates, pleural effusion), an improvement in laboratory parameters were noted. The authors of this study did not find any side effects.
MP is also used in the treatment of chronic obstructive pulmonary disease (COPD).In particular, in the placebo-controlled study SCCOPE (Systemic Corticosteroids in Chronic Obstructive Pulmonary Disease Exacerbations Trial), this GC was administered intravenously at a dose of 125 mg every 6 hours for 3 days, followed by a switch to oral prednisolone and a gradual dose reduction. On the first day of treatment, the MP group showed a greater increase in FEV 1 (per 100 ml) than in the placebo group. The use of GC made it possible to significantly reduce the duration of inpatient treatment (8.5 versus 9.7 days) and reduce the number of cases of therapy ineffectiveness (Erbland M.L. et al., 1998).
Comparison of MP and dexamethasone prescription for 7-14 days against the background of basic therapy (antibiotics, bronchodilators, oxygen therapy) for exacerbations of COPD showed that in the MP group FEV 1 increased much more significantly (from 46.7 ± 10.6 to 67.5 ± 12.4%) than in the dexamethasone group (from 50.1 ± 7.6 to 58.9 ± 10.8%). The difference turned out to be statistically significant (p <0.05). The authors of the work concluded that the use of MP can reduce the inflammatory response in the airways and eliminate bronchospasm faster than the use of dexamethasone (LiH.et al., 2003).
Patients with Crohn’s disease who do not improve on the background of diet, intake of antidiarrheal drugs, sulfasalazine or metronidazole, should be treated with GC, including MP (Cronstein B. N., 1995). The first generations of HA have been used to induce remission in patients with inflammatory bowel disease since the 1970s. (Dubois-Camacho K. et al., 2017). In the multicenter, double-blind study, the European Cooperative Crohn’s Disease Study (ECCDS; Malchow H.et al., 1984) evaluated the effects of sulfasalazine, 6-MP, and their combination in patients (n = 452) with Crohn’s disease. Participants were assigned to high-dose 6-MP, 6-MP plus 3 g sulfasalazine, sulfasalazine monotherapy (3 g / day), or placebo; the treatment lasted 6 weeks, then the drugs were prescribed in maintenance doses. When analyzing all patients and individual subgroups (active disease, disease of certain parts of the intestine), it was found that 6-MP is the most effective drug.Sulfasalazine monotherapy was found to be the least effective regimen.
Intravenous administration of MP has an antiemetic effect in patients undergoing chemotherapy. In a double-blind, randomized study, F. Roila et al. (1988) compared the antiemetic efficacy of intravenous drugs MP and metoclopramide in 67 patients with breast cancer who received intravenous cyclophosphamide, methotrexate and 5-fluorouracil. MP has been shown to be as effective in preventing vomiting as metoclopramide, while being better tolerated.MP is also used as a palliative therapy that improves the quality of life of patients with end-stage cancer. T. Popiela et al. (1989) found that MP at a dose of 125 mg for 56 consecutive days significantly improved the quality of life of such patients according to their own assessment of symptoms (nausea, vomiting, pain, appetite and sleep disorders, weakness, anxiety, etc.).
Meniere’s disease is a disease of the inner ear manifested by frequent dizziness (96.2%), tinnitus (91.1%), sensorineural hearing loss (87.7%) (CraneB.T., MinorL. B., 2015). In the study by E. Masoumi et al. (2017), with the participation of 80 patients with Meniere’s disease, it was shown that intratympanic administration of MP (40 mg / dL 3 r / wk) was accompanied by a more favorable dynamics of symptoms than the administration of dexamethasone (4 mg / dl 3 r / wk). Although after 1 month the percentage of vertigo control on a numerical scale in the dexamethasone group was 75%, and in the MP group – 66%, after 6 months in the dexamethasone group the indices returned to the initial level, while in the MP group, higher values remained.Thus, in Meniere’s disease, the effect of MP is more stable than the effect of dexamethasone.
Treatment of headache associated with drug misuse requires immediate discontinuation of the causative drugs and, in some cases, a detoxification protocol to avoid withdrawal. In a study by M. Paolucci et al. (2017) bridge therapy, consisting of intravenous administration of MP and diazepam for 5 days, led to a significant decrease in the frequency of headaches both during detoxification and in the first 3 months after stopping the use of the causative medication.After 3 months, the number of days with headache per month in the MP group was 3.0, while in the group whose participants simply stopped taking drugs, it was 9.4.
According to the clinical trials registry clinicaltrials.gov, at the moment, studies of the use of MP in various fields of medicine are ongoing, including in the treatment of Friedreich’s ataxia, ankylosing spondylitis, Raynaud’s phenomenon, acute respiratory distress syndrome, Charcot’s arthropathy and other complications of diabetes mellitus, metastatic prostate cancer, acute alcoholic hepatitis, polycystic ovary syndrome, nephrotic syndrome, as well as during in vitro fertilization.
Thus, 60 years of clinical experience in the use of MP in various diseases (rheumatic, allergic, neurological, etc.) provides strong evidence of the efficacy and safety of this HA. The MP forms present on the Ukrainian pharmaceutical market (tableted – Medrol, injectable – Solu-Medrol, long-acting suspension for injections – Depo-Medrol) allow you to choose the optimal route of administration for any pathological condition that requires the appointment of HA.
Prepared Larisa Strilchuk
Medicna newspaper “Zdorovya Ukrainy 21 storichchya” No. 6 (427), birch 2018 p.
Intoxication with oil products
Gasoline is a liquid with a pungent odor, it is mainly a mixture of products of gasoline distillate of oil. Gasoline evaporates easily at medium temperatures.
Gasoline vapors are heavier than air and therefore stay in the lower layers of the room.
The maximum permissible concentration of gasoline in the air is 0.3 mg / m3
It is used as a fuel for cars, airplanes, as a solvent for rubber, fats, varnishes, for washing parts, for making some quickly drying paints.
Routes of entry into the body
- The main route of entry of gasoline into the body is the respiratory system.
- As a good solvent for fats, gasoline also has the ability to penetrate the skin, stomach and mucous membranes, causing a number of general and local effects.
- Leaded gasoline containing tetraethyl lead is especially hazardous to health.
- Gasoline is excreted through:
- lungs with exhaled air,
- partly with urine in the form of various hydrocarbons.
Gasoline belongs to the general toxic narcotic poisons that cause predominant disturbances in the functional state of the central nervous system with early symptoms of disorders of higher nervous activity.
In industry, with unfavorable sanitary and hygienic conditions, both acute and chronic intoxication with gasoline can be observed.
Clinic of acute poisoning
In case of acute poisoning of mild and moderate degree under the influence of low concentrations of gasoline, phenomena of intoxication are usually observed:
- mental agitation,
- unsteady gait,
- euphoria, violent laughter, dizziness
- nausea, vomiting,
- sometimes unconsciousness.
In severe cases, there are:
- tonic and clonic convulsions,
- increased tendon reflexes,
- hyperthermia, the temperature rises to 39-40 °.
At very high concentrations of gasoline vapors (cleaning of tanks, tanks, in case of accidents with appropriate apparatus, when pouring gasoline without taking precautions), a “lightning-fast” form of poisoning with sudden loss of consciousness and respiratory arrest can be observed.
- there is hyperemia of the mucous membranes and skin of the face, hyperemia of the pharynx, cough,
- enlargement and soreness of the liver,
- lability of the cardiovascular system,
- mild and rapidly transient albuminuria.
Of particular interest is the “gasoline” pneumonia observed in acute poisoning. We are talking about cases when gasoline in a liquid state, usually in drivers, when sucked through a hose, penetrates into the lung and causes direct damage to the lung tissue, more often the right lung.These cases give a peculiar clinical picture, depending, apparently, on the unusual route of penetration of the poison.
On the first day, usually 3-6 hours after the penetration of gasoline into the bronchopulmonary system, the temperature rises to 38-39 °, the appearance of a sharp pain in the side, and a cough.
On the 2nd day – with a cough, rusty sputum begins to separate, breathing becomes shallow, rapid (50-60 per minute). Dullness is found over the affected area of the lung, bronchial breathing and crepitant rales are heard.
The pulse is usually quickened (100-120 beats per minute), in the blood – leukocytosis (12,000-15,000), ESR acceleration to 35-50 mm per hour.
With fluoroscopy, by the end of the first day, sometimes on the 2nd day, an intense darkening is found, capturing more or less part of the lobe.
Clinical symptomatology in these early days so resembles croupous pneumonia , and if you do not know the anamnesis, you can make a diagnostic error.
Peculiarities of “gasoline” pneumonia:
- high temperature, as well as phenomena in the lungs last for a much shorter time – already on the 4-5th day the temperature decreases, and this drop occurs lytically,
- the general condition improves,
- pain in the side and shortness of breath stop,
- general clinical symptoms disappear relatively quickly.
- Radiological changes remain a little longer.
- cases of transition of “gasoline” pneumonia into lung gangrene with a lethal outcome are known.
When gasoline is swallowed, abdominal pain, nausea, vomiting appear, possibly with blood, later, as absorption and penetration into the blood (through the mucous membranes), yellowness of the skin appears, soreness and enlargement of the liver, urobilin is determined in the urine – it develops toxic hepatopathy.
When gasoline is inhaled in order to induce euphoria and hallucinations, addiction develops quickly. Gasoline substance abuse is common among teenagers.
Gasoline substance abuse quickly enough leads to severe damage to the central nervous system, psychoorganic syndrome, irreversible decline in intelligence and disability.
If you inhale gasoline vapors for a long time during its evaporation in a closed room without ventilation, you can lose consciousness, tonic and clonic convulsions, hemiparesis appear.
Chronic gasoline intoxication
Chronic intoxication does not give a clearly defined clinical symptomatology and is characterized by:
- various functional disorders of the nervous system:
- asthenic state,
- a change of mental depression and excitement, hysterical reactions.
- complaints of headache, dizziness, general weakness, lethargy, sleep disturbance.
- catarrhal symptoms appear
- anemia and chronic hepatitis may develop.
- in women, the menstrual cycle is disturbed, in men, potency decreases.
Prolonged application of gasoline may cause skin irritation – dermatitis. Gasoline-related skin diseases can occur with prolonged contact with clothing soaked in gasoline.
First aid to the victim in case of acute intoxication
The patient must be taken out or taken out of the polluted room into fresh air, ensure peace, give a warm drink, activated charcoal – 20-30 tablets, vegetable oil – 50-70 grams; if possible, inhalation with oxygen.
If gasoline is drunk, do not specifically induce vomiting, as vomit containing gasoline can enter the lungs and cause toxic pneumonia. The stomach needs to be flushed through a tube.
If vomiting is spontaneous, you can give 2-3 glasses of a weak solution of soda to drink – 2 grams per glass of water (teaspoon – 5 grams).
For acute intoxications, it is recommended:
- rest, warmth,
- oxygen inhalations,
- intravenous glucose infusions, cardiovascular drugs,
- in severe cases – artificial respiration.
With the development of “gasoline” pneumonia, therapeutic agents (antibiotics, cardiovascular drugs) usually used for the corresponding diseases are indicated.
For chronic intoxications:
- fortifying treatment,
- physiotherapy (baths, oxygen foam, etc.)
- sanatorium treatment in the middle lane, on the Black Sea coast of Crimea and the Caucasus.
- sealing of production processes
- improvement of ventilation,
- combating high temperatures in the production environment,
- the use of hose gas masks when cleaning tanks, various tanks containing gasoline.
- Systematic periodic medical examinations are required – once every 2 years – with the participation of a neuropathologist and therapist (a blood test for hemoglobin, leukocytes, ROE, general urine analysis is mandatory).
- In the presence of pronounced changes in the nervous system, it is recommended to transfer to work that excludes contact with toxic substances.
Kerosene is a clear, colorless or yellowish liquid with a bluish tint and a characteristic odor.
It is used as a fuel for jet engines, internal combustion engines and for domestic needs.
Kerosene is less toxic than gasoline, its lethal dose when ingested is 300-500 ml, narcotic and local irritating effect is weaker than that of gasoline.
Kerosene poisoning occurs quite often when people use it for “medicinal” purposes on the advice of some acquaintance (as it used to be used to remove lice from the head).
Clinic for acute poisoning with kerosene
When taken orally in small amounts, there are:
– nausea, belching with kerosene, vomiting
– abdominal pain
– short-term euphoria
– general weakness
– dizziness when taken
- indomitable vomiting develops rapidly (vomit and flushing water, exhaled air smells of kerosene)
- abdominal pain
- coma, there may be visual and auditory hallucinations convulsions
- cyanosis of the mucous membranes, limbs
- in the lungs against the background of hard breathing, dry and wet rales are heard, pneumonia often develops, which is prone to abscess formation
- death can occur from acute cardiovascular failure
In chronic poisoning with kerosene, bronchitis and chronic inflammation in the lungs develop as a complication, which can lead to death.
In acute poisoning with kerosene through the mouth, it is recommended:
- gastric lavage after preliminary administration of 100-200 ml of petroleum jelly or vegetable oil
- oxygen therapy
- antibiotics (from the group of penicillins)
- glucocorticosteroids (prednisolone), hydrocortisone
- cardiovascular means
Complications of hemorrhoids – Clinic Health 365 Yekaterinburg
Anemia. One of the common complications of hemorrhoids . Chronic blood loss from hemorrhoids can lead to anemia, in which the number of healthy red blood cells that can carry oxygen to the cells of the body decreases, leading to symptoms such as fatigue and weakness. With severe anemia, dizziness and fainting may occur.
Infringement of internal hemorrhoids. If blood flow to an internal hemorrhoid is reduced, the node may be “pinched”, causing severe pain and tissue death (gangrene).When straining during bowel movements (stool discharge), the nodes fall out of the rectum, then edema of the fallen nodes develops. Spasm of the sphincter of the rectum (the muscle that closes the entrance to the rectum) increases edema, causes additional stagnation of blood in the rectal plexus of veins and thrombosis of external hemorrhoids. At the same time, there are complaints of a sharp bursting pain in the anus, edema, a feeling of a foreign body. When the node dies off, discharge from the rectum with an unpleasant odor and difficulty in defecation are noted, there may be bleeding.
Thrombosis of external hemorrhoids usually occurs after errors in diet, exercise. The patient experiences a painful, grape-sized foreign body in the anus (anus). There are sharp pains in the anus, which can worsen even with little physical exertion, coughing.
Infectious complications – perianal abscess and paraproctitis. There are small glands that open inside the anus, they produce a special lubricant, helping the passage of feces through the rectum.With hemorrhoids, there is a chronic disturbance of the blood supply, both in the area of these glands and in the fatty tissue around the rectum. Infection with microorganisms can occur if the opening of one of these glands becomes clogged as a result of inflammation, a perianal abscess (around the anus) forms. Then the infection spreads from the inflamed gland to the fatty tissue surrounding the rectum, and paraproctitis occurs. Paraproctitis is an acute or chronic inflammation of the peri-rectal fatty tissue, an accumulation of pus in the deep tissues surrounding the rectum.Both of these processes require immediate treatment. A delay in treatment can lead to serious deterioration and unnecessary complications.
Symptoms of paraproctitis:
Pain in the anus or buttocks
Feeling of a lump in the anal area
Painful intestinal cramps
Pain in the lower abdomen
Edema in the anus or buttocks
Some people are more prone to developing perrectal and perianal abscesses, including those with the following medical problems:
AIDS or HIV infection with a low level of leukocytes in the blood
Crohn’s disease or ulcerative colitis.
People receiving medications that suppress the body’s immune system, such as glucocorticosteroids (prednisolone, methylprednisolone), chemotherapy drugs for cancer
90,000 Prednisolone 5 mg No. 30 tab.
Instructions for medical use
of the medicinal product
International non-proprietary name
PREDISOLON 5 MG,
AUXILIARY SUBSTANCES: MAGNESIUM STEARATE, TALC, CORN STARCH, LACTOSE MONOHYDRATE, STARCH PRESELATINIZED.
TABLETS WHITE, ROUND SHAPE, FLAT ON BOTH SIDES WITH BEVELED EDGES, WITH “PD” AND “5.0” ENGRAVES AND RISK BETWEEN THEM.
CORTICOSTEROIDS FOR SYSTEMIC USE. GLUCOCORTICOIDS. PREDISOLON. CODE
ATX H02AV06 Pharmacological properties Pharmacokinetics
INTAKE: 90,190 prednisolone When ingestion rapidly and completely absorbed from the gastrointestinal tract (the presence of up to 85% of the dose), bioavailability, lower at higher doses.THE MAXIMUM CONCENTRATIONS IN BLOOD PLASMA ARE REACHED AFTER 1-2 HOURS. HOWEVER, THE MAXIMUM BIOLOGICAL EFFECT IS ACHIEVED SIGNIFICANTLY LATER (AS A RULE, NOT EARLIER AFTER 4-8 HOURS).
FEEDING DELAYS THE REACH OF THE MAXIMUM CONCENTRATION OF PREDISOLONE IN BLOOD PLASMA, BUT DOESN’T AFFECT THE GENERAL BIOAVAILABILITY.
AS A RULE, THE BINDING OF PRENISOLONE IS 90-95%, WHICH OCCURRES PREVENTLY WITH THE CORTICOSTEROID-BINDING GLOBULIN (TRANSCORTINOZHLAMA)
ONLY 5-10% OF PREDISOLONE ARE IN AN UNCONNECTED FORM AND BIOLOGICALLY ACTIVE.
PRENIZOLONE IS THE MAIN ACTIVE METABOLITE OF PRENIZOLONE. PREDISOLONE FIRST OF ALL METABOLIZES IN THE LIVER; 25% IS EXTRACTED IN AN UNCHANGEED FORM THROUGH THE KIDNEY.
BIOLOGICAL SEMI-EXPIRATION IS 18-36 HOURS. THE PERIOD OF SEMI-REMOVAL FROM BLOOD PLASMA IS 2 – 4 HOURS, WHICH IS REDUCED BY MEDICINAL PREPARATIONS INDUCING LIVER ENZYMES.
PHARMACOKINETICS IN SPECIAL GROUPS OF PATIENTS:
IN PATIENTS WITH SEVERE LIVER DISEASES (HEPATITIS, CIRROSIS). FREE ACTIVE FRACTION CAN BE SIGNIFICANTLY INCREASED IN PATIENTS WITH LIVER DISEASES ASSOCIATED WITH HYPOALBUMINEMIA. PATIENTS WITH SEVERE LIVER DISORDERS MAY ALSO DECREASE BIOAVAILABILITY.
PREDISOLONE 5MG IN TABLETS IS A CORTICOSTEROID WITH GLUCOCORTICOID, ANTI-INFLAMMATORY, AND ALSO MINERALO-CORTICOID ACTIVITY IN AT LEAST.LIKE OTHER CORTICOSTEROIDS, PREDISOLONE NIKOMED INDUCTS SEVERAL MECHANISMS, INCLUDING ANTI-INFLAMMATORY ACTIVITY, IMMUNOSUPPRESSIVE PROPERTIES, AND ANTIPROLIFERATIVE EFFECTS. OTHER MECHANISMS INCLUDE INFLUENCE ON CARBOHYDRATE METABOLISM, FAT DISTRIBUTION, HEMATOLOGICAL PARAMETERS, CALCIUM EXTRACTION, GROWTH, MOOD AND SUPPRESSION OF THE HYPOTHALAMO-HYPOPHYSICAL ADRENAL. THE THRESHOLD DOSE FOR THE DEVELOPMENT OF CUSHING SYNDROME IS 7.5 MG / DAY.
1. ANTI-INFLAMMATORY EFFECT IS ACHIEVED BY DECREASING THE FORMATION AND DECREASED ACTIVITY OF INFLAMMATION MEDIATORS (QUININE, HISTAMINA, LIPOSOMAL ENZYMS, PROSTAGLANDINENE VOCHALIENOVATEL).PREDISOLONE REDUCES CELL MIGRATION INTO THE AFFECTED AREAS, REDUCES VASCULAR EXPANSION AND INCREASED VESSEL PERMEABILITY IN THESE ZONES. VASCULAR EFFECT DECREASES VASCULAR PERMEABILITY DUE TO WHAT THE MOTION OF BLOOD SERUM THROUGH THE VESSELS WALLS INTO INTERCELERAL SPACES DECREASES AND AS A CONSEQUENCE, DECREASES THE DISEASE.
2. IMMUNOSUPPRESSIVES properties reduce RESPONSE TO DELAYED HYPERSENSITIVITY REACTIONS AND IMMEDIATE types (Types III and IV) BY INHIBITION TOXIC antigen-antibody complexes, which cause allergic vasculitis in the vessel wall skin as well as by inhibiting lymphokines, target cells, and macrophages (CAUSING ALLERGIC CONTACT DERMATITIS IN JOINT ACTION).
3. The antiproliferative effect reduces inflammation, expression of crusting on the skin formed as a result HIGH POLIFERATIVNOY activity of white blood cells – lymphocytes and excessive formation of fine capillaries in the superficial skin layer, the dermatological diseases (such as psoriasis).
INDICATIONS 90,190 Pharmacodynamic Therapy
– RHEUMATIC DISEASES INCLUDING collagenosis
– allergic diseases (hay fever, bronchial asthma, urticaria, drug allergies)
– respiratory diseases: chronic bronchitis (administered with antibiotic treatment)
– lung fibrosis, SARKAIDOZ
– ULCERATIVE ileitis / COLITIS
– proliferative glomerulonephritis (lipoid nephrosis) nephrotic syndrome
– acute severe dermatoses (pemphigus vulgaris, erythrodermic, Syndrome Lyell)
– thrombocytopenic purpura, chronic LIMFADENOZ with autoimmune PHENOMENOM (HEMOLYTIC ANEMIA, THROMBOPENIA)
– TUMORS (USED IN COMBINATION WITH CHEMOTHERAPY)
– PRIMARY INSUFFICIENCY CHNIKOV (ADDISON’S DISEASE) AND HYPOPITUITARISM (SHIKHANA’S SYNDROME)
METHOD OF APPLICATION AND DOSES
AT THE BEGINNING OF THERAPY, ANY CORTICOSTEROID SHOULD BE TAKEN INTO ACCOUNT.THE INITIAL DOSE MUST BE RIGHT TO ACHIEVE THE DESIRED THERAPEUTIC EFFECT AND WILL DEPEND ON THE CLINICAL RESPONSE. PERIODICALLY IT IS NECESSARY TO EVALUATE THIS DOSE, BECAUSE THE EXPRESSION OF THE MAIN DISEASE CAN CHANGE, OR COMPLICATIONS MAY DEVELOP DURING THERAPY. THE DOSE SHOULD BE GRADUALLY REDUCED TO THE MINIMUM VALUE TO PROVIDE AND MAINTAIN A SATISFACTORY CLINICAL RESPONSE TO TREATMENT. MAY BE REQUIRED TO INCREASE THE DOSE DURING LONG-TERM THERAPY OR IN THE CASE OF EXCERVATION OF THE MAIN DISEASE.
IF THE LONG-TERM THERAPY WITH PRENISOLONE (NORMALLY MORE THAN 3 WEEKS) MUST BE DISCONTINUED, THE CANCELLATION SHOULD BE CARRIED OUT GRADUALLY AND STEP BY STEP TO AVOID THE “CANCELLATION SYNDROME”. ABSTRACT CUTTING THERAPY CAN BE FATAL. DOSE SHOULD BE REDUCED OVER WEEKS OR EVEN MONTHS DEPENDING ON THE DOSE VALUE, DURATION OF THERAPY, THE MAIN DISEASE OF THE PATIENT AND THE INDIVIDUAL RESPONSE OF THE PATIENT TO TREATMENT. UNLIKELY THAT abrupt withdrawal of treatment with prednisolone Nicomedia spends less than 3 weeks, WILL result in a clinically significant suppression of the hypothalamic-pituitary-adrenal system in most patients, but consider that the reaction to corticosteroids and tolerability of their withdrawal can vary widely.SO, IT IS NECESSARY TO CONSIDER THE QUESTION OF A GRADUAL REDUCTION OF THE DOSE WHEN DISCONTINUING THE MEDICINE AFTER SHORT COURSES OR WHEN TAKING HIGHER DOSES AND IN PATIENTS WITH OTHER PHYSICS OF RISKOVIROS.
THE DOSING REGIME FOR GRADUAL DOSE REDUCTION SHOULD BE SELECTED INDIVIDUALLY. THE MOST OF PATIENTS WELL RESOLVE A DOSE REDUCTION OF PRENIZOLONE NIKOMED BY 2.5 MG EVERY 3-7 DAYS UP TO REACHING A DOSE OF PREDISOLONE NIKOMED 5-10 MG / DAY. HIGHER DOSES SHOULD BE REDUCED GRADUALLY OVER 9-12 MONTHS.
WITH A GRADUAL DOSE REDUCTION, THE EVENING DOSE SHOULD BE MISSED FIRST, AND THEN THE DOSES THAT SHOULD BE TAKEN AT NOON, AFTER DINNER OR EVENING, THEN THERE IS THAT IS THEREFORE. LONG PERIODIC TREATMENT WITH GLUCOCORTICOID THERAPY (1 DOSE EVERY DAY IN THE MORNING) HAS BEEN EFFICIENT DUE TO THE ABSENCE OF ADRENAL CORK SUPPRESSION.
METHOD OF APPLICATION: TAKE INSIDE TOGETHER WITH A SMALL AMOUNT OF LIQUID AFTER A FOOD.
ADULTS: NORMAL DOSE RANGES FROM 5 TO 60 MILLIGRAMS / DAY DEPENDING ON THE DISEASE TREATED FOR. IN GENERAL, THE ENTIRE DAILY DOSE SHOULD BE TAKEN IN THE MORNING BETWEEN 6 AM AND 8 AM. (CIRCADIC THERAPY – DAILY SECRETARY RHYTHMS SHOULD BE CONSIDERED WHEN PRESCRIBING).
SUBSTITUTIONAL THERAPY: THE RECOMMENDED INITIAL DOSE IS 5 MG, TAKEN GENTLY IN THE MORNING AND EVENING.
DOSES FOR SPECIFIC GROUPS OF PATIENTS
DOSAGE IN PATIENTS WITH HYPOTHYROSIS: IN PATIENTS WITH HYPOTHYROSIS, DOSE REDUCTION MAY BE REQUIRED.
DOSAGE IN PATIENTS WITH LIVER IMPAIRMENT: PATIENTS WITH LIVER IMPAIRMENT are MORE PROBABLE TO DEVELOP SEVERE ADVERSE REACTIONS DUE TO DECREASED MUFFICIENCY. DOSE ADJUSTMENT MAY BE NECESSARY.
DOSAGE IN PATIENTS WITH RENAL FAILURE: IN PATIENTS WITH RENAL FAILURE, DOSE ADJUSTMENT IS NOT REQUIRED.
DOSAGE IN ELDERLY PATIENTS: DOSE CORRECTION IS NOT REQUIRED, HOWEVER, IT SHOULD BE CONSIDERED THAT LONG-TERM ADMINISTRATION OF CORTICOSTEROIDS IN ELDERLY PATIENTS MAY CAUSE EXCERNATIVE EXCERNATION OF SACHES
DOSES FOR CHILDREN: NO EXPERIENCE IN CHILDREN. CHILDREN ARE CONSIDERED ESPECIALLY AT RISK IN RELATION TO DELAYED GROWTH, THEREFORE THE INDICATION FOR USE OF THE PREPARATION REQUIRES A PARTICULARLY STRICT CHILDREN’S CONDITION.
IN CHILDREN DURING GROWTH, TREATMENT SHOULD BE BASICALLY PERIODIC OR INTERRUPTED. A GRADUAL DOSE REDUCTION TO A DOSE PROVIDING A SATISFACTORY CLINICAL RESPONSE AND CAUSING THE MINIMUM SIDE EFFECTS IS NECESSARY.
ANTI-INFLAMMATORY OR IMMUNOSUPPRESSIVE EFFECTS: USUALLY THE DOSE OF PREDISOLONE IS 0.1-2 MG / KG / DAY.THE DOSE CAN BE BROKENED INTO 1-4 DEPOSITS PER DAY. THE LOWEST EFFECTIVE DOSE IS USUALLY DETERMINED BY CLINICAL RESPONSE.
EXCERVATION OF BRONCHIAL ASTHMA: USUALLY THE DOSE OF PREDISOLONE IS 1-2 MG / KG / DAY; THIS DOSE CAN BE BROKEN IN 1-2 TAKES / DAY WITHIN 3-5 DAYS.
SUBSTITUTION THERAPY: REGULAR DOSE IS 4 TO 5 MG / m2 / DAY.
NEPHROTIC SYNDROME: THE NORMAL DOSE IS 2 MG / KG / DAY (MAXIMUM DOSE 60-80 MG / DAY), WHICH IS GIVEN IN 2-4 TAKES.
VERY FREQUENTLY (> 1/10), FREQUENTLY (> 1/100, <1/10), RARE (> 1/1000, <1/100), RARE (> 1/10000, <1 / 1000), VERY RARE (<1/10000), UNKNOWN (CANNOT BE ASSESSED BASED ON AVAILABLE DATA).
IN GENERAL, THE FREQUENCY OF DEVELOPMENT OF PREDICTED SIDE EFFECTS, INCLUDING SUPPRESSION OF THE HYPOTHALAMO-HYPOPHYSICAL-ADRENAL SYSTEM, DEPENDS ON THE DOSE, TIME OF ADMISSION AND DURATION. SIDE EFFECTS MAY BE REDUCED TO A MINIMUM IF USE THE LOWEST EFFECTIVE DOSE FOR THE MINIMUM PERIOD OF TIME.
– increased susceptibility to infection, aggravation without infection, activation of latent infection and masking symptoms of infection (due to immunosuppressive and anti-inflammatory effects prednisolone)
– reduction in the number of eosinophils and lymphocytes
– MASKING or exacerbation of existing disease
– Adrenal insufficiency (starting with SUPPRESSION WORK hypothalamus and ends TRUE atrophy of the adrenal cortex) at constant use of oral prednisone withdrawal symptoms due to insufficient adrenal (headache, nausea, dizziness, anorexia, fatigue, emotional instability, apathy, and an inadequate response to a stressful situation) “STEROID DIABETES MELLITUS” WITH LOW SENSITIVITY TO INSULIN, INCREASED BLOOD SUGAR LEVEL IN PATIENTS ALREADY SUFFERING WITH DIABETES MELLITUS (100%), DELAYED GROWTH IN CHILDREN LTATE impaired secretion of growth hormone, and reduced susceptibility to HIM
– increased intraocular pressure (up to 40% of patients treated with oral medication), cataract (30% of patients UNDER LONG-TERM oral treatment drug)
– lung abscess (12%)
– Oral candidiasis, particularly in cancer patients (33%)
– fungal infections of mucous membranes (30%)
– Osteoporosis causes pain, back pain, limited mobility, acute pain, vertebral crush fractures and loss of height, fractures of long BONE (25% long-term treatment of oral preparations), myopathy (10%) IN THE TREATMENT OF HIGH-DOSE
– increased number of leukocytes and platelets
– Cushing’s syndrome, including changes CHARACTER fat deposition (moon face, truncal obesity, ” Bull’s Hump “) WHEN Continuous use of oral doses above the physiological (typically more than 50 mg per day), hypokalemia DUE sodium retention and excretion of potassium, amenorrhea in women of childbearing age, high cholesterol, triglycerides and lipoprotein AT treatment with high doses taken by mouth, increased appetite and weight gain
– euphoria, depression, psychosis (induced by corticosteroids)
– Hypertension (due to sodium retention, which leads to fluid retention), worsening of congestive heart failure (due to delay sodium)
– increased risk of developing tuberculosis
– increased symptoms and Increased risk of gastrointestinal perforation, colitis, ileitis, diverticulitis
– stretch marks, acne-like rash, bruising, dermatitis, ecchymosis, facial erythema, atrophy, hirsutism, slow wound healing, increased sweating, telangiectasia and thinning of the skin, Masking or worsening of existing diseases LEATHER
– increasing the frequency of nighttime urination
– ALLERGIC REACTIONS
– diabetes (<1%) IN THE TREATMENT OF SMALL oral doses, increased cholesterol, triglycerides and lipoprotein IN THE TREATMENT OF LOW oral doses
– insomnia, mood swings, changes in personality, mania and hallucinations
– respiratory muscle myopathy
– gastric ulcer or duodenal ulcer while receiving acetylsalicylic acid or nonsteroidal antiinflammatory drugs (NSAIDs), gastrointestinal bleeding (0.5%) , GASTROINTESTINAL PERFORATIONS
– ASEPTIC BONE TISSUE NECROSIS
– URINARY STONES DUE TO INCREASED EXCRETION OF CALCIUM AND PHOSPHATE
– RARE RICE
TROPOSTA Bani BLOOD
– changes in thyroid function
– possibility of extending the COMA in cerebral malaria, cognitive disorders (eg, poor memory), dementia, epidural lipomatosis
– HIGH RISK OF DESTRUCTION cornea WITH SIMULTANEOUS herpetic infection of the eye (due to masking this infection), glaucoma (with prolonged oral treatment drug)
– ketoacidosis and hyperosmolar coma, manifestations of latent hyperparathyroidism, propensity to porphyria, the syndrome of tumor lysis, inappropriate secretion of sex hormones (DISORDERS of menstruation, hirsutism, impotence)
– MANIFESTATION OF LATENT EPILEPSY, PSEUDOTUMOR OF THE BRAIN (BENEFICIAL INTRACRANIAL HYPERTENSION WITH SYMPTOMS SUCH AS HEADACHE, BLUE VISION AND VISUAL IMPAIRMENT
VISUAL DISORDERS –
Cardiomyopathy with risk reduction of cardiac activity, arrythmias due to hypokalemia, vascular collapse
– Pancreatitis (AFTER A LONG treatment with high doses)
– epidermal necrolysis, Stevens-Johnson syndrome
– Achilles tendinopathy and patellar tendons
– an increased risk of atherosclerosis and thrombosis, vasculitis (MAY ALSO OCCUR AS A withdrawal syndrome after prolonged therapy)
– ulcers and esophageal candidiasis
– muscular atrophy, a disease tendons, tendinitis, tendon rupture
– delayed wound healing, eating disorders
WITH AN EXCESSIVE RAPID DOSE REDUCTION AFTER PROLONGED TREATMENT PROBLEMS MAY DEVELOP MUSCLE AND JOINT PAIN, FEVER, RHINITIS, CONJUNCTIVITIS AND WEIGHT LOSS.
prednisolone NYCOMED contraindicated in the following conditions / disorders:
– hypersensitivity to prednisone NYCOMED or any auxiliary substances in preparations
– systemic mycosis
– vaccination with live viral or bacterial vaccine is contraindicated DURING immunosuppression corticosteroids (not a full immune response may allow a live attenuated vaccine caused infectious diseases)
during prolonged therapy:
– ULCERS 12 duodenal ulcer
– stomach ulcers
– severe forms of osteoporosis
– HEAVY myopathy (EXCEPT myasthenia gravis )
– PSYCHIATRIC ANAMNESIS
– ACUTE VIRAL INFECTIONS (SHEALING HERPES, SIMPLE HERPES, FLARE POISON)
– Chronic active hepatitis (C HBS AG-positive)
GLAUCOMA – Poliomyelitis
– LYMPHADENITIS after vaccination with BCG
– pre- and post-vaccination period (8 weeks before and 2 weeks post vaccination)
MEDICINAL INTERACTION CORTICOID EFFECT IS DECLINED BY THE APPLICATION OF CYP3A4 INDUCTORS SUCH AS RIFAMPICIN, PHENYTOIN, PRIMIDON, BARBITURATES, CARBAMAZEPINE AND AMINOGLUTHETHYMIDE.
CORTICOID EFFECT IS INCREASED WITH THE APPLICATION OF SUBSTANCES BLOCKING CYP3A4: (KETOCONAZOL, RITONAVIR), ERYTHROMYCIN, TROLEANDROMYCIN.
GASTROINTESTINAL TRACT ORGANS AND METABOLISM
PREVISOLONE NIKOMED PREVENTS THE EFFECT OF HYPOGLYCEMIC PREPARATIONS PURPOSE. ADVERSE EFFECT: INCREASED RISK OF HYPERGLYCEMIA.
POTASSIUM EXTRACTING DIURETICS (THIAZIDES, FUROSEMIDE, ETC.
EFFECT OF ADDITIONAL LOSS OF POTASSIUM IN THE KIDNEY. ADVERSE EFFECT: INCREASED RISK OF HYPOCALYEMIA AND CONSEQUENTED CARDIAC ARRHYTHMIAS.
GLYCOSIDE EFFECT DUE TO POTASSIUM DEFICIENCY.
ANGIOTENSIN-CONVERSING ENZYME (ACE) INHIBITORS
INCREASED RISK OF BLOOD FORMULA CHANGE.
REDUCTION OF ALREADY REDUCED BLOOD PRESSURE.
HORMONES FOR SYSTEMIC APPLICATION
THE LEVEL OF PREDISOLONE IN BLOOD SERUM MAY INCREASE DUE TO ITS REDUCED METABOLISM.ADVERSE EFFECT: INCREASED RISK OF DEVELOPMENT OF SIDE EFFECTS OF CORTICOSTEROIDS. EXCESSIVE USE OF GLUCOCORTICOIDS CAN SUPPRESS THE EFFECT OF SOMATOTROPINE, WHICH INCREASES GROWTH.
INCREASING THE METABOLISM OF PREDISOLONE. ADVERSE EFFECT: REDUCED EFFICIENCY OF PRENIZOLON.
EFFECT OF ADDITIONAL LOSS OF POTASSIUM IN THE KIDNEY. ADVERSE EFFECT: INCREASED RISK OF HYPOCALYEMIA AND CONSEQUENTED CARDIAC ARRHYTHMIAS.
ADVERSE EFFECT: INCREASED RISK OF RUPTURE OF TENDONS.
ADVERSE EFFECT: MAY INCREASE THE EFFECTS OF PREDISOLONE.
MEANS FOR THE MUSCLE, JOINT AND BONE SYSTEM
ACETYL SALICYLIC ACID (ACC)
IT IS KNOWN THAT ACETYL SALICYLIC ACID IRRITATES THE VENTRICULAR, MAY BE PRESENTED THE MECHANISM IS NOT KNOWN. INCREASED CLEARANCE OF ACETYL SALICYLIC ACID DUE TO EXPOSURE OF PREDISOLONE HAS BEEN REPORTED.THERE IS AN INCREASED RISK OF DEVELOPMENT OF GASTROINTESTINAL BLEEDING AND ULTRA, AS WELL AS A RISK OF DECREASING THE EFFICIENCY OF ACETYL SALICYLIC ACID. THUS, SALICILATE SIDE EFFECTS WILL BE MANIFESTED WHEN PREDISOLONE IS CANCELLED.
NON-STEROID ANTI-INFLAMMATORY DRUGS (NSAIDs)
NSAIDs IRRITATE THE STOMACH, AND PRONISOLONE CAN MASK THESE ADVERSE EFFECTS. ADVERSE EFFECT: INCREASED RISK OF GASTROINTESTINAL BLEEDING AND ULTRA FORMATION.
NON-DEPOLARIZING MUSCLE RELAXANTS
ADVERSE EFFECT: LONG-TERM RELAXATION OF MUSCLES.
CENTRAL NERVOUS SYSTEM
BARBITURATES STIMULATE LIVER ENZYMES AND INCREASE METABOLISM OF PREDISOLONE. ADVERSE EFFECT: REDUCED EFFICIENCY OF PRENIZOLON.
PHENYTOIN AND PHOSPHENYTOIN
INCREASED METABOLISM OF PREDISOLONE IN THE LIVER. ADVERSE EFFECT: REDUCED EFFICIENCY OF PRENIZOLON.
INDUCTION OF P450-MEDIATED METABOLISM OF QUETIAPINE INDUCED BY CORTICOSTEROIDS. ADVERSE EFFECT: LOWERING THE LEVEL OF QUETIAPIN IN THE BLOOD SERUM.
INCREASED QUETIAPINE DOSE MAY BE REQUIRED TO MAINTAIN SCHIZOPHRENIA SYMPTOMS CONTROL.
SIMULTANEOUS USE TOGETHER WITH SYSTEMIC GLUCOCORTICOIDS CAN INCREASE THE RISK OF DEVELOPMENT OF SEIZURES.
MECHANISM UNKNOWN. STRENGTHENING THE ACTION OF THE PRESOLONE.
PREVISOLONE CAN INCREASE THE LEVEL OF CYCLOSPORIN IN BLOOD PLASMA.
EFFECTS ON LABORATORY TESTS AND STUDIES
SKIN REACTIONS TO ALLERGIC TESTS MAY BE SUPPRESSED.THE REDUCTION OF THYROTROPIC HORMONE (TSH) INCREASES.
REDUCED IMMUNE RESPONSE GIVES THE POSSIBILITY OF INFECTIONS CAUSED BY LIVE VACCINES, AND CAN ALSO DECREASE IN EFFICIENCY.
THERE IS AN INCREASED RISK OF GENERALIZED, POTENTIALLY LIFE-THREATENING INFECTIONS WHEN VACCINED WITH LIVE VACCINES.
THE METABOLISM OF GLUCOCORTICOIDS MAY BE ACCELERATED AND, CONSEQUENTLY, THEIR EFFICIENCY MAY DECREASE.
RELAXING AND BETA SYMPATOMETICS
INCREASE IN POTASSIUM LOSS.
CHLOROQUINE, HYDROXYCHLOROQUINE, MEFLOQUINE
INCREASED RISK OF MYOPATHIES, CARDIOMYOPATHY
UNWANTED EFFECT: INCREASED CLEARANCE DURING TREATMENT WITH PREDISOLONE.
SINGLE DOSES OF PREDISOLONE CAN INHIBIT THE ACTIVATION OF CYCLOPHOSPHAMIDE, BUT THE LEVEL OF ACTIVATION INCREASES AFTER PROLONGED USE.
CAN INCREASE THE EFFECT OF PRENISOLONE.
POSSIBLE REDUCTION OF PRASIKVANTEL CONCENTRATION IN BLOOD DUE TO CORTICOSTEROIDS.
ADVERSE EFFECT: INCREASED INTRAOCULAR PRESSURE IS POSSIBLE WHEN ADMINISTRATED WITH PREDISOLONE.
INHIBITION OF CORTICOSTEROID METABOLISM BY LICRICE. ADVERSE EFFECT: INCREASED RISK OF CORTICOSTEROID SIDE EFFECTS.
– Patients with certain physical problems, such as fever, trauma or surgery, during treatment may take time CORRECTION OF DAILY corticoid DOSE
– the risk of disease tendons, tendinitis or tendon rupture will increase with the simultaneous use of fluoroquinolones and corticosteroids
– Long-term use should be accompanied by examination by an ophthalmologist every three months
– Long-term use may be associated with rapid progression of Kaposi’s sarcoma
– EXCEPT replacement therapy corticosteroids do not possess curative, A palliative effect thanks to its anti-inflammatory and immunosuppressive properties …LONG-TERM RECEPTION, DEPENDING ON THE DOSE AND DURATION OF TREATMENT, IS ASSOCIATED WITH AN INCREASED FREQUENCY OF UNWANTED EFFECTS. Patients who are receiving long-term corticosteroid therapy system actions, must be supervised in order to identify SUPPRESSION hypothalamic-pituitary-adrenal (HPA) axis (adrenal insufficiency), Cushing’s syndrome, hyperglycemia, and glucosuria
– after long-term corticosteroid therapy, treatment should be withdrawn SOFT TO PREVENT “CANCELLATION SYNDROME”.ADRENOCORTICAL INSUFFICIENCY MAY BE CONSERVED FOR MONTHS AFTER CORTICOSTEROID TREATMENT IS STOPPED, AND DURING STRESS PERIODS (SURGICAL OPERATION, DISEASE) MAY REQUIRE NECESSARY. Risk of adrenal insufficiency can be reduced prescribing THROUGH THE DAY instead of daily doses administered
– in connection with anti-inflammatory and immunosuppressive EFFECTS Corticosteroids THEIR used in doses higher than necessary for replacement therapy, susceptibility to infections, exacerbate AVAILABLE INFECTION DISEASES AND ACTIVATION OF LATENT INFECTIONS.ANTI-INFLAMMATORY EFFECT MAY LEAD TO MASKING SYMPTOMS UNTIL THE PERIOD, UNTIL THE INFECTIOUS DISEASE PROVES TO THE RELATED STAGE. IF NEW INFECTIONS ARISE DURING TREATMENT, THE FACT SHOULD BE CONSIDERED THAT IT WILL BE IMPOSSIBLE TO LOCALIZE SUCH INFECTION
– IN PATIENTS WITH LATENT TESUME TUBERCULES TUBERCULES TUBERCULES. SUCH PATIENTS SHOULD BE CAREFULLY OBSERVED FOR TB REACTIVATION AND IF LONG-TERM CORTICOSTEROID TREATMENT IS REQUIRED, ANTITUBERCULOSIS CHEMOTHERAPY MAY BE INDICATED.The use of corticosteroids in patients with active tuberculosis should be restricted to cases LIKE exacerbation or dissemination of TB if their use to treat diseases PLANNED together with a suitable anti-tuberculosis therapy
– Systemic corticosteroid therapy may increase the risk of severe or lethal infection in persons exposed VIRAL DISEASES SUCH AS CHICKEN POISON OR MEASLES (PATIENTS SHOULD BE WARNED TO AVOID SUCH RISK AND TO CONTACT A DOCTOR IMMEDIATELY IF IT IS PRESENT).CORTICOSTEROIDS CAN PROMOTE BACTERIAL AND FUNGAL INFECTIONS (CANDIDA INFECTIONS). CORTICOIDS CAN ACTIVATE LATENT AMEOBIC INFECTIONS, SO IT IS VERY IMPORTANT TO REMOVE THEM BEFORE STARTING CORTICOID THERAPY
– PREDISOLONE INCREASES GLUCONEOGENESIS. APPROXIMATELY 20% OF PATIENTS TREATED WITH HIGH DOSES OF STEROIDS DEVELOP BENEFITS “STEROID DIABETES” WITH LOW INSULIN SENSITIVITY AND LOW RENAL GLUCOSIS. THE CONDITION IS REVERSIBLE WHEN THE THERAPY IS DISCONTINUED.IN CONFIRMED DIABETES MELLITUS TREATMENT WITH CORTICOSTEROIDS USUALLY LEADS TO IMPAIRMENT OF THE BALANCE, THAT CAN BE COMPENSATED BY CORRECTING THE DOSE OF INSULINA
– LONG-LONG PREVENTIONAL CAPACITY. Prednisone reduces the level of calcium and phosphate, which affects the level of vitamin D, thereby causing a dose-dependent reduction LEVEL osteocalcin in serum (Protein bone matrix, which correlates with bone formation)
– THERAPY prednisolone within weeks cause children RISK DEVELOPMENT growth retardation associated with a reduction in growth hormone secretion and reduce PERIPHERAL sensitivity to this hormone
– corticosteroids can cause mental disorders, including euphoria, insomnia, mood swings, personality changes, depression and psychotic tendencies
– Long corticosteroids SYSTEM OF MAY CAUSE A POSTER SUBCAPSULAR CATARACT AND GLAUCOMA (DUE TO INCREASED INTRACULAR PRESSURE), AS WELL AS AN INCREASED RISK OF EYE INFECTION.OPHTHALMOLOGICAL EXAMINATION AND TREATMENT IN THE CASE OF GLAUCOMA, ULTRA AND CORNEAL INJURY MUST BE SHOWN. PATIENTS WITH HERPETIC INFECTION HAVE AN INCREASED RISK OF DEVELOPING CORNEAL INJURY, BECAUSE PREDISOLONE CAN MASK THE INFECTION.
Corticosteroids should be used with caution in the following conditions:
– gastro-intestinal diseases such as ulcerative colitis and diverticulitis at the possibility of perforation of the colon, abscess COLON OR OTHERWISE pyogenic infections, obstruction of the colon, EXPRESS fistulas, and sinus TRACTS, FRESH INTESTINAL ANASTOMOSIS AND LATENT PEPTIC ULTRA.Inflammatory properties Glucocorticoids can mask SIGNS gastrointestinal perforations and thus leads to a delay DIAGNOSTICS and, consequently, to potentially fatal
– High blood pressure or congestive cardio-vascular system (due to mineralocorticoid EFFECT prednisolone, which may lead to RETENTION OF LIQUID AND SALT)
– OSTEOPOROSIS (BECAUSE CORTICOSTEROIDS CAN INCREASE THE SYMPTOMS OF OSTEOPOROSIS)
– KNOWN AND PROSPECTED INFECTIONS
Treatment in a polyclinic for erosive and ulcerative lichen planus with total damage to all parts of the oral mucosa
Lichen planus is a chronic polyetiologic disease with rash of papules on the mucous membranes and skin.Isolated lesions of lichen planus of the oral mucosa are observed in 75% of cases. It is one of the most common diseases of the oral mucosa.
The appearance of lichenoid rashes in the oral cavity, as a rule, is associated with emotional stress, neuropsychic shock, negative emotions. Disturbance of neuroendocrine regulation (early onset of menopause) is important.
The erosive and ulcerative form of lichen planus of the oral mucosa, being a precancerous disease, requires close attention and qualified treatment from the dentist.When a dentist detects a total lesion of the oral mucosa with an erosive and ulcerative form of lichen planus, the patient is referred for inpatient treatment to a clinic for skin diseases.
In a hospital, as a rule, the patient receives large doses of corticosteroid drugs and other drugs by mouth. At the same time, less attention is paid to the local treatment of erosive and ulcerative lesions of the oral mucosa [1-6].
Purpose of the study – to develop an effective method for the treatment of erosive and ulcerative lichen planus in a polyclinic with total damage to the mucous membrane of the oral cavity, gums and lips.
Material and Methods
Clinical examination and treatment of patients was carried out on the basis of the Department of Diseases of the Oral Mucosa of the Department of Hospital Therapeutic Dentistry, Periodontology and Geriatric Dentistry.
7 patients (1 man and 6 women) aged from 46 to 71 years with an erosive and ulcerative form of lichen planus were under observation (see table).
Complaints upon admission
Patients complained of an unusual appearance of the oral mucosa, loss of taste, burning sensation, pain when eating and brushing teeth, roughness and tightness of the oral mucosa.
All patients had anxiety-suspicious syndrome, negative psychoemotional states with a tendency to depression, carcinophobia. The disease proceeded with alternating periods of remission and exacerbation.The exacerbation was always preceded by stress.
Examination of the skin of 3 patients revealed single papules on the skin of the forearms. Examination of the oral mucosa revealed multiple papular rashes on the dorsal surface of the tongue, the mucous membrane of the cheeks, lips, and the vestibular surface of the gums (Fig. 1, 2). Figure 1. Lichen planus, erosive-ulcerative form. Patient A., 52 years old. Figure 2. Lichen planus, erosive and ulcerative form. Patient B., 46 years old.
On the mucous membrane of the transitional folds of the cheeks and the ventral surface of the tongue against the background of bright hyperemia, sharply painful extensive erosions and ulcers were determined (Fig.3) Figure 3. Lichen planus, erosive and ulcerative form. Patient G., 68 years old.
The essence of the method lies in the combined use of steroid drugs – both as a general course (prednisolone) and topically (diprospan). A complex of therapeutic measures was carried out in the oral cavity. In addition, after consultation with a neuropsychiatrist, patients were prescribed daily antidepressants: fluoxetine 20 mg, 1 capsule in the morning, or cipralex – 10 mg, 1 tablet in the morning.
The course of treatment with antidepressants depended on the duration of the disease, the severity of psychoemotional changes and was 3-6 months.
Successful cure of patients in our group without prescribing oral prednisolone is currently not possible. But our task was to use this drug in sparing doses.
Such a scheme was proposed earlier by prof. A.L. Mashkelleison:
1. Prednisolone 0.005 g
Scheme: 1st week – 4 tablets per day, every other day;
2nd week – 3 tablets a day, every other day;
3rd week – 2 tablets a day, every other day;
4th week – 1 tablet a day, every other day.
2. Delagil 0.25 g 1 tablet 2 times a day, daily, course 4 weeks.
3. Vitamin PP 0.05 g 1 time per day, after meals, course 4 weeks.
4. Vitamin A, oil solution, 8-10 drops on rye bread 2 times a day, course 4 weeks.
We attached great importance to this stage of treatment. Eliminated traumatic factors, carried out hygiene correction, professional hygiene, replacement of prostheses made of dissimilar metals.Candidiasis was ruled out. Antiseptic treatment of erosions and ulcers was carried out, followed by rubbing in prednisolone ointment, and after 10 minutes – Cholisal or Kamistad gel.
With preliminary premedication (sedatives, antihistamines), diprospan 1 dose and 4 ml of 2% lidocaine solution (without a vasoconstrictor) were injected with an insulin needle under the elements of lesions of the oral mucosa (foci of exudation and hyperemia, erosion, ulcers).
If necessary, the injection of diprospan was repeated after 4-6 weeks.
Characteristics of medicinal products
1. Cipralex, fluoxetine
Daytime antidepressants. Eliminate depressive reactions of various origins, panic disorders, anxiety, phobias. Improves mood.
The therapeutic effect develops after 3-4 weeks of constant admission. Does not cause sedation.
Fluoxetine 20 mg, 1 capsule in the morning, regardless of the meal.Then the dose is gradually increased to 2 capsules – a double dose in the morning. The course of treatment is 3-6 months.
Cipralex – 10 mg, 1 tablet in the morning.
Diprospan * is a glucocorticosteroid drug. International (non-proprietary) name: betamethasone *.
Manufacturer: Schering-Plow Labo, Belgium.
Dosage form – suspension for injection.1 ml of a suspension of diprospan contains 6.43 mg of betamethasone dipropionate and 2.63 mg of betamethasone sodium phosphate. The combined composition of the drug has significant advantages when used in a clinical setting. One of the components of the drug (betamethasone sodium phosphate) is highly soluble and easily absorbed from the injection site, which provides anti-inflammatory and analgesic effects within 1-3 hours. Another component of the drug (betamethasone dipropionate) is poorly soluble and slowly absorbed from the depot formed at the injection site.The latter provides a prolonged (up to 4-6 weeks) effect of the drug after administration.
Diprospan has a high glucocorticosteroid activity, but unlike its predecessors (hydrocortisone, prednisolone, kenalog), it has a number of advantages:
– a slight mineralocorticosteroid effect, fast and at the same time prolonged powerful anti-inflammatory and analgesic effect;
– does not cause local fine crystalline reactions;
– does not have a local dystrophic effect on tissues;
– assigned both once and repeatedly (if indicated).
3. Prednisolone is a synthetic analogue of the steroid hormone of the adrenal cortex, hydrocortisone. Glucocorticosteroids have anti-inflammatory, desensitizing, anti-allergic, anti-shock and anti-toxic effects.
Prescribed for neurodermatitis, dermatoses, eczema, allergic shock, etc. In the treatment of erosive and ulcerative forms of lichen planus used in combination with delagil. Assign from 2.5 mg and gradually reduce the dose until the complete cessation of the drug.
Release form: tablets containing 0.001 g and 0.005 g of prednisolone.
4. Hingamin (delagil) – antimalarial drug. Hingamin quickly causes the death of asexual erythrocyte forms of all types of plasmodia. The spectrum of action of hingamine is not limited to the effect on the malaria plasmodium. It has an inhibitory effect on the synthesis of nucleic acids, the activity of certain enzymes, and immune processes. As a result, the drug has found wide application in the treatment of collagen diseases (systemic lupus erythematosus, scleroderma, rheumatoid arthritis) and dermatoses (lichen planus).The drug is well and quickly absorbed and slowly excreted from the body.
Release form: tablets of 0.25 g; powder; ampoules of 5 ml of 5% solution.
In the treatment of erosive and ulcerative lichen planus, it is used in combination with steroid preparations, 0.25 g 2 times a day for 1 month.
5. Nicotinic acid (vitamin PP, vitamin B3) – belongs to the vitamins of group B. Nicotinic acid plays an essential role in the life of the body.It is a prosthetic group of codehydrase enzymes I and II, which play the role of hydrogen carriers and take part in redox processes.
Nicotinic acid is prescribed to normalize redox processes in the body and vasodilation. For these purposes, vitamin PP is prescribed in the treatment of lichen planus.
Release form: powder and tablets of 0.05 g and ampoules containing 1 ml of 0.17% sodium nicotinate solution, which corresponds to 0.1% nicotinic acid.In the treatment of lichen planus, vitamin PP is prescribed at 0.05 g 1-2 times a day after meals for 1 month. Also, injections of a solution of vitamin PP under the elements of the lesion.
When using niacin on an empty stomach, redness of the face and upper half of the body, dizziness may occur. Nicotinamide should be prescribed for persons with an increased sensitivity to nicotinic acid.
6. Retinol (vitamin A) normalizes metabolic processes in the epithelium, the function of cell membranes, stimulates the regeneration of epithelial cells.
Vitamin A is found in animal products (butter, egg yolk, liver).
The daily requirement for vitamin A for an adult is 1.5 mg, or 5000 IU.
In the treatment of lichen planus, 8-10 drops of an oil solution of vitamin A are prescribed orally 2-3 times a day for a course of 1.5 months; topically in the form of applications of an oil solution of vitamin A to the affected areas 2-3 times a day for 15 minutes for a course of 1.5 months.
7.Oral gels Holisal, Kamistad
Anti-inflammatory, analgesic effect.
Treatment results and discussion
After the completion of the course of treatment, the patients did not show any complaints. Examination of the oral mucosa showed the disappearance of foci of exudation, hyperemia, complete epithelization of erosions, ulcers, and a significant decrease in lichenoid eruptions (Fig. 4). Figure 4.Lichen planus, erosive and ulcerative form. Patient B., 46 years old. After treatment.
In 2 patients, on the background of stress, 1-1.5 months after treatment, an exacerbation occurred (exudation, hyperemia and single small erosions appeared on the mucous membrane of the cheeks). These patients underwent a course of general and local treatment again.
When examining a group of patients 6 months after completion of the course of treatment, there were no complaints. Single papules were identified on the unchanged oral mucosa.The psychoemotional state of the patients has improved markedly.
The method of treatment that we offer allows you to avoid hospitalization, which is a significant advantage. In addition, the effectiveness of local administration of diprospan allows for the prescription of sparing doses of prednisolone and reduces the risk of complications.
With local administration of diprospan with lidocaine, pain symptoms are quickly eliminated, which, combined with the action of daytime antidepressants, leads to a noticeable improvement in the psychoemotional state of patients.
Thus, the effectiveness of the treatment of the erosive and ulcerative form of lichen planus with total damage to all parts of the oral mucosa increases significantly due to the combined use of steroid drugs, as well as local therapeutic measures in the oral cavity. Our experience confirms the real possibility of treating patients with this disease in a polyclinic.
90,000 Neuritis: description of the disease, causes, symptoms, cost of treatment in Moscow
The optic nerve refers to the accumulation of nerve cells in the inner lining of the eye – the retina.A similar structure of a huge number of neurites forms a nerve disc, which has protection in the form of various sheaths.
With neuritis of a spherical formation in the orbit, the disease is difficult to miss, because it progresses at a significant rate. For this reason, the patient urgently makes a visit to the ophthalmologist.
The main contingent of persons faced with a similar problem is patients 30-50 years old. In isolated cases, optic neuritis is diagnosed in the elderly or children.
During the progression of the pathology, two points are recorded: the inflammatory process and damage to the structure (sheath / tissue) of the optic nerve. One of the main provoking factors for the onset of the disease is the destruction of the fibers of the vitreous body of the eye.
In the overwhelming majority of cases, part of the nerve territory is affected. Its complete destruction is a rare case.
It is necessary to dwell in more detail on the types of pathology, depending on their localization:
one.Inside the skull. Intracranial (optochiasmal) neuritis changes the visual field and is often quite severe. It is not always possible to determine it at the initial stage, which can lead to an increase in atrophy.
2. Outside the skull. Retrobulbar neuritis has orbital (inside the orbit), axial (behind the eyeball), transverse (along the perimeter of all fibers) and interstitial (fibers – glial cells) forms.
The axial shape implies the defeat of the corresponding beam.Central vision with it sharply decreases to a critical point. The variety is considered the most common retrobulbar neuritis.
The orbital form is much less common and is incurable in the chronic course of the disease. It arises due to infection of the body by external and internal factors-provocateurs.
The interstitial form is unpredictable in that we are talking about a lesion of the lining of the brain.
Causes of optic nerve neuritis:
one.Viruses. The most dangerous are herpes simplex, Filatov’s disease (mononucleosis), chickenpox and encephalitis.
2. Fungi. We are talking about pathological microorganisms, which, when the human body is damaged, are difficult to treat.
3. Bacteria. Untreated sinusitis (sinusitis) and frontal sinusitis (frontal sinusis) result in optic neuritis. The most dangerous in this case is meningitis, when the lining of the brain is seriously affected.
4.Eye pathologies. Most often, uevit is considered a provoking factor in pathology, which causes inflammation of the ocular choroid.
5. Inflammations of a specific nature. A common mistake of non-specialists is to confuse them with the defeat of the body by bacteria and fungus. In fact, it is granulomatosis in the form of sarcoidosis, which most often affects the lungs and eyes.
6. Sexually transmitted diseases. The optic nerve is especially at risk in gonorrhea, genital herpes and syphilis.Dangerous is the neglected form of sounded genitourinary infections, from which a person can go blind.
7. Intoxication. In this case, we are talking not only about the poisoning of the body with poisons, but also about the consequences of alcoholism. Long-term use of strong tobacco is also hazardous to the eyes.
8. Taking certain medications. These usually include Quinine tablets and powders. A number of antibiotics, which were taken on their own, are clearly dangerous for the optic nerve.
9. Special cases. With traumatic brain injury and abnormal pregnancy, the risk of rapid development of optic neuritis increases.
10. Problems with teeth and gums. Periodontitis and caries can provoke a voiced problem with the organs of vision.
11. Unexplained occurrence. In some cases, the reason for diagnosing optic neuritis in a patient remains a rhetorical question.
The forms of pathology are based on the cause of their occurrence, and doctors voice them as follows:
one.Infectious. Infection with pathogenic microorganisms often leads to optic neuritis.
2. Parainfectious. A postponed viral disease or a vaccination that was not done according to the rules is the main provocateurs of eye problems.
3. Ischemic. The source of the disease in this case is a stroke or heart attack.
4. Autoimmune. The intense production of auto-aggressive antibodies often affects the eyes.
five.Toxic. Methyl alcohol is the main cause of the onset of pathology. When using drugs or working with chemists, you should expect a similar result.
6. Demyelinating. With this form, the disc of the eye is rapidly damaged.
The severity of the clinical picture of the disease:
1. Weak regression. The boundaries of the optic nerve disc (optic nerve head) are not clearly expressed. Arteries and veins are enlarged.
2.Pronounced pathology. The border between the retina and the disc is not visible. There is a large number of hemorrhages and the appearance of white spots in this area.
3. The beginning of atrophy. The disc, as the nerve sheath is destroyed, turns pale with narrowing of the arteries.
It is not difficult to detect a disease that proceeds according to the classical scheme. It reveals itself rapidly and with a pronounced clinical picture. Difficulties in the examination begin with a sluggish pathology.Some people confuse pseudoneuritis with optic neuritis. However, the treatment of both diseases is carried out according to a different scheme. It is easy to distinguish them, because with pseudoneuritis, a person’s vision remains unchanged.
Diagnosis of pathology is carried out in the complex:
1. Initial inspection. The ophthalmologist examines the affected eye for visual pathological changes. Next, the doctor gives a referral for a detailed blood test to see the complete clinical picture.
2. Ophthalmoscopy. A similar study of the fundus is carried out in order to assess the integrity of the structures of the organ of vision. With the help of a special apparatus of two types (electronic or mirror), the reaction of the eye to a light stimulus is checked. The first version of the ophthalmoscope is most appropriate for research, because it allows you to take a picture for further examination by a doctor.
3. Tables of Golovin, Snellen or Sivtsev. They are used to test visual acuity, which drops sharply with neuritis of the optic nerve.More modern methods of such diagnostics are skiascopy and refractometry.
4. MRI. The purpose of this study is to identify the stage and the affected area of the problem area. In this way, the presence / absence of a tumor in the brain is also determined.
5. Ultrasound of the optic nerve. It should be noted that this type of diagnosis can hardly be called traditional. Ultrasound is an auxiliary element of the general examination system.
Even in the presence of a genetic predisposition to the disease (or rather, especially with it), it is worth adhering to the following preventive program:
regular examination and consultation with an ophthalmologist;
refusal to perform actions that could cause a head injury or eye injury;
ban on self-treatment of colds of varying complexity;
restriction on sedentary work in order to avoid the consequences of physical inactivity;
minimizing bad habits with the preference for a complete rejection of them;
food not in a hurry, but with a choice of a menu rich in proteins and minerals;
compliance with the visual regime without abuse of the use of a PC;
development of your own daily routine with the main condition to sleep at least 7 hours;
regular tests for UAC and urine to identify abnormalities in health;
hiking in the fresh air away from the polluted area;
change in the field of activity, which implies excessive visual stress;
regular visits to the dentist for the prevention of periodontitis and caries.
Proper nutrition for the prevention of optic neuritis involves more than smart diet planning. The toxic form of the disease is not always associated with nicotine and alcohol poisoning. Food products must be purchased from trusted manufacturers. Pathogenic microorganisms can be found in regular milk from the spontaneous market.
List of Prescribed Drugs Before Diagnosis:
one.Antibiotics They are administered intramuscularly or with the help of droppers. Medicines with an ototoxic spectrum of action are banned. The reason for the refusal is that, in addition to hearing loss and disorders of the vestibular apparatus, they can cause nystagmus and dizziness. If you suspect neuritis of the optic nerve, involuntary eye movement will complicate the situation. Ototoxic drugs include Gentamicin, Streptomycin and Neomycin.
2. Corticosteroids. They are injected retrobulbar, which implies an injection under the skin of the lower eyelid.Therapy with Prednisolone is carried out for 5 days with a gradual decrease in the daily dosage of the drug.
3. Diuretics. Perfectly eliminates edema Diakarb, which is taken together with Panangin. Usually a diuretic is used according to the scheme of 3 days of intake – 2 days off.
4. Antiseptics. Hexamethylenetetramine solution is a disinfectant that is used against some microorganisms.
5. Nootropics. They are necessary in order for the metabolism to be restored in the nerve cells.Most often, experts recommend Piracetam to achieve this goal.
6. Stimulants of regeneration. Solcoseryl is used in the form of an ointment or gel for wounds and burns. If you suspect optic neuritis, it is administered intramuscularly.
7. Antispasmodics. Dibazol has a short-term effect, but still promotes the expansion of the vessels of the brain.
8. Vitamins. Usually, organic substances of group B are prescribed, but it does not hurt to use them in combination with ascorbic acid and retinol.
You should forget about traditional medicine, because they are not able to solve the main problem. At best, they will mask the symptoms of pathology for a short time, which is very dangerous for the eyes.
Decompression of the optic nerve is a complex process that consists of many stages:
1. Sphenoetmoidectomy. The procedure is called total, although during the operation of the affected optic nerve, the turbinates remain intact.
2. Identification. It is carried out in order to establish the direction of the nerve. It is also necessary to examine the paranasal (sphenoid) sinus, where the ICA (internal carotid artery) protrusion is located.
3. Using an endoscope. It is used to detect the localization of the thalamus (optic tubercle). Not far from it (1 cm), the plate rises backward.
4. Dissection. In this case, the surgeon is interested in the distance between the periorbital zone and the sounding plate.Dissection takes place up to the thalamus.
5. Using a diamond cutter. In the absence of pressure on the optic nerve, the bone above the thalamus is thinned from the medial (middle) side and removed. As a result, the inflamed area of the visual pathway is exposed, which is processed.
6. Special cut. The need for a sheath-like opening of the nerve sheaths remains at the discretion of the surgeon and ophthalmologist. If the incision is appropriate, then it is urgently treated with fibrin glue.Otherwise, a fistula may form at the site of the autopsy.
Discomfort after decompression of the optic nerve
In some cases, the patient may experience the following inconveniences:
painful sensations in the eye area;