Antimicrobials, Antitussives/expectorants, Bronchodilators, Corticosteroids, Systemic, Corticosteroids, Inhaled, Antiviral Agents, Analgesics/antipyretics

Author

Jazeela Fayyaz, DO Attending Physician, Department of Pulmonary and Sleep Medicine, Medical Director of Sleep Lab, Unity Hospital

Jazeela Fayyaz, DO is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Roger B Olade, MD, MPH Medical Director, Genesis Health Group

Roger B Olade, MD, MPH is a member of the following medical societies: American College of Occupational and Environmental Medicine, American College of Physicians

Disclosure: Nothing to disclose.

Klaus-Dieter Lessnau, MD, FCCP Former Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory, Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women’s Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

Paul Blackburn, DO, FACOEP, FACEP, is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

webmd.com”>Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD, is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Lippincott textbook royalty; Wiley textbook royalty

Ali Hmidi, MD Resident Physician, Department of Internal Medicine, Brooklyn Hospital Center, Weill Cornell Medical College

Disclosure: Nothing to disclose.

Jeffrey Nascimento, DO, MS Fellow, Department of Pulmonary Medicine, Lenox Hill Hospital

webmd.com”>Jeffrey Nascimento, DO, MS, is a member of the following medical societies: American College of Chest Physicians, American Medical Association, American Osteopathic Association, American Thoracic Society, New York County Medical Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Robert E O’Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O’Connor, MD, MPH, is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

webmd.com”>Disclosure: Nothing to disclose.

Samuel Ong, MD Visiting Assistant Professor, Department of Emergency Medicine, Olive View-UCLA Medical Center

Disclosure: Nothing to disclose.

Samer Qarah, MD Pulmonary Critical Care Consultant, Department of Internal Medicine, Division of Pulmonary and Critical Care, The Brooklyn Hospital Center and Cornell University

Samer Qarah, MD, is a member of the following medical societies: American College of Critical Care Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

webmd.com”>Disclosure: Medscape Salary Employment

Steroid tablets | Asthma UK

How do steroids help asthma?

The steroids used to treat asthma are known as corticosteroids. Corticosteroids are copies of hormones your body produces naturally.

Steroids help asthma by calming inflamed airways and stopping inflammation. This helps ease asthma symptoms such as breathlessness and coughing. It will also help prevent your lungs reacting to triggers.

“You’re more likely to avoid high doses of steroids if you take your preventer inhaler every day as prescribed,” says Dr Andy Whittamore, Asthma UK’s in-house GP.

Video: steroids for asthma and their side effects 

Video: Steroids for asthma and their side effects

Asthma UK’s in-house GP Dr Andy Whittamore explains how steroids work to help control asthma and why you shouldn’t worry about side effects.

Transcript for steroids for asthma and their side effects

0:00
As a GP, I do get people coming to see me worried about taking steroids for their asthma.

0:06
I do reassure them that the low doses we prescribe in inhalers is usually enough to control their asthma

0:13
without causing any major problems.

0:15
So they’re very safe, and trust me that they’re the most effective thing we have. Steroids work by calming down the

0:22
inflammation in the lungs. It’s that inflammation that not only causes symptoms such as cough, wheeze and

0:28
breathlessness, but it’s also inflammation that really gets flared up by pollens, pollution, stress, exercise, things like

0:36
that. So, by treating that underlying inflammation with a low-dose steroid inhaler, what we can do is help prevent people having symptoms and massive

0:46
flare-ups that end up with them being in hospital. If you need steroid tablets, whether they’re on a short-term basis or a very occasionally long-term, it’s again to treat the inflammation in the lungs, it’s just is having to treat a lot more

1:00
inflammation to try and keep you safe, and keep you well. For people who are

1:05
taking an inhaled steroid, so the brown preventer medication, for example, I do reassure them the low doses generally don’t cause a problem, but if they do get

1:14
problems, for example with the sore mouth, then to rinse their mouth out after they use their inhaler, to help prevent this, but if it’s still causing a problem then to speak to their GP or nurse about

1:24
different medications. Finally, the key thing is that steroid treatment is essential in the management of asthma.

1:31
Taking a regular preventative containing steroid can keep your lungs well, can keep you healthy and keep you doing the things that you enjoy doing.

When will your doctor prescribe steroids for your asthma?

Your doctor will prescribe steroids for your asthma if you need extra help with symptoms. They’ll prescribe the lowest dose of steroid medicines you need to treat your asthma symptoms and keep you well.

For example, your GP will prescribe steroid medicine if:  

• you’re taking your reliever inhaler three or more times a week. Most people with asthma are prescribed a steroid preventer inhaler to use every day. It stops inflammation building up in your airways and cuts your risk of symptoms. So, if you’ve only been given a reliever inhaler, and you’re using it three or more times a week, see your GP.

• you’ve had an asthma attack. You might be given a short course of steroid tablets (prednisolone) to take until your symptoms are fully under control. These can quickly get the swelling in your airways back down again if you have an asthma attack.

• you’re getting asthma symptoms even when you’re taking your preventer inhaler as prescribed. This is when a course of steroid tablets may be what you need to get your asthma back under control.

If your asthma is still not well controlled in spite of high dose inhaled steroids, keep taking them until you can discuss your treatment with your GP. Use our severe asthma tool to find out if you need a referral to a severe asthma specialist.

Steroid preventer inhalers for asthma

Preventer inhalers contain a low dose of steroids to prevent inflammation in your airways over time. This means you’re less likely to react to your asthma triggers.

“If you’ve been prescribed a preventer inhaler and are using it correctly, you’re less likely to need to take steroid tablets,” says Dr Andy.  “Also, there’s very clear evidence that if you don’t smoke, your preventer inhaler works better, so you’re less likely to need steroid tablets.” 

Your steroid preventer inhaler is an essential part of your asthma care. It lowers your risk of symptoms and an asthma attack. You need to take it every day as prescribed, even if you feel well, to keep your airways protected. This is because it works away in the background to prevent inflammation building up in your airways. If you stop taking it that protection will stop.

Don’t stop taking your steroid preventer inhaler before speaking to your GP or asthma nurse. You need your preventer every day to keep the inflammation down in your airways and lower your risk of an asthma attack.

“If you’re on a high dose, your body can really miss it if you stop it suddenly,” says Dr Andy.

“Always talk to your GP first before stopping any medicine they have prescribed. And remember to collect your repeat prescription before your inhaler runs out.”

Steroid tablets for asthma

Steroid tablets also come in a soluble or liquid form. They contain a higher dose of steroids than a preventer inhaler.

Your GP will work out how much you need to take, and for how long, depending on your symptoms and how long it takes you to recover.

• For adults, steroid tablets are usually prescribed for at least five days.
• For children, steroid tablets are usually prescribed for at least three days.
• If you need a longer course of steroid tablets, your GP or asthma nurse will make sure these are prescribed at the lowest possible dose. You may need to take them for weeks or a few months at a time, depending on the number of steroid tablets you’re prescribed, or how long it takes you to fully recover.

“Your course of steroids may be longer depending on how long it takes you or your child to fully recover,” says Dr Andy. “It’s important that you come off them gradually if you’ve taken them for three weeks or more.” 

Getting the best from your steroid tablets 

“It’s important that steroid tablets are taken as prescribed, and that you see the course out,” says Dr Andy.

“You also need to carry on with your preventer inhaler so you can benefit from a lower dose of steroid tablets and give yourself more chance of a quick recovery.”

As well as this:

• Don’t be tempted to stop taking your steroid tablets before the course is finished. If you don’t finish the course your airways may still be inflamed. This means your asthma symptoms could come back again, putting you at risk of what could be a life-threatening asthma attack. Your GP can support you in coming off steroids gradually to cut your risk of symptoms
• Make sure you’re fully recovered.This means few, or no, symptoms (cough, wheeze, tightness in your chest, difficulty breathing) and not needing to use your reliever inhaler.“If you use a peak flow meter and your reading is back to above 75% of your personal best, that’s a good indication you’ve recovered too,” says Dr Andy.
• If you haven’t fully recovered, see your GP as soon as possible as you may need another course of steroid tablets to get the inflammation in your airways right down. It should be started as soon as you finish the first course – or as soon as possible. This is to make sure the inflammation in your lungs, which the steroid tablets are helping to control, doesn’t build back up again.
• Make sure your GP knows about other conditions you have like high blood pressure, stomach ulcer or diabetes. And any other other medicines you’re taking, like aspirin, ibuprofen or anti-coagulants, which could react with the oral steroids.   

Side effects of steroids

Like all prescription drugs, there is a risk of side effects when you take steroids. But your GP will only ever prescribe them if the benefits outweigh the risks.

It’s also worth remembering that you’ll be kept on the lowest possible dose of steroids to manage your asthma, which will help minimise the chances of having side effects.

Side effects from your steroid preventer inhaler

Inhaled steroids (the ones found in your preventer inhaler) are usually in a very low dose and have few or no side effects. However, they can sometimes cause side effects like a sore throat or thrush.

“Using your inhaler in the best way, with a spacer, and rinsing your mouth out, cuts your risk of side effects – the steroid medicine you’re inhaling goes straight down into the airways and very little is absorbed into the rest of the body,” says Dr Andy. “If you’re taking a higher dose your GP or asthma nurse will keep a closer eye on you to monitor side effects. ”

Find out more about your preventer inhaler and possible side effects here.

Side effects from a short course of steroid tablets

Most people who take a short course of oral steroids won’t experience significant side effects. You’re more likely to notice side effects if you’re on a high dose.

Although the dose of steroid going into your body is higher if you’re taking them in tablet form, any side effects like stomach upset, increased appetite, and mood swings are usually temporary and will stop once the course of tablets has finished.

Taking steroid tablets can also mean you’re more at risk from colds and viruses.

“Catching chickenpox when you’re taking steroids can cause you to become really unwell,” says Dr Andy. “If you’ve been around someone with chickenpox, see your GP to check your immunity.”

If you’re worried about any side effects, tell your GP or asthma nurse as soon as possible. They can give advice on how to reduce them. For example, if your stomach is upset after taking steroids, your GP may suggest taking the tablet with meals or after food.

“If you do get side effects from taking steroid tablets, it’s important to remember that the benefits far outweigh the risks, and your GP or asthma nurse will aim to get you on the lowest doses that will completely control your symptoms,” says Dr Andy.  

Side effects from taking steroid tablets longer-term

If you take steroid tablets for three months or more continuously, or you have three to four courses a year, you’re more likely to get side effects. 

These can include risk of infection, increased appetite, higher blood pressure, mood swings and depression.

“I’ve been taking steroid tablets for severe asthma for 11 years. I used to hate taking them and a few years ago decided to stop all my medication. I was in hospital 36 hours later. Even though the high dose of steroids I take causes some side effects, without them I wouldn’t breathe as well or have such a good quality of life. You need to balance it up.” – Jenny, diagnosed with severe asthma

Never stop taking your steroid medicines suddenly. Keep taking the course as prescribed, and talk to your GP about any side effects you’re worried about.

Find out more about taking steroid tablets in the long term and how to manage side effects.

Side effects for your child with asthma

If you’re worried about your child taking steroid inhalers, or side effects from steroid tablets, speak to your GP or asthma nurse. You can also get some advice and reassurance about Common concerns about your child’s medicines.

Steroids FAQs

In this section we answer some of your common concerns about taking steroids. 

Will steroids affect my bone health?

The use of steroids has been associated with a risk of reduced bone density in some people. At your annual asthma review, your GP or asthma nurse can talk to you about your individual risk and what you can do to reduce this risk.

Will steroids make my face fat?

Some people who take steroids, particularly oral or injected steroids in the long term, may find they put on weight and notice they develop a “moon-shaped” face. This side effect is usually temporary and will stop once the course has finished. Your GP or asthma nurse will monitor this.

Will steroids cause diabetes?

The use of steroids, especially if you’re taking high doses, has been linked to an increased risk of developing diabetes. 

Your GP or asthma nurse will keep an eye on your blood-sugar levels if you’re taking high doses of steroids by arranging blood tests and by testing your urine for glucose. 

I’m pregnant. Is it safe to use my preventer inhaler, or take steroid tablets if I need them?

The medicines used to treat asthma are generally safe in pregnancy and won’t harm your baby. This includes your preventer inhaler and steroid tablets. There are more risks to both you and your baby if you don’t take your medicines and your asthma gets worse.

Do I need to carry a steroid emergency card?

Some people who take medicines containing steroids may need a steroid emergency card. It depends on what total daily dose of steroid medicine you’re taking, and for how long.

For example, your doctor may ask you to carry a steroid card if:

• you need oral steroids (for example prednisolone) for longer than four weeks
• you’ve needed several short courses of oral steroids in a year
• your preventer inhaler contains high doses of steroid medicine. Different preventer inhalers have different doses that are considered high, so you need to check with your GP or asthma nurse and pharmacist if you’re not sure.
• you’re taking other types of steroid medicine, for example steroid nasal drops or steroid creams, alongside your steroid inhaler, which could add up to a high overall dose.

A steroid emergency card lets health care professionals and emergency doctors know you take steroids. It is useful in emergency situations. This is because when you’re on high doses of steroids your body may stop producing enough of its own natural steroids to deal with illness or injury. In this situation, doctors will need to give you extra corticosteroids.

At your next appointment, ask your doctor or asthma nurse what your total daily dose of steroid medicine is, from your preventer medicine, and any other steroid medicines you’re taking. They can let you know if you should be carrying a steroid card.

If you do need a steroid card, make sure you always carry it with you. If you lose it, you can get a replacement from your pharmacy or GP.

Do not stop steroids suddenly

If you’ve been prescribed steroids, whether as tablets, liquid or in an inhaler, make sure you take them every day as prescribed. Do not stop taking your steroid medication suddenly unless you have been told to by your GP or asthma nurse.

Talk to our asthma nurses

If you have any concerns or are worried about taking steroids, you can call the Asthma UK Helpline on 0300 222 5800 to talk to one of our respiratory nurse specialists. You can also message them via WhatsApp on 07378 606 728 (Monday-Friday, 9am-5pm).

Last updated August 2019

Next review due August 2022

When a cough is not just a cough

When Cheryl Daigle started coughing in February 2013, she chalked it up to the sneezing and sniffles that had held her hostage for the past week. After all, it seemed like everyone around her was sick.

Yet as days turned into weeks, Daigle’s cough only worsened, and each fit began to usher in a frightening inability to take a deep breath. Things reached a tipping point when she couldn’t catch her breath while driving the 40 miles to work. She pulled over into a parking lot and called her husband for help.

“I called my husband and said, ‘You gotta come get me,’” Daigle said. “He told me to call 911.”

advertisement

Daigle, now 57, landed in a New Hampshire emergency department, where doctors treated her with antibiotics for bronchitis. When her symptoms didn’t improve, her primary care doctor prescribed a few days of steroid pills, possibly thinking Daigle’s lingering cough and trouble breathing stemmed from asthma or decades of smoking cigarettes, although Daigle had quit about five years earlier.

Over the next year, Daigle was in and out of the emergency room. She underwent X-rays of the lungs and evaluations by specialists, but there were few answers. Each time, a few days of steroid pills helped her symptoms. Yet when she stopped taking them, “the cough would come right back,” Daigle told STAT.

advertisement

She also felt breathless, even at rest. “I had trouble getting enough air in,” she said.

Because lying down worsened the shortness of breath, Daigle slept in a recliner. And she continued to have a runny nose.

Then Daigle’s doctor in New Hampshire referred her to Dr. Laura Brenner, a lung specialist at Massachusetts General Hospital. When the two first met in the spring of 2014, the effects of the steroids struck Brenner more than Daigle’s breathing symptoms.

“My face was swollen, I’d gained 25 pounds, and the skin on my arms and the backs of my hands was very fragile,” said Daigle. “I had areas where the skin would just peel back on my hands, and if I touched things too hard, it would bruise or rip open.” The steroids had also wreaked havoc on her body’s ability to process sugar in the blood, precipitating diabetes that required treatment with insulin.

As Daigle described her breathing symptoms in Brenner’s office, the list of possible causes in the doctor’s mind was relatively short – but they extended beyond run-of-the-mill asthma.

“Her symptoms, and how much steroid she needed, was a lot for asthma,” Brenner said in an interview. “It’s also rare for an adult to develop new asthma, so I wondered if something else was at play.”

A disease called allergic bronchopulmonary aspergillosis, an allergic reaction to a fungus ubiquitous in the environment, was one possibility. Another option was a vasculitis — inflammation in the walls of the body’s blood vessels — called eosinophilic granulomatosis with polyangiitis, or EGPA, formerly known as Churg-Strauss syndrome.

Nothing quite fit

Blood tests showed sky-high levels of white blood cells called eosinophils — a sign of an ongoing allergic response — and of immunoglobulin E, an antibody involved in allergic reactions that can also be high in certain autoimmune diseases. Blood testing for other antibodies, including anti-neutrophil cytoplasmic antibody, or ANCA, came up negative. That pointed away from an autoimmune disease, but didn’t make it impossible. Tests for infections also were unrevealing.

Lung function testing showed her lungs had trouble both inflating and emptying out. She underwent a lung biopsy, which showed she had a disease called non-specific interstitial pneumonia. As the name implies, it can have a wide range of underlying causes, from autoimmune diseases to exposures to toxins, and the results corroborated the findings of a CT of the chest.

That spurred Brenner to send Daigle to see Dr. Eli Miloslavsky, a rheumatologist and vasculitis expert at Mass. General. He, too, was struck by how dependent Daigle was on steroids to keep her symptoms manageable.

“She probably had the most severe asthma I’ve seen in terms of how she couldn’t get off of steroids at all,” Miloslavsky told STAT.

Brenner tried omalizumab, a medicine that binds to the immunoglobulin E so prevalent in Daigle’s bloodstream, preventing it from activating a cascade of effects. When that didn’t help, Daigle switched to an inhaled steroid, an anti-inflammatory antibiotic, and a medicine called montelukast, which decreases airway inflammation.

Yet as always, once on a lower dose of steroid pill, Daigle’s troubling symptoms rebounded.

“I was extremely frustrated because I couldn’t get any answers as to what was wrong with me,” Daigle said. She pushed through her daily 40-mile commute and long days at work, but it was hardly bearable.

The ineffectiveness of this arsenal of anti-asthma drugs begged the question as to whether this was asthma at all, and it brought EGPA back to the forefront of Miloslavsky’s mind.

In some ways, EGPA fit Daigle’s story to a T: This autoimmune disease tends to start around age 50, and it can cause asthma that starts late in life, a runny nose, and high levels of eosinophils in the blood. It’s quite rare; in Europe and the United States, fewer than two people in a million are diagnosed with the disease each year.

Yet the breathing problems found in EGPA usually are accompanied by signs of vasculitis, including skin rash and numbness or tingling in the legs and feet. Daigle didn’t have those symptoms or signs of a vasculitis on her lung biopsy. Still, Miloslavsky theorized, it was possible to develop the breathing problems that can come with EGPA well before developing vasculitis.

When treatment guides diagnosis

Miloslavsky and Brenner knew Daigle had been suffering for years. So even without a firm diagnosis, they decided to treat her as though she had EGPA, hoping her symptoms would respond.

“Sometimes you make a diagnosis, and treatment follows from that — but we looked at her the other way,” Miloslavsky said. “We thought, ‘What do you need to be better? We can’t offer anything else for your asthma, but here’s another way to treat you.’”

Miloslavsky selected the injectable medicine rituximab. This drug would suppress the autoimmune response, hopefully allowing Daigle to stop the steroids.

Indeed, after starting the rituximab, Daigle successfully came off of the steroids, and she’s been breathing easy ever since. In fact, she feels as good as she did before it all began in 2013.

“It was such a relief,” said Daigle, whose energy has returned now that she sleeps through the night, free from the coughing fits that used to wake her. She hasn’t needed to use an inhaler for two years, and she’s back to shopping, playing with her granddaughter, and nurturing her flower garden.

The memory of how bad things were still haunts her, however.

“I worry that it’s going to come back,” Daigle said. And some of the effects of the steroids linger; although she’s lost 40 pounds and her skin isn’t as fragile anymore, she continues to have diabetes.

The remarkable response Daigle had to rituximab makes Brenner and Miloslavsky think she had EGPA the whole time, even though her symptoms were not textbook.

“This was one of the most dramatic responses of the asthma component of EGPA that I’ve seen,” Miloslavsky said.

Daigle’s harrowing journey taught her the importance of persistence, even when all hope seems lost.

“Just keep pushing,” she said. “Just keep trying to live your life.”

Allison Bond is a hospitalist at Massachusetts General Hospital. If you have dealt with a diagnostic puzzle that has been solved, either as a caregiver or a patient, please email Allison at [email protected].

Zithromax (Z-Pak) | Uses, Dosage & Azithromycin Interactions

What Is a Z-Pak?

Zithromax (azithromycin), also known as Z-Pak, is an antibiotic used to treat bacterial infections by inhibiting the growth of bacteria in the body. A Z-Pak is typically taken over a five-day course to treat infections such as bronchitis, pneumonia, and infections of the ears, lungs and other organs. First approved by the FDA in 1991 to treat certain respiratory and skin infections, its use has since expanded to include a wide variety of bacterial infections. These include sexually transmitted diseases, bacterial inflammation and middle-ear infections in children.

COVID-19 Alert

Medical providers are experimenting with azithromycin plus hydroxychloroquine to treat COVID-19.

Learn More

Zithromax has been highly profitable for its manufacturer, Pfizer. At the height of sales in 2002, it brought in over $1 billion for Pfizer. Although the wide availability of generics reduced the company’s revenue, sales still totaled $435 million in 2012.

This antibiotic is popular because it treats infections in adults and children. But, the drug is not without side effects — including fatal heart-related risks.

Zithromax also led to some legal trouble for Pfizer. The company was forced to pay millions to several states to settle allegations that it used misleading tactics to market the drug to children.

How Zithromax Works

Zithromax belongs to a class of antibiotics called macrolides, which are bacteriostatic — meaning they treat infections by preventing bacteria from multiplying and producing the proteins that are essential for their growth. Eventually, the remaining bacteria die or are killed by the immune system, not by the drug itself. This is in contrast to bactericidal antibiotics, which kill bacteria. Bactericidal drugs include fluoroquinolones and penicillin.

Zithromax does not break down in the body as quickly as other antibiotics. Instead of floating freely in the blood, the drug molecules are picked up by white blood cells that fight bacteria. The white blood cells take the medicine to the front lines of their struggle with germs, where it becomes concentrated in the tissues surrounding the infection. That concentration helps it remain in the body longer, which means patients need fewer doses to beat their infections.

Zithromax and Z-Pak Dosage

Zithromax is most familiar to the public as the “Z-Pak,” a convenient five-day pill regimen with a dose of 500 mg (2 tablets of 250 mg) the first day and 250 mg for the remaining four days. But, Zithromax comes in several dosages and forms, including oral tablets and liquids for oral use, injections and intravenous drips.

Dosage forms and strengths

Tablets

250 mg, 500 mg, 600 mg

Oral suspension (liquid)

100 mg/5 mL, 200 mg/5 mL, 1,000 mg/5 mL

Injection and IV

10 mL vial of 500 mg

A doctor determines the dose depending on the infection being treated. For example, for pneumonia, pharyngitis or skin infections the recommended dose is the standard 500 mg for the first day and 250 mg for the remaining 4 days.

For more a complicated disease such as acute sinusitis, doctors prescribe 500 mg a day for three days. In the case of sexually transmitted diseases, the dose is 1 gram, or 1,000 mg, in a single dose.

Who Shouldn’t Take Zithromax?

According to the medication insert, certain people should not take Zithromax. Patients with allergies to azithromycin, erythromycin, or any macrolide or ketolide should not take Zithromax. People with liver problems or who had jaundice with prior use of Zithromax should not take it again.

Sexually Transmitted Infections

Antibiotics used at high doses for short periods of time may mask or delay the symptoms of incubating gonorrhea or syphilis (meaning the disease is already present and developing in the body but symptoms have not yet appeared). Therefore, Zithromax, at the recommended dose, should not be relied upon to treat gonorrhea or syphilis, two types of sexually transmitted diseases (STDs) caused by bacterial infections.

All patients who are diagnosed with or suspected of having sexually transmitted urethritis (urethral inflammation) or cervicitis (irritation or infection of the cervix) should also be tested for gonorrhea and syphilis prior to starting treatment with Zithromax. If infection is confirmed, treatment for those diseases should be initiated with a more appropriate antibacterial drug.

Pregnancy

In animal studies on mice and rats, researchers did not find evidence of birth defects at 3.2 times the human daily dose of 600 mg. But, because there are no actual studies on pregnant humans, pregnant mothers should only use Zithromax while pregnant if necessary. Since it can pass into breast milk, health care providers should use caution in administering Zithromax to breastfeeding mothers, according to the medication label.

Seniors

In clinical trials, 9 percent of patients were at least 65 years of age, and 3 percent were at least 75 years of age. Researchers did not find any differences in effectiveness or safety between young patients and seniors.

Side Effects

In most cases, patients don’t experience side effects from Z-Paks. In clinical trials, adverse reactions occurred in about 12 percent of patients, and less than 10 percent of the reactions were severe.

The most common side effects were gastrointestinal and included diarrhea, stomach pain and nausea. Generally, side effects were more severe with a higher dose.

Serious side effects are rare but can be life-threatening. These include severe allergic reactions, liver injury and diarrhea associated with antibiotic-resistant bacteria.

In March 2013, the FDA warned azithromycin, including brand names Zithromax, Zmax, Azithrocin and Azin, “can cause abnormal changes in the electrical activity of the heart that may lead to a potentially fatal irregular heart rhythm. ”

More recently, in August 2018, the FDA warned long-term use of Zithromax can cause cancer relapse and death in people who have had blood or lymph node cancer and have received donor stem cell transplants.

Zithromax Drug Interactions

In clinical trials, Zithromax had the potential to interact with two different types of drugs. Taking Zithromax with alcohol could also intensify side effects.

Drugs that react to Zithromax include:

Nelfinavir

is a drug doctors prescribe to treat HIV infections. This drug can increase the amount of Zithromax in the blood. The medication insert does not recommend the use of these two drugs together. Health care providers should check for liver abnormalities and hearing impairment.

Warfarin

is a blood thinner. Taking Warfarin with Zithromax increased the blood thinning effect. Doctors should monitor patients taking both drugs.

Macrolides

are a class of antibiotic, and Zithromax belongs to this class. Researchers observed interactions between other macrolides and two drugs: digoxin and phenytoin. Patients who use Zithromax with digoxin and phenytoin should be carefully monitored for drug interactions.

Zithromax Effectiveness in Clinical Trials

In clinical trials, Zithromax was effective at fighting bacterial infection, including some antibiotic-resistant strains.

Studies conducted before approval of the drug measured its minimum inhibitory concentration (MIC) in relation to a host of bacteria. MIC is the lowest concentration of an antibiotic that will inhibit the growth of bacteria and thereby kill them. A lower MIC means a more effective antibiotic.

In a 1991 study in the European Journal of Clinical Microbiology and Infectious Diseases, researchers found Zithromax had a markedly low MIC against some bacteria compared with three other types of antibiotics, meaning it was highly effective — for example, resolving 92 percent of gonorrhea infections treated.

Zithromax Litigation

In 2003, Pfizer agreed to pay $6 million to settle deceptive Zithromax marketing allegations from 19 states. Oregon’s attorney general at the time, Hardy Myers, led the investigation. According to court documents, Pfizer misrepresented the effectiveness of Zithromax in its ads and failed to disclose the risks of antibiotic overuse.

Pfizer Settlement

Pfizer admitted no wrongdoing and said the FDA approved its advertising and promotional materials. It claimed it was settling to avoid unnecessary costs.

The drugmaker created a mascot for Zithromax, a zebra named Max, to use in its marketing. Pfizer sent plastic zebras that hang on stethoscopes and medical journals wrapped in zebra stripes to pediatricians. It also donated a zebra named Max to the San Francisco Zoo and invited children to a naming celebration.

The 2013 FDA heart rhythm warning prompted some lawyers to investigate and file Zithromax lawsuits. According to plaintiffs, Zithromax caused abnormal heart rhythms. But there have been no settlements or trial dates set.

Steroids for the common cold

Review question

We reviewed the evidence for using steroid medications to improve symptoms in patients who have a common cold.

Background

Common colds are experienced by over half a billion patients annually in the USA alone and result in significant loss of productivity. Although there are a number of medications used to help improve the symptoms of the common cold, none have good evidence of benefit. Steroids (corticosteroids) have been shown to help relieve symptoms in other types of upper respiratory tract infections by reducing the inflammation of the lining of the nose and throat, which means they might also improve the symptoms of the common cold.

Study characteristics

Our evidence is current to May 2015. We found three trials in total. Two trials recruited adults from the general population or from among hospital staff in Finland. These trials (total 253 adults) compared intranasal steroid sprays, which allow steroids to be puffed into the nostrils, to sprays containing placebo only. We found a third trial, which recruited 100 children referred to outpatient clinics in an Iranian paediatric hospital. This trial compared intranasal steroid spray to no spray and gave oral antibiotics to all participants.

Key results and quality of the evidence

Neither of the two trials comparing steroid spray to placebo spray in adults showed a benefit of steroids across a range of different measures. The trial comparing steroid spray to no spray in children did find some evidence of benefit but we rated the quality of the evidence from this trial as very poor and the results were unclear. We could not combine the results of the trials to assess this question further. There were no reports of adverse events.

Conclusion

The available evidence suggests that we should not use intranasal steroids for the common cold. However, as we found only three small trials, we cannot be sure that there is no effect without performing larger, well-designed trials.

What Corticosteroid is Most Appropriate for treating Acute Exacerbations of CoPD?

Case

A 66-year-old Caucasian female with moderate chronic obstructive pulmonary disease (COPD) (FEV1 55% predicted), obesity, hypertension, and Type 2 diabetes mellitus on insulin therapy presents to the ED with four days of increased cough productive of yellow sputum and progressive shortness of breath. Her physical exam is notable for an oxygen saturation of 87% on room air, along with diffuse expiratory wheezing with use of accessory muscles; her chest X-ray is unchanged from previous. The patient is given oxygen, nebulized bronchodilators, and one dose of IV methylprednisolone. Her symptoms do not improve significantly, and she is admitted for further management. What regimen of corticosteroids is most appropriate to treat her acute exacerbation of COPD?

Overview

COPD is the fourth-leading cause of death in the United States and continues to increase in prevalence.1 Acute exacerbations of COPD (AECOPD) contribute significantly to this high mortality rate, which approaches 40% at one year in those patients requiring mechanical support.¹ An exacerbation of COPD has been defined as an acute change in a patient’s baseline dyspnea, cough, and/or sputum beyond day-to-day variability sufficient to warrant a change in therapy.² Exacerbations commonly occur in COPD patients and often necessitate hospital admission. In fact, COPD consistently is one of the 10 most common reasons for hospitalization, with billions of dollars in associated healthcare costs.³

The goals for inpatient management of AECOPD are to provide acute symptom relief and to minimize the potential for subsequent exacerbations. These are accomplished via a multifaceted approach, including the use of bronchodilators, antibiotics, supplemental oxygen, noninvasive positive pressure ventilation in certain circumstances, and systemic corticosteroids.

The administration of systemic steroids in AECOPD has been prevalent for several decades, with initial studies showing positive effects on lung function, specifically FEV1.⁴ Studies have demonstrated the benefit of steroids in prolonging the time to subsequent exacerbation, reducing the rate of treatment failure, and reducing length of stay (LOS).⁵ Corticosteroids have since become an essential component of the standard of care in AECOPD management.

Despite consensus that systemic steroids should be used in COPD exacerbations, a great deal of controversy still surrounds the optimal steroid regimen.⁶ Steroid use is not without risk, as steroids can lead to adverse outcomes in medically complex hospitalized patients (see Table 1, below). Current guidelines provide limited guidance as to the optimal route of administration, dosing regimen, or length of therapy; clinical practice varies widely.

Review of the Data

Administration route: intravenous (IV) vs. oral. The use of steroids in AECOPD began with such IV formulations as methylprednisolone, and this became the typical method of treating hospitalized patients. This practice was validated in a multicenter Veterans Affairs trial, which demonstrated decreased risk of treatment failure (defined as all-cause mortality, need for intubation, readmission for COPD, or intensification of pharmacologic therapy) for patients randomized to receive an IV-to-oral steroid regimen compared with those randomized to placebo.5 Patients receiving steroids also had shorter LOS and improvements in FEV1 after the first day of treatment. Subsequent randomized controlled trials in patients with AECOPD demonstrated the benefit of oral regimens compared with placebo with regard to FEV1, LOS, and risk of treatment failure.^6,7,8

Similarities in the bioavailability of oral and IV steroids have been known for a long time.⁹ Comparisons in efficacy initially were completed in the management of acute asthma exacerbations, with increasing evidence, including a meta-analysis, demonstrating no difference in improvement in pulmonary function and in preventing relapse of exacerbations for oral compared with IV steroids.¹⁰ However, only recently have oral and IV steroids been compared in the treatment of AECOPD. De Jong et al randomized more than 200 patients hospitalized for AECOPD to 60 mg of either IV or oral prednisolone for five days, followed by a week of an oral taper.¹¹ There were no significant differences in treatment failure between the IV and oral groups (62% vs. 56%, respectively, at 90 days; one-sided lower bound of the 95% confidence interval [CI], −5.8%).

A large observational study by Lindenauer et al, including nearly 80,000 AECOPD patients admitted at more than 400 hospitals, added further support to the idea that oral and IV steroids were comparable in efficacy.¹² In this study, multivariate analysis found no difference in treatment failure between oral and IV groups (odds ratio [OR] 0.93; 95% CI, 0.84-1.02). The authors also found, however, that current clinical practice still overwhelmingly favors intravenous steroids, with 92% of study patients initially being administered IV steroids.¹²

Based on the evidence from de Jong and Lindenauer, it appears that there is no significant benefit to the use of IV over oral steroids. Additionally, there is evidence for oral administration being associated with beneficial effects on cost and hospital LOS.¹² Oral steroids, therefore, are the preferred route of administration to treat a hospitalized patient with AECOPD, unless the patient is unable to tolerate oral medications. Current guidelines support the practice of giving oral steroids as first-line treatment for AECOPD (see Table 2, above).

High dose vs. low dose. Another important clinical issue concerns the dosing of steroids. The randomized trials examining the use of corticosteroids in AECOPD vary widely in the dosages studied. Further, the majority of these trials have compared steroids to placebo, rather than comparing different dosage regimens. The agents studied have included prednisone, prednisolone, methylprednisolone, and hydrocortisone, or combinations thereof. In order to compare regimens of these different drugs, steroid doses often are converted into prednisone equivalents (see Table 3, below). Though no guidelines define “high dose” and “low dose,” some studies have designated doses of >80 mg prednisone equivalents daily as high-dose and prednisone equivalents of ≤80 mg daily as low-dose.^13,14

Starting doses of systemic corticosteroids in the treatment of AECOPD in clinical studies range from prednisone equivalents of 30 mg daily to 625 mg on the first day of treatment.^5,8 No randomized studies of high- versus low-dose steroid regimens have been conducted. One retrospective chart review of 145 AECOPD admissions evaluated outcomes among patients who were given higher (mean daily dose >80 mg prednisone equivalent) and lower (mean daily dose of ≤80 mg prednisone) doses.¹⁴ The authors found that patients who received higher doses of steroids had significantly longer LOS compared with those who received lower doses, especially among the subset of patients who were admitted to the floor rather than the ICU, though this analysis did not adjust for severity of illness. In this study, the most striking finding noted by the authors was the wide variability in the steroid doses prescribed for the inpatient treatment of AECOPD.

More recently, the study by Lindenauer et al examined outcomes between patients treated with high-dose IV steroids (equivalent of 120 mg-800 mg of prednisone on the first or second day of treatment) compared to low-dose oral steroids (prednisone equivalents of 20 mg-80 mg per day).¹² The authors found no differences between the two groups regarding the rate of treatment failure, defined by initiation of mechanical ventilation after the second hospital day, in-hospital mortality, or readmission for COPD within 30 days of discharge. After multivariate adjustment, including the propensity for oral treatment, the low-dose oral therapy group was found to have lower risk of treatment failure, shorter LOS, and lower total hospital cost.

Despite the heterogeneity of the published data and the lack of randomized trials, the existing evidence suggests that low-dose prednisone (or equivalent) is similar in efficacy to higher doses and generally is associated with shorter hospital stays. Recognizing these benefits, guidelines do favor initiating treatment with low-dose steroids in patients admitted with AECOPD. The most recent publications from the American Thoracic Society/European Respiratory Society Task Force (ATS/ERS), the Global Initiative for Chronic Obstructive Lung Disease (GOLD), the National Clinical Guidelines Centre in the United Kingdom, and the Canadian Thoracic Society all recommend equivalent dosing of prednisone in patients admitted with AECOPD who are able to tolerate oral intake (see Table 2).^1,2,15,16

Duration. As with the dosing of systemic corticosteroids in AECOPD, the optimal duration of treatment is not well-established. National and international consensus panels vary in their recommendations, as outlined in Table 2. This may be related to the variability in length of treatment found in the literature.

Treatment durations ranging from one day to eight weeks have been studied in inpatients with AECOPD. The landmark randomized controlled trial by Niewoehner and colleagues compared two-week and eight-week courses of systemic corticosteroids and found no difference in the rates of treatment failure, which included death, need for mechanical ventilation, readmission for COPD, and intensification of pharmacologic therapy.⁵ Based on these results, many experts have concluded that there is no benefit to steroid courses lasting beyond two weeks.

Although improvements in outcomes have been demonstrated with corticosteroid regimens as short as three days compared with placebo, most of the randomized controlled trials have included courses of seven to 14 days.⁴ Given the risks of adverse events (e.g. hyperglycemia) that are associated with systemic administration of steroids, the shortest effective duration should be considered.

In both clinical practice and clinical studies, steroid regimens often include a taper. A study by Vondracek and Hemstreet found that 79% of hospital discharges for AECOPD included a tapered corticosteroid regimen.¹⁴ From a physiologic standpoint, durations of corticosteroid treatment approximately three weeks or less, regardless of dosage, should not lead to adrenal suppression.¹⁷ There also is no evidence to suggest that abrupt discontinuation of steroids leads to clinical worsening of disease, and complicated steroid tapers are a potential source of medication errors after hospital discharge.¹⁸ Furthermore, the clinical guidelines do not address the tapering of corticosteroids. Therefore, there is a lack of evidence advocating for or against the use of tapered steroid regimens in AECOPD.

Back to the Case

In addition to standard treatment modalities for AECOPD, our patient was administered oral prednisone 40 mg daily. She experienced steroid-induced hyperglycemia, which was corrected with adjustment of her insulin regimen. The patient’s pulmonary symptoms improved within 72 hours, and she was discharged home on hospital day four to complete a seven-day steroid course. At hospital discharge, she was administered influenza and pneumococcal vaccinations, and she was instructed to resume her usual insulin dosing once she finished her prednisone course.

Overview

In the management of AECOPD, there remains a lack of consensus in defining the ideal steroid regimen. Based on current literature, the use of low-dose oral corticosteroids, such as prednisone 40 mg daily, for a seven- to 14-day course is recommended. TH

Dr. Cunningham is an assistant professor of internal medicine and academic hospitalist in the section of hospital medicine at Vanderbilt University School of Medicine in Nashville, Tenn. Dr. LaBrin is an assistant professor of internal medicine and pediatrics and academic hospitalist at Vanderbilt University School of Medicine.

References

1. From the Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2010. Global Initiative for Chronic Obstructive Lung Disease website. Available at: www.goldcopd.org/GuidelineItem.asp?intId=989. Accessed Feb. 21, 2011.
2. Celli BR, MacNee W, ATS/ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J. 2004;23:932-946.
3. Morbidity and mortality: 2009 chart book on cardiovascular, lung, and blood diseases. National Institutes of Health’s National Heart, Lung, and Blood Institute website. Available at: www.nhlbi.nih.gov/resources/docs/2009_ChartBook.pdf. Accessed Feb. 24, 2011.
4. Albert RK, Martin TR, Lewis SW. Controlled trial of methylprednisolone in patients with chronic bronchitis and acute respiratory insufficiency. Ann Intern Med. 1980;92(6):753-758.
5. Niewoehner DE, Erbland ML, Deupree RH, et al. Effect of systemic glucocorticoids on exacerbations of chronic obstructive pulmonary disease. Department of Veterans Affairs Cooperative Study Group. N Engl J Med. 1999;340(25):1941-1947.
6. Thompson WH, Nielson C, Carvalho P, Charan NB, Crowley JJ. Controlled trial of oral prednisone in outpatients with acute COPD exacerbation. Am J Respir Crit Care Med. 1996;154:407-412.
7. Seemungal TA, Donaldson GC, Bhowmik A, Jeffries DJ, Wedzicha JA. Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2000;161:1608-1613.
8. Davies L, Angus RM, Calverley PM. Oral corticosteroids in patients admitted to hospital with exacerbations of chronic obstructive pulmonary disease: a prospective randomised controlled trial. Lancet. 1999;354(9177):456-460.
9. Al-Habet S, Rogers HJ. Pharmacokinetics of intravenous and oral prednisolone. Br J Clin Pharmacol. 1980;10(5):503-508.
10. Rowe BH, Keller JL, Oxman AD. Effectiveness of steroid therapy in acute exacerbations of asthma: a meta-analysis. Am J Emerg Med. 1992;10:301-310.
11. De Jong YP, Uil SM, Grotjohan HP, Postma DS, Kerstjens HA, van den Berg JW. Oral or IV prednisolone in the treatment of COPD exacerbations: A randomized, controlled, double-blind study. Chest. 2007;132(6):1741-1747.
12. Lindenauer PK, Pekow PS, Lahti MC, Lee Y, Benjamin EM, Rothberg MB. Association of corticosteroid dose and route of administration with risk of treatment failure in acute exacerbation of chronic obstructive pulmonary disease. JAMA. 2010;303(23):2359-2367.
13. Manser R, Reid D, Abramsom MJ. Corticosteroids for acute severe asthma in hospitalized patients. Cochrane Database Syst Rev. 2000;(2):CD001740.
14. Vondracek SF, Hemstreet BA. Retrospective evaluation of systemic corticosteroids for the management of acute exacerbations of chronic obstructive pulmonary disease. Am J Health Syst Pharm. 2006;63:645-652.
15. Chronic obstructive pulmonary disease: management of chronic obstructive pulmonary disease in adults in primary and secondary care. National Institute for Health and Clinical Excellence website. Available at: guidance.nice.org.uk/CG101/Guidance/pdf/English. Accessed Feb. 21, 2011.
16. O’Donnell DE, Aaron S, Bourbeau J, et al. Canadian Thoracic Society recommendations for management of chronic obstructive pulmonary disease—2007 update. Can Respir J. 2007;14 Suppl B:5B-32B.
17. Webb J, Clark TJ. Recovery of plasma corticotrophin and cortisol levels after three-week course of prednisolone. Thorax. 1981;36:22-24.
18. O’Driscoll BR, Kalra S, Wilson M, Pickering CA, Carroll KB, Woodcock AA. Double-blind trial of steroid tapering in acute asthma. Lancet. 1993; 341:324-7.

Z-pack heart rhythm warning: FDA warns azithromycin “Z-pack” antibiotics could lead to deadly heart rhythms for some

Azithromycin, a commonly-prescribed antibiotic, may trigger a potentially deadly irregular heart rhythm for some patients, the Food and Drug Administration (FDA) warned Tuesday. The antibiotic that’s sold as Zithromax, Zmax or sometimes referred to as a “Z-Pack” is prescribed to treat bacterial infections such as bronchitis, pneumonia, or ear infections.

The FDA is warning the public that the pills can cause abnormal changes in the heart’s electrical activity that may lead to a fatal heart rhythm. Not everyone is at risk. Patients with known risk factors such as existing QT interval prolongation, low blood levels of potassium or magnesium, a slower than normal heart rate, or those who use  certain drugs to treat abnormal heart rhythms, or arrhythmias face the greatest risk.

“Health care professionals should consider the risk of fatal heart rhythms with azithromycin when considering treatment options for patients who are already at risk for cardiovascular events,” the FDA said in its March 12th update.

The new guidance was prompted by a May 2012 study and another study by the antibiotic’s manufacturer, Pfizer, that looked at risks to electrical activity of the heart in azithromycin-takers.

Last May, a New England Journal of Medicine study paid for by the National Heart, Lung and Blood Institute found there would be 47 extra heart-related deaths per one million course of treatment with five days of Zithromax, as compared to 10 days of amoxicillin and other antibiotics. The risks of cardiovascular death associated with levofloxacin (Levaquin) treatment were similar to those associated with azithromycin treatment, according to the FDA.

“People need to recognize that the overall risk is low,” Dr. Harlan Krumholz, a Yale University health outcomes specialist who was not involved in the study, told the Associated Press last May. He added more research was needed but patients with heart disease “should probably be steered away” from Zithromax for now.

The FDA also issued a statement last May following the study saying the agency was aware of the findings, and it would review the results and communicate any new information.

Sales of Zithromax, one of the U.S.’ top-selling antibiotics, totaled $464 million in 2011 according to health care information company IMS Health, the AP reported.

More Z-pack news

Trending News

Ryan Jaslow

Ryan Jaslow is CBSNews.com’s health editor.

90,000 RINZASIP® with vitamin C | RINZA®

In case of overdose, consult a doctor immediately. Prompt medical attention is critical, even if you don’t notice any signs or symptoms.

Ascorbic acid

Symptoms of acute overdose: diarrhea and other gastrointestinal disorders.

Symptoms of chronic intoxication with ascorbic acid: impaired renal excretory function, formation of kidney stones, decreased capillary permeability (possible deterioration of tissue trophism, increased blood pressure, hypercoagulation, development of microangiopathies, impaired iron metabolism), erosion of tooth enamel.

Caffeine

Symptoms of acute overdose: abdominal pain, nausea, vomiting, fever, chills, headache, agitation, insomnia, irritability, loss of appetite, weakness, tremor, anxiety, altered consciousness, delirium, hallucinations, increased blood pressure followed by hypotension , tachycardia, tachypnea, hypokalemia, hyponatremia, hyperglycemia, metabolic acidosis, epileptic seizures, convulsions, myoclonus and rhabdomyolysis, supraventricular and ventricular arrhythmias.

Symptoms of chronic intoxication with caffeine, (“caffeinism”): irritability, insomnia, anxiety, emotional lability, chronic abdominal pain.

Pheniramine

Symptoms: CNS depression, hyperthermia, anticholinergic syndrome (mydriasis, flushing, fever, dry mouth, urinary retention, intestinal paresis), tachycardia, hypotension, hypertension, nausea, vomiting, psychomotor agitation, hallucinations psychosis, convulsions, arrhythmias.Rarely, patients with agitation, seizures, or coma develop rhabdomyolysis and renal failure.

Phenylephrine

Symptoms: headache, nausea, vomiting, irritability, agitation, insomnia, psychosis, convulsions, palpitations, tachycardia, increased blood pressure, reflex bradycardia.

Paracetamol

Symptoms, appear after ingestion of more than 7.5-10 g: during the first 24 hours after ingestion – pallor of the skin, nausea, vomiting, anorexia, abdominal pain, increased prothrombin time, impaired glucose metabolism, hypokalemia, metabolic acidosis ( incl.including lactic acidosis). Symptoms of liver dysfunction may appear 12-48 hours after an overdose: increased activity of “hepatic” transaminases, hepatonecrosis. In severe cases – liver failure with progressive encephalopathy, coma. Rarely, liver failure develops lightning fast and may be complicated by renal failure (tubular necrosis).

The overdose threshold can be lowered in elderly patients and children, in patients taking certain medications (for example, inducers of liver microsomal enzymes), alcohol or suffering from wasting.

Treatment: gastric lavage, the appointment of activated charcoal in the first 6 hours after the overdose, the introduction of SH-group donors and precursors of the synthesis of glutathione – methionine 8-9 hours after the overdose and acetylcysteine ​​- after 12 hours. The need for additional therapeutic measures ( further administration of methionine and acetylcysteine) depends on the concentration of paracetamol in the blood, as well as on the time elapsed after taking it. Symptomatic therapy.

From the circulatory system: Paracetamol overdose in people with glucose-6-phosphate dehydrogenase deficiency can cause hemolytic anemia.

up

Grippoflu for colds and flu instructions for use: indications, contraindications, side effects – description Grippoflu Cold and Flu Powder for oral solution (25290)

Paracetamol

Enhances the effects of MAO inhibitors, sedatives, ethanol.

The risk of hepatotoxic action of paracetamol increases with the simultaneous use of barbiturates, phenytoin, phenobarbital, carbamazepine, rifampicin, isoniazid, zidovudine and other inducers of liver microsomal enzymes.

With long-term regular use of paracetamol, the anticoagulant effect of warfarin and other coumarins may increase, while the risk of bleeding increases. A single use of paracetamol has no significant effect.

Metoclopramide increases the rate of absorption of paracetamol and reduces the time to reach its C _max in blood plasma.Likewise, domperidone may increase the rate of absorption of paracetamol.

Paracetamol can lead to an increase in Tmax _1/2 chloramphenicol.

Paracetamol is able to reduce the bioavailability of lamotrigine, while it is possible to reduce the effectiveness of lamotrigine due to the induction of its metabolism in the liver.

Absorption of paracetamol can be reduced when used simultaneously with cholestyramine, but the decrease in absorption is insignificant if cholestyramine is taken an hour later.

Regular use of paracetamol with zidovudine may cause neutropenia and increase the risk of liver damage.

Probenecid affects the metabolism of paracetamol. In patients concomitantly using probenecid, the dose of paracetamol should be reduced.

Hepatotoxicity of paracetamol increases with prolonged excessive use of ethanol (alcohol).

Paracetamol may interfere with the uric acid test using the phosphotungstate precipitating reagent.

Pheniramine

It is possible to increase the effect of other substances on the central nervous system (for example, MAO inhibitors, tricyclic antidepressants, alcohol, antiparkinsonian drugs, barbiturates, tranquilizers and drugs). Pheniramine can inhibit the action of anticoagulants.

Phenylephrine

Phenylephrine can potentiate the action of MAO inhibitors and cause a hypertensive crisis.

The simultaneous use of phenylephrine with other sympathomimetic drugs or tricyclic antidepressants (for example, amitriptyline) may increase the risk of adverse reactions from the cardiovascular system.

Phenylephrine may reduce the effectiveness of beta-blockers and other antihypertensive drugs (eg, debrisoquine, guanethidine, reserpine, methyldopa). There may be an increased risk of hypertension and other cardiovascular side effects.

The simultaneous use of phenylephrine with digoxin and cardiac glycosides may increase the risk of cardiac arrhythmias or myocardial infarction.

Concomitant use of phenylephrine with ergot alkaloids (ergotamine and methysergide) may increase the risk of ergotism.

With simultaneous use with barbiturates, primidone increases the excretion of ascorbic acid in the urine.

Ascorbic acid

With the simultaneous use of oral contraceptives, the concentration of ascorbic acid in the blood plasma decreases. It is possible to increase the concentration of ethinyl estradiol in the blood plasma with its simultaneous use as part of oral contraceptives.

When used simultaneously with iron preparations, ascorbic acid, due to its regenerating properties, converts trivalent iron into bivalent, which improves its absorption.

With simultaneous use with warfarin, it is possible to reduce the effects of warfarin.

With the simultaneous use of ascorbic acid increases the excretion of iron in patients receiving deferoxamine.

With simultaneous use with tetracycline, the excretion of ascorbic acid in the urine increases.

NeoLab

Schedule of intake points for the holiday on March 8!

NeoLab Company congratulates you on the coming spring holiday!

Strive for new goals, new knowledge, love with all your heart.Strength, health and inspiration to you.

Please be informed that on holidays the pick-up points will work according to the following schedule:

• Kiev, st. Nikolay Amosov, 5a

March 3.8 – day off

March 9 – from 8:00 to 17:00

• Kiev, st. North, 4A

March 3 – from 8:00 to 12:00

March 8 – day off

March 9 – from 8:00 to 15:00

• Kiev, st. Rizhskaya, 1

March 3 – from 9:00 to 12:00

March 8 – day off

March 9 – from 8:00 to 16:00

• Kiev, st.Solomenskaya, 17

March 3.8 – day off

March 9 – from 8:00 to 15:00

• Kiev, st. Nikolay Amosov, 6

March 3 – from 8:00 to 16:00

March 8.9 – day off

• Kiev, st. People’s militia, 5

March 3.8 – day off

March 9 – from 8:00 to 16:00

• Kiev, st. Tymoshenko, 21

March 3 – from 7:00 to 15:00

March 8 – from 7:00 to 15:00

March 9 – from 7:00 to 18:00

• Kiev, st.Dekabristov, 9

March 3 – from 7:00 to 15:00

March 8 – from 7:00 to 15:00

March 9 – from 7:00 to 18:00

• Irpin, st. Pushkinskaya, 78

March 3 – from 7:00 to 15:00

March 8 – from 7:00 to 15:00

March 9 – from 7:00 to 18:00

• Novoukrainka, lane, Hospital, 1

March 3.8 – day off

March 9 – from 8:00 to 12:00

• Fastov, st. Leo Tolstoy, 24

March 3.8 – day off

March 9 – from 8:00 to 15:00

• Obukhov, st.Chestnut, 52

March 3 – from 8:00 to 12:00

March 8 – day off

March 9 – from 8:00 to 15:00

• White Church, st. Semashko, 9

March 3 – from 7:00 to 12:00

March 8 – day off

March 9 – from 7:00 to 16:00

• White Church, st. Yaroslav the Wise, 44

March 3.8 – day off

March 9 – from 8:00 to 15:00

• Rokitnoe, st. Vokzalnaya, 86

March 3.8 – day off

March 9 – from 8:00 to 15:00

• Kropyvnytskyi, st.Korolenka, 56

March 3 – from 8:00 to 14:00

March 8.9 – day off

• Boryspil, st. Kotlyarevsky, 1

March 3 – from 7:00 to 13:00

March 8 – day off

March 9 – from 7:00 to 15:00

• Borodyanka, st.