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Elevated liver enzymes and enlarged spleen: 18-Year-Old Woman With Fever, Abdominal Pain, and Elevated Liver Enzymes

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Enlarged Liver: Symptoms, Causes, Treatments

Overview

What is an enlarged liver?

The liver is an essential organ in many of the body’s functions. An enlarged liver (hepatomegaly) is swollen beyond its normal size for any reason.

An enlarged liver is a symptom of an underlying problem, but is not a disease itself. An enlarged liver may occur along with other symptoms, depending on the underlying disease that is causing it.

Symptoms and Causes

What causes an enlarged liver?

Several diseases or conditions can cause the liver to enlarge. For some people, an enlarged liver results from consuming too many toxins, including alcohol, medications such as acetaminophen (Tylenol®) or supplements. Long-term exposure to high doses of toxic substances (including alcohol), medications or supplements can cause cirrhosis (scarring) of the liver.

Other diseases and medical conditions that can cause the liver to enlarge include:

  • Cancers, including liver cancer or cancer from other organs metastasizing (spreading) to the liver, especially colon cancer, pancreatic cancer and lung cancer
  • Benign (non-cancerous) liver tumors
  • Blood backflow from the heart as a result of congestive heart failure or other diseases affecting the valves of the heart
  • Budd-Chiari syndrome (blood clots in the blood vessels that drain the liver)
  • Recurrent alcohol use causing inflammation of the liver
  • Excess fat in the liver, usually as a result of obesity, alcohol use or diabetes
  • Genetic (inherited) disorders that cause fatty or sugary substances to build up in the liver, such as Gaucher disease and alpha-1 antitrypsin deficiency
  • Polycystic liver disease (several benign cysts in the liver)
  • Acute fatty liver of pregnancy (abnormal fat accumulation in the liver during pregnancy)

What are the symptoms of an enlarged liver?

An enlarged liver often does not cause any symptoms. Doctors often detect it when treating a patient for another, unrelated condition.

An enlarged liver may occur along with other symptoms, especially if the underlying cause is a primary liver disease. These symptoms may include:

  • Fatigue
  • Jaundice (yellowing of the whites of the eyes and skin)
  • Nausea and vomiting
  • Pain in the upper middle or upper right side of the abdomen
  • Filling up quickly after meals

If you have any of these symptoms, especially if they persist, contact your doctor.

Diagnosis and Tests

How is an enlarged liver diagnosed?

A doctor can diagnose an enlarged liver with a physical examination and imaging tests, such as such as CT scan, ultrasound or MRI. The doctor will likely need to order some blood tests to determine what is causing the liver enlargement. In some cases, a liver biopsy (a small sample of the liver to be examined under the microscope) might be needed.

Management and Treatment

How is an enlarged liver treated?

Treatment for an enlarged liver depends on what is causing it. Lifestyle changes can help when the liver enlargement is a result of fat accumulation in the liver or consuming alcohol. Lifestyle changes include:

  • Losing weight
  • Cutting back or eliminating alcohol
  • Eating a healthy diet
  • Increasing exercise and physical activity

Treatment for other causes of liver enlargement depends on the underlying disease that caused it.

Living With

When should I call the doctor about symptoms of an enlarged liver?

If you have symptoms that may indicate an enlarged liver, such as pain in the upper abdomen, persistent nausea and vomiting, or jaundice, contact your doctor.

Enlarged spleen ,high liver enzymes

My hubby has been diagnosed since April 2012. His diagnosis came out of the blue when he started vomiting blood one night and in hospital he had an ultrasound, lots of bloods, an endoscopy and eventually a biopsy & from those it was obvious he had cirrhosis. He is life long t-total and his issues are due to auto immune liver disease. His bleeding was due to burst varices caused by portal hypertension – he underwent an aggressive banding regime, also had aneurysms on his spleen due to P/H. He was listed for transplant in 2014 but stabilized and was delisted in 2015.

He has issues but is stable and currently has none of the decompensated liver cirrhosis symptoms.

Ok that’s good he is doing well now

Have they given you any information on if he will have future problems ?

I find it strange as my dad has had similar symptoms on and off through his life even when he was tea total other than the odd beer

So I’m wondering if it could be something hereditary?

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I wouldn’t say he’s doing well as such but is making the most of each day as his energy levels and health allow. When he was delisted from transplant list we were told it wasn’t a matter of if he’ll need a t/p but when. So he will probably would need one at some point but he’s currently stable so we make the most of that. He has issues with sleep deprivation, chronic fatigue, cognitive function and such like.

Sometimes you can have a propensity for liver issues and if you’ve added to that ‘a few drinks in the evening’ then you might be drinking in excess of guideline levels and this can exacerbate underlying issues. If your father had liver issues/symptoms then it would be something I would be mentioning to your doctors for possible follow up.

Alcohol is only one cause of liver issues – there are countless others such as auto immune, hereditary, viral, lifestyle related even medications can cause liver issues.

Katie

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Ok thanks

Only long term medication I have had was antibiotics I was on years when I was young for acne

I’m taking bisoprolol 2.5 now I’m not sure if this is due to liver ?

I will just have to wait for the fibroscan and specialist however long that will be

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We wonder if it was a long term antibiotic my hubby took for acne which caused his issues. He has always been fit and healthy but his GP kept prescribing an antibiotic for adult acne. His AIH is deemed burned out which points to him having a liver injury in the past but no active inflammation now (which is an unusual presentation for AIH).

Wait for your appointments, antibody blood tests should reveal whether there is something auto immune going on.

Katie

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Sleep deprivation? From insomnia? As I suffer from insomnia too

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while ago I also suffered some episodes that I was told could be A fibrillation

Is this a sign of liver problems?

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Hi I’ve always been t-total, except the odd glass of wine once or twice a year. I have always been overweight though. As I was adopted I had no idea if any of my numerous ailments were due to genetics, but over the past few years I have met members of my birth family and even though we are all of a similar body frame, none of them have suffered with issues with their liver. I had NASH, which went to cirrosis, portal hypertension and eventually Heptatic Encephalopathy. Which then made me require a liver transplant which after a year on the list I had 3 weeks ago. I asked in the beginning of my condition was heriditary, as my daughter is a similar build to me. and he said no, he elaborated that it was just had luck, and there was nothing I could have done to prevent the series of events. He said, however. it was exasperated by me being overweight, and I may have had a normal lifespan despite the liver damage. And would have probably died from an unrelated condition in old age.

I think with liver diease people always assume it’s down to alcohol or drug abuse, but there are over 100 various medical conditions that can damage your liver, so it’s probably better to not assume as your dad’s symptoms are similar they are due to the same condition as the other person. Just ask your father’s consultant who will be able to exactly diagnose the root of his problem, doctors don’t always openly offer information because some people don’t want to know, so if you are Frank with him about all of your fears then he will honestly give you the tryth, as it’s their duty. Good luck and I wish you well.

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Spleen problems and spleen removal

Some people are born without a spleen or need to have it removed because of disease or injury.

The spleen is a fist-sized organ found in the upper left side of your abdomen, next to your stomach and behind your left ribs. 

It is an important part of your immune system but you can survive without it. This is because the liver can take over many of the spleen’s functions.

What does the spleen do?

The spleen has a few important functions:

  • It fights any invading germs in the blood (the spleen contains infection-fighting white blood cells).
  • It controls the level of blood cells. The spleen controls the level of white blood cells, red blood cells and platelets (small cells that form blood clots)
  • It screens the blood and removes any old or damaged red blood cells.

If the spleen doesn’t work properly, it may start to remove healthy blood cells. This can lead to:

  • anaemia, from a reduced number of red blood cells
  • an increased risk of infection, from a reduced number of white blood cells
  • bleeding or bruising, from a reduced number of platelets

Spleen problems

Spleen pain

Spleen pain is usually felt as a pain behind your left ribs. It may be tender when you touch the area. This can be a sign of a damaged, ruptured or enlarged spleen.

A damaged or ruptured spleen

The spleen can become damaged or may rupture (burst) after a forceful blow to the abdomen, car accident, sporting accident or fracture to the ribs. 

Rupture can happen straight away or it may happen weeks after the injury.

Signs of a ruptured spleen are:

  • pain behind your left ribs and tenderness when you touch this area
  • dizziness and a rapid heart rate (a sign of low blood pressure caused by blood loss)

Sometimes, if you lie down and raise your legs, the pain can be felt at the tip of your left shoulder.

A ruptured spleen is a medical emergency, as it can cause life-threatening bleeding. Go straight to A&E if you think you’ve ruptured or damaged your spleen.

Enlarged spleen

The spleen can become swollen after an infection or injury. It can also become enlarged as a result of a disease such as cirrhosis, leukaemia or rheumatoid arthritis.

An enlarged spleen doesn’t always cause symptoms. Otherwise, look out for:

  • feeling full very quickly after eating (an enlarged spleen can press on the stomach)
  • feeling discomfort or pain behind your left ribs 
  • anaemia and/or fatigue
  • frequent infections
  • easy bleeding

Doctors can often tell if you have an enlarged spleen by feeling your abdomen. A blood test, CT scan or MRI scan would confirm the diagnosis.

The spleen is not usually removed if it’s just enlarged. Instead, you’ll receive treatment for any underlying condition and your spleen will be monitored. Antibiotics may be prescribed if there’s an infection.

You’ll need to avoid contact sports for a while, as you’ll be at greater risk of rupturing the spleen while it is enlarged.

Surgery is only necessary if the enlarged spleen is causing serious complications or if the cause can’t be found.

Splenectomy (having the spleen removed)

An operation to remove the spleen, known as a splenectomy, may be needed if the spleen is damaged, diseased or enlarged.

It may sometimes be more appropriate to have just part of your spleen removed – a partial splenectomy.

If there’s time, you’ll be advised to have a series of immunisations before the operation.

Laparoscopy

Most splenectomies are carried out using laparoscopy (keyhole surgery).

A laparoscope is long, thin, flexible instrument with its own light source. It is attached to a camera and will relay high definition, magnified pictures back to a TV screen to guide the surgeon’s instruments.

Laparoscopic splenectomy allows a surgeon to access the inside of your abdomen without having to make large incisions (cuts) in your skin. However, you will still need a general anaesthetic.

The procedure involves:

  • Making several incisions in your abdomen (tummy area).
  • Guiding a laparoscope into your body through one of the incisions, so doctors can see what they’re doing. 
  • Passing thin instruments into your abdomen through the other incisions, to remove your spleen. Gas will be pumped into your abdomen to make this easier.

The incisions will then be stitched up or sometimes glued together. You may be able to go home the same day, or may need to stay in hospital overnight. If you go home the same day, someone will need to stay with you for the first 24 hours.

Open surgery

Open surgery, where one large incision is made, may be needed if the spleen is too large or too damaged to be removed via keyhole surgery. Often, in emergencies, this will be the preferred method to rapidly control bleeding.

You’ll need a general anaesthetic and may need to stay in hospital for a few days to recover.

Afterwards

It’s normal to feel sore and be bruised after a splenectomy, but you’ll be given pain relief medication.

You should be able to eat and drink as normal soon after the operation.

Like any operation, a splenectomy carries a small risk of complications, including bleeding and infection.

Your doctor will run through these risks with you.

You should be given breathing and leg movement exercises to do at home, to reduce your risk of getting a blood clot or a chest infection.

Another risk is the surgical wound becoming infected. If you spot any signs of infection, contact your GP or hospital immediately, as you may need antibiotics.

Recovery usually takes a few weeks. Your doctor or nurse will advise when you can go back to your usual activities, such as driving.

Living without a spleen

If your spleen needs to be removed, other organs such as the liver can take over many of the spleen’s functions.  

This means you will still be able to cope with most infections. However, there is a small risk that a serious infection may develop quickly. This risk will be present for the rest of your life.

Risk of infection

Young children have a higher risk of serious infection than adults, but the risk is still small. The risk is also increased if you have a medical condition such as sickle cell anaemia, coeliac disease or a condition that affects your immune system, such as HIV.

This risk can be minimised by following simple precautions to prevent infection.

Vaccinations

Make sure you have had all your routine childhood vaccinations. You should also be vaccinated against:

Antibiotics

It’s recommended that you take low-dose antibiotics for the rest of your life to prevent bacterial infections. Antibiotics are particularly important:

  • for children under the age of 16
  • for the first two years after your spleen is removed 
  • if your immune system doesn’t work properly

Be alert for signs of infection

Watch out for signs of infection, such as:

  • high temperature (fever)
  • sore throat 
  • cough
  • severe headache 
  • headache with drowsiness or a rash 
  • abdominal pain 
  • redness and swelling around the surgical wound

Your GP can prescribe a course of antibiotics for you to use if you get an infection. You should start taking them at the first sign of an infection, so see your GP as soon as possible.

If your infection becomes serious, you will be admitted to hospital.

Animal and tick bites

Bites from animals and ticks (small blood-sucking parasites) can cause infections.

If you get bitten by an animal, particularly a dog, start your course of antibiotics and seek medical advice urgently.

If you go trekking or camping regularly, you may be at risk of babesiosis, which is a rare disease transmitted by ticks. Try to avoid tick bites by wearing clothes that cover your skin, particularly long trousers. If you become ill, get medical advice straight away.

Telling medical staff about your condition

Healthcare professionals will mark your health records to show that you don’t have a working spleen. However, always remember to tell any medical professionals that you see, including your dentist.

Carry medical ID

It’s a good idea to carry or wear some medical ID. For example:

  • if your spleen is removed, the hospital may give you a splenectomy card to take home with you
  • you may want to buy your own medical ID, such as a MedicAlert or Medi-Tag bracelet or pendant 

If you need help or emergency treatment, your medical ID will alert the staff to your condition.

Travel abroad

If you’re travelling abroad:

  • you may be advised to take a course of antibiotics with you
  • find out if you need an extra meningitis vaccination (types ACWY) 
  • check if you need any travel vaccinations 

People without a working spleen have an increased risk of developing a severe form of malaria. If possible, avoid countries where malaria is present. If you can’t, speak to your GP or local pharmacist about anti-malaria medicine before you travel. You should also use mosquito nets and insect repellent. 

Scars

The scars from your operation will gradually fade.

Hepatosplenomegaly – Gaucher Disease News

Hepatosplenomegaly — a condition where both the liver and spleen are enlarged — is an early and the most common symptom of Gaucher disease. An enlarged spleen is observed in more than 90% of patients and is often the first sign of the disease. In some cases, spleen size may be as much as 15 times larger than normal. This enlargement generally causes abdominal distension and pain. An enlarged liver is seen in 60%–80% of Gaucher disease patients.

Causes of hepatosplenomegaly

Hepatosplenomegaly occurs when Gaucher cells accumulate in the liver and spleen, resulting in an abnormal increase in their size. Gaucher cells contain large amounts of glucocerebroside, a complex lipid molecule that accumulates inside cells due to the beta-glucocerebrosidase enzyme not functioning properly in Gaucher disease patients.

Gaucher cells are predominantly immune cells called macrophages because they engulf and ingest old red and white blood cells, which are sources for large amounts of glucocerebroside.

Management of hepatosplenomegaly

Several treatments for Gaucher disease to help manage hepatosplenomegaly are summarized below.

Enzyme replacement therapy

The most effective treatment that decreases the size of the liver and spleen in Gaucher disease patients is enzyme replacement therapy (ERT). Such therapies approved by the U.S. Food and Drug Administration (FDA) include Cerezyme (imiglucerase), Elelyso (taliglucerase alfa), and VPRIV (velaglucerase alfa). When infused into a patient, the recombinant beta-glucocerebrosidase enzyme enters the patient’s cells and metabolizes glucocerebroside. ERT thus helps to alleviate disease symptoms, including hepatosplenomegaly.

Substrate reduction therapy

When enzyme replacement therapy is ineffective, substrate reduction therapy can be used. These small molecule inhibitors reduce the production of the substrate of the faulty enzyme, glucocerebroside, thus alleviating disease symptoms including hepatosplenomegaly. FDA-approved substrate reduction therapeutics include Cerdelga (eliglustat) and Zavesca (miglustat).

Splenectomy

Before the development of ERT, splenectomy or the surgical removal of the spleen was the main treatment for splenomegaly and severe hypersplenism (overactive spleen). However, splenectomy is now rarely performed in Gaucher disease patients because it may lead to substantial worsening of the disease in other organs. The operation is only performed if patients have severe cytopenia (reduction in the number of mature blood cells) due to splenomegaly and are not responding to ERT.

Liver transplant

A liver transplant can be performed to treat Gaucher disease patients who have complications caused by an enlarged liver such as portal hypertension, where blood flow through the portal vein (the blood vessel that carries blood to the liver) is obstructed because of massive infiltration of Gaucher cells.

***

Gaucher Disease News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

Spleen in dogs and cats.

It is not uncommon for us to encounter problems with the spleen. Sometimes it just enlarges without any major problems, sometimes it twists on itself, sometimes it causes internal bleeding, and oftentimes it becomes cancerous. This page will emphasize cancer of the spleen, called hemangiosarcoma.

A rupturing spleen is a medical emergency requiring immediate veterinary care. These dogs can collapse and go into life-threatening shock. The Long Beach Animal Hospital, staffed with emergency vets, is available until the evenings 7 days per week to help if your pet is having any problems, especially shock, seizures, pain, difficulty breathing, or bleeding.

Think of us as your Long Beach Animal Emergency Center to help when you need us for everything from minor problems to major a major emergency. We serve all of Los Angeles and Orange county with our Animal Emergency Center Long Beach, and are easily accessible to most everyone in southern California via Pacific Coast Hwy or the 405 freeway.

If you have an emergency that can be taken care of by us at the Animal Emergency Hospital Long Beach always call us first (562-434-9966) before coming.  This way our veterinarians can advise you on what to do at home and so that our staff and doctor can prepare for your arrival. To learn more please read our Emergency Services page.

In breeds that have a high incidence of splenic tumor we recommend yearly exams starting at 5 years of age,  with radiographs and ultrasounds to catch this problem early before complications and spread, since the prognosis is poor in most cancerous spleens because they have already spread by the time of diagnosis.

Unfortunately, some pets, especially large breed dogs, will not show any symptoms until the spleen is huge. This occurred with a Labrador Retriever that was presented to us with the owner telling us “he just wasn’t doing right”.  He was eating good, was not vomiting, had no diarrhea, and was not coughing. This owner was astute and brought him in for an exam just in case.

A thorough exam and blood panel revealed no problems, so a radiograph was taken. This radiograph revealed a large abdominal mass. This could have been coming from the liver, spleen, intestines, kidneys, pancreas, or mesenteric lymph nodes. An ultrasound revealed it was from the spleen. The next day we removed an 8 pound rupturing spleen! You can see pictures of the surgery to remove this large mass in the surgery section later in this page, along with pictures of a dog with an even larger spleen!

Graphic surgical photos are on this page, especially of surgery which tends to be bloody.

Nomenclature

We will use some medical terms regarding the spleen:

  • Extra medullary hematopoeisis- The making of red blood cells outside of the bone marrow
  • Reticuloendothelial system- in regards to the spleen, it is the system that recycles red blood cells
  • Anemia- a low amount of red blood cells or hemoglobin
  • Thrombocytopenia- a decrease in thrombocytes, which are an important part of the clotting factors when there is bleeding.
  • Hemoabdomen- free blood in the abdomen
  • Splenomegaly- enlargement of the spleen as a result of any cause
  • Splenectomy- removal of the spleen
  • Hypersplenism- an enlarged spleen that is normal and not causing any problem

Spleen Anatomy

The spleen is an elongated and relatively flat organ that resides in the abdomen of mammals along the outer edge of the stomach. It has a tremendous blood supply that is closely attached to the blood supply supporting the stomach. It is the largest filter of blood in the body.

It has an outer capsule composed of smooth muscle and elastic fibers. The internal part of the spleen (called the parenchyma) has white pulp and red pulp. The white pulp is lymphatic tissue and the red pulp is part of the venous blood system. In between these pulps is elastic tissue that can fill up as needed.

A normal spleen in a cat

A normal spleen in a  small dog

A normal spleen in a medium sized dog

A swollen spleen in a medium sized dog

The blood supply to the spleen is closely adjoined to the stomach. You can see the dark vertical blood vessels in this photo as they enter fat between the stomach and a very enlarged and dark spleen in a semi-circle at the far right.

Physiology

The spleen has many functions. The four primary ones are:

  • Storage of cells
  • Production of red blood cells
  • Filtration of the bloodstream
  • Production of cells for the immune system

Iron that has been recycled from old red blood cells is stored in the spleen where it awaits transport to the bone marrow.

Fortunately, the body can get by without a spleen in most cases, so if there is a serious problem, and all other factors are equal, we will remove it. We tend to remove only spleens that are cancerous, rupturing, or have a torsion.

Diseases

Splenomegaly

Splenomegaly is a generalized term that simply means enlargement of the spleen. In some species, like ferrets, an enlarged spleen can be normal, and is called hypersplenism. A spleen can be enlarged diffusely or it might  have nodules in certain areas.

There are many causes for an enlarged spleen. The most common and important are listed in more detail below. Some of the more uncommon ones are due to infectious agents (erlichiosis, babesia, hemobartonella), FIP, medications, and immune mediated diseases.

This spleen has splenomegaly in addition to numerous nodules

Splenic Torsion

In this problem the spleen twists on itself, compromising the blood supply. When the spleen twists the blood keeps on pumping into it by the arterial system, but this same blood is not able to leave through the venous system, and the spleen becomes grossly engorged.

It can occur on its own, after excessive exercise, or due to trauma. It can occur in conjunction with Gastric Dilatation Volvulus (GDV), also known as bloat. We tend to see this torsion, along with GDV, in large and deep chested breeds.

If the torsion is chronic, there might be no symptoms at all, or there might be:

    • poor appetite (anorexia)
    • weight loss
    • discolored urine
    • vomiting- might be intermittent
    • weakness
    • weight loss.
    • collapse
    • death

Examination of a pet with splenic torsion might reveal:

    • pale mucous membranes (gums)
    • rapid heart rate (tachycardia)
    • painful abdomen
    • a large mass in the abdomen upon palpation
    • fever
    • dehydration
    • jaundice (icterus)

Icterus, also known as jaundice, is a yellow discoloration

A blood panel might reveal:

    • anemia
    • low platelets (thrombocytopenia)
    • elevated white blood cells (leukocytosis),
    • elevated liver enzyme tests,
    • hemoglobin in the urine (hemoglobinuria)

This disease is diagnosed by imaging tests when the above symptoms are present. A radiograph might reveal a mass in the abdomen with the spleen abnormally located. Ultrasound can confirm the problem and give us an idea of its severity.

A splenic torsion is considered an emergency, so the treatment of choice is surgical removal after a pet has been stabilized by treating for shock. On the deep chested breeds we might even tack the stomach to the abdomen to help prevent potential GDV in the future.

Splenic Cancer

Some splenic masses that are cancerous are classified as benign, meaning they do not generally spread (metastasize), and only take up extra space within the abdomen. Even though they do not spread, sometimes this extra space they take up can interfere with other organs.

Some benign cancerous masses include lipoma (fatty tumors), hemagioma (associated with vasculature), and plasmacytosis (infiltration of plasma cells throughout the splenic nodule or tissue in general). Unfortunately, when a spleen has cancer it commonly is the malignant version and not this benign version.

 The most common malignant tumor in the spleen is the hemangiosarcoma (HSA). It is also called malignant hemangioendothelioma). The cause is not known. It can spread to many different organs, making it highly malignant:

      • heart
      • lungs
      • muscle
      • skin
      • bones
      • abdomen
      • diaphragm
      • brain
      • kidney

HSA can also cause complications, such as disruption of the coagulation cascade which causes a mixture of abnormal clot formation as well as inability to control internal bleeding (known as disseminated intravascular coagulation, DIC).

Symptoms of HSA vary, and range from mild to severe. In extreme cases sudden blood loss can lead to sudden death.

These large nodules on this spleen are a malignant cancer called hemangiosarcoma

Another common type of malignant splenic cancer is lymphosarcoma, a type of cancer that can have a primary tumor in any other organ (i.e. lung, gastrointestinal tract, liver). Lymphosarcoma is one of the more common tumor types observed in the spleen of cats. Sometimes the tumor within the spleen is not even the primary tumor, but rather a single nodule or multiple nodules due to metastasis from a distant primary tumor.

Hematoma

Hematomas are one of the most common causes of an enlarged spleen in dogs, representing over 50% of splenomegaly cases. This type of splenic mass is basically an accumulation of pooled blood within the splenic tissue; many stop growing and are then resorbed after a period of time, but others grow exponentially and eventually rupture. A ruptured hematoma originating from the spleen is an emergency, and often the pet experiences an acute collapsing episode followed by a significant loss of blood into the abdomen (hemoabdomen). You can see the surgery of a dog with an 8 pound hematoma later in this page

Other causes

Congestions of the spleen can occur from iatrogenic causes, which are those associated with administration of certain drugs (i.e. anesthetic agents or tranquilizers). Congestion can also occur due to increased blood pressure within the vasculature of the liver (known as portal hypertension), which can occur secondary to congestive heat failure among others.  The spleen can over-react to particular conditions, resulting in a disease process known as hyperplastic, or reactive, splenomegaly. A spleen can become reactive when there is excessive stimulation of the immune system from conditions such as immune-mediated disease, bacterial infections, tick-borne diseases, and many more.

This spleen has a laceration

Diagnosis

Signalment

Dogs, cats, and ferrets can get splenic diseases, although it is much more of a problem in dogs. Splenomegaly itself can occur in most any age due to the numerous causes of the condition. For instance, if the cause of splenic enlargement is infectious, then the pet may be quite young. However, if the enlargement is cancerous, the pet tends to be middle aged (average 10 years in dogs). Due to the wide range of causes, there is no known gender predilection (males tend to be affected equally as often as females). Certain disease processes tend to be over-represented by specific breeds:

Splenic torsion tends to occur in large breed, deep-chested dogs:

Splenic tumors like HSA tend to occur in several breeds. It can be some common in some breeds that we  recommend physical exams, blood work, abdominal radiographs, and especially abdominal ultrasounds, yearly in these dogs as they reach 5 years of age:

    • German Shepherds
    • Golden Retrievers
    • Portugese Water Dogs
    • Boxers
    • English setters
    • English pointers
    • Great Danes
    • Skye Terriers
    • Bernese Mountain Dogs
History

In many cases, a patient with splenic disease has very little or no specific clinical signs. Observations made by owners at home might include non-specific indicators of illness:

    • lethargy
    • inappetence
    • weight loss
    • diarrhea
    • vomiting
    • collapse
    • discolored urine
    • abdominal distention
Physical Exam

Upon palpation of the abdomen, significant abnormalities of the spleen can usually be detected, especially when a large mass is present within the cranial aspect of the abdomen (toward the chest). However, a mass or enlarged organ in the cranial abdomen cannot always be differentiated from a mass or enlargement of the liver. In some cases, decreased pallor (pale gums) can be a sign of anemia or shock, which in combination with an abdominal mass can indicate a ruptured splenic mass or torsion. We confirm this with an ultrasound before surgery.

If the gums are pale, certain diseases of the spleen may lead to free blood in the abdomen, which can sometimes but not always be detected by palpation of a fluid wave. Other generalized signs might include weakness, fever, dehydration, poor pulses, increased heart rate (tachycardia), increased bleeding at site of blood draw (due to coagulopathy), and/or increased size of peripheral lymph nodes.

Diagnostic Tests

Some diagnostic tests which provide significant information include radiographs, blood work, ultrasonography, evaluation of the cells (cytology) through a fine-needle aspirate sample, and surgical exploration.

Radiography

The arrow points to what a spleen looks like on a radiograph. It is enlarged, although a lobe of the liver can easily overlap the spleen and make the spleen look enlarged. So in this case, technically its called hepatosplenomegaly.

Here is a dog with an enlarged spleen. Can you see it?

The red circle delineates the enlarged spleen.

L.I. – Large Intestine

Pr- Prostate

Blood Panel

Blood work (clinical chemistry and complete blood counts) is a crucial component for detection of compromised organ function. Splenic involvement might reveal anemia (decreased red blood cells), thrombocytopenia (decreased platelets for clotting), leukopenia (decreased white blood cells) and reticulocytosis (increased immature red blood cells to indicate that the body is trying to compensate for the loss of mature red blood cells).

This is a blood panel that might be seen with splenic disease, although many other diseases can also cause this type of blood panel. The primary problem in this blood panel is anemia.

Fluid Analysis

If abdominal fluid is present we can remove it and analyze it. This is called abdominocentesis. There is no guarantee this will make a diagnosis since many cancers, including HSA, might not be found in this fluid.

Ultrasonography

Ultrasonography has revolutionized diagnosis in animals, and prevented many unnecessary exploratory surgeries (called celiotomies or laparotomies), while at the same time alerted us to the fact that we need to do immediate surgery. Keep in mind, our patients do not talk to us, and  an enlarging tumor in the abdomen in one of us humanoids would be uncomfortable, and cause us to seek medical care long before we see a dog or cat with a tumor growing in the abdomen.

Ultrasonography of the abdomen is an important modality for diagnosis of splenic disease because of its sensitivity to changes of organ size, shape, location, and even texture. An ultrasonographic examination in combination with radiographs provides a comprehensive understanding of which organs are involved and often helps to narrow the possibilities down to a select few differentials.

We use ultrasound to confirm our suspicions of a splenic tumor based on the breed, history, exam findings, and blood panels and radiographs. Ultrasound confirms the diagnosis, lets us know if the spleen is already rupturing, tells us the size of the spleen, and if there are any other internal organ problems. A critical component of the ultrasonographic exam in HSA is echocardiography (evaluation of the heart). A key site of metastasis associated with hemangiosarcoma is the right atrium. HSA that has spread to the right atrium of the heart is a serious sign, and the prognosis is not good. This is important information if we are thinking of surgical removal of the spleen.

The lines demarcate the margins of this spleen

Do you see the spleen in this picture without the demarcation?

A typical ultrasound report on a dog with a cancerous spleen

This ultrasound of the heart (echocardiogram) shows spread of the tumor to the right atrium, which is a poor prognosis

RV- Right ventricle

RA- Right atrium

Cytology

Aspiration of the cells in an organ for cytological exam by a pathologist is an important part of most abdominal ultrasounds. It helps prevent an exploratory surgery, and can lead to a diagnosis in many cases. Cytologic evaluation of splenic problems is not always indicated and can sometimes be contraindicated depending on certain disease processes. Certain cancers of the spleen as well as hematomas may result in significant blood loss if stuck with a needle due their fragile nature. Even though the ultrasound guides the biopsy location, if the disease process only involves a small portion of the splenic tissue, or is sporadically located throughout, then a small needle-sized sample may not obtain the affected tissue at all.

ECG (Electrocardiogram)

This tests the electrical activity of the heart. I some HSA’s there will be an arrhythmia

Definitive Diagnosis

Histopathology is the analysis of the spleen after it is removed. This gives us our final diagnosis.

Histopathology

Treatment

Surgery is a common treatment for splenic disease. This is called a splenectomy. If there is trauma or a problem in only a small part of the spleen, we might do a partial splenectomy since we always want to preserve as much function of the spleen as possible. This partial splenectomy is not common.

We do the surgery to remove the tumor, and if malignant add chemotherapy to help prevent spread after we do the surgery. Prior to surgery we do an ultrasound of the heart as already mentioned, and also take chest radiographs to check for spread of a tumor. We also perform a clotting panel since blood loss is common in this surgery and we do not want post operative bleeding.
Unfortunately, survival time for dogs and cats with surgery alonge HSA is only 1-3 months, with most dogs dying due to spread of the HSA to other organs, causing these organs to malfunction. This emphasizes the need for an early diagnosis in the breeds prone to this cancer.

Dogs that have surgery to remove the spleen, and that are also treated with chemotherapy, might survive up to 9 months. This depends on whether the tumor has spread, and again emphasizes the need for an early diagnosis. Dogs and cats have less side effects than people on chemotherapy, and their quality of life is high if this therapy is instituted immediately after surgery.

Dogs that are diagnosed at a young age, have had the HSA rupture prior to surgery, have evidence of spread to other organs when the splenectomy is performed, or have a more aggressive grade of tumor, do not tend to live 9 months after surgery.

The primary chemotherapy drug for HSA is Adriamycin (doxorubicin). It will slow the disease process, but it will not cure your pet of this disease. The doctors at the Veterinary Cancer Group in Tustin institute this therapy.

If a pet is anemic, or we anticipate significant blood loss during surgery, we will give a blood transfusion prior to surgery or during the procedure. Post operatively if a pet is not doing well we will give a blood transfusion also.

After doing a cross match to ensure compatibility we obtain whole blood for the transfusion

Splenectomy

A splenectomy is performed to treat and sometimes cure this problem. It is sometimes done as an emergency procedure if the spleen has ruptured and there is significant internal bleeding.

Pre-anesthetic preparation is important in every surgery we perform, no matter how routine, because surgery is not an area to cut corners.  Once a pet is anesthetized, prepared for surgery, and had its monitoring equipment hooked up and reading accurately, the surgery can begin.

This is a sterile abdominal surgery, and our surgeons scrubs with a special antiseptic soap prior to gowning and gloving

While our patient is being anesthetized our surgeon is already in our surgical suite setting up instruments. Our surgeon is ready to start before our patient is at a proper plane of anesthesia. Once the anesthetist gives the green light the surgery starts immediately. We want our surgeon waiting for his patient, not the other way around.  All of this is to minimize anesthetic time.

We keep a close tab on important physiologic parameters for all of our surgeries. Monitors like this give us an early warning of an impending problem.

This machine monitors:

Temperature
Heart Rate
Heart rhythm
Oxygen saturation
Carbon dioxide level
Respiratory rate

In addition to our monitoring equipment our anesthetist stays “hands on” in monitoring important physiologic parameters.  In addition to our monitoring equipment our anesthetist stays “hands on” in monitoring important physiologic parameters. Our anesthetist is using a special stethoscope (esophageal), that is passed down the esophagus and lays right over the heart. This gives us a clear sound of the heart and how it is beating.

To minimize anesthetic time we routinely have 2 doctors working as a team performing the splenectomy.  They work together as a well orchestrated team.Our patient is under anesthesia and our surgeons are completing the draping process while our anesthetist is adjusting the surgical lights.

By working together early in the surgery we minimize anesthetic time.

For a pet that might already be anemic it is important to minimize blood loss during surgery. Special care is taken on entering the abdomen to minimize loss. There is minimal bleeding at this point as our surgeon gently dissects the sub Q (subcutaneous) tissue just under the skin.

As the surgery progresses we sometimes encounter significant bleeding from blood vessels in the sub Q fat and from muscles that are cut. All of them are clamped or cauterized before proceeding further. For a pet that might already be anemic this added blood loss is important to control, and it is stopped immediately.

When all bleeders are under control (called hemostasis) we enter the abdomen. We make our incision at a specific spot in the abdominal muscles called the linea alba. It is at this spot that there are minimal blood vessels. The linea also has strong tendinous attachments to the muscle, so when we sew it back together these tendons attachments have more holding ability than the abdominal muscles alone. This will prevent a hernia.

Our first view of the spleen once we have entered the abdomen. It is the round and reddish structure at the top of the abdominal opening and just to the left of our surgeon’s finger.

A spleen that is not healthy is friable and can easily rupture when handled. Our surgeon has to gently coax it out to prevent  this from happening.

Once it is finally exteriorized the problem is obvious. At this point we do not know if it is cancerous or not. We do know it is in the process of rupturing and glad we are getting it out now.

Now that we have it ready for removal we have to ligate its blood supply. As you remember from your surgical anatomy above the blood vessels to the spleen are closely related stomach. It is important to ligate the blood supply very close to the spleen so as not to compromise the blood supply to the stomach, leading to serious consequences.

This blood supply can be surrounded by fat. We have to isolate segments before we ligate.

In the center of this picture you can see one blood vessel that is already ligated. On the right our surgeon is in the process of ligating another blood vessel.

We have completed 3 ligations at this point, with many more to go.

Our surgeons work simultaneously, each starting at a different end of the spleen, so they can complete this tedious part of the surgery sooner. Its all about secure ligation of these blood vessels and minimal anesthetic time.

As part of the natural healing process there is a tissue in the abdomen called omentum. It is like a net, and surrounds an organ that might be diseased. For example, a ruptured intestine that is leaking intestinal fluid (extremely irritating to the abdomen and will cause a peritonitis), will have this net surround the intestine to wall off the leak.

In the case of this rupturing spleen the omentum covered the spleen to help prevent further blood loss. These are clots on the omentum from that. At this point in time during the surgery we cannot determine for sure if these are clots or spread of tumor. The report from the pathologist will tell us for sure. It turns out that this time they are clots.

When the spleen is completely removed we complete our exploratory surgery by checking the other internal organs, especially the liver. Once this check is complete we suture the muscle layer (the linea alba) closed. Again, we work as a team, with each surgeon (they are both lefties) suturing the linea until they meet in the center.

Once we have finished suturing our patient, who is already on a pain patch (Duragesic or Fentanyl patch- which is removed in 3 days), is given an additional pain injection and carefully monitored post-operatively. As part of the monitoring we perform a simple blood panel to make sure there was no problem with blood loss during surgery. If the blood loss is significant we will give a blood transfusion with the blood we have already set aside specifically for this patient.

Post operatively we take radiographs of the chest and perform and ultrasound every 2 months for cases of HSA looking for distant and local metastasis.

Occasionally we come across a spleen that is so large it is hard to believe it can get this big. The following spleen was over 8 pounds, removed for a 65 pound labrador named Jake.  Dr. P and Dr. R had to do this one together.  Removing it was like delivering a baby!

The size was obvious as soon as we entered the abdomen. At this point in time we were not sure if it was a boy or a girl! Dr. P is coaxing it out of the abdomen at the beginning of the surgery, being very careful not to rupture it.

We had to be very gentle  because it was quite delicate(friable) and already rupturing

Ligating the blood vessels to the spleen was more difficult than usual because of the size, scar tissue, and omental tissue that covered the rupturing spleen

It turns out that this was a hematoma and the dog did fine for several more years. Lucky this spleen did not rupture before the surgery.  Most likely, with a hematoma this large, death would have ensued rapidly.

We also took out a spleen with a large hematoma on this dog named Colt that weighed 14 pounds

You can learn all the details of this case, and see his surgery, by following this Had to make it live for you to see it. spleen hematoma link. Its a case study and very informative, with lots of cool pictures.

Ancillary Treatment

After surgery we will consult with the oncologists at the Veterinary Cancer Group for further treatment

Post Surgical Treatment

Prognosis

A successful outcome from surgery depends on what disease process is present and how long it has been present.

Splenic Hematoma- good

Splenic Torsion- good

Hemangiosarcoma – guarded to poor.

Return to Canine Diseases Page.

Can mononucleosis damage the liver? : Nursing2021

I recently cared for a 36-year-old man with jaundice and lymphadenopathy whose liver enzymes were elevated. Later, he was diagnosed with mononucleosis. I thought this disease affected the spleen. Can it affect the liver too?—D.C., CALIF.

Clinical Queries. Terry J. Jenkins is a post-master’s graduate student at Vanderbilt University School of Nursing.

SELECTED REFERENCE


Tierney L, et al. Current Medical Diagnosis and Treatment. New York, N.Y., Lange Medical Books, 2005.

Biliary Atresia | Symptoms and Treatment

What Causes Biliary Atresia?

The causes of biliary atresia are not completely understood. For some children, biliary atresia may occur because the bile ducts did not form properly during pregnancy. For other children with biliary atresia, the bile ducts may be damaged by the body’s immune system in response to a viral infection acquired after birth.

Who Is at Risk for Biliary Atresia?

Biliary atresia is a rare disorder. About one in 15,000 to 20,000 babies do not have complete bile ducts.

Biliary atresia seems to affect girls more than boys. Within the same family, it is common for only one child in a pair of twins or only one child within the same family to have the disease. Asians and African-Americans are affected more frequently than Caucasians.

There does not appear to be any link to medications taken during pregnancy.

Do Children with Biliary Atresia Have Other Associated Abnormalities?

Ten to 15 percent of infants with biliary atresia may be born with other problems in the:

  • Heart
  • Spleen (polysplenia)
  • Blood vessels (inferior vena caval anomalies, preduodenal portal vein)
  • Intestine (situs inversus or malrotation)

What Are the Symptoms of Biliary Atresia?

Babies with biliary atresia usually appear healthy when they are born. Symptoms of the disease typically appear within the first two weeks to two months of life. Symptoms include:

  • Jaundice a yellow coloring of the skin and eyes due to a very high level of bilirubin (bile pigment) in the bloodstream.
    Jaundice caused by an immature liver is common in newborns. It usually goes away within the first week to 10 days of life. A baby with biliary atresia usually appears normal at birth, but develops jaundice at two or three weeks after birth.
  • Dark urine caused by the buildup of bilirubin (a breakdown product from hemoglobin) in the blood. The bilirubin is then filtered by the kidney and removed in the urine.
  • Acholic stools (white or clay-colored stools) because no bile or bilirubin coloring is being emptied into the intestine. Bile gives stool its green or brown color, and without such, stool is without color (often white or gray).
  • Weight loss and irritability develop when the level of jaundice increases.

How Is Biliary Atresia Diagnosed?

Jaundice may be present with other liver disorders, so several tests are needed to get the correct diagnosis.

  • Blood tests are done to tell if there are liver function abnormalities. They may also identify the cause (etiology) of jaundice.
  • X-rays of the abdomen look for an enlarged liver and spleen.
  • An abdominal ultrasound can tell if there is a small gall bladder or none at all. The gall bladder is the organ that stores bile. If this organ is missing or absent since birth, that often indicates biliary atresia.
  • A liver biopsy tells if an infant is likely to have biliary atresia. In a liver biopsy, a tiny sample of the liver is removed with a needle. That sample is then looked at under a microscope. A liver biopsy is very reliable. If the biopsy shows that the infant probably has biliary atresia, further surgery will confirm the diagnosis and treat the condition.
  • Diagnostic surgery confirms if an infant has biliary atresia. Surgery allows doctors to see if there is an injured piece of the bile ducts going from the liver to the intestine. This could prevent normal bile flow from the liver.
  • An operative cholangiogram is done during the surgery to confirm the diagnosis of biliary atresia.

A cholangiogram is a procedure done at time of operation. This procedure involves a dye that is injected through the gall bladder and goes through the bile ducts. An X-ray is done to learn if the dye flows normally into the intestine and the liver. In infants with biliary atresia, the dye does not usually flow out of the gall bladder due to the blocked ducts.

If the ducts are normal or open (patent) and the dye flows the way it should, biliary atresia is ruled out. A bigger liver biopsy (tissue sample) is then done to find the cause of the liver disorder.

Biliary atresia is diagnosed when the cholangiogram shows that the bile ducts are not open. Then infants usually undergo an operation called the Kasai procedure.

How Is Biliary Atresia Treated?

Biliary atresia cannot be treated with medication. A Kasai procedure (also known as a or hepatoportoenterostomy) is done. The Kasai procedure is an operation to re-establish bile flow from the liver into the intestine. It is named after the surgeon who developed it.

The surgeon removes the damaged ducts outside of the liver (called extrahepatic ducts) and identifies smaller ducts that are still open and draining bile. The surgeon then attaches a loop of intestine to this portion of the liver, so that bile can flow directly from the remaining healthy bile ducts into the intestine.

After this procedure, infants are usually in the hospital for seven to 10 days to heal. Long-term antibiotic therapy is given to reduce the risk of infection, and additional medications may be used to promote bile flow and maximize the success of the operation

With an experienced surgeon, the Kasai procedure is successful in 60 to 85 percent of the patients. This means that bile drains from the liver and the jaundice level goes down.

The Kasai procedure is not a cure for biliary atresia, but it does allow babies to grow and have fairly good health for several, sometimes for many years. About 25% of patients who undergo a Kasai procedure do not go on to require a liver transplant.

In 15-40 percent of patients the Kasai procedure does not work. If this is the case, liver transplantation can correct this problem.

Success with the Kasai procedure is related to:

  • Age. The younger an infant at the time of surgery, the more likely the surgery will be successful. By the time an infant is older than about 3 to 4 months old, surgery is unlikely to be helpful.
  • Extent of cirrhosis (scarring and damage to liver tissue) at the time of surgery.
  • The number and size of microscopic ducts in the scarred tissue that can drain bile.
  • The nutritional status of the baby at time of transplant (sufficient vitamins, high calorie diet)
Nutrition and Biliary Atresia

Children with liver disease have a faster metabolism than healthy children. This means that children with biliary atresia may require more calories.

A child with biliary atresia and jaundice cannot properly digest fats. This is because not enough bile gets to the intestine. Due to liver damage, there may also be a loss of vitamins and protein.
Guidelines from your doctor for your child’s nutrition may include:

  • A well-balanced diet, consisting of three meals a day plus small snacks in between meals
  • Vitamin supplements (Specifically Vitamins A, D, E, and K as these are absorbed in fat, and children with biliary atresia cannot absorb these well)
  • Adding medium-chain triglyceride (MCT) oil to foods and liquids or infant formulas. MCT adds extra calories that will help your child grow.
  • High-calorie liquid feedings may be recommended if your child is too ill to eat normally. Feedings are given through a special tube (nasogastric tube) that is placed in the nose and guided down the esophagus and into the stomach.

Although digestion may return to normal after surgery, extra vitamins or MCT oil may be needed.

What Are the Complications of Biliary Atresia and What Can Be Done for Them?

Complications right after surgery are low. Most problems that develop are due to progression of the liver disease.

  • After the Kasai procedure, it is common to get an infection in the bile ducts. This is usually treated using intravenous antibiotics. Treatment may continue with oral antibiotics.
  • Jaundice or itching may occur. These can often be treated successfully with medications such as cholestyramine and ursodeoxycholic acid (for itching).
  • Many patients with cirrhosis have changes in blood flow through the liver and intestines. These changes may produce problems such as easy bruising of the skin, nosebleeds, retention of body fluid and enlarged veins (varices) in the stomach and esophagus.

Increased pressure in these veins can cause a sudden and large amount of bleeding in the stomach and intestines. Although this can be a very serious complication, with prompt and experienced medical care, bleeding can usually be stopped.  Sometimes that requires specialized procedures in which a hardening (sclerosing) agent is injected into the abnormal vessels.

  • If retention of body fluid occurs, it can be treated with diuretics (medicine that helps remove excess water from the body).

As the disease gets worse, other complications of cirrhosis may also occur.

What Is the Long-Term Outlook?

Long-term survival after the Kasai procedure is affected by the presence of progressive liver disease (cirrhosis) and the development of portal hypertension (high blood pressure in the portal vein that carries blood to the liver).

Nearly half of all infants who have had a Kasai procedure require liver transplantation before age 5. Older children may continue to have good bile drainage and no jaundice.

Some children may develop portal hypertension and have gastrointestinal bleeding, accumulation of fluid in the abdomen (ascites) and enlargement of the spleen (hypersplenism).

Eighty-five percent of all children who have biliary atresia will need to have a liver transplant before they are 20 years old. The remaining 15 percent have some degree of liver disease. Their disease can be managed without having a transplant.

Liver Transplant

If there is still not enough bile flow with the Kasai procedure, ultimately, liver transplantation will be considered. A liver transplant operation removes the damaged liver and replaces it with a new liver from a donor.

After a transplant, ongoing lifelong care is required. Frequent contact with physicians and other members of the transplant team is also necessary.

Treatment of secondary iron overload syndrome St. Petersburg

Early detection and treatment of secondary iron overload syndrome in patients with chronic liver disease prevents the progression of liver disease to cirrhotic stage and significantly reduces the risk of liver cancer. We successfully treat patients with obesity and non-alcoholic fatty hepatosis (non-alcoholic fatty liver disease) and chronic hepatitis C in combination with secondary iron overload syndrome.

The center’s gastroenterologists have created an author’s method of identifying and treating secondary overload syndrome in patients with chronic liver diseases. Our gastroenterologists share their experience in scientific and practical seminars and in scientific articles.

Treatments for secondary iron overload syndrome in chronic liver disease include :

  • treatment of the underlying disease;
  • 90,011 strict abstinence from alcohol;

  • adherence to a diet with limited iron content to 8-10 mg / day.;
  • therapeutic phlebotomy in the absence of contraindications;
  • use of antioxidants.

Specializes in the diagnosis and treatment of secondary iron overload syndrome in patients with chronic diseases in our center, Candidate of Medical Sciences, Associate Professor of the Department of Hospital Therapy, St. Petersburg State Medical University. Academician I.P. Pavlova, hepatologist Mekhtieva Olga Alexandrovna .

Once diagnosed with iron overload syndrome, treatment options are fairly straightforward for most people.However, without treatment for this condition, life-threatening damage to organs and tissues, especially the liver, can develop. Thus, it is important to detect iron overload before organ and tissue damage due to iron accumulation occurs.

There are a number of laboratory tests that are used to detect iron overload. These are, first of all, the level of ferritin and the percentage of saturation of transferrin with iron in the blood serum. All patients with elevated values ​​of these indicators should undergo genetic testing to exclude the primary syndrome of iron overload – hereditary hemochromatosis.All tests for the diagnosis of iron overload syndrome can be taken in our center.

The patient will receive

as a result of treatment

  1. No symptoms and improved quality of life.
  2. Prevention of complications and improvement of well-being.
  3. Normalization of laboratory analysis indicators.
  4. Elimination of risk factors for the development of dangerous diseases.
Tips and Tricks

With iron overload syndrome, it will help to reduce the amount of excess iron in the liver diet with limited intake of iron .

Diet with iron overload

Increased bilirubin: causes, consequences, treatment

Bilirubin is a bile pigment that is formed during the breakdown of hemoglobin, or rather
heme – an iron-containing protein in the composition of hemoglobin contained in erythrocytes.
In an adult, about 1-2×10 11 erythrocytes are destroyed during the day.

Basically, the breakdown of red blood cells occurs in the spleen, bone marrow and, to a lesser extent, in the liver.In the process of destruction of the erythrocyte, hemoglobin is released, which further breaks down into heme and globin. After a series of transformations, biliverdin (a yellow pigment) is formed from heme, and subsequently the red-yellow pigment bilirubin. This chain of chemical reactions can be seen by observing the change in the color of the hematoma (bruise): depending on the stages of the decay of the heme, the bruise changes color several times – it “fades”. From the spleen, bilirubin is transported by the blood protein albumin to the liver. This fraction of bilirubin (in conjunction with albumin) is called indirect (free or unconjugated).So biliburin enters the liver, where it binds with glucuronic acids and enters bile. This fraction of bilirubin is called direct (conjugated). With bile, conjugated bilirubin enters the intestinal lumen, where, with the participation of intestinal microflora, it turns into a colorless pigment urobilinogen, part of which is excreted in the feces, and part is absorbed back into the blood and excreted in urine. Intestinal urobilinogen under the influence of intestinal microflora turns into stercobilin – a brown pigment.

With premature pathological destruction of erythrocytes, impaired binding of bilirubin with glucuronic acids or the release of bilirubin from the liver into the intestines, jaundice can be observed – staining of the skin and mucous membranes in yellow.

Norms of bilirubin 4 :

Normal indicators of total serum bilirubin are 3.4–20.4 μmol / L , indirect bilirubin – up to 6.5 μmol / L 1, direct – up to 5.1 μmol / L .
Jaundice can be observed with bilirubin values ​​at the level of 40–70 µmol / L .

An increase in the level of bilirubin in the blood is medically called hyperbilirubinemia. It is important for the doctor to know which fraction of bilirubin is increased, as this can play a decisive role in the diagnosis.

There are several types of jaundice 1 :

Suprahepatic jaundice develops with accelerated massive pathological destruction of erythrocytes and is manifested, as a rule, by anemia.The breakdown of erythrocytes can be associated, for example, with a defect in the erythrocyte membrane6, with the development of an infectious disease7, with transfusion of incompatible blood groups, etc. An increase in the fraction of indirect bilirubin is observed.

Hepatic (hepatocellular or parenchymal) jaundice is associated with damage to liver cells, which leads to the inability of liver cells to both bind bilirubin from the blood and release bilirubin bound to glucuronic acids into bile.Among the causes of hepatic jaundice are viral hepatitis, toxic liver damage, including medicinal, primary biliary cirrhosis, etc. In this case, hyperbilirubinemia is observed due to both (indirect and direct) fractions of bilirubin.

Subhepatic jaundice , as a rule, is associated with a violation of the discharge of bile from the liver into the intestine along the biliary tract. Obstruction or a sharp narrowing of the lumen of the biliary tract, for example, a stone, a tumor of the head of the pancreas, tumor metastases, can lead to the development of subhepatic jaundice.With a complete blockage, bilirubin does not enter the intestines, while it is completely absorbed into the blood. The concentration of direct bilirubin in the blood can be significantly higher than normal.

Especially often diagnosed in premature babies 3 , however, according to some data, it is observed in 60% of full-term babies 9 . The symptoms of jaundice usually appear on the 2nd day from birth and persist up to 3 weeks in premature babies and up to 2 weeks in full-term babies 3 . It is worth noting that prolonged jaundice may indicate the development of certain diseases, for example, thyroid pathology (secondary hypothyroidism) 5 or infectious diseases 3 .

Normally, with neonatal jaundice, the concentration of bilirubin in the blood does not exceed 205 μmol / l 3 . When the level of free (indirect) bilirubin exceeds 340 mmol / L, there is a risk of developing bilirubin encephalopathy, since indirect bilirubin is able to penetrate the blood-neophal barrier and have a toxic effect on the brain 1 . According to other sources, the concentration of bilirubin above 250 μmol / l can already lead to the development of deafness, cerebral palsy, seizures and mental retardation 3 .In order to diagnose pathology in a timely manner, doctors monitor the condition of newborns, assess the dynamics of symptoms and, if necessary, take urgent measures to reduce the level of bilirubin. Early diagnosis and timely treatment of neonatal jaundice in children contribute to the prevention of the development of bilirubin encephalopathy 8 .

Diagnosis of elevated bilirubin:
analyzes and results

The concentration of total, direct and indirect bilirubin is assessed by a biochemical blood test.The most common and widely used for the quantitative determination of total and direct bilirubin are chemical colorimetric and spectrophotometric methods. The use of non-invasive (percutaneous) methods for determining bilirubin is relevant, since in comparison with the usual invasive method it helps to avoid punctures and possible infection 8.9 .

With the development of hepatic and subhepatic jaundice, darkening of urine may be observed, and feces, on the contrary, may become less colored and even colorless, which is explained by an increase in the level of urobilin and conjugated bilirubin in urine and the absence of urobilinogen in feces 1 .

Since an increase in bilirubin is usually a symptom of a certain disease, the first step is to determine the cause of hyperbilirubinemia. Hyperbilirubinemia can be a symptom of cytolysis 2 (damage and destruction of liver cells) and hepatocellular failure syndrome 2 (liver dysfunction). In addition to specific treatment aimed at eliminating the cause of hyperbilirubinemia (for example, antiviral drugs in the treatment of hepatitis C or surgical treatment if a tumor or metastases is detected), pathogenetic therapy can be used: for example, in newborns, phototherapy is used in the treatment of jaundice to remove bilirubin from the skin, since under the influence of ultraviolet radiation, the pigment is destroyed.

If the cause of hyperbilirubinemia is a liver disease (for example, in chronic hepatitis, cirrhosis), essential phospholipid preparations can be used as part of the complex therapy of these diseases, which help restore liver cells 10 .

Date of publication of the material: November 17, 2020

MAT-RU-2003445-1.00-11 / 2020

90,000 5 products useful for the liver – Rossiyskaya Gazeta

The liver is often called the main “filter” and “chemical laboratory” of the body.Its most important function is to neutralize and remove harmful substances from the body. But this organ not only helps to get rid of toxins, but itself needs our support. One of the important points of such help is proper nutrition.

Medical Daily named five types of foods that are good for liver health.

1. Garlic. This vegetable helps the liver activate enzymes that help flush out toxins. In addition, it is rich in compounds like allicin and selenium, which help in cleansing the liver.Allicin has antioxidant, antibiotic and antifungal properties, and selenium, in turn, enhances the effect of antioxidants.

However, it is worth remembering that this vegetable has its own contraindications. For example, it is not recommended for gastritis, stomach and duodenal ulcers, as well as other diseases of the digestive system.

2. Coffee. Scientists have found that this drink can reduce the risk of liver disease. One study found that two extra cups of coffee a day were associated with a 44 percent reduction in the risk of developing cirrhosis and an almost 50 percent reduction in the risk of dying from cirrhosis.In addition, the coffee drink may have a protective effect against non-alcoholic fatty liver disease.

3. Avocado. This overseas “superfruit” can also be very beneficial for the liver. Its inclusion in the diet promotes the production of an antioxidant called glutathione, which is needed to filter out harmful substances from the liver and protect organ cells from damage. Avocados are rich in vitamins C and E, which neutralize free radicals. In addition, the fruit has anti-inflammatory properties that also support liver health.

4. Turmeric. Researchers believe this spice can help reduce free radical damage. In addition, turmeric helps the body metabolize fats and stimulate bile production and supports natural liver cleansing.

5. Grapefruit. Not only does it taste good, it also helps prevent liver damage. Drinking grapefruit juice helps the liver eliminate carcinogens and toxins. This fruit is also rich in vitamin C and antioxidants. However, grapefruit is contraindicated in people with liver failure.

90,000 Patients with Gilbert’s syndrome: a new management approach

Authors:
M.B. Shcherbinina

M.B. Shcherbinina, MD, Professor, Medical Center for Outpatient Services for Children and Adults, Dnepropetrovsk

In 1900, Nicolas Auguste Gilbert described congenital benign jaundice, which was later named after him – Gilbert’s disease or syndrome (SG).This is one of the most common variants of functional (non-hemolytic) hyperbilirubinemia. SJ accompanies a person all his life, falling into the field of vision of doctors of various specialties. The management of such patients usually raises many questions. Previously, it was assumed that SF does not have adverse health effects and does not require treatment. However, in recent years, many new things have appeared in the concept of the disease. We would like to consider this through examples of clinical analysis of patients.

Clinical case No. 1
A woman, 23 years old, complained of the appearance of jaundice against the background of ARVI and taking a combined drug used for the treatment of colds for 2 days. The drug includes paracetamol, the total dose of which was 4 g / day.
Prior to this, the patient had no episodes of jaundice. She considered herself healthy.
Does not abuse alcohol. I do not smoke. From the hereditary history it was possible to find out that the paternal grandfather periodically developed jaundice, which the family spoke of as “non-contagious jaundice.”
Normosthenic physique. Body mass index (BMI) 22.4 kg / m 2 . The skin is subicteric, the sclera and oral mucosa are icteric.
The abdomen is soft, painless on palpation. The edge of the liver is 1 cm below the costal arch along the mid-clavicular line, painless, elastic. The spleen is not palpable.
In the research results, an increase in total (78.2 μmol / l) and indirect bilirubin (61.6 μmol / l), ALT (54 IU). Other indicators of the general analysis of blood and hepatic complex are not changed.

Clinical case No. 2
A man, 27 years old, complained of severity, recurrent pain in the right hypochondrium after taking alcohol, fatty and / or fried foods, increased fatigue.
Considers himself ill for 10 years, when, after intense sports training, he began to notice yellowing of the sclera, drowsiness, severe weakness. SJ was first established in 2004
Alcohol is not abused. I do not smoke. Hereditary history is not burdened.
Asthenized. The physique is hyposthenic. BMI 20.6 kg / m 2 . Skin, sclera and oral mucosa with slight yellowness.
On palpation of the abdomen – pain in the right hypochondrium. The boundaries of the liver are normal. The spleen is not palpable.
The research results show an increase in total (52.4 μmol / l) and indirect bilirubin (41.3 μmol / l). Other indicators of the general analysis of blood and hepatic complex are not changed.

Clinical case No. 3
A man, 31 years old, presented with a dull, almost constant pain in the right hypochondrium, worsening after eating, a feeling of bitterness in the mouth, severe weakness.
Suffers from hemolytic anemia. The diagnosis was established at the age of 18 based on the results of sternal puncture, a positive Coombs’ reaction, an increase in the level of reticulocytes in the peripheral blood. Hormone therapy courses were prescribed periodically. Deterioration of well-being is noted after severe stress. Hyperbilirubinemia due to indirect bilirubin was not adequately corrected with corticosteroids.
Does not abuse alcohol. I do not smoke. Hereditary history is not burdened.
Normosthenic constitution, BMI 23.8 kg / m 2 .The skin is subicteric, the sclera and oral mucosa are icteric. The abdomen is soft, painful in the right hypochondrium, the edge of the liver is 2 cm below the costal arch along the mid-clavicular line, painful, indurated. An enlarged spleen is palpated.
Esophagogastroduodenoscopy: signs of anemia of the gastric mucosa.
Ultrasound examination (ultrasound). The size of the liver – the right lobe 150 mm, the left lobe 96 mm, the structure is heterogeneous; portal vein – 13 mm. The size of the spleen is 148 × 61 mm, the splenic vein is 10 mm.The dimensions of the gallbladder are 100 × 38 mm, the wall is thickened to 3.5 mm, there is thick bile in the lumen of the bladder, flakes, parietal suspension, no calculi. Conclusion: hepatosplenomegaly with initial signs of portal hypertension, chronic cholecystitis.
The research results show a decrease in hemoglobin (89 g / l), an increase in total (104 µmol / l) and indirect bilirubin (87.7 µmol / l). After inclusion in therapy of phenobarbital at a dose of 3 mg / kg / day, a positive dynamics of the level of bilirubin parameters was noted.After 5 days of therapy, total bilirubin was 40.9 μmol / L, indirect bilirubin – 30.6 μmol / L.

Clinical case No. 4
Man, 24 years old, worried about periodically increasing yellowness of the skin and sclera, general weakness, emotional lability.
Suffers from the abdominal form of Wilson-Konovalov’s disease. She constantly takes penicillamine at a dose of 0.75 g / day, vitamin B 6 100 mg / day, methylprednisol at a dose of 8 mg / day.
Does not abuse alcohol.I do not smoke. The patient’s father died at the age of 36 from liver cirrhosis of unclear etiology, had no bad habits.
Asthenized. The physique is hyposthenic. BMI 19.6 kg / m 2 . The skin is subicteric, the sclera and oral mucosa are icteric.
The abdomen is soft, painful in the right hypochondrium, the edge of the liver is 2 cm below the costal arch along the mid-clavicular line, painful, indurated. An enlarged spleen is palpated.
In the research results, a decrease in hemoglobin (108 g / l), an increase in total (76.1 µmol / l) and indirect bilirubin (53.3 µmol / l), ALT (48 IU).
ultrasound. The size of the liver – the right lobe is 154 mm, the left lobe is 98 mm, the structure is heterogeneous; portal vein – 14 mm. The size of the spleen is 148 × 63 mm, the splenic vein is 10 mm. The size of the gallbladder is 110 × 41 mm, the wall is thickened to 3.5 mm, in the lumen of the bladder there is thick bile, parietal suspension, no calculi. Conclusion: hepatosplenomegaly, signs of chronic hepatitis with transformation into liver cirrhosis, chronic cholecystitis.


So, all patients have manifestations of jaundice due to an increase in the content of the indirect fraction of bilirubin in the blood.Each patient underwent laboratory tests to exclude syphilis, HIV, viral, including acute hepatitis in the 1st case, primarily cholestatic and hereditary (Wilson-Konovalov disease, hemochromatosis) liver diseases. At the same time, negative results were obtained for all markers in the first 3 cases and characteristic changes for Wilson-Konovalov disease in the 4th – blood ceruloplasmin 146 mg / l (norm 281-334 mg / l), daily copper excretion in urine 382 μg / day (the norm is less than 50 mcg / day).Studies concerning hemolytic anemia confirmed this diagnosis in the 3rd case.

Thus, jaundice appeared for the first time in the 1st clinical case and requires clarification. The rest of the patients were diagnosed. However, for a patient with SF, the question arises about the possible addition of concomitant gastroenterological pathology. In the last two clinical cases, it should be analyzed why the treatment prescribed for the underlying pathology does not completely stop the manifestations of jaundice.Is it possible for these patients to have SF?

FS has a high prevalence
Prior to genetic diagnosis, FS was thought to be a rare disease. Currently, according to epidemiological studies, SD occurs from 5 to 10% in the world population. This is every tenth inhabitant of the globe. According to some reports, the number of heterozygous carriers can reach 40%. A high frequency of detection of SF was found among the population of African countries (up to 36%), Germany (11%), Scotland (10-13%), Spain (9%), low – among Asians (about 3%).
Men prevail among patients with GS (10: 1).

Typical clinical manifestations and changes in laboratory and instrumental parameters in patients with SJ
In most cases, SJ is detected in patients aged 12-30 years in the form of persistent or recurrent jaundice of the sclera and skin. In this regard, if SJ is suspected, it is recommended to examine the patient in daylight. The yellowness of the skin and visible mucous membranes becomes clearly visible when the level of bilirubin in the blood serum reaches 43-50 μmol / L and above.As a rule, the intensity of jaundice with SJ is low. Maximum – icterus of the sclera, oral mucosa and sub-icteric skin. Particular attention should be paid to identifying staining of the feet, palms, nasolabial triangle, armpits.
The appearance or intensification of jaundice is provoked by physical or psycho-emotional overstrain, starvation, food errors, intercurrent diseases, taking certain medications (sulfamides, salicylates, etc.), hyperinsolation. These episodes are accompanied by weakness, increased fatigue, emotional lability, dyspepsia (discomfort and unexpressed pain in the right hypochondrium, epigastric region).It is also possible that there are no complaints at all and / or visual manifestations of the disease.
The size of the liver most often remains within the normal range or slightly increased. In laboratory tests, an increase in bilirubin by 2-5 times (rarely more) with a significant predominance of the indirect fraction, the rest of the biochemical parameters of blood and liver tests are not changed.
With SG, in 30% of cases, hemoglobin increased by more than 160 g / l, in 15% of patients mild reticulocytosis is detected, in 12% – a decrease in the osmotic resistance of erythrocytes.An increase in the content of hemoglobin in the blood is associated with its excessive synthesis with an increased level of bilirubin in the blood and tissues. The question of the presence of latent hemolysis in SF (reticulocytosis, decreased osmotic resistance of erythrocytes) is the topic of many years of discussion.
A large number of functional tests (hypocaloric, rifampicin, with nicotinic acid and phenobarbital) are used to diagnose SF. Let’s take a hypocaloric test as an example. Restricting the diet to 400 kcal for 72 hours causes an increase in bilirubin levels in all people.In the absence of a gene defect, the level of bilirubin rarely increases by more than 9.6 μmol / L in men and 4.1 μmol / L in women. This effect is more pronounced in individuals with FS, while the test is more sensitive in men than in women.

Modern ideas about the pathogenesis of SG
During the day, the human body produces from 200 to 450 mg of bilirubin. In the blood, bilirubin is present in two fractions – indirect bilirubin (formed during the breakdown of hemoglobin and enzyme systems with the participation of heme, insoluble in water, but highly soluble in fats, toxic) and direct (soluble in water, less toxic, excreted from the body with bile ).Direct bilirubin is produced in the liver after binding with glucuronic acid, therefore it is also called bound or conjugated. The key in this process is the enzyme uridine diphosphate glucuronyl transferase (UDPGT). In conditions of a lack of UDFGT, indirect bilirubin cannot be bound in the liver, which leads to its increase in the blood and the development of jaundice.
UDFGT deficiency is a hallmark of SF and is associated with mutations in the UGT1A1 gene encoding the enzyme located on the 2nd pair of chromosomes (2q37).In patients with FS, the sequence of thymidine-adenine (TA) repeats, which serves as an attachment site for DNA-dependent RNA polymerase, contains one extra TA repeat (7 instead of 6). As a result, gene expression is reduced. In a homozygous state, this leads to a decrease in the functional activity of the enzyme by about 30%, in heterozygous carriers – by 14%.
SJ can develop during liver transplantation to a recipient from a donor with a genetic defect. In these patients, after surgery, an isolated increase in bilirubin due to the indirect fraction is detected, which indicates the dominant role of hepatic UDFGT in the metabolism of bilirubin.

Genetic analysis for SF
Currently, scientists have the opportunity of objective genetic analysis, which confirms or does not confirm the diagnosis of SF. The material for research is blood plasma. Detection of the mutant gene is carried out by direct DNA diagnostics by analyzing the promoter region of the UGT1A1 gene for the number of TA repeats. Normally (TA) 6 / (TA) 6 – 6 TA repeats, corresponds to the normal genotype; (TA) 6 / (TA) 7 – dinucleotide insert (7 TA repeats) in heterozygous form; (TA) 7 / (TA) 7 – dinucleotide insert (7 TA repeats) in homozygous form.7 TA repeats in the promoter region of the UGT1A1 gene indicate a decrease in the functional activity of the UDPGT enzyme and indicate the presence of SF.
This disorder is inherited in an autosomal recessive manner. Below are some of the options for transmitting SF to offspring. If both parents suffer from SD, then all of their children will be sick. If one of the parents is a carrier of the abnormal gene, and the other is sick, then the probability of the disease in the child will be 50%. If one of the parents is a carrier and the other is healthy, then 50% of the children will be carriers, and 50% will be healthy.If both parents are carriers of this syndrome, then the probability of having sick children will be 25%, carriers will be 50%, and the remaining 25% will be healthy.

SJ in the aspect of pharmacogenetics
In general, the group of UDFGT enzymes is involved in the metabolism of a large number of substances: hormones (steroid hormones, thyroid hormones), catecholamines, endogenous metabolites (bile acids, bilirubin), drugs and their metabolites, as well as toxins, including carcinogens.In this regard, in individuals with an insertion in the UGT1A1 gene promoter, when taking many drugs, the so-called aglucones, the manifestation of SF is possible. To be excreted from the body, they must, like bilirubin, combine with glucuronic acid, loading the same enzyme – UDFGT, and, accordingly, displacing bilirubin. As a result, jaundice appears. By the way, the inhibition of glucuronization processes by their own steroid hormones also explains the high frequency of the prevalence of SF among men with manifestation of the disease during puberty.
With regard to clinical trials of drugs, it is important for pharmacologists to distinguish between the true hepatotoxicity of a drug and the response of individual patients with FS. Thus, in the trial of tocilizumab, a promising drug for the treatment of rheumatoid arthritis, 2 of 1,187 participants had a high rise in bilirubin levels. Subsequently, it turned out that both patients suffered from GS (Lee J.S., Wang G., Martin N. et al., 2011). This removed the drug from suspicion of true hepatotoxicity. Another example is antiviral therapy of chronic hepatitis C with interferons with ribavirin.In the course of treatment, a 17-fold increase in the bilirubin level was observed in 2 patients with FS. Cancellation of ribavirin led to the normalization of bilirubin parameters (Deterling K. et al., 2009).

Combination of SF with diseases of the gastrointestinal tract
Most often, with SF, diseases of the esophagus, stomach, duodenum and biliary tract are detected. This is due to the embryogenetic affinity and functional relationship between the liver, biliary tract and the upper digestive tract, a violation of the composition and rheological properties of bile, characteristic of SF, as well as a decrease in the detoxification function of the liver.It was found that SF makes a significant contribution to the development of cholelithiasis (GSD). In particular, a 2009 study, during which 198 patients with cholelithiasis and 152 people without it were genetically examined for SG with separation (TA) 6 / (TA) 6 – homozygotes without pathology; (TA) 6 / (TA) 7 – heterozygotes for SD; (TA) 7 / (TA) 7 – homozygotes for SD. The first group included (TA) 6 / (TA) 6 – 30.0%, (TA) 6 / (TA) 7 – 46.5%, (TA) 7 / (TA) 7 – 23.3%, in the second (TA) 6 / (TA) 6 – 48.5%, (TA) 6 / (TA) 7 – 33.5%, (TA) 7 / (TA) 7 – 17.8%.Thus, among those who have SJ, with a high reliability (p = 0.01), gallstone disease is more common (Tsezou A., Tzetis M., Giannatou E., 2009). In 2010, a meta-analysis was published, which included 2816 patients with cholelithiasis and 1617 people without it (Buch S., Schafmayer C., Volzke H. et al., 2010). It turned out that patients with FS have a high risk of cholelithiasis (p = 0.018). At the same time, the risk of gallstones in men increases by 21.2% (p = 0.046).
Disorders from the lower parts of the digestive tract in SF are more often of a functional nature.In the literature, there were publications about a rarer occurrence among patients with FS of colorectal cancer and Crohn’s disease.

Results of the diagnostic search in the given clinical cases
Our patients belong to the representatives of the European population, therefore, they have a high risk of SD. All participants are young patients with low intensity of jaundice due to the indirect fraction of bilirubin. In each case, the factor that provokes the appearance or intensification of jaundice with symptoms of general asthenization is clear.In the 1st and 4th cases, a hereditary history is traced.

Clinical case No. 1
After the onset of jaundice in a woman, the paracetamol-containing cold remedy was canceled. Detoxification therapy was carried out. In a control study of the hepatic complex 2 weeks after recovery from acute respiratory viral infections, the indices of bilirubin and ALT corresponded to the norm. Ultrasound of the abdominal organs did not reveal any abnormalities.
Taking into account the hereditary history, the woman underwent a genetic examination, which confirmed the presence of SG – (TA) 7 / (TA) 7.
Conclusion: SJ manifested against the background of acute respiratory viral infections and the use of a high dose of paracetamol, one of the main metabolic pathways of which is conjugation with glucuronides in the liver.

Clinical case No. 2
The patient underwent additional studies. Ultrasound of the abdominal organs. The dimensions of the gallbladder are 81 × 28 mm, the wall is thickened to 3 mm, the contents are thick bile, multiple stones, the maximum diameter is 6 mm. Conclusion: gallstone disease, signs of chronic cholecystitis.
Conclusion: a young man with SJ developed gallstone disease, which led to an increase in pain and dyspeptic manifestations.

Clinical case No. 3
The patient’s intake of phenobarbital for 5 days made it possible to achieve a decrease in the level of indirect bilirubin in the blood. This can be regarded as a positive result confirming the presence of SG. The action of phenobarbital is based on enzymatic induction and activation of the enzyme UDPGT. The manifestation of SD was probably caused by the severe stress experienced by the patient.
Conclusion: The presence of hemolytic anemia in patients does not exclude SF, but only makes it worse.

Clinical case No. 4
Considering the complexity of the diagnostic process and hereditary history, the man underwent a genetic examination, which confirmed the presence of both Wilson-Konovalov disease and SD – (TA) 7 / (TA) 7. In this case, there is a constantly elevated level of bilirubin due to the indirect fraction with an increase in their content in the blood and increased jaundice in response to typical provoking factors in SF.
Conclusion: SJ can be combined with other hereditary diseases. So, combinations of SD with Marfan, Ehlers-Danlos syndromes are described.

Features of management tactics patients with SJ
Thus, SJ is a hereditary disorder of bilirubin metabolism, the timely recognition and correction of which is essential for the patient. In the cases presented by us, known clinical and laboratory criteria were used to make a diagnosis.The modern stage in the development of medicine, which made it possible to objectively confirm the diagnosis of SF by genetic methods, puts its diagnosis on a new level. From the above examples, it can be seen that even phenotypically (outwardly) healthy parents can have a child with SF. Therefore, if there are cases of this disease in a person’s pedigree, it is recommended to undergo a genetic examination for mutations in the genes responsible for the development of FS. Based on the results of the tests, the geneticist can determine whether a person is a carrier and how the syndrome will be inherited.
Given the high incidence of FS in the population, genetic analysis is also recommended before starting treatment with drugs with hepatotoxic effects. In particular, this allows predicting the risk of complications during irinotecan therapy in patients with cancer.
Non-drug treatment and prevention of complications of FS include the elimination of risk factors: maintaining a correct lifestyle (rejection of bad habits, proper nutrition, etc.)etc.), combating stress (autogenous training), increasing immunity. It is very important for the patient to minimize drug exposure. First of all, this concerns the intake of anabolic steroids, glucocorticoids, androgens, rifampicin, cimetidine, chloramphenicol, streptomycin, sodium salicylate, ampicillin, caffeine, ethinyl estradiol, paracetamol, diacarb, menthol, as well as a number of other drugs, in the metabolism of which UD is involved.
Episodes of jaundice, as a rule, resolve on their own, without the use of drugs.However, if the bilirubin level exceeds 50 μmol / l and is accompanied by poor health, it is possible to take phenobarbital in a short course (1.5-2.0 mg / kg, or 30-200 mg / day in 2 doses for 2-4 weeks). Phenobarbital is a part of drugs such as corvalol, barboval, valocordin, therefore these drugs are often used (20-30-40 drops 3 r / day for 1 week), although the effect due to a low dose of phenobarbital is observed only in some patients. The inducers of enzymes of the monoxidase system of hepatocytes, in addition to phenobarbital, include flumecinol, prescribed in a dose of 0.4-0.6 g (4-6 drops) once a week or 0.1 g 3 times a day for 2-4 weeks (not registered in Ukraine).Under the influence of these drugs, the level of bilirubin in the blood decreases, dyspeptic symptoms disappear, but in the course of treatment, lethargy, drowsiness, and ataxia occur. In such cases, these drugs are prescribed in minimal doses before bedtime, which allows them to be taken for a long time.
The excretion of direct bilirubin is possible with the help of enhanced diuresis, the use of activated carbon or other sorbents that adsorb bilirubin in the intestine. Through phototherapy, the destruction of indirect bilirubin fixed in tissues is achieved, thereby releasing peripheral receptors that can bind new portions of bilirubin, preventing its penetration through the blood-brain barrier.
The benign quality of SF, consisting in the absence of an outcome in liver cirrhosis, does not exclude the aggravation of the phenomena of dysfunction of the biliary system, the development of chronic cholecystitis and the formation of cholelithiasis. This is clearly confirmed by three of the above clinical cases. In this regard, patients with FS are individually prescribed hepatoprotectors – ursodeoxycholic acid (UDCA) preparations, phospholipids, silibinin, milk thistle fruit extract, artichoke leaf extract, as well as vitamin therapy, especially B vitamins.
In our opinion, in order to prevent or reduce damage to the biliary tract against the background of FS, it is most advisable to use UDCA. In addition to its known positive effects, it was shown in an experiment on rats that UDCA is able to reduce the sensitivity of nerve cells to the damaging effect of indirect bilirubin. So, in the work (Silva R.F., Rodrigues C.M., Brites D.Y., 2001), apoptosis in the culture of nerve cells (neurons and astrocytes) was assessed after incubation with indirect bilirubin without and in the presence of UDCA.In the first variant, an increase in cell apoptosis was observed up to 7 times. The presence of UDCA provided protection for 60% of nerve cells in culture, and the level of apoptosis increased by a little over 6%. This is a relevant moment, given that patients with FS are prone to psychosomatic disorders.
UDCA is used at a dose of 10-12 mg / kg per day. It is possible to prescribe it in the form of a treatment course until the process is resolved, for example, elimination of biliary sludge, with preventive courses for 3 months 2 times a year (spring-autumn), or in the form of a constant prophylactic dose of 250 mg / day once in the evening.
In conclusion, it is necessary to note a gradual increase in the number of latent metabolic defects among the population, which sooner or later may manifest themselves. Scientists are faced with the task of creating conditions for a reasonable and at the same time sufficiently safe intervention in the material basis of heredity in order to correct such defects. This is a direction for future research.

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90,000 Liver diseases in cats and their treatment with dietary cat food

What is liver disease?

The liver is an extremely important organ that performs many functions, such as breaking down and converting nutrients, removing toxic substances from the blood, and storing vitamins and minerals.Since the liver is responsible for the elimination of various substances from the body, it is susceptible to a variety of negative external influences. Diseases of the liver lead to liver inflammation known as hepatitis. If left untreated, it can lead to loss of organ function, as it replaces healthy liver cells with scar tissue. Diseases and damage to other organs and tissues can also adversely affect liver function.

Fortunately, liver diseases can be effectively controlled and their progression significantly reduced.Many cats continue to live happily after years of diagnosis. Proper nutrition and regular consultation with your veterinarian are the keys to treating your cat’s liver disease.

What can cause liver disease?

The following are some of the risk factors for liver disease in cats:

Age. Some diseases, including liver failure, are common in older cats

Breed. Certain breeds, such as Siamese, are often born with or have a predisposition to certain liver problems.

Obesity. Overweight cats are more likely to develop liver disease.

Medicines and chemicals. Medicines containing acetaminophen can cause liver damage in cats

Does my cat have liver disease?

The symptoms of liver disease can be very similar to those of other diseases.If you notice any of the following symptoms in your cat, see your veterinarian for a complete examination of the animal.

Symptoms to watch for:

  • Poor appetite or loss of appetite
  • Dramatic weight loss
  • Weight Loss
  • Jaundice (yellowing of the gums, whites of the eyes or skin)
  • Increased Thirst
  • Vomiting or diarrhea
  • Changes in behavior
  • Excessive salivation
  • Loss of energy or depression

Other possible symptoms of liver disease include dark urine, pale gums, or fluid buildup in the abdomen, which can be mistaken for sudden weight gain.Your veterinarian may order a variety of diagnostic tests to check for liver disease in your cat.

IMPORTANT. Symptoms of liver disease are not very specific, which complicates their diagnosis. If overweight cats stop eating, they can develop life-threatening complications. Cats that lose their appetite for two to three days may have liver lipidosis, a condition associated with excessive accumulation of fat in the liver that interferes with normal liver function.If your cat refuses to eat, contact your veterinarian immediately.

The importance of nutrition

If your cat has been diagnosed with liver disease, you are probably wondering, “How do you care for her?” Treatment for any liver disease aims to give the liver a “rest” and minimize its stress associated with the processing of fats, proteins, carbohydrates and drugs. It is especially important to feed the cat correctly.Give her food with easy-to-digest carbohydrates, high-quality fats, and limited amounts of salt to control existing liver damage and improve liver function.

Always consult your veterinarian for an accurate diagnosis and the correct treatment to recommend the best food for your pet’s liver health.

Ask your veterinarian:

  1. What foods should I not give my cat due to her health condition?
    • Ask how human food can affect the health of a cat?
  2. Would you recommend Hill’s Prescription Diet for my cat?
    • Ask about special foods for your cat.
    • How much and how many times a day should you feed your cat with the recommended food?
    • Discuss what treats you can give your cat with the recommended food.
  3. How quickly will the first signs of improvement appear in my cat?
  4. Can you provide me with written instructions or a brochure with information about the liver disease diagnosed in my cat?
  5. What is the best way to contact you or your veterinary clinic if I have any questions (email / phone)?
    • Ask if your cat needs follow-up.
    • Specify if a reminder or email notification will be sent to you.

Biochemical blood test

Biochemical blood test allows you to diagnose the work of human internal organs.
A blood test is performed on an empty stomach. A person should not eat for six to twelve hours before collecting blood. It is allowed to drink water from liquids. For biochemical analysis, blood is taken from a vein.

With a classified approach to deciphering the LHC and knowledge of medical standards, it is possible to accurately determine the imbalance of trace elements, infections and inflammation, disorders in organs such as the liver, heart, spleen, kidneys, etc.

Biochemical blood test: diagnosis and decoding

Total protein
Total protein reflects the total amount of proteins in the blood. Consists of amino acids. Total protein maintains Ph blood, moves and clots blood, and participates in immune responses.
Medical norm: from sixty four to eighty four g / l.
An overestimated level of protein is a symptom of such diseases as rheumatism, arthritis, cancer, infectious diseases
If the level of protein is too low, then this indicates diseases of the kidneys, intestines, liver, and oncological diseases.

Hemoglobin
Hemoglobin is a protein of red blood cells that transports oxygen throughout the body.
Medical norm: men – from one hundred thirty to one hundred and sixty g / l, women – from one hundred twenty to one hundred fifty g / l
Decreased hemoglobin is a sign of anemia.

Haptoglobin
This is a protein that binds hemoglobin. The main function of haptoglobin is to store iron in the body.
Medical norm: children – from two hundred and fifty to one thousand three hundred and eighty mg / l, adults – from one hundred fifty to two thousand mg / l, elderly – from three hundred fifty to one thousand seven hundred and fifty mg / l.
A decreased concentration of haptoglobin in the blood is a symptom of liver disease, enlargement of the spleen, autoimmune disease, and a defect in the erythrocyte membrane.
An increased concentration of haptoglobin indicates the presence of malignant tumors such as lung cancer, breast cancer and genetics

Glucose
Glucose is involved in carbohydrate metabolism, glycogen formation and nutrition of brain tissues.
Medical norm: from 3, 30 to 5, 50 mmol / l
High blood glucose is a sign of the risk of diabetes mellitus, indicates an intolerance of the body to glucose.

Urea
Is the main product of the breakdown of proteins
Medical standard: from two and a half to eight points, three tenths of mmol / l
The curtailed urea level indicates diseases of the cardiovascular system, tumors, intestinal and urinary tract obstruction.

Creatinine
Creatinine reflects the state of the kidneys and takes part in the energy metabolism of tissues.
Medical norm: for men – from sixty two to one hundred and fifteen micromol / l, for women – from fifty three to ninety seven micromol / l.
Elevated creatinine indicates hyperthyroidism or renal failure.

Cholesterol
Takes part in the formation of the synthesis of sex hormones and vitamin D. Distinguish between total cholesterol, high density lipoprotein cholesterol and low density lipoprotein
A high amount of cholesterol in the blood indicates an increased risk of liver and cardiovascular diseases

Bilirubin
Bilirubin is formed during the breakdown of hemoglobin.Bilirubin is concentrated from direct and indirect bilirubin.
Medical norm: from five to twenty μmol / l.
If the bilirubin content is high, there is a risk of jaundice. Also, an increased content of bilirubin is the cause of liver diseases, heart disease, hepatitis, cirrhosis and cholelithiasis.

ALT (ALT) Alanine aminotransferase
Alanine aminotransferase is used to diagnose liver function. It is found in the cells of the liver, kidneys and heart.When cells of any of the above organs are destroyed, this enzyme enters the bloodstream.
Medical norm: men – up to forty-one units / l, women – up to thirty-one units / l.
A high level reports such diseases as cirrhosis, liver cancer, heart attack, cirrhosis, myocarditis.

AST (AST) Aspartate aminotransferase
Aspartate aminotransferase is found in the cells of the kidneys, heart and liver. Takes part in the exchange of amino acids.
Medical norm: men – up to forty units / l, women – up to thirty-one units / l
A high level of AST indicates the potential for heart attack, hepatitis, pancreatitis, heart failure and liver problems.

Lipase
The enzyme is designed to break down triglycerides. Pancreatic lipase is of particular importance.
Medical norm: from zero to one hundred and ninety units / l.
A high concentration of lipase in the blood indicates diseases of the pancreas.

Amylase
Amylase digests and breaks down carbohydrates from food. Distinguish between alpha-amylase (diastase) and pancreatic amylase
Medical standard: alpha-amylase – from twenty-eight to one hundred units / l.
Medical standard: pancreatic amylase: from zero to fifty units / l.
An excess of the amylase norm indicates the possible presence of such diseases as peritonitis, pancreatitis, diabetes mellitus, pancreatic cyst, stone, cholecystitis or renal failure.

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