essay on the liver

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Liver: Anatomy and Functions

Anatomy of the liver.

The liver is located in the upper right-hand portion of the abdominal cavity, beneath the diaphragm, and on top of the stomach, right kidney, and intestines.

Shaped like a cone, the liver is a dark reddish-brown organ that weighs about 3 pounds.

There are 2 distinct sources that supply blood to the liver, including the following:

Oxygenated blood flows in from the hepatic artery

Nutrient-rich blood flows in from the hepatic portal vein

The liver holds about one pint (13%) of the body's blood supply at any given moment. The liver consists of 2 main lobes. Both are made up of 8 segments that consist of 1,000 lobules (small lobes). These lobules are connected to small ducts (tubes) that connect with larger ducts to form the common hepatic duct. The common hepatic duct transports the bile made by the liver cells to the gallbladder and duodenum (the first part of the small intestine) via the common bile duct.

Functions of the liver

The liver regulates most chemical levels in the blood and excretes a product called bile. This helps carry away waste products from the liver. All the blood leaving the stomach and intestines passes through the liver. The liver processes this blood and breaks down, balances, and creates the nutrients and also metabolizes drugs into forms that are easier to use for the rest of the body or that are nontoxic. More than 500 vital functions have been identified with the liver. Some of the more well-known functions include the following:

Production of bile, which helps carry away waste and break down fats in the small intestine during digestion

Production of certain proteins for blood plasma

Production of cholesterol and special proteins to help carry fats through the body

Conversion of excess glucose into glycogen for storage (glycogen can later be converted back to glucose for energy) and to balance and make glucose as needed 

Regulation of blood levels of amino acids, which form the building blocks of proteins

Processing of hemoglobin for use of its iron content (the liver stores iron)

Conversion of poisonous ammonia to urea (urea is an end product of protein metabolism and is excreted in the urine)

Clearing the blood of drugs and other poisonous substances

Regulating blood clotting

Resisting infections by making immune factors and removing bacteria from the bloodstream

Clearance of bilirubin, also from red blood cells. If there is an accumulation of bilirubin, the skin and eyes turn yellow. 

When the liver has broken down harmful substances, its by-products are excreted into the bile or blood. Bile by-products enter the intestine and leave the body in the form of feces. Blood by-products are filtered out by the kidneys, and leave the body in the form of urine.

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The Liver: A ‘Blob’ That Runs the Body

By Natalie Angier

• June 12, 2017

To the Mesopotamians, the liver was the body’s premier organ, the seat of the human soul and emotions. The ancient Greeks linked the liver to pleasure: The words hepatic and hedonic are thought to share the same root .

The Elizabethans referred to their monarch not as the head of state but as its liver, and woe to any people saddled with a lily-livered leader, whose bloodless cowardice would surely prove their undoing.

Yet even the most ardent liverati of history may have underestimated the scope and complexity of the organ. Its powers are so profound that the old toss-away line, “What am I, chopped liver?” can be seen as a kind of humblebrag.

After all, a healthy liver is the one organ in the adult body that, if chopped down to a fraction of its initial size, will rapidly regenerate and perform as if brand-new. Which is a lucky thing, for the liver’s to-do list is second only to that of the brain and numbers well over 300 items, including systematically reworking the food we eat into usable building blocks for our cells; neutralizing the many potentially harmful substances that we incidentally or deliberately ingest; generating a vast pharmacopoeia of hormones, enzymes, clotting factors and immune molecules; controlling blood chemistry; and really, we’re just getting started.

“We have mechanical ventilators to breathe for you if your lungs fail, dialysis machines if your kidneys fail, and the heart is mostly just a pump, so we have an artificial heart,” said Dr. Anna Lok, president of the American Association for the Study of Liver Diseases and director of clinical hepatology at the University of Michigan.

“But if your liver fails, there’s no machine to replace all its different functions, and the best you can hope for is a transplant.”

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The Many Vital Functions of the Liver

The liver is the heaviest organ in the body and one of the largest. It's located in the upper right portion of your belly under the ribs and is responsible for functions vital to life.

The liver primarily processes nutrients from food, makes bile, removes toxins from the body, and builds proteins. It metabolizes many drugs. It breaks down fat and produces cholesterol. It converts glycogen into glucose. It creates immune factors necessary to fight infection.

It's easy to see how inflammation of the liver , or hepatitis , interferes with these important functions and can lead to poor health. Fortunately, the liver is extremely resilient and most cases of liver inflammation don't even come to medical attention, but in cases of severe liver disease , there can be a serious interruption of these essential liver functions. Let's look at each of these functions a little closer.

Processing Nutrients from Food

The digestive system immediately begins to break down the food that we eat into smaller and smaller pieces. Eventually, these nutrients will enter the blood and travel to the liver through the hepatic portal system , the major pathway that blood takes from the ​ digestive system to the liver.

The liver will then process these nutrients in different ways, depending on the body's needs. It usually stores some of the nutrients in a form that the body can use for quick energy. The rest will be used to make other important chemicals the body needs.

When the liver is severely damaged, such as in liver failure , it can't continue to process nutrients from the blood that the body must have. Without aggressive medical care, the absence of these essential liver functions can result in signs of serious illness like brain damage and coma .

Making Bile

Bile is a thick, green-yellow fluid that the liver produces to help digest food, especially fat, as it passes from the stomach to the intestines. This fluid is made in the liver but is stored in a nearby sac called the gallbladder. When a person eats a meal heavy in fat, like a juicy steak, the body will use its store of bile to help break down the fats in the steak for digestion.

Removing Toxins From the Blood

All of the blood in the body will eventually pass through the liver. This is important because the liver needs to pull out any bad things in the blood, such as toxins, and remove them from the body. It metabolizes many drugs and alcohol and helps remove other toxins such as damaged cells, proteins, and old hormones.

The liver prepares all of these types of toxins to be removed from the body. However, when the liver is damaged, these toxins can't be removed and they start to accumulate creating problems.

Building Proteins

A protein is a complex chemical that is essential to living things, like plants, animals, and people. Proteins are everywhere in the body and need to be constantly produced to sustain life. The liver is in charge of building many kinds of proteins that the body uses every day.

For instance, there are many proteins produced by the liver that are responsible for blood clotting. When the liver is damaged , sometimes the body isn't able to clot blood effectively. In mild cases, it just takes a long time for bleeding to stop. However, in severe cases, the blood wouldn't be able to clot. A simple cut on the skin would lead to continued bleeding (though not necessarily a dangerous amount), and possibly bruises.

Gastrointestinal Society: Canadian Society of Intestinal Research. The liver - An amazing organ .

Centers for Disease Control and Prevention. What is viral hepatitis ?

Johns Hopkins Medicine. Liver: Anatomy and functions .

National Institute of Diabetes and Digestive and Kidney Diseases. Your digestive system and how it works .

American Liver Foundation. The progression of liver disease .

Johns Hopkins Medicine. Biliary system anatomy and functions .

Center for Liver Disease and Transplantation. The liver and its functions .

MedlinePlus. Loss of brain function - liver disease .

By Charles Daniel  Charles Daniel, MPH, CHES is an infectious disease epidemiologist, specializing in hepatitis.

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The Liver and Its Functions

The liver is the largest solid organ in the body. It removes toxins from the body’s blood supply, maintains healthy blood sugar levels, regulates blood clotting, and performs hundreds of other vital functions. It is located beneath the rib cage in the right upper abdomen.

• The liver filters all of the blood in the body and breaks down poisonous substances, such as alcohol and drugs.
• The liver also produces bile, a fluid that helps digest fats and carry away waste.
• The liver consists of four lobes, which are each made up of eight sections and thousands of lobules (or small lobes).

Functions of the Liver

The liver is an essential organ of the body that performs over 500 vital functions. These include removing waste products and foreign substances from the bloodstream, regulating blood sugar levels, and creating essential nutrients. Here are some of its most important functions:

• Albumin Production : Albumin is a protein that keeps fluids in the bloodstream from leaking into surrounding tissue. It also carries hormones, vitamins, and enzymes through the body.
• Bile Production : Bile is a fluid that is critical to the digestion and absorption of fats in the small intestine.
• Filters Blood : All the blood leaving the stomach and intestines passes through the liver, which removes toxins, byproducts, and other harmful substances.
• Regulates Amino Acids : The production of proteins depend on amino acids. The liver makes sure amino acid levels in the bloodstream remain healthy.
• Regulates Blood Clotting : Blood clotting coagulants are created using vitamin K, which can only be absorbed with the help of bile, a fluid the liver produces.
• Resists Infections : As part of the filtering process, the liver also removes bacteria from the bloodstream. 
• Stores Vitamins and Minerals : The liver stores significant amounts of vitamins A, D, E, K, and B12, as well as iron and copper.
• Processes Glucose : The liver removes excess glucose (sugar) from the bloodstream and stores it as glycogen. As needed, it can convert glycogen back into glucose.

Anatomy of the Liver

The liver is reddish-brown and shaped approximately like a cone or a wedge, with the small end above the spleen and stomach and the large end above the small intestine. The entire organ is located below the lungs in the right upper abdomen. It weighs between 3 and 3.5 pounds.

The liver consists of four lobes: the larger right lobe and left lobe, and the smaller caudate lobe and quadrate lobe. The left and right lobe are divided by the falciform (“sickle-shaped” in Latin) ligament, which connects the liver to the abdominal wall. The liver’s lobes can be further divided into eight segments, which are made up of thousands of lobules (small lobes). Each of these lobules has a duct flowing toward the common hepatic duct, which drains bile from the liver.

The following are some of the most important individual parts of the liver:

• Common Hepatic Duct : A tube that carries bile out of the liver. It is formed from the intersection of the right and left hepatic ducts.
• Falciform Ligament : A thin, fibrous ligament that separates the two lobes of the liver and connects it to the abdominal wall.
• Glisson’s Capsule : A layer of loose connective tissue that surrounds the liver and its related arteries and ducts.
• Hepatic Artery : The main blood vessel that supplies the liver with oxygenated blood.
• Hepatic Portal Vein : The blood vessel that carries blood from the gastrointestinal tract, gallbladder, pancreas, and spleen to the liver. 
• Lobes : The anatomical sections of the liver.
• Lobules : Microscopic building blocks of the liver.
• Peritoneum : A membrane covering the liver that forms the exterior.

Maintaining a Healthy Liver

The best way to avoid liver disease is to take active steps toward a healthy life. The following are some recommendations that will help keep the liver functioning as it should:

• Avoid Illicit Drugs : Illicit drugs are toxins that the liver must filter out. Taking these drugs can cause long-term damage.
• Drink Alcohol Moderately : Alcohol must be broken down by the liver. While the liver can moderate amounts, excessive alcohol use can cause damage.
• Exercise Regularly : A regular exercise routine will help promote general health for every organ, including the liver.
• Eat Healthy Foods : Eating excessive fats can make it difficult for the liver to function and lead to fatty liver disease .
• Practice Safe Sex : Use protection to avoid sexually transmitted diseases such as hepatitis C .
• Vaccinate : Especially when traveling, get appropriate vaccinations against hepatitis A and B , as well as diseases such as malaria and yellow fever, which grow in the liver.

If you need help for a liver condition, give us a call at (877) LIVER MD/ (877) 548-3763 or get in touch using our online request form .

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Liver histology

Author: Adrian Rad, BSc (Hons) • Reviewer: Uruj Zehra, MBBS, MPhil, PhD Last reviewed: August 08, 2023 Reading time: 14 minutes

The liver is the largest internal organ of the human body, weighing approximately 1.5 kg. Embryologically it develops from the foregut and it spans the upper right and part of left abdominal quadrants. Anatomically the liver consists of four lobes: two larger ones (right and left) and two smaller ones (quadrate and caudate).

Histologically speaking, it has a complex microscopic structure, that can be viewed from several different angles. Physiologically speaking, the liver also performs many essential functions and it is your best friend when you are enjoying some beers with your friends. This article will examine every histological component of the liver, its macroscopic and microscopic vascular supply, and the biliary system.

Functions and physiology

Histological components, hepatic (classic) lobule, portal lobule  , liver acinus, hepatocytes, perisinusoidal space (space of disse), biliary tree, hepatic cirrhosis.

The liver performs several important functions in the human body, such as given below:

• Plasma protein synthesis - albumins, lipoproteins, glycoproteins, prothrombin, fibrinogen
• Vitamin storage and modification - vitamins A, D, and K
• Iron storage and metabolism - transferrin, haptoglobin, hemopexin, ferritin
• Drugs and toxins degradation
• Bile production
• Carbohydrate metabolism

The liver consists of the following major histological components:

• Parenchyma , which is represented by hepatocytes
• Stroma , which is a continuation of the surrounding capsule of Glisson. It consists of connective tissue and contains the vessels. The capsule is also covered by a layer of mesothelium , arising from the peritoneum covering the liver. The connective tissue of the stroma is type III collagen (reticulin), which forms a meshwork that provides integrity for the hepatocytes and sinusoids.

• Sinusoids , which are capillaries travelling between hepatocytes
• Spaces of Disse (perisinusoidal spaces), which are located between the hepatocytes and the sinusoids.

Feeling a little perplexed? Don't worry - liver histology is a complex topic! Why not try learning with flashcards?  They're a well known tool for learning faster and more effectively. 

In histological terms, the liver consists of a large number of microscopic functional units that work in unison to ensure the overall, proper activity of the entire organ. There are three possible ways of describing one such unit, as given below:

• Portal lobule

The classic lobule is the traditional description and the one that you have most likely heard of the most. It consists of hexagonal plates of hepatocytes stacked on top of each other. Within each plate, the hepatocytes radiate outwards from a central vein. As they extend towards the periphery, the hepatocytes are arranged into strips, similar to the spokes of a cartwheel. Hepatic sinusoids travel between the strips of hepatocytes, draining into the central vein .

One portal canal is located at each corner of the hexagonal classic lobule, making a total of six for each lobule. These portal canals are composed of the portal triads , which are surrounded by loose stromal connective tissue . A periportal space ( space of Mall ), where lymph is produced, is sandwiched between the connective tissue of the portal canals and the hepatocytes.

While connective tissue is present around the portal canals, the interlobular quantity is very small in humans. This can make routine histological visualizations of the classic lobule difficult.

While the classic lobule view focuses on the blood supply and hepatic mass arrangement, the portal lobule view underlines the exocrine function of the liver i.e. bile secretion. In this case, each functional unit is a triangle, having a central axis through a portal field and the imaginary vertices through the three different but closest portal canals surrounding it. The area covered by the triangle represents the hepatic regions that secrete bile into the same bile duct .

The focus of this description is the perfusion, metabolism and pathology of hepatocytes, providing a more accurate description of the physiology of the liver. A liver acinus functional unit is in the shape of an oval. The short axis is represented by a shared border between two adjacent lobules together with the portal canals. The long axis is an imaginary line between two adjacent central veins.

Each half of the liver acinus can be divided into three zones:

• Zone 1 - It is the one closest to the short axis, hence to the portal canals and supply of arterial blood. The hepatocytes in zone 1 receive the highest amount of oxygen.

• Zone 2 - It is the one located between zones 1 and 3.

• Zone 3 - It is the one furthest from the short axis but closest to the central vein, hence the hepatocytes receive the least amount of oxygen.

These large and polyhedral (six surfaces) cells make up 80% of the total cells of the liver. They can contain between two and four nuclei , which are large and spherical, occupying the centre of the cells. Each nucleus has at least two nucleoli . The typical lifespan of a hepatocyte is five months. The adjacent hepatocytes leave a very small space between them known as bile canaliculi which are almost 1.0-2.0 μm in diameter. The cell membranes near these canaliculi are joined by tight junctions.

The cytoplasm is acidophilic in routine H&E staining, dotted with basophilic regions represented by rough endoplasmic reticulum (rER) and ribosomes. In addition, hepatocytes contain the following organelles:

• Smooth endoplasmic reticulum (sER), which is essential in toxin degradation and conjugation, as well as cholesterol synthesis.
• Mitochondria (up to 1000/cell)
• Golgi network , which is composed of approximately 50 small Golgi units. They contain granules with very low density lipoprotein and bile precursors.
• Peroxisomes , which contain oxidases and catalases. These enzymes are responsible for detoxification reactions taking place in the liver, for example, that of alcohol.
• Glycogen deposits , which are lost in during H&E preparations, leaving irregular stained areas.
• Lipid droplets
• Lysosomes , which are responsible for iron storage under the form of ferritin.

This space is situated between the layers of hepatocytes and the sinusoidal endothelial cells. The hepatocytes extend villi into the perisinusoidal space, increasing the extent and rate of material exchange, together with the microvilli .

The perisinusoidal space contains a specific type of cell called Ito, or hepatic stellate , cells. Their role is the storage of hepatic vitamin A inside lipid droplets, which is subsequently released as retinol. However, Ito cells are also responsible for hepatic fibrosis, since they are the ones secreting large amounts of collagen during liver injury.

Vasculature

The liver, as an organ, receives blood from two different sources. The major one is via the hepatic portal vein (75%), which carries venous blood from the intestines , pancreas and spleen . Despite the lack of oxygen, this blood contains high amount of nutrients, endocrine secretions, broken down erythrocytes, but also ingested toxins. The second major source is via the hepatic artery (25%), which brings oxygenated blood to the liver.

Together with the bile duct, the hepatic portal vein and hepatic artery form the portal triad . Those structures supply blood to the sinusoids and the hepatocytes, subsequently draining into the central vein followed by the sublobular veins. The second drainage pattern is via the hepatic veins , which end up in the inferior vena cava .

Interlobular vessels connect the portal triads and sinusoids, transporting the blood into the latter. The hepatic sinusoids have a discontinuous epithelium due to the presence of fenestrae and gaps between endothelial cells and constitute a low-resistance vascular channel. A basement membrane is also absent. The sinusoids appear as pale spaces between the hepatocytes in routine hematoxylin and eosin (H&E) staining. The endothelial cells display flat and condensed nuclei, with poorly stained cytoplasm.

The name of the blood vessels travelling through the portal canals are called interlobular vessels . They send blood into the sinusoids, either directly if they are really small, or by branching into distributing vessels first, which in turn empty into the sinusoids via inlet vessels . From the sinusoids, the blood drains into the central vein , which occupies the central axis of the classic liver lobule. The endothelial cells forming the central veins are surrounded by a small quantity of connective tissue fibers.

As they travel through the parenchyma, the central veins become larger, subsequently emptying into the sublobular veins . The endothelial lining of the sublobular veins is surrounded by a high quantity of connective tissue fibers, consisting of a layer of both collagenous and elastic fibers. Several sublobular veins then converge into larger and valveless hepatic veins , which ultimately empty into the inferior vena cava .

The sinusoids also receive arterial blood from the hepatic arteries . The latter have a thick muscular wall and also supply the connective tissue and various structures in the portal canals.

In addition, sinusoids contain a specific cell type called Kupffer cell , containing ovoid nuclei. These monocyte derivatives of the mononuclear phagocytic system are part of the sinusoid lining from which they extend processes into the lumen . Therefore, Kupffer cells continuously sample the blood travelling through the sinusoids, phagocytosing antigens, microorganisms, and damaged red blood cells .

This is a system consisting of channels that carries bile from the source, this being the hepatocytes, all the way to the gallbladder and intestines. The epithelial cells lining this system are called cholangiocytes . They range in shape from cuboidal in small ductules, to columnar in large ductules. Cholangiocytes have several histological features, such as:

• Few organelles
• Presence of tight junctions between the cells
• Microvilli on their apical domains
• Primary cillium

The hepatocytes secrete bile into the bile canaliculi , which are the smallest channels of the biliary tree. The secretion into these canaliculi is an active process. They partially loop around the hepatocytes and become the canals of Hering close to the portal canal.

These canals are lined by both hepatocytes and cuboidal cholangiocytes. The flow of bile is opposite to that of the blood and the canals of Hering are capable of contracting and assisting this flow towards the portal canal. The canals of Hering also posses hepatic stem cells , which represent the source of hepatocytes and cholangiocytes.

The canals of Hering flow into intrahepatic bile ductules in the periportal space (of Mall), which are completely lined by cholangiocytes. In turn, the intrahepatic bile ductules flow into interlobular bile ducts , which are lined by cuboidal to columnar cholangiocytes and form part of the portal triad. As these ducts travel towards the porta hepatis , they increase in diameter and become invested inside dense connective tissue composed of elastic fibers. Finally, these interlobular ducts join to form the right and left hepatic ducts , which in turn merge to form the common hepatic duct . This duct is lined by columnar epithelial cells. The cystic duct branches from the common hepatic duct, carrying bile to and from the gallbladder.

As the last step in studying liver histology, test your new knowledge with our quiz.

Clinical points

This condition is characterised by aggregates of regenerated hepatic cells that are separated by bands of scar tissue (deposited collagen tissue). These two processes take place in response to some extent of hepatocyte destruction , resulting in their damage and subsequent death. Some causes include:

• Chronic alcoholism
• Hepatitis B or C infection
• Certain autoimmune conditions
• Some genetic metabolic diseases that result in an excessive storage of copper and iron

The scar tissue negatively impacts the blood flow from the sinusoids to the hepatocytes, resulting in a decrease in function. As a result, portal hypertension develops because the blood cannot drain from the portal vein.

This condition classically manifests itself as a yellow discoloration of tissues, which is due to excessive levels of bilirubin ( hyperbilirubinaemia ) and deposited bile pigments. Jaundice can have a variety of causes, two common ones being hepatic and biliary tract diseases.

If the ability of the liver to excrete conjugated bilirubin is exceeded, prehepatic jaundice takes place. This type is related to diseases characterised by a high amount of red blood cell breakdown, like sickle cell anaemia (a major source of bilirubin is red blood cell breakdown).

If the liver is damage such that it cannot effectively metabolise and excrete bilirubin, hepatic jaundice occurs. In contrast to the prehepatic type, this kind of jaundice exhibits both conjugated and unconjugated hyperbilirubinaemia.

Posthepatic (obstructive) jaundice is due to a chemical blockage in the biliary system, mostly due to gallstones.

References:

• Ross M. H., Pawlina W.: Histology: A text and atlas: With Correlated Cell and Molecular Biology, 6th edition, Lippincott Williams & Wilkins
• Young B., Woodford P., O’Dowd G.: Wheater’s Functional Histology: A Text and Colour Atlas, 6th edition, Churchill Livingstone Elsevier
• Mescher Anthony L.: Junqueira’s Basic Histology: Text and Atlas, 13th edition, McGraw-Hill Education

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Your liver is the largest organ inside your body. It helps your body digest food, store energy, and remove poisons.

There are many kinds of liver diseases:

• Diseases caused by viruses, such as hepatitis A , hepatitis B , and hepatitis C
• Diseases caused by drugs, poisons, or too much alcohol. Examples include fatty liver disease and cirrhosis .
• Liver cancer
• Inherited diseases, such as hemochromatosis and Wilson disease

Symptoms of liver disease can vary, but they often include swelling of the abdomen and legs, bruising easily, changes in the color of your stool and urine, and jaundice , or yellowing of the skin and eyes. Sometimes there are no symptoms. Tests such as imaging tests and liver function tests can check for liver damage and help to diagnose liver diseases.

• Liver Disease (Mayo Foundation for Medical Education and Research) Also in Spanish
• Progression of Liver Disease to Liver Cancer (American Liver Foundation)
• Abdominal Ultrasound (American College of Radiology; Radiological Society of North America) Also in Spanish

• Magnetic Resonance Cholangiopancreatography (MRCP) (American College of Radiology; Radiological Society of North America) Also in Spanish
• Needle Biopsy (Mayo Foundation for Medical Education and Research) Also in Spanish
• 25 Ways to Love Your Liver Health (American Liver Foundation)
• Careful: Acetaminophen in Pain Relief Medicines Can Cause Liver Damage (Food and Drug Administration)
• Cirrhosis and Portal Hypertension (American Academy of Family Physicians) Also in Spanish
• Acute Liver Failure (Mayo Foundation for Medical Education and Research) Also in Spanish
• Benign Liver Tumors (American Liver Foundation) Also in Spanish
• Enlarged Liver (Mayo Foundation for Medical Education and Research) Also in Spanish
• Gilbert Syndrome (Mayo Foundation for Medical Education and Research) Also in Spanish
• Liver Cysts: A Cause of Abdominal Pain? (Mayo Foundation for Medical Education and Research) Also in Spanish
• Liver Hemangioma (Mayo Foundation for Medical Education and Research) Also in Spanish
• Portal Hypertension (Merck & Co., Inc.) Also in Spanish
• Primary Sclerosing Cholangitis (PSC) (American Liver Foundation) Also in Spanish
• FastStats: Chronic Liver Disease and Cirrhosis (National Center for Health Statistics)

Journal Articles References and abstracts from MEDLINE/PubMed (National Library of Medicine)

• Article: Improved liver disease prediction from clinical data through an evaluation of...
• Article: Mental health and quality of life in patients with chronic liver...
• Article: Biological Functions and Potential Therapeutic Significance of O-GlcNAcylation in Hepatic Cellular...
• Liver Diseases -- see more articles
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• Alagille Syndrome (American Liver Foundation) Also in Spanish
• Biliary Atresia (Nemours Foundation) Also in Spanish
• Galactosemia (American Liver Foundation) Also in Spanish
• Glycogen Storage Disease Type 1 (von Gierke) (American Liver Foundation) Also in Spanish
• ALP isoenzyme test (Medical Encyclopedia) Also in Spanish
• Ascites (Medical Encyclopedia) Also in Spanish
• Diet - liver disease (Medical Encyclopedia) Also in Spanish
• Enlarged liver (Medical Encyclopedia) Also in Spanish
• Liver disease (Medical Encyclopedia) Also in Spanish
• Liver scan (Medical Encyclopedia) Also in Spanish
• Loss of brain function - liver disease (Medical Encyclopedia) Also in Spanish

The information on this site should not be used as a substitute for professional medical care or advice. Contact a health care provider if you have questions about your health.

• DOI: 10.1111/jdv.20110
• Corpus ID: 269919257

Assessment of metabolic dysfunction-associated steatotic liver disease in patients with hidradenitis suppurativa: A cross-sectional study.

• N. Omari , S. Simonsen , +5 authors C. Näslund-Koch
• Published in Journal of the European… 19 May 2024

8 References

Bioskin: a protocol for the copenhagen translational skin immunology biobank and research programme, phosphatidylethanol (peth) in blood as a marker of unhealthy alcohol use: a systematic review with novel molecular insights, a multi-society delphi consensus statement on new fatty liver disease nomenclature., risk of liver dysfunction and non-alcoholic fatty liver diseases in people with hidradenitis suppurativa: a systematic review and meta-analysis of real-world evidences, easl clinical practice guidelines (cpgs) on non-invasive tests for evaluation of liver disease severity and prognosis- 2020 update., hidradenitis suppurativa: an update on epidemiology, phenotypes, diagnosis, pathogenesis, comorbidities and quality of life, high prevalence of non‐alcoholic fatty liver disease among hidradenitis suppurativa patients independent of classic metabolic risk factors, development and validation of the international hidradenitis suppurativa severity score system (ihs4), a novel dynamic scoring system to assess hs severity, related papers.

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Chronic liver disease.

Ashish Sharma ; Shivaraj Nagalli .

Affiliations

Last Update: July 3, 2023 .

• Continuing Education Activity

Chronic liver disease is a progressive deterioration of liver functions. Liver functions include the production of clotting factors and other proteins, detoxification of harmful products of metabolism, and excretion of bile. This is a continuous process of inflammation, destruction, and regeneration of liver parenchyma leading to fibrosis and cirrhosis. Cirrhosis is a final stage of chronic liver disease that results in disruption of liver architecture, the formation of widespread nodules, vascular reorganization, neo-angiogenesis, and deposition of an extracellular matrix. The underlying mechanism of fibrosis and cirrhosis at a cellular level is the recruitment of stellate cells and fibroblasts that cause fibrosis, while parenchymal regeneration relies on hepatic stem cells. This activity reviews the evaluation and treatment of chronic liver disease and highlights the role of the healthcare team in evaluating and treating patients with this condition.

• Identify the etiology of chronic liver disease.
• Outline the appropriate evaluation of chronic liver disease.
• Review the treatment options available for chronic liver disease.
• Describe interprofessional team strategies for improving care coordination and communication to advance chronic liver disease and improve outcomes.
• Introduction

Chronic liver disease (CLD) is a progressive deterioration of liver functions for more than six months, which includes synthesis of clotting factors, other proteins, detoxification of harmful products of metabolism, and excretion of bile. CLD is a continuous process of inflammation, destruction, and regeneration of liver parenchyma, which leads to fibrosis and cirrhosis. The spectrum of etiologies is broad for chronic liver disease, which includes toxins, alcohol abuse for a prolonged time, infection, autoimmune diseases, genetic and metabolic disorders. Cirrhosis is a final stage of chronic liver disease that results in disruption of liver architecture, the formation of widespread nodules, vascular reorganization, neo-angiogenesis, and deposition of an extracellular matrix. The underlying mechanism of fibrosis and cirrhosis at a cellular level is the recruitment of stellate cells and fibroblasts, resulting in fibrosis, while parenchymal regeneration relies on hepatic stem cells. Chronic liver disease is an extremely common clinical condition, and the focus is done on the common etiologies, clinical manifestations, and management.

The following are the most common etiologies:

Alcoholic Liver Disease

Alcoholic liver disease is a spectrum of disease which includes alcoholic fatty liver with or without hepatitis, alcohol hepatitis (reversible because of acute ingestion) to cirrhosis (irreversible). Patients with severe alcohol use disorder mostly develop chronic liver disease; this is the most frequent cause of CLD.

Non-alcoholic Fatty Liver Disease (NAFLD/NASH)

NAFLD has an association with metabolic syndrome (obesity, hyperlipidemia, and diabetes mellitus). Some of these patients develop non-alcoholic steatohepatitis, which leads to fibrosis of the liver. All the risk factors of metabolic syndrome can aggravate the disease process.

Chronic Viral Hepatitis

Chronic hepatitis B, C, and D infections are the most common causes of chronic liver disease in East Asia and Sub-Saharan Africa. There are various genotypes of hepatitis C. In Europe and North America, genotype 1a and 1b are more prevalent, while in Southeast Asia, genotype 3 is more common. A molecular epidemiological study revealed a high prevalence of HCV genotype 4, subtype 4a among Egyptian patients living in Sharkia governorate, Egypt. Chronic hepatitis C, if not treated, may lead to hepatocellular carcinoma.

Genetic Causes

• Alpha-1 antitrypsin deficiency:  This is the most common genetic cause of CLD among children.
• Hereditary hemochromatosis:  It is an autosomal recessive disorder of iron absorption. Here due to a mutation involving the HFE gene that regulates the iron absorption from the intestine, excessive iron is absorbed from the gastrointestinal tract. As a result, there is a pathological increase in total body iron (such as ferritin and hemosiderin). This process leads to the generation of hydroxyl free radicals, which in turn causes organ fibrosis.
• Wilson disease:  Autosomal recessive disorder leading to copper accumulation

Autoimmune Causes

Autoimmune hepatitis is a rare disease in which there is the destruction of liver parenchyma by autoantibodies. Most of the patients who present with this disease have already developed cirrhosis. Females are more commonly affected than males.

• Primary biliary cirrhosis (PBC): This is an autoimmune and progressive disease of the liver, which is the destruction of intrahepatic biliary channels and portal inflammation and scarring. It leads to cholestatic jaundice and fibrosis of liver parenchyma. PBC is more common in middle-aged women. Alkaline phosphatase levels increase in PBC.
• Primary Sclerosing Cholangitis (PSC): commonly associated with ulcerative colitis. This condition is characterized by a decrease in the size of intrahepatic and extrahepatic bile ducts due to inflammation and fibrosis. 
• Autoimmune hepatitis (AIH): This is a form of chronic inflammatory hepatitis, more common in women than men, and is characterized by elevated autoantibodies such as antinuclear antibodies, anti-smooth muscle antibodies, and hypergammaglobulinemia. 

Other Causes of Chronic Liver Disease

• Drugs - amiodarone, isoniazid, methotrexate, phenytoin, nitrofurantoin.
• Vascular. Budd-Chiari syndrome.
• Idiopathic/cryptogenic, around 15%
• Epidemiology

Chronic liver disease is one of the frequent causes of death, especially in the developing world. The increasing prevalence of chronic liver disease has been noted in recent times. The majority of chronic liver diseases in the developed world include alcoholic liver disease, chronic viral hepatitis, including hepatitis B and C, non-alcoholic fatty liver disease (NAFLD), and hemochromatosis. [1] In the United States, according to the National Vital Statistics Report 2017 from the Center for Disease Control and Prevention, approximately 4.5 million adults had chronic liver disease and cirrhosis, which is 1.8 percent of the adult population. There were 41,473 deaths (12.8 deaths per 100,000 population) from chronic liver disease and cirrhosis. 

• Pathophysiology

Chronic liver disease represents a continuous and progressive process of hepatic fibrosis, liver tissue architectural distortion, and regeneration nodule formation. While fibrosis is usually irreversible, but it can be reversible in the initial stage of development. The transition time point of reversible fibrosis to irreversible fibrosis is still not completely understood. In chronic liver disease, if not treated, the endpoint is usually irreversible fibrosis, regeneration nodule formation, and development of cirrhosis liver. The development rate of fibrosis is dependent on the underlying etiologies, environmental, and host factors. The evolution of liver fibrosis was studied in 4852 patients with different underlying etiology in one study. The author observed significant differences in the rate of development of fibrosis and its progression. The rate was most rapid in patients with coinfection with HIV- HCV, while primary biliary cirrhosis was the slowest. Fibrosis progression rate was higher with increasing age, and females demonstrated a more gradual progression of liver fibrosis in all but alcoholic liver disease. [2]  Similarly, in another study, genetic polymorphism was attributed as an underlying factor for the difference in fibrosis rate progressions and the development of more severe disease in some individuals compared to others with the same underlying etiology. [3]

Hepatic fibrosis is the deposition of extracellular matrix (ECM) in response to chronic liver injury by any etiology. The common pathway is initiated by hepatic stellate cells (HSC), which usually are vitamin A storing dormant cells found in space between sinusoids and hepatocytes. In response to chronic liver injury, HSC gets activated into proliferative fibrogenic myofibroblast and upregulates the expression of inflammatory receptors such as chemokine receptors, ICAM-1, and other inflammatory mediators by releasing chemokines and other leukocyte chemoattractants. This pro-inflammatory phase or initiation phase also changes gene and phenotypic expression of the liver cells, making them more responsive to these inflammatory cytokines, and perpetuation of activated HSC cells results in the accumulation of ECM and progressive fibrosis. [4]

• Histopathology

The stellate cells are thought to be the source of collagen in pathological conditions. Chronic liver injury activates hepatic stellate cells, which are activated and transformed into a myofibroblast-like phenotype. They then lay down the extracellular matrix. Chronic inflammation, cytokine production by damaged parenchymal cells, and disruption of the extracellular matrix are well-characterized stimuli to stellate cells. 

The etiology affects the patterns of liver fibrosis. Chronic hepatotropic virus infection causes portal expansion followed by periportal fibrosis, septal (bridging) fibrosis, and cirrhosis. Alcoholic liver disease and adult non-alcoholic fatty liver disease cause fibrosis, starting with a centrilobular perivenular distribution and sinusoidal fibrosis. Pediatric fatty liver disease is similar to hepatotropic virus infection with a periportal distribution. Perisinusoidal or perivenular fibrosis is usually not apparent.

Biliary tract disease cirrhosis is characterized by feathery degeneration of periseptal hepatocyte leasing to the presence of prominent “halos” and irregular-shaped nodules (“jigsaw” micronodular pattern). Fibrosis progressively links the adjacent central veins and portal tracts in venous outflow obstruction, resulting inveno-portal cirrhosis or veno-centric (“reversed lobulation” cirrhosis). [5]

• History and Physical

Clinical Manifestations

Signs and symptoms of CLD can be nonspecific, such as fatigue, anorexia, weight loss, or depend upon the complication that the patient has developed. The three significant complications are because of portal hypertension (esophageal varices, ascites), hepatocellular insufficiency (e.g., jaundice, hepatic encephalopathy), and hepatocellular carcinoma. Decompensated chronic liver disease can present with one of the following complications.

Portal Hypertension

Portal hypertension is a result of resistance to portal blood flow because of cirrhotic and noncirrhotic etiology. A portal venous pressure above seven mmHg is considered portal hypertension; however, clinical features or complications do not develop until portal pressure is higher than 12 mmHg. Portal hypertension causes can divide into prehepatic (e.g., portal vein thrombosis), hepatic (e.g., cirrhosis), and post hepatic (e.g., Budd Chiari syndrome). Cirrhosis and hepatic schistosomiasis remain the most common cause of portal hypertension, with cirrhosis being more common in developed countries. The following are the consequences of long-standing portal hypertension.

• Esophageal varices: It presents with melena or upper GI bleed. Cirrhosis of the liver leads to raised portal pressure, which can cause esophageal or gastric varices. Esophageal variceal bleeding is the most common life-threatening complication of CLD.
• Caput medusae
• Rectal hemorrhoids
• Ascites: It is an accumulation of fluid in the peritoneal cavity because of raised portal pressure (increased hydrostatic pressure), decreased albumin (reduced oncotic pressure), and splanchnic vasodilation (due to the release of nitric oxide). Most of the patients develop ascites in the later stages of cirrhosis. Clinical findings in such patients are abdominal distension, shifting dullness, and a fluid wave. Tense ascites can lead to shortness of breath or early satiety.

Hepatocellular Insufficiency

Hepatic Encephalopathy

This is a neuropsychiatric syndrome caused by hepatic dysfunction. Detoxification of harmful products of metabolism, e.g., ammonia, occurs in the liver. In a patient with cirrhosis, the removal of these substances from the body is impaired, leading to an increased level of ammonia. Raised levels of ammonia can impair consciousness. Almost 50% of patients with DCLD can develop hepatic encephalopathy. 

According to AASLD guidelines, depending upon the severity of the disease, there are different grades of hepatic encephalopathy. [6]

• Grade 0/Minimal : Subclinical, normal mental status with minimal changes in memory, coordination, intellectual function, concentration.
• Grade 1:  Trivial lack of awareness, euphoria or anxiety, shortened attention span, impairment of addition or subtraction, altered sleep rhythm.
• Grade 2:  Lethargy or apathy, disorientation to time, personality change, inappropriate behavior, dyspraxia, asterixis.
• Grade 3:  Somnolence to semi-stupor, responsive to stimuli, confused, gross disorientation, bizarre behavior.
• Grade 4:  Coma

The patient can present in any of these symptoms. Most of the patients with hepatic encephalopathy present with altered sensorium. Infections, GI bleed, hyperkalemia, TIPS [7] , sedating agents, and alkalosis can aggravate hepatic encephalopathy.

Jaundice is a yellowish discoloration of the eyes, skin, and mucous membrane because of overproduction or under clearance of bilirubin. Metabolism of hemoglobin or myoglobin produces bilirubin in the spleen. Bilirubin then circulates in the body, bound to albumin. The liver dissociates this complex and converts unconjugated bilirubin to conjugated bilirubin. Jaundice is clinically visible when total bilirubin is greater than 2 mg/dl. As in chronic liver disease, there is the destruction of liver parenchyma, and it does not conjugate bilirubin, which deposits in various tissues of the body. There is pruritus because of the accumulation of bile salts.

Spontaneous Bacterial Peritonitis (SBP)

It is one of the acute and painful complications of chronic liver disease. Bacteria ( E. coli, Klebsiella, Streptococcus pneumonia ) seep through the gastrointestinal tract and infect the ascitic fluid. The infection spread through the fluid to the peritoneal membrane, causing inflammation. SBP presents with fever, generalized abdominal pain, tenderness, and absent bowel sounds.

Hyperestrinism

In chronic liver disease, the catabolism of estrogen becomes impaired, resulting in excess estrogen in the body. This manifests as palmar erythema, spider angiomas (dilated cutaneous arterioles with a central red spot and red extensions that radiate outward like a spider's web in the territory of SVC), gynecomastia (enlarged tender subareolar tissue), and testicular atrophy.

Hepatorenal Syndrome (HRS)

Hepatorenal syndrome is a functional renal failure as kidneys are normal, where there is a gradual loss of renal function. It is a diagnosis of exclusion. Vasoconstrictors are released in CLD, which is responsible for the narrowing of renal vessels. The following criteria have been described:

• Chronic liver disease with portal hypertension or advanced liver failure
• Continuous rising in creatinine, usually more than 0.3 mg/dl within 48 hours or doubling from baseline within seven days. 
• Oliguria with the absence  or minimal proteinuria
• Urine sodium less than 10 meq/L
• Failure to improve with volume expansion and stopping the diuretics.
• Absence of shock
• No recent use of the nephrotoxic drug
• Absence of renal parenchymal disease

Coagulopathy

The liver produces clotting factors, so the patients with CLD have coagulopathies and manifest or contribute to easy bruising and bleeding per gastrointestinal tracts. Hence, PT/INR (intrinsic pathway) and APTT (extrinsic pathways) are prolonged.

The diagnosis of chronic liver disease depends upon the etiology and complications of the disease. An outline regarding the diagnosis for various CLD appears below.

• Viral hepatitis B and C: Serology, PCR (quantitative and qualitative) with genotype
• Alcoholic liver disease: Elevated levels of AST>ALT with a history of chronic alcohol intake. Usually, AST: ALT ratio is 2 to 1 in alcoholic liver disease.
• Hemochromatosis: Raised serum iron, ferritin, decreased TIBC, and liver biopsy. Genetic testing can detect a mutation in the HFE gene, especially C282Y.
• Wilson disease: Raised urine copper, decreased serum ceruloplasmin, and liver biopsy. Genetic testing for the ATP7B gene.
• Non-alcoholic fatty liver disease: Diagnosis of exclusion and ALT>AST. Ultrasonography of the liver is informative. 
• Autoimmune hepatitis: Raised ANA, ASMA, and LKM-1
• Alpha 1 antitrypsin deficiency: Decreased levels of alpha one antitrypsin
• Primary biliary cirrhosis: Markedly raised alkaline phosphatase levels with an antimitochondrial antibody
• Budd-Chiari and veno-occlusive disease: CBC, clotting profile, and imaging studies like ultrasound doppler or computed tomography with contrast study

  Laboratory Findings

In chronic liver disease, there is inflammation and destruction of hepatocytes that leads to the release of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), hence the high levels of these markers in the blood. Other parameters (ALP and GGT) of LFTs also appear elevated in cholestatic conditions like PBC. AST and ALT are usually elevated two to three times of normal limit, but normal levels of these markers do not rule out cirrhosis. [8] As in compensated CLD LFTs may be normal in cirrhosis. Bilirubin (unconjugated> conjugated) levels are elevated in jaundice. There is reduced production of clotting factors leading to raised PT/INR and APTT.

Because of hepatocellular insufficiency in cirrhosis, albumin level drops, and ammonia raises, causing ascites and hepatic encephalopathy. The increased concentration of ammonia, tryptophan metabolites, short-chain fatty acids, octopamine, mercaptans, increased oxidative stress, and increase intracellular osmolality are among many which have been proposed as the mechanism of developing hepatic encephalopathy. [9] [10] [11] [12] [13] In the case of ascites, diagnostic paracentesis is an investigation of choice to see whether ascites are because of raised portal pressure or another cause. By doing a biochemical and cytological analysis of ascitic fluid, we calculate the serum ascites albumin gradient (serum albumin-ascitic fluid albumin). If this gradient is greater than 1.1, then portal hypertension is a likely cause, but if it is less than 1.1, portal hypertension is unlikely. WBC greater than 500/microliter or PMN greater than 250/microliter and fluid cultures will be positive in patients with SBP. [14] Ultrasound of the abdomen and serum AFP levels can help diagnose the presence of hepatocellular carcinoma. In hepatorenal syndrome, creatinine usually is elevated to more than1.5 g/dl. Thrombocytopenia is an indirect measure of splenomegaly, which occurs in CLD because of raised portal pressure.

Radiologic Investigations

It includes an abdominal ultrasound, CT scan, fibro scan, hepatic wedge pressure, endoscopy, EEG, TIPS, triphasic CT, and Doppler scan.

• Ultrasound abdomen  is one of the most common and affordable imaging studies in the case of chronic liver disease. Ultrasound detects the size, echogenicity nodularity of the liver, thereby diagnosing liver cirrhosis. Other benefits of ultrasound in CLD include measurement of portal vein diameter as portal vein diameter increases in portal HTN and assessment of a clot in the hepatic vein (Budd-Chari) and portal vein in portal vein thrombosis.
• Computed tomography  scan can show a lesion in the liver or obstruction of biliary channels in a more precise way, but triphasic CT is the test of choice in diagnosing hepatocellular carcinoma. 
• Transient elastography  (TE) detects early stages of cirrhosis. It can also detect cardiovascular damage in patients with NAFLD. [15] It works on two physical principles; strain displacement and shear wave imaging and quantification. The latter includes point shear wave elastography. It measures the velocity of low frequency (50 Hz) elastic shear waves propagating through the liver. The stiffer the tissue, the faster the elastic shear wave propagates. It can easily work on an ultrasound machine. According to the European association of study for the Liver (EASL), TE is the most effective approach to diagnose cirrhosis in chronic liver disease.
• Wedge hepatic venous pressure  measures portal venous pressure in CLD.
• Doppler scan  can help in diagnosing Budd-Chiari and portal vein thrombosis.
• EEG  shows delta waves in hepatic encephalopathy.
• An upper endoscopy  can diagnose and treat esophageal varices. On endoscopy, we can measure the size of varices. Small varices are less than 5 mm, and large varices are greater than 5 mm.
• A liver biopsy  can confirm the diagnosis of chronic liver disease. Various techniques to perform a liver biopsy are by laparoscope, transjugular, or percutaneously.
• Treatment / Management

Treatment and Prophylaxis

The treatment goal is to stop the progression of the disease and complications and require a multidisciplinary approach. The principle of management is mainly underlying cause correction, Portal hypertension management, and specific treatments for individual disease. A brief outline regarding treatment for various CLD and related complications is given below. For more comprehensive details, please see individual topics in the Statpearls glossary.

General Management

Patients with chronic liver disease mostly present with one of the complications.

Esophageal varices - Varices related bleeding are one of the deadly complications, and the treatment includes aggressive fluid resuscitation, vasopressors (octreotide, terlipressin), and endoscopy. Endoscopic band ligation and injection sclerotherapy are the usual modalities to treat variceal bleed in an emergency. In some patients, early transjugular intrahepatic portosystemic shunt (TIPS) can increase the survival rate. Propranolol is used for primary and secondary prophylaxis for esophageal varices. Diuretics (furosemide, spironolactone) and sodium restriction are essential treatment options for ascites. For tense ascites, therapeutic paracentesis is done. Albumin infusion can also be considered. Initially, broad-spectrum antibiotics are the treatment of choice for SBP and then specific antibiotics after culture. 

Hepatic encephalopathy - The basic principle of treatment is to address the precipitating factors. Patients with hepatic encephalopathy usually improve with precipitating cause correction along with rifaximin and lactulose. [16] [17] Lactulose acts by converting ammonia to ammonium ions and decreases its absorption from the gastrointestinal tract. Lactulose also relieves constipation through its osmotic effect, which further helps to ease the symptoms of hepatic encephalopathy. Rifaximin is used to decrease ammonia production by gut flora. Liver transplant is a curative treatment in patients with hepatorenal syndrome.

Hepatorenal syndrome - HRS based on severity divided into two categories. HRS 1 is more severe compared to HRS 2 (less severe). The primary goal is to correct underlying cause correction to reverse acute kidney injury. Treatment modalities depend on the severity and location of the patient. Treatment modalities include norepinephrine or terlipressin with albumin infusion or midodrine, octreotide with albumin infusion. TIPS procedure in some patients can help and liver transplantation the only definite treatment in the patient who fails to respond to all other treatments. [18] [19] [20]   

Hepatocellular carcinoma (HCC) - Treatment is based on the Barcelona clinic liver cancer staging system in the management of HCC:

• Initial stage (single HCC lesion): Resection and ablation.
• Intermediate stage: Transarterial chemoembolization and radio-embolization. [21]
• Metastatic disease: Sorafenib [22]

Specific Treatment

Viral Hepatitis

• Continuous viral suppression with nucleoside and nucleotide analogs 
• Direct-acting antivirals achieving HCV eradication 
• Interferon-alpha

Alcoholic liver disease:  Alcohol abstinence

Non-alcoholic fatty liver disease:  Treatment of metabolic syndrome components

Autoimmune hepatitis:  Corticosteroids and other immunosuppressive drugs

Hereditary hemochromatosis:  Phlebotomy, iron-chelators 

Copper overload (Wilson disease):  Copper chelators 

Alpha-1-antitrypsin deficiency:  Transplant

Drugs and toxins:  Identify and stop the factor

Primary biliary cholangitis (PBC):  Ursodeoxycholic acid (UDCA) [23]  

Primary sclerosing cholangitis : Transplant

Budd-Chiari syndrome:  Anticoagulation, thrombolysis or angioplasty with or without stenting, TIPS, or liver transplant

• Differential Diagnosis
• Constrictive pericarditis
• Cor-pulmonale
• Dilated cardiomyopathy
• Inferior vena cava thrombosis
• Nodular regenerative hyperplasia
• Sarcoidosis
• Schistosomiasis

Stages of liver disease

• Hepatitis or steatosis or hepatosteatosis
• Hepatocellular carcinoma (HCC)

Compensated chronic liver disease (who has not developed significant complications) usually carries a better prognosis than decompensated liver cirrhosis. Decompensated liver cirrhosis patients (who have developed variceal bleeding, ascites, HCC, SBP, and hepatorenal syndrome) have a poor prognosis. Mean survival of about six months if Child-Pugh score of 12 or greater or MELD score of 21 or higher.

There are various scoring systems used to assess the severity of chronic liver disease.

1.  The Child-Pugh score  uses ascites, bilirubin, albumin, PT, and encephalopathy.

• Class A (score 5-6): well-compensated disease.
• Class B (score 7-9): functional compromise.
• Class C (score 10-15): decompensated disease.

2.  MELD  (model of end-stage liver disease) uses bilirubin, serum creatinine, and INR. The MELD score was initially used to predict mortality within three months after the TIPS procedure and now used to prioritize patients for receipt of a liver transplant.

• Complications

The following are the complications of chronic liver disease.

• Variceal bleeding
• Ascites and spontaneous bacterial peritonitis (SBP)
• Hepatic encephalopathy
• Hepatorenal syndrome
• Hepatopulmonary syndrome
• Consultations
• Gastroenterology/hepatology consultation for patients with decompensated chronic liver disease
• Nephrology consultation in patients with hepatorenal syndrome
• Dietician consultation for advice on the diet
• Referral to a transplant center in patients needing a liver transplant
• Deterrence and Patient Education

Patient education is one of the critical factors that can play a pivotal role in the prevention of chronic liver disease. Most of the causative factors of chronic liver disease damage the liver over a long period; therefore, it is necessary to stop its progression to avoid cirrhosis and its complications.

Recommendations for Preventive Care in Chronic Liver Disease

• Avoid various types of alcohol (wine, liquor, mixed drinks, beer).
• Regular screening for hepatitis B and hepatitis C
• Vaccination against hepatitis A and B
• Avoid iron supplementation unless there is an iron deficiency.
• Avoid over-the-counter painkillers (aspirin, acetaminophen) and other hepatotoxic drugs.
• Maintain a good lipid profile to avoid metabolic syndrome and NAFLD.
• Pearls and Other Issues

To prevent complications, patients with chronic liver disease will need surveillance. These patients should undergo routine monitoring of their CBC, CMP, and prothrombin time at least 3 to 4 times per year.

Routine diagnostic endoscopy should be performed for asymptomatic esophageal varices, and a follow-up endoscopy should be done in 2 years if varices are not present. Treatment with a nonselective beta-blocker to reduce heart rate by 25% in patients with esophageal varices, offers primary prophylaxis with variceal bleeding. [24]  Patients with large esophageal varices should have prophylactic endoscopic variceal banding to avoid the risk of rupture and bleeding.

• The incidence of hepatocellular carcinoma has risen in the United States, and patients with cirrhosis should undergo surveillance with ultrasonography every six months. [25]  A 4-phase CT scan or an MRI scan should be done to rule out hepatocellular carcinoma in patients with a liver nodule on the ultrasound.
• Enhancing Healthcare Team Outcomes

An interprofessional team that provides a holistic and integrated approach is needed for a patient with chronic liver disease to achieve the best possible outcomes. The earlier signs and symptoms of a complication are identified, the better is the prognosis and outcome. The team consists of primary care physicians, gastroenterologists/hepatologists, dieticians as needed, and a social worker and community nurses who can monitor the patient and make referrals as necessary to prevent the development of complications. Routine labs and endoscopy and the ultrasound as appropriate are required. The liver transplant team should closely monitor patients who are transplant candidates.

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Disclosure: Ashish Sharma declares no relevant financial relationships with ineligible companies.

Disclosure: Shivaraj Nagalli declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Sharma A, Nagalli S. Chronic Liver Disease. [Updated 2023 Jul 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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COVID-19: Long-term effects

Some people continue to experience health problems long after having COVID-19. Understand the possible symptoms and risk factors for post-COVID-19 syndrome.

Most people who get coronavirus disease 2019 (COVID-19) recover within a few weeks. But some people — even those who had mild versions of the disease — might have symptoms that last a long time afterward. These ongoing health problems are sometimes called post- COVID-19 syndrome, post- COVID conditions, long COVID-19 , long-haul COVID-19 , and post acute sequelae of SARS COV-2 infection (PASC).

What is post-COVID-19 syndrome and how common is it?

Post- COVID-19 syndrome involves a variety of new, returning or ongoing symptoms that people experience more than four weeks after getting COVID-19 . In some people, post- COVID-19 syndrome lasts months or years or causes disability.

Research suggests that between one month and one year after having COVID-19 , 1 in 5 people ages 18 to 64 has at least one medical condition that might be due to COVID-19 . Among people age 65 and older, 1 in 4 has at least one medical condition that might be due to COVID-19 .

What are the symptoms of post-COVID-19 syndrome?

The most commonly reported symptoms of post- COVID-19 syndrome include:

• Symptoms that get worse after physical or mental effort
• Lung (respiratory) symptoms, including difficulty breathing or shortness of breath and cough

Other possible symptoms include:

• Neurological symptoms or mental health conditions, including difficulty thinking or concentrating, headache, sleep problems, dizziness when you stand, pins-and-needles feeling, loss of smell or taste, and depression or anxiety
• Joint or muscle pain
• Heart symptoms or conditions, including chest pain and fast or pounding heartbeat
• Digestive symptoms, including diarrhea and stomach pain
• Blood clots and blood vessel (vascular) issues, including a blood clot that travels to the lungs from deep veins in the legs and blocks blood flow to the lungs (pulmonary embolism)
• Other symptoms, such as a rash and changes in the menstrual cycle

Keep in mind that it can be hard to tell if you are having symptoms due to COVID-19 or another cause, such as a preexisting medical condition.

It's also not clear if post- COVID-19 syndrome is new and unique to COVID-19 . Some symptoms are similar to those caused by chronic fatigue syndrome and other chronic illnesses that develop after infections. Chronic fatigue syndrome involves extreme fatigue that worsens with physical or mental activity, but doesn't improve with rest.

Why does COVID-19 cause ongoing health problems?

Organ damage could play a role. People who had severe illness with COVID-19 might experience organ damage affecting the heart, kidneys, skin and brain. Inflammation and problems with the immune system can also happen. It isn't clear how long these effects might last. The effects also could lead to the development of new conditions, such as diabetes or a heart or nervous system condition.

The experience of having severe COVID-19 might be another factor. People with severe symptoms of COVID-19 often need to be treated in a hospital intensive care unit. This can result in extreme weakness and post-traumatic stress disorder, a mental health condition triggered by a terrifying event.

What are the risk factors for post-COVID-19 syndrome?

You might be more likely to have post- COVID-19 syndrome if:

• You had severe illness with COVID-19 , especially if you were hospitalized or needed intensive care.
• You had certain medical conditions before getting the COVID-19 virus.
• You had a condition affecting your organs and tissues (multisystem inflammatory syndrome) while sick with COVID-19 or afterward.

Post- COVID-19 syndrome also appears to be more common in adults than in children and teens. However, anyone who gets COVID-19 can have long-term effects, including people with no symptoms or mild illness with COVID-19 .

What should you do if you have post-COVID-19 syndrome symptoms?

If you're having symptoms of post- COVID-19 syndrome, talk to your health care provider. To prepare for your appointment, write down:

• When your symptoms started
• What makes your symptoms worse
• How often you experience symptoms
• How your symptoms affect your activities

Your health care provider might do lab tests, such as a complete blood count or liver function test. You might have other tests or procedures, such as chest X-rays, based on your symptoms. The information you provide and any test results will help your health care provider come up with a treatment plan.

In addition, you might benefit from connecting with others in a support group and sharing resources.

• Long COVID or post-COVID conditions. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects.html. Accessed May 6, 2022.
• Post-COVID conditions: Overview for healthcare providers. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-care/post-covid-conditions.html. Accessed May 6, 2022.
• Mikkelsen ME, et al. COVID-19: Evaluation and management of adults following acute viral illness. https://www.uptodate.com/contents/search. Accessed May 6, 2022.
• Saeed S, et al. Coronavirus disease 2019 and cardiovascular complications: Focused clinical review. Journal of Hypertension. 2021; doi:10.1097/HJH.0000000000002819.
• AskMayoExpert. Post-COVID-19 syndrome. Mayo Clinic; 2022.
• Multisystem inflammatory syndrome (MIS). Centers for Disease Control and Prevention. https://www.cdc.gov/mis/index.html. Accessed May 24, 2022.
• Patient tips: Healthcare provider appointments for post-COVID conditions. https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/post-covid-appointment/index.html. Accessed May 24, 2022.
• Bull-Otterson L, et al. Post-COVID conditions among adult COVID-19 survivors aged 18-64 and ≥ 65 years — United States, March 2020 — November 2021. MMWR Morbidity and Mortality Weekly Report. 2022; doi:10.15585/mmwr.mm7121e1.

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