This Web Site is committed to the memory of Janis Morrow.

   

Your Liver Functions

 

---

 

 

The Liver

The characteristic structure and organization of the liver enables it to perform vital roles in regulating, synthesizing, storing, secreting, transforming, and breaking down many different substances in the body. In addition, the liver's ability to regenerate lost tissue helps maintain these functions, even in the face of moderate damage. This section of the module focuses on the structural aspects of the liver and its ability to regenerate.

Liver Functions

The body depends on the liver to perform a number of vital functions , and although there is substantial overlap, they can be divided into three basic categories:

regulation, synthesis, and secretion of many substances important in maintaining the body's normal state
storage of important nutrients such as glycogen (glucose), vitamins, and minerals,  purification, transformation, and clearance of waste products, drugs, and toxins
Disease or traumatic injury can greatly reduce the liver's ability to carry out these normal activities. Thus, most of the clinical manifestations of liver dysfunction (discussed later in this module) stem from cell damage and impairment of the normal liver capacities. For example, viral hepatitis causes damage and death of hepatocytes. In this case, manifestations may include increased bleeding (due to decreased synthesis of clotting factors), jaundice (yellow pigmentation due to decreased clearance of bilirubin ), and increased levels of circulating hepatocyte enzymes (released from dead liver cells).

1. Regulations, Synthesis, and Secretion. Hepatocytes are metabolically active cells that serve many functions. For example, they take up glucose, minerals, and vitamins from portal and systemic blood and store them. In addition, hepatocytes can produce many important substances needed by the body, such as blood clotting factors, transporter proteins, cholesterol, and bile components. Finally, by regulating blood levels of substances such as cholesterol and glucose, the liver helps maintain body homeostasis.

a. Glucose. The liver plays a major role in maintaining blood concentrations of glucose, by storing or releasing glucose as needed.

b. Proteins. Most blood proteins (except for antibodies) are synthesized and secreted by the liver. One of the most abundant serum proteins is albumin. Impaired liver function that results in decreased amounts of serum albumin may lead to edema, swelling due to fluid accumulation in the tissues.

The liver also produces most of the proteins responsible for blood clotting, called coagulation or clotting factors. If the blood cannot clot normally due to a decrease in the production of these factors, excessive bleeding may result.

c. Bile. Bile is a greenish fluid synthesized by hepatocytes and secreted into biliary ducts. It then leaves the liver to be temporarily stored in the gallbladder before emptying into the small intestine. The major components of bile include cholesterol, phospholipids, bilirubin (a metabolite of red blood cell hemoglobin), and bile salts. Importantly, bile salts act as "detergents" that aid in the digestion and absorption of dietary fats. Liver damage or obstruction of a bile duct (e.g., gallstone) can lead to cholestasis, (the blockage of bile flow, which causes the malabsorption of dietary fats), steatorrhea (foul-smelling diarrhea caused by non-absorbed fats), and jaundice.

d. Lipids. Cholesterol, a type of lipid, is a substance found in cell membranes that helps maintain the physical integrity of cells. The liver synthesizes cholesterol, which is then packaged and distributed to the body to be sued or excreted into bile for removal from the body. Increased cholesterol concentrations in bile may predispose to gallstone formation.

The liver also synthesizes lipoproteins, which are made up of cholesterol, triglycerides (containing fatty acids), phospholipids, and proteins. Lipoproteins circulate in the blood and shuttle cholesterol and fatty acids (an energy source) between the liver and body tissues. Most liver diseases do not significantly affect serum lipid levels, with the exception of cholestatic diseases, which may be associated with increased levels.

2. Storage. As mentioned above, the liver is designed to store important substances such as glucose (in the form of glycogen). The liver also stores fat-soluble vitamins (vitamins A, D, E and K), folate, vitamin B ₁₂ , and minerals such as copper and iron. However, excessive accumulation of certain substances can be harmful. For example, patients with an inherited condition known as Wilson's disease cannot secrete copper into bile normally and usually have a low blood level of the copper-binding protein ceruloplasmin. Retained copper accumulates in the liver (leading to cirrhosis and in the central nervous system (resulting in neuropsychiatric symptoms).

3. Purification, Transformation, and Clearance. The liver removes harmful substances (such as ammonia and toxins) from the blood and then breaks them down or transforms them into less harmful compounds. In addition, the liver metabolizes most hormones and ingested drugs to either more or less active products.

a. Ammonia. The liver converts ammonia to urea, which is excreted into the urine by the kidneys. In the presence of severe liver disease, ammonia accumulates in the blood because of both decreased blood clearance and decreased ability to form urea. Elevated ammonia levels can be toxic, especially to the brain, and may play a role in the development of hepatic encephalopathy.

b. Bilirubin. Bilirubin is a yellow pigment formed as a breakdown product of red blood cell hemoglobin. The spleen, which destroys old red cells, releases "unconjugated" bilirubin into the blood, where it circulates in the blood bound to albumin (Figure 7). The liver efficiently takes up bilirubin and chemically modifies it to "conjugated," or water-solube, bilirubin that can be excreted into bile. Increased production or decreased clearance of bilirubin results in jaundice, a yellow pigmentation of the skin and eyes from bilirubin accumulation.

c. Hormones. Since the liver plays important roles in hormonal modification and inactivation, chronic liver disease may cause hormonal imbalances. For example, the masculinizing hormone testosterone and the feminizing hormone estrogen are metabolized and inactivated by the liver. Men with cirrhosis, especially those who abuse alcohol, have increased circulating estrogens relative to testosterone derivatives, which may lead to body feminization.

d. Drugs. Nearly all drugs are modified or degraded in the liver. In particular, oral drugs are absorbed by the gut and transported via the portal circulation to the liver. In the liver, drugs may undergo first-pass metabolism, a process in which they are modified, activated, or inactivated before they enter the systemic circulation, or they may be left unchanged.

Alcohol is primarily metabolized by the liver, and accumulation of its products can lead to cell injury and death.

In patients with liver disease, drug detoxification and excretion may be dangerously altered, resulting in drug concentrations that are too low or too high or the production of toxic drug metabolites. Therefore, medications that are metabolized by the liver must be used with caution in patients with hepatic disease; these patients may need lower doses of the drug.

e. Toxins. The liver is generally responsible for detoxifying chemical agents and poisons, whether ingested or inhaled. Pre-existing liver disease may inhibit or alter detoxification processes and thus increase the toxic effects of these agents. Additionally, exposure to chemicals or toxins may directly affect the liver, ranging from mild dysfunction to severe and life-threatening damage.

Summary

From its sheltered position in the abdominal cavity, the liver filters blood from both the portal and systemic circulations. The body depends on the liver to regulate, synthesize, store, and secrete many important proteins and nutrients and to purify, transform, and clear toxic or unneeded substances. To carry out these functions, hepatocytes are organized for optimal contact with sinusoids (leading to and from blood vessels) and bile ducts. A special feature of the liver is its ability to regenerate, but this capacity can be exceeded by repeated or extensive damage.

---

The Liver

 

The liver is the largest gland in the body (approximately 1500 grams) and is located in the right upper quadrant of the adodomen. It is glossy in appearance and dark red in color from the rich supply of blood flowing through it. Approximately 25% of the cardiac output flows to the liver. It performs many important functions:
1) the uptake, storage, and disposal of nutrients (protein, glucose and fat), drugs and toxins and 2) the production of synthesis proteins critical for blood clotting) and metabolism of substances produced by the body (Vitamins A, B, D, B-12, K)

Click on Image to Enlarge

Anatomy of the Liver

The anterior surface of the liver is triangular in shape, made of two lobes. The right lobe is the larger of the two, measuring 6 to 7 inches in length. The left lobe is closer to 3 inches in length.

Click on Image to Enlarge

Ligaments connect the upper surface of the liver to the diaphragm and the abdominal wall and the under surface to the stomach and duodenum. The gall bladder is located on the under surface of the right lobe of the liver. Neighboring organs include the colon, the intestines, and the right kidney.

The Liver Up Close

When viewed under a microscope, the liver is seen as large network of units called hepatic lobules. The hepatic lobule is very small and looks like a six-sided cylinder

Click on Image to Enlarge

The lobule itself is surrounded by connective tissue and has 5 to 7 clusters of vessels around its edges. These vessels include a branch of the portal vein, a branch of the   hepatic artery, and a bile duct.

A central vein runs through the middle of the lobe and is surrounded by cords of liver cells that radiate out in all directions. Between these cords are wide thin-walled blood vessels called sinusoids.

Digestive Function of the Liver

Sometimes referred to as the "great chemical factory" of the body, the liver creates, regulates, and stores a variety of substances used by the gastrointestinal system , and it serves a number of important digestive functions.

Click on Image to Enlarge

The main digestive chemical synthesized by the liver is bile. During a meal, bile is secreted by liver cells and travels through the hepatic duct system into the small intestine where it is used to break down fat molecules.

Between meals, bile is stored in the gall bladder. Bile further serves as a waste disposal system for toxins removed from the blood by the liver.

The liver also plays a major role in the regulation of blood glucose (blood sugar). The liver synthesizes, dissolves, and stores amino acids, protein, and fat. It stores several important vitamins like B-12 and Vitamin A. The liver also disposes of cellular waste and breaks down harmful substances like alcohol, disposing of them into the bile.

Circulatory Function of the Liver

While the liver is technically part of the gastrointestinal system, it also plays an important role in blood circulation. The liver has been called the "antechamber of the heart" because it collects and processes all of the gastrointestinal blood through the portal vein and delivers it to the right side of the heart. The liver receives blood through two vascular systems, the portal vein and hepatic artery.

Click on Image to Enlarge

 

The portal vein is formed by multiple branches of veins (superior and inferior mesenteric, splenic) that supply the small and large intestine. Thus, all blood leaving the intestine will flow into the portal vein and then into the liver. This helps to explain how colon cancer cells leave the intestine and travel, via the portal vein, to the liver and then grow into tumors. About 75% of the total blood flow to the liver comes from the portal vein.

Click on Image to Enlarge

The hepatic artery arises from a branch (celiac) of the aorta (the main artery leading from the heart). The hepatic artery supplies "oxygen-rich" blood to the liver and represents 25% of the total blood flow to the liver.

The blood drains from the liver into the hepatic veins. These veins drain into the inferior vena cava and finally into the right atrium of the heart. The liver processes so much blood that at one time more than 25% of the total blood output from the heart is flowing through its tissues!

The liver is a complex and unique organ serving many functions vital to sustaining life. From digestion to circulation, the liver is constantly processing blood for use by the rest of the body.

The liver is the most resilient of all of the body's organs. It is capable of regenerating itself. When part of the liver is removed, a healthy organ will often grow back to its original size.
 
 

---

 

---

 

What does it all mean? (Interpreting Liver Function Tests)

Special Considerations in Interpreting Liver Function Tests.

Author/s: David E. Johnston
 

A number of pitfalls can be encountered in the interpretation of common blood liver function tests. These tests can be normal in patients with chronic hepatitis or cirrhosis. The normal range for aminotransferase levels is slightly higher in males, nonwhites and obese persons. Severe alcoholic hepatitis is sometimes confused with cholecystitis or cholangitis. Conversely, patients who present soon after passing common bile duct stones can be misdiagnosed with acute hepatitis because aminotransferase levels often rise immediately, but alkaline phosphatase and g-glutamyltransferase levels do not become elevated for several days. Asymptomatic patients with isolated, mild elevation of either the unconjugated bilirubin or the g-glutamyltransferase value usually do not have liver disease and generally do not require extensive evaluation. Overall hepatic function can be assessed by applying the values for albumin, bilirubin and prothrombin time in the modified Child-Turcotte grading system.

The commonly used liver function tests (LFTs) primarily assess liver injury rather than hepatic function. Indeed, these blood tests may reflect problems arising outside the liver, such as hemolysis (elevated bilirubin level) or bone disease (elevated alkaline phosphatase [AP] level).

Abnormal LFTs often, but not always, indicate that something is wrong with the liver, and they can provide clues to the nature of the problem. However, normal LFTs do not always mean that the liver is normal. Patients with cirrhosis and bleeding esophageal varices can have normal LFTs. Of the routine LFTs, only serum albumin, bilirubin and prothrombin time (PT) provide useful information on how well the liver is functioning.

The general subject of LFTs1,2 and the differential diagnosis of abnormal LFTs in asymptomatic patients3-5 have been well reviewed. This article discusses some common pitfalls in the interpretation of LFTs. Hints for interpreting these tests are presented in Table 1.

Markers of Hepatocellular Injury

The most commonly used markers of hepatocyte injury are aspartate aminotransferase (AST, formerly serum glutamic-oxaloacetic transaminase [SGOT]) and alanine aminotransferase (ALT, formerly serum glutamate-pyruvate transaminase [SGPT]). While ALT is cytosolic, AST has both cytosolic and mitochondrial forms.

Hepatocyte necrosis in acute hepatitis, toxic injury or ischemic injury results in the leakage of enzymes into the circulation. However, in chronic liver diseases such as hepatitis C and cirrhosis, the serum ALT level correlates only moderately well with liver inflammation. In hepatitis C, liver cell death occurs by apoptosis (programmed cell death) as well as by necrosis. Hepatocytes dying by apoptosis presumably synthesize less AST and ALT as they wither away. This probably explains why at least one third of patients infected with hepatitis C virus have persistently normal serum ALT levels despite the presence of inflammation on liver biopsy.6,7 Patients with cirrhosis often have normal or only slightly elevated serum AST and ALT levels. Thus, AST and ALT lack some sensitivity in detecting chronic liver injury. Of course, AST and ALT levels tend to be higher in cirrhotic patients with continuing inflammation or necrosis than in those without continuing liver injury.

As markers of hepatocellular injury, AST and ALT also lack some specificity because they are found in skeletal muscle. Levels of these aminotransferases can rise to several times normal after severe muscular exertion or other muscle injury, as in polymyositis,8 or in the presence of hypothyroidism, which can cause mild muscle injury and the release of aminotransferases. In fact, AST and ALT were once used in the diagnosis of myocardial infarction.

Slight AST or ALT elevations (within 1.5 times the upper limits of normal) do not

necessarily indicate liver disease. Part of this ambiguity has to do with the fact that unlike the values in many other biochemical tests, serum AST and ALT levels do not follow a normal bell-shaped distribution in the population.9 Instead, AST and ALT values have a skewed distribution characterized by a long "tail" at the high end of the scale (Figure 1).5 For example, the mean values for ALT are very similar from one population to another, but the degree to which the distribution is skewed varies by gender and ethnicity. The ALT distributions in males and nonwhites (i.e., blacks and Hispanics) tend to have a larger tail at the high end, so that more values fall above the upper limits of normal set for the average population.10,11

AST and ALT values are higher in obese patients, probably because these persons commonly have fatty livers.12 ALT levels have been noted to decline with weight loss.13 Depending on the physician's point of view, the upper limits of normal for AST and ALT levels could be set higher for more obese persons.

Rare individuals have chronically elevated AST levels because of a defect in clearance of the enzyme from the circulation.14 For both AST and ALT, the average values and upper limits of normal in patients undergoing renal dialysis are about one half of those found in the general population.15 Mild elevations of ALT or AST in asymptomatic patients can be evaluated efficiently by considering alcohol abuse, hepatitis B, hepatitis C and several other possible diagnoses (Table 2).5

Various liver diseases are associated with typical ranges of AST and ALT levels (Figure 2). ALT levels often rise to several thousand units per liter in patients with acute viral hepatitis. The highest ALT levels-often more than 10,000 U per L-are usually found in patients with acute toxic injury subsequent to, for example, acetaminophen overdose or acute ischemic insult to the liver. AST and ALT levels usually fall rapidly after an acute insult.

Lactate dehydrogenase (LDH) is less specific than AST and ALT as a marker of hepatocyte injury. However, it is worth noting that LDH is disproportionately elevated after an ischemic liver injury.16

It is especially important to remember that in patients with acute alcoholic hepatitis, the serum AST level is almost never greater than 500 U per L and the serum ALT value is almost never greater than 300 U per L. The reasons for these limits on AST and ALT elevations are not well understood. In typical viral or toxic liver injury, the serum ALT level rises more than the AST value, reflecting the relative amounts of these enzymes in hepatocytes. However, in alcoholic hepatitis, the ratio of AST to ALT is greater than 1 in 90 percent of patients and is usually greater than 2.17 The higher the AST-to-ALT ratio, the greater the likelihood that alcohol is contributing to the abnormal LFTs. In the absence of alcohol intake, an increased AST-to-ALT ratio is often found in patients with cirrhosis.

The elevated AST-to-ALT ratio in alcoholic liver disease results in part from the depletion of vitamin B6 (pyridoxine) in chronic alcoholics.18 ALT and AST both use pyridoxine as a coenzyme, but the synthesis of ALT is more strongly inhibited by pyridoxine deficiency than is the synthesis of AST. Alcohol also causes mitochondrial injury, which releases the mitochondrial isoenzyme of AST.

Patients with alcoholic hepatitis can present with jaundice, abdominal pain, fever and a minimally elevated AST value, thereby leading to a misdiagnosis of cholecystitis. This is a potentially fatal mistake given the high surgical mortality rate in patients with alcoholic hepatitis.19

Markers of Cholestasis

Cholestasis (lack of bile flow) results from the blockage of bile ducts or from a disease that impairs bile formation in the liver itself. AP and g- glutamyltransferase (GGT) levels typically rise to several times the normal level after several days of bile duct obstruction or intrahepatic cholestasis. The highest liver AP elevations-often greater than 1,000 U per L, or more than six times the normal value-are found in diffuse infiltrative diseases of the liver such as infiltrating tumors and fungal infections.

Diagnostic confusion can occur when a patient presents within a few hours after acute bile duct obstruction from a gallstone. In this situation, AST and ALT levels often reach 500 U per L or more in the first hours and then decline, whereas AP and GGT levels can take several days to rise.

Both AP and GGT levels are elevated in about 90 percent of patients with cholestasis.20 The elevation of GGT alone, with no other LFT abnormalities, often results from enzyme induction by alcohol or aromatic medications in the absence of liver disease. The GGT level is often elevated in persons who take three or more alcoholic drinks (45 g of ethanol or more) per day.21 Thus, GGT is a useful marker for immoderate alcohol intake. Phenobarbital, phenytoin (Dilantin) and other aromatic drugs typically cause GGT elevations of about twice normal. A mildly elevated GGT level is a typical finding in patients taking anticonvulsants and by itself does not necessarily indicate liver disease.22,23

Serum AP originates mostly from liver and bone, which produce slightly different forms of the enzyme. The serum AP level rises during the third trimester of pregnancy because of a form of the enzyme produced in the placenta. When serum AP originates from bone, clues to bone disease are often present, such as recent fracture, bone pain or Paget's disease of the bone (often found in the elderly). Like the GGT value, the AP level can become mildly elevated in patients who are taking phenytoin.22,23

If the origin of an elevated serum AP level is in doubt, the isoenzymes of AP can be separated by electrophoresis. However, this process is expensive and usually unnecessary because an elevated liver AP value is usually accompanied by an elevated GGT level, an elevated 5[acute accent]-nucleotidase level and other LFT abnormalities.

In one study,24 isolated AP elevations were evaluated in an unselected group of patients at a Veterans Affairs hospital. Most mild AP elevations (less than 1.5 times normal) resolved within six months, and almost all greater elevations had an evident cause that was found on routine clinical evaluation.

Persistently elevated liver AP values in asymptomatic patients, especially women, can be caused by primary biliary cirrhosis, which is a chronic inflammatory disorder of the small bile ducts. Serum antimitochondrial antibody is positive in almost all of these patients.

Indicators of How Well the Liver Functions

Bilirubin

Bilirubin results from the enzymatic breakdown of heme. Unconjugated bilirubin is conjugated with glucuronic acid in hepatocytes to increase its water solubility and is then rapidly transported into bile. The serum conjugated bilirubin level does not become elevated until the liver has lost at least one half of its excretory capacity. Thus, a patient could have obstruction of either the left or right hepatic duct without a rise in the bilirubin level.

Because the secretion of conjugated bilirubin into bile is very rapid in comparison with the conjugation step, healthy persons have almost no detectable conjugated bilirubin in their blood. Liver disease mainly impairs the secretion of conjugated bilirubin into bile. As a result, conjugated bilirubin is rapidly filtered into the urine, where it can be detected by a dipstick test. The finding of bilirubin in urine is a particularly sensitive indicator of the presence of an increased serum conjugated bilirubin level.

In many healthy persons, the serum unconjugated bilirubin is mildly elevated to a concentration of 2 to 3 mg per dL (34 to 51 [micro sign]mol per L) or slightly higher, especially after a 24-hour fast. If this is the only LFT abnormality and the conjugated bilirubin level and complete blood count are normal, the diagnosis is usually assumed to be Gilbert syndrome, and no further evaluation is required. Gilbert syndrome was recently shown to be related to a variety of partial defects in uridine diphosphate-glucuronosyl transferase, the enzyme that conjugates bilirubin.25

Mild hemolysis, such as that caused by hereditary spherocytosis and other disorders, can also result in elevated unconjugated bilirubin values, but hemolysis is not usually present if the hematocrit and blood smear are normal. The presence of hemolysis can be confirmed by testing other markers, such as haptoglobin, or by measuring the reticulocyte count.

Severe defects in bilirubin transport and conjugation can lead to markedly elevated unconjugated bilirubin levels, which can cause serious neurologic damage (kernicterus) in infants. However, no serious form of liver disease in adults causes elevation of unconjugated bilirubin levels in the blood without also causing elevation of conjugated bilirubin values.

When a patient has prolonged, severe biliary obstruction followed by the restoration of bile flow, the serum bilirubin level often declines rapidly for several days and then slowly returns to normal over a period of weeks. The slow phase of bilirubin clearance results from the presence of delta-bilirubin, a form of bilirubin chemically attached to serum albumin.26 Because albumin has a half-life of three weeks, delta-bilirubin clears much more slowly than bilirubin-glucuronide. Clinical laboratories can measure delta-bilirubin concentrations, but such measurements are usually unnecessary if the physician is aware of the delta-bilirubin phenomenon.

Albumin

Although the serum albumin level can serve as an index of liver synthetic capacity, several factors make albumin concentrations difficult to interpret.27 The liver can synthesize albumin at twice the healthy basal rate and thus partially compensate for decreased synthetic capacity or increased albumin losses. Albumin has a plasma half-life of three weeks; therefore, serum albumin concentrations change slowly in response to alterations in synthesis. Furthermore, because two thirds of the amount of body albumin is located in the extravascular, extracellular space, changes in distribution can alter the serum concentration.

In practice, patients with low serum albumin concentrations and no other LFT abnormalities are likely to have a nonhepatic cause for low albumin, such as proteinuria or an acute or chronic inflammatory state. Albumin synthesis is immediately and severely depressed in inflammatory states such as burns, trauma and sepsis, and it is commonly depressed in patients with active rheumatic disorders or severe end-stage malnutrition. In addition, normal albumin values are lower in pregnancy.

Prothrombin time

The liver synthesizes blood clotting factors II, V, VII, IX and X. The prothrombin time (PT) does not become abnormal until more than 80 percent of liver synthetic capacity is lost. This makes PT a relatively insensitive marker of liver dysfunction. However, abnormal PT prolongation may be a sign of serious liver dysfunction. Because factor VII has a short half-life of only about six hours, it is sensitive to rapid changes in liver synthetic function. Thus, PT is very useful for following liver function in patients with acute liver failure.

An elevated PT can result from a vitamin K deficiency. This deficiency usually occurs in patients with chronic cholestasis or fat malabsorption from disease of the pancreas or small bowel. A trial of vitamin K injections (e.g., 5 mg per day administered subcutaneously for three days) is the most practical way to exclude vitamin K deficiency in such patients. The PT should improve within a few days.

Blood ammonia

Measurement of the blood ammonia concentration is not always useful in patients with known or suspected hepatic encephalopathy. Ammonia contributes to hepatic encephalopathy; however, ammonia concentrations are much higher in the brain than in the blood and therefore do not correlate well.28 Furthermore, ammonia is not the only waste product responsible for encephalopathy. Thus, blood ammonia concentrations show only a mediocre correlation with the level of mental status in patients with liver disease. It is not unusual for the blood ammonia concentration to be normal in a patient who is in a coma from hepatic encephalopathy.

Blood ammonia levels are best measured in arterial blood because venous concentrations can be elevated as a result of muscle metabolism of amino acids. Blood ammonia concentrations are most useful in evaluating patients with stupor or coma of unknown origin. It is not necessary to evaluate blood ammonia levels routinely in patients with known chronic liver disease who are responding to therapy as expected.

Grading Liver Function by Child-Turcotte Class

In communicating among themselves, many physicians use the Child-Turcotte class as modified by Pugh, often termed the "Child class," to convey information about overall liver function and prognosis (Table 3).29 This grading system can be used to predict overall life expectancy and surgical mortality in patients with cirrhosis and other liver diseases.30

For elective general abdominal surgery, perioperative mortality is in the neighborhood of several percent for patients who fall into the Child class A, 10 to 20 percent for those in class B and approximately 50 percent for those in class C.31 These percentages must be balanced by prognostic considerations when transplantation becomes an option. The presence of cirrhosis by itself is not an indication for liver transplantation, and transplantation is rarely performed in patients who fall into Child class A. For example, the 10-year survival rate is as high as 80 percent in patients with hepatitis C and cirrhosis who have Child class A liver function and no variceal bleeding.32 However, once patients with any type of liver disease fall into the Child-Turcotte class B or class C category, survival is significantly reduced and transplantation should be considered.

REFERENCES

1.Kaplan MM. Laboratory tests. In: Schiff L, Schiff ER, eds. Diseases of the liver. 7th ed. Philadelphia: Lippincott, 1993:108-44.

2.Kamath PS. Clinical approach to the patient with abnormal liver function test results. Mayo Clin Proc 1996;71:1089-94.

---

 

Tylenol/Acetaminophen HCV and your liver

 

 

Other Pages Of Interest :

Visit Janis and Friends Blog

2010 Hepatitis C News Around the World

New Hepatitis C Drugs In Devolvement