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Liver disease and

Hepatitis C infection has an unpredictable natural history with significant potential for causing severe liver disease and variable response to current therapy based on pretreatment factors. Therefore, HCV is an excellent model to describe the... [Pg.44]

Another common liver disease, alcoholic liver damage produced by moderate to heavy alcoholic intake, is also reflected by an elevation of the serum GOT and GPT activities. The serim glutamyl transferase activity is reported to be a sensitive index of alcoholic intake and can serve to monitor persons on alcoholic withdrawal programs (60). The LD-5 isoenzyme arises mainly from liver tissue, but has a short half-life (61), which is about 1/5 and 1/2 of the half life of the transaminases, GPT and GOT respectively. Some authors consider that a normal LD-5 isoenzyme activity in a jaundiced patient is sufficient evidence to exclude primary liver disease and that obstruction is probably responsible for the jaundice (62). In hemolytic jaundice the LDH-1 and 2 isoenzymes are elevated. [Pg.208]

Liver transplantation is increasingly used for treatment of end-stage liver disease and thousands of transplants are... [Pg.241]

Cirrhosis is the result of long-term insult to the liver, so damage is typically not evident clinically until the fourth decade of life. Chronic liver disease and cirrhosis combined were the 12th leading cause of death in the United States in 2002. In patients between the ages of 25 and 64, damage from excessive alcohol use accounted for over one-half of the deaths.2 Alcoholic liver disease and viral hepatitis are the most common causes of cirrhosis in the United States and worldwide. [Pg.323]

This isotonic volume expander contains sodium, potassium, chloride, and lactate that approximates the fluid and electrolyte composition of the blood. Ringer s lactate (also known as lactated Ringer s or LR) provides ECF replacement and is most often used in the perioperative setting, and for patients with lower GI fluid losses, burns, or dehydration. The lactate component of LR works as a buffer to increase the pH. Large volumes of LR may cause metabolic alkalosis. Because patients with significant liver disease are unable to metabolize lactate sufficiently, Ringer s lactate administration in this population may lead to accumulation of lactate with iatrogenic lactic acidosis. The lactate is not metabolized to bicarbonate in the presence of liver disease and lactic acid can result. [Pg.406]

Disulfiram works by irreversibly blocking the enzyme aldehyde dehydrogenase, a step in the metabolism of alcohol, resulting in increased blood levels of the toxic metabolite acetaldehyde. As levels of acetaldehyde increase, the patient experiences decreased blood pressure, increased heart rate, chest pain, palpitations, dizziness, flushing, sweating, weakness, nausea and vomiting, headache, shortness of breath, blurred vision, and syncope. These effects are commonly referred to as the disulfiram-ethanol reaction. Their severity increases with the amount of alcohol that is consumed, and they may warrant emergency treatment. Disulfiram is contraindicated in patients who have cardiovascular or cerebrovascular disease, because the hypotensive effects of the disulfiram-alcohol reaction could be fatal in such patients or in combination with antihypertensive medications. Disulfiram is relatively contraindicated in patients with diabetes, hypothyroidism, epilepsy, liver disease, and kidney disease as well as impulsively suicidal patients. [Pg.543]

Asterixis Abnormal posture and movements that may occur in advanced liver disease and a few other circumstances. [Pg.1560]

Martinot, M, etal, (1997). Influence of hepatitis G virus infection on the severity of liver disease and response to interferon-a in patients with chronic hepatitis C. Ann. Intern. Med. 126,874-881. [Pg.234]

Copper is associated with two important life-threatening diseases in man, the pathologies of both being due to defective intracellular copper transport. Menke s disease is characterized by progressive cerebral degeneration, essentially due to insufficient copper absorption, and Wilson s disease is due to excessive copper accumulation in liver, accompanied by liver disease and haemolytic crises. [Pg.322]

Obesity may also contribute to gallbladder disease, gout, breathing problems, increased incidence of infections, liver diseases, and increased pain, especially in the lower back and knees. [Pg.12]

Education, simple rules of personal hygiene and safe food preparation can prevent many diarrheal diseases. Hand washing with soap is an effective step in preventing spread of illness. Human feces must always be considered potentially hazardous. Immunocompromised persons, alcoholics, persons with chronic liver disease and pregnant women may require additional attention, and health care providers can play an important role in providing information about food safety. These populations should avoid undercooked meat, raw shellfish, raw dairy products, French-style cheeses and unheated deli meats [114]. [Pg.31]

The metabolic encephalopathies comprise a series of neurological disorders not caused by primary structural abnormalities rather, they result from systemic illness, such as diabetes, liver disease and renal failure. Metabolic encephalopathies usually develop acutely or subacutely and are reversible if the systemic disorder is treated. If left... [Pg.594]

Lockwood, A. H., Yap, E. W. H. and Wong, W. H. Cerebral ammonia metabolism in patients with severe liver disease and minimal hepatic encephalopathy. /. Cereb. Blood Flow Metab. 11 337-341,1991. [Pg.602]

Acetaminophen is usually well tolerated, but potentially fatal hepatotoxicity with overdose is well documented. It should be used with caution in patients with liver disease and those who chronically abuse alcohol. Chronic alcohol users (three or more drinks daily) should be warned about an increased risk of liver damage or GI bleeding with acetaminophen. Other individuals do not appear to be at increased risk for GI bleeding. Renal toxicity occurs less frequently than with NSAIDs. [Pg.25]

Potentially important laboratory abnormalities occurring with niacin therapy include elevated liver function tests, hyperuricemia, and hyperglycemia. Niacin-associated hepatitis is more common with sustained-release preparations, and their use should be restricted to patients intolerant of regular-release products. Niacin is contraindicated in patients with active liver disease, and it may exacerbate preexisting gout and diabetes. [Pg.119]

Type A HE is induced by acute liver failure, Type B results from portal-systemic bypass without intrinsic liver disease, and Type C occurs with cirrhosis. HE may be classified as episodic, persistent, or minimal. [Pg.253]

Elevations of serum bilirubin are common in end-stage liver disease and obstruction of the common bile duct, but other causes of hyperbilirubinemia are numerous. [Pg.254]

Therapy with INH results in a transient elevation in serum transaminases in 12% to 15% of patients and usually occurs within the first 8 to 12 weeks of therapy. Risk factors for hepatotoxicity include patient age, preexisting liver disease, and pregnancy or postpartum state. INH also may result in neurotoxicity, most frequently presenting as peripheral neuropathy or, in overdose, seizures, and coma. Patients with pyridoxine deficiency, such as alcoholics, children, and the malnourished, are at increased risk, as are patients who are slow acetylators of INH and those predisposed to neuropathy, such as those with diabetes. [Pg.555]

Patients with chronic conditions that cause limited immune deficiency (e.g., renal disease, diabetes, liver disease, and asplenia) and who are not receiving immunosuppressants may receive live attenuated and killed vaccines, and toxoids. [Pg.569]

Medical indications Persons with chronic liver disease and persons who receive clotting factor concentrates. [Pg.1067]

Anhaptoglobinemia or subnormal Hp values, often found in acute and chronic liver disease, and in mononucleosis, may also be caused by an increased consumption and not by decreased synthesis. In both disorders there exists a tendency for the development of splenomegaly, i.e., a tendency to retarded splenic blood flow with slightly shortened survival time of the red cells as a consequence. If we do not presume a half-life of Hp in normals below one day, the main part of the Hp catabolism must be secondary to Hb release. Hence, subnormal Hp values will probably appear in conditions with no clinically observable increased hemolysis or slightly decreased Hp synthesis. The latter may be a con-... [Pg.175]

Cataracts in early childhood 1 1 Cataracts often within a few days of birth Vomiting and diarrhea after milk ingestion Jaundice and hyperbilirubinemia Hypoglycemia may be present Liver disease and cirrhosis Lethargy, hypotonia Mental retardation... [Pg.171]

The main indications for liver transplantation include chronic hepatitis C, alcoholic liver disease, nonalcoholic fatty liver disease, and cryptogenic cirrhosis. [Pg.403]

Statins should be avoided in active liver disease and unexplained raised serum transaminases. Some antihistamines, such as diphenhydramine and promethazine, should be used with caution in mild-to-moderate liver disease. Selective serotonin re-uptake inhibitors should be used at a reduced dose or avoided in hepatic impairment. [Pg.118]

Hepatitis B vaccine schedule consists of three injections given at time 0, 1 month after the first injection and a third injection given 6 months after the first injection. Patients at high risk are given a booster after 5 years to maintain the immunity profile. Patients receiving blood transfusions, haemophilia patients, patients with chronic liver disease, and haemodialysis patients are among the high-risk patients who should be vaccinated. [Pg.335]

Vulnerability of the liver to injury necessitates routine evaluation of hepatic function in patients and asymptomatic individuals to avert or control adverse clinical conditions. Thus, a plethora of methods has been developed for the diagnosis of liver diseases and dysfunctions. One such method uses physical palpation to determine alterations or changes in the orientation of the liver, which provides valuable information about the organ status but the quality of information is subjective and imprecise [3]. Another common method for the diagnosis of more serious hepatic injuries involves liver biopsies coupled with biochemical tests to determine the extent of liver injury and prognosis [4-7]. However, in acute and some chronic hepatic disorders, dynamic and continuous hepatic function monitoring would be advantageous. [Pg.35]

B15. Black, M., and Billing, B. H., Hepatic bilirubin UDP-gluouronyl-transferase activity in liver disease and Gilbert s syndrome. New Engl. J. Med. 280,1266-1271 (1969). [Pg.279]

Drug/Lab test interactions Asympiomai c reversible increases in AST and ALT aminotransferase levels have occurred in patients treated with LMWHs and heparin. Because aminotransferase determinations are important in the differential diagnosis of Ml, liver disease, and PE, interpret elevations that might be caused by LMWHs with caution. [Pg.126]


See other pages where Liver disease and is mentioned: [Pg.302]    [Pg.455]    [Pg.154]    [Pg.66]    [Pg.739]    [Pg.435]    [Pg.792]    [Pg.228]    [Pg.360]    [Pg.243]    [Pg.20]    [Pg.177]    [Pg.327]    [Pg.357]    [Pg.318]    [Pg.254]    [Pg.115]    [Pg.83]    [Pg.107]    [Pg.351]    [Pg.606]   
See also in sourсe #XX -- [ Pg.318 ]




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