|
Natalie Cole Optimistic About Her Battle with Hepatitis C
Although currently recovering from combination therapy's side effects, the well-respected vocalist Natalie Cole may have conquered the Hepatitis C virus....
Hep C and Fatty Liver Disease Linked
Pittsburgh researchers have found an enzyme known to participate in fat production is elevated in those with Hepatitis C. Further exploration of this enzyme could help physicians better predict which HCV patients are at risk of developing fatty liver disease....
Anadys' ANA773 Hepatitis C Phase I Trials in Netherlands
Reducing the dosing schedule in half, Anadys Pharmaceuticals continues its investigation of ANA773, a Toll-Like Receptor-7 agonist prodrug. Approaching the Hepatitis C virus differently from most other contenders, Phase I clinical trials evaluating the safety, tolerability and viral-load decline associated...
|
|
|
University of Iowa Family Practice Handbook, 3rd Edition, Chapter 4
Gastroenterology: Alcoholic Liver Disease, Liver Failure and Chronic Liver
Disease
Peter P. Toth, M.D., Ph.D.
Department of Family Medicine
University of Iowa
Peer Review Status: Externally Peer Reviewed by Mosby
Alcoholic Liver Disease
- Cause is chronic alcohol ingestion.
- See chronic liver disease below for symptoms and signs.
- Clinically resembles hepatitis and progresses to cirrhosis.
- Must abstain from alcohol.
- See chronic liver disease below for manifestations and treatment.
Liver Failure and Chronic Liver Disease
- Cirrhosis
Cirrhosis is a diffuse process consisting of islands of regenerated liver
surrounded by dense fibrosis that occurs after a protracted insult (such as
alcohol, chronic active hepatitis).
- Symptoms of Cirrhosis
Weight loss, malnutrition, fatigue, easy bruising (caused by reduced levels
of factors II, VII, IX, and X), jaundice, encephalopathy, pruritus, edema,
and ascites. The patient may also have GI bleeding from esophageal varices
(caused by portal hypertension) or coma. Look for fetor hepaticus, asterixis,
and hyperreflexia. GI bleeding is a common cause of encephalopathy and coma
in liver failure patients because of the large gastrointestinal protein load.
- Laboratory Evaluation
Laboratory evaluation may show normal liver enzymes in end-stage disease because
of the small amount of residual hepatic tissue. These patients will usually
have low serum levels of total protein and albumin. Anemia and thrombocytopenia
may also be present. Blood ammonia levels may be elevated, but these correlate
poorly with clinical manifestations of coma. Electrolyte abnormalities include
hyponatremia, hypokalemia, and water overload (see also sections on these
topics). There may also be concomitant acidosis or alkalosis.
- Treatment
Consists in removal of the offending agent (such as alcohol).
- Acute treatment (for coma or encephalopathy).
- Clean bowels with enemas.
- Neomycin 4 to 6 g PO QD in divided doses to reduce bacterial toxins.
May be given via NG tube.
- Lactulose 30 to 45 g PO TID to produce two or three loose stools
per day.
- Limit total protein intake to 20 to 40 g/day.
- Vitamin K 5 to 10 mg/day for 2 or 3 days may help coagulation.
- Potassium supplements may be used for hypokalemia.
- Potassium-sparing diuretics such as spironolactone 100 to 300 mg/day
divided into 2 or 3 doses will reduce ascites without decreasing potassium.
Hydrochlorothiazide or furosemide may be added to this regimen if
needed (see section on ascites below).
- Chronic treatment. Chronic treatment includes the prevention of coma
or encephalopathy with the measures outlined above as well as chronic
management of electrolyte disorders.
- Watch for spontaneous peritonitis, which can occur with
ascites (see section on ascites).
- Acetaminophen toxicity is common in this population with doses that
are generally considered nontoxic.
table Of Contents
|
|