Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of 18 chronic alcoholic patients who had sclerosing hyaline necrosis in noncirrhotic livers was compared with a group of 12 similar individuals with acute alcoholic hepatitis, but no centrilobular fibrosis. In cases with sclerosing hyaline necrosis, the most characteristic features were portal hypertension with very large, tender livers and unusually high glutamic-oxalacetic transaminase values; these were associated with centrilobular fibrosis and abundant alcoholic hyalin. Three of these patients died within two years and in two of these, early cirrhosis was found at necropsy. In the cases of acute alcoholic hepatitis, hepatomegaly was the most conspicuous finding, and only a single patient died; death here was unrelated to hepatic disease, the liver being unremarkable at necropsy. Patients who had sclerosing hyaline necrosis tended to remain ill for significantly longer periods. These observations, in conjunction with evidence gathered from the literature, seem to suggest that sclerosing hyaline necrosis is an obligatory step in the natural evolution of alcoholic hepatic disease, especially in cases that evolve into cirrhosis.
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PMID:Sclerosing hyaline necrosis in noncirrhotic chronic alcoholic hepatitis. 6 9

Acute alcoholic hepatitis is an anatomical (fatty liver with sclerosing hyaline necrosis) and a clinical (hepatomegaly with a variety of symptoms of hepatic failure) entity arising out of chronic alcoholism, and of a typically 'pre-cirrhotic' state. Although fatal in 25% of acute cases due to failure of homeostasis, it often leaves a centrilobular scarring necrosis which in more than 60% of cases progresses to nodular cirrhosis. Continued alcoholism worsens the prognosis. Alcoholic hepatitis may be confused with acute abdominal catastrophes or with a hepatoma. The characteristic Mallory bodies found on liver biopsy are found rarely in non-alcoholic hepatitis. There is no effective treatment for this disease except reduction of alcohol intake; indeed, the disease may become self-perpetuating.
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PMID:[Acute alcoholic hepatitis]. 92 58

In a group of 1,025 cases of alcoholic liver the authors detected 28 cases (2.73%) of acute alcoholic hepatitis on the basis of the morphologic examination, 75% were males, mean age 45 +/- 18 years. The mean amount of alcohol consumed daily was 106.7 g for a mean duration of 19.78 years. The hepatic lesional substrate was hepatic steatosis and cirrhosis in 7 cases (25%) and steatofibrosis in the other 14 cases (50%). The triggering factors were the abuse of alcohol in 27 cases and a pneumonia in the last case. The disease was characterized by fever, encephalopathy, hepatomegaly, hepatocytolytic-cholestatic syndrome. The evolution was dictated by the gravity of the background hepatic lesional substrate.
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PMID:[Acute alcoholic hepatitis]. 257 74

We report a case of Zieve's Syndrome that developed after an important alcohol consumption in a 32-yr-old female patient. She was admitted to the hospital with anorexia, asthenia and jaundice. Physical examination showed liver stigmata and hepatomegaly. Laboratory tests demonstrated increased aminotransferase levels, hyperbilirubinemia, hyperlipidemia and normocytic and normochromic anemia with dianocytes in peripheral blood smear. Ultrasonography showed a hyperechoic liver and a liver biopsy showed acute and chronic alcoholic liver disease. Clinical evolution was satisfactory and the therapy consisted of blood transfusion, parenteral fluids, B-complex vitamin and a fatty free diet. Jaundice, hyperlipidemia and haemolytic anemia define Zieve's Syndrome (Z.S.) There is a pathogenetic relationship among the clinical and biological phenomena in this syndrome, whose starter is an acute alcohol intake. Haemolysis is the distinctive feature with respect to the classical acute alcoholic hepatitis, and it is due to erythrocyte's metabolic and osmotic instability in relation to lipids abnormalities. Its clinical resolution precedes the normalization of serum lipids levels. Therapy is similar to that for acute alcoholic hepatitis although sometimes the anemia requires blood transfusion.
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PMID:[Zieve's syndrome. A case report]. 864 20

A 47-year-old female with a history of chronic alcoholism presented with nausea, vomiting and mild epigastric tenderness. She reported subjective fever, abdominal fullness and loose, watery stools and had stable vitals on arrival. Examination was positive for mild epigastric tenderness with hepatic enlargement. Computed tomography of the abdomen showed circumferential thickening of the stomach wall, lower esophagus and the first part of the duodenum in addition to peritoneal ascites. She was admitted for alcohol-related gastritis, acute alcoholic hepatitis, and acute kidney injury. She was started on fluid resuscitation and supportive management. After 8-hours, the patient became hemodynamically unstable with subsequent intubation and fluid resuscitation. She was started on empiric antibiotics. Blood and ascitic fluid cultures were obtained showing group A beta-hemolytic streptococci (GAS). The patient was diagnosed with primary GAS peritonitis along with diffuse gastritis and streptococcal toxic shock syndrome. No cutaneous source of Streptococcus pyogenes was identified, and there was no personal or family history of streptococcal pharyngitis. Antibiotics were switched to IV ampicillin and clindamycin. However, the patient continued to deteriorate and succumbed to death within 2-days.
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PMID:Streptococcal toxic shock syndrome with primary group A streptococcus peritonitis in a healthy female. 3035 61