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)

Hepatitis A is an acute, necroinflammatory disease of the liver which results from infection by the hepatitis A virus (HAV). The mean incubation period is approximately 30 days. Although the disease is usually self-limited, the severity of illness is age-dependent. In children, hepatitis A is usually asymptomatic, while in adults, symptomatic infection is characteristic and jaundice is common. Fulminant hepatitis A is rare and is also age-dependent. The onset of hepatitis A is often abrupt and characteristic prodromal symptoms are followed, within a few days to a week, by dark urine and jaundice. Mild to moderate tenderness over an enlarged liver is usually detected. Serum alanine and aspartate aminotransferase levels usually both rise rapidly during the prodromal period, reach peak levels and then decrease by approximately 75% per week. Serum bilirubin concentrations reach peak levels later and decline less rapidly than serum aminotransferases. Nonetheless, the period of jaundice persists for < 2 weeks in approximately 85% of cases. Nearly all adult patients with clinically apparent disease experience complete clinical recovery with restoration of normal serum bilirubin and aminotransferase values by 6 months. Relapses and prolonged cholestasis are unusual manifestations of hepatitis A, and even in these circumstances, recovery is the rule and chronic hepatitis is not seen. The diagnosis of hepatitis A requires the detection of immunoglobulin M antibody to HAV in a patient who presents with, or has recently had, clinical features of hepatitis (icteric or anicteric disease) or in an individual with inapparent, asymptomatic infection in whom serum aminotransferase elevations may be detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical manifestations and diagnosis of hepatitis A virus infection. 133 49

A case report is presented of a 43-year-old woman with generalized peliosis hepatitis that developed during longterm use of oral contraceptives (OCs). The patient had been in good health until the last 2 years when she began to experience vague epigastric pains and a feeling of abdominal distension. Several months prior to admission, she had started to complain of itching and fatigue. There was no history of dark urine, white stools, or hepatitis. On physical examination, no jaundice or cutaneous stigmata of chronic liver disease were observed. Laboratory studies showed a normal erythrocyte sedimentation rate and hematological blood count. A radionuclide study of the liver showed hepatomegaly; especially the left lobe was enlarged. A computerized tomographic scan of the liver showed multiple areas of decreased density in both of the enlarged lobes. There was no evidence of a tumor. Selective transfemoral angiography of the celiac artery also showed hepatic enlargement but no signs of a space-occupying lesion. At laparoscopy, the liver was grossly enlarged and had a lumpy appearance, but again there were no signs of a tumor. No evidence of veno-occlusive disease or hepatocellular adenoma was found. The diagnosis was peliosis hepatitis. The OCs were withdrawn, and the patient was discharged. Regular follow-up in the outpatient department showed no decrease in the size of the liver. The alkaline phosphatase level rose. The fatigue became worse, and cholestyramine was prescribed for progressive itching. In September 1980, the patient was admitted for reevaluation. A repeated CT scan and angiography of the liver again yielded no evidence of a tumor. Esophagoscopy showed the presence of varices grade 2. The liver at laparoscopy had the same appearance as it had in 1976. Histological examination of a biopsy specimen showed occasional dilated sinusoids and locally marked periportal and intralobular fibrosis. No regeneration nodules were found. The diagnosis was liver fibrosis. The patient's condition deteriorated gradually in the following years. She experienced increasing fatigue. Steatorrhea developed, and the patient lost weight. She needed increasing doses of cholestyramine and oral supplementation of vitamins A, D, and K. She was admitted for a 3rd time in February 1985. Esophagoscopy revealed varices grade 4. A CT scan of the liver showed no change. The patient successfully underwent an orthotopic liver transplantation in January 1987. The diagnosis of peliosis hepatis was well documented in this patient.
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PMID:Generalized peliosis hepatis and cirrhosis after long-term use of oral contraceptives. 312 33

A case is described wherein a 29 year old woman was admitted to the hospital because of the possibility of a hepatic tumor; symptoms included abdominal pain, diffuse hepatic enlargement and absence of uptake in an area of the right hepatic lobe. After a normal pregnancy and delivery 11 years earlier the patient used oral contraceptives (OCs) composed of norethindrone with mestranol until 8 years before entry; 5 years before admission she resumed use of an OC containing norethindrone and ethinyl estradiol. She smoked 1.5 packages of cigarettes and drank 1 glass of wine daily, and there was no history of nausea, vomiting, melena, jaundice, dark urine, light stools, hepatitis, or blood transfusions. Benign lesions which are known to be caused by OCs fall into 2 groups: designated focal nodular hyperplasia and liver-cell adenoma. The evidence linking the latter with OCs is more convincing since in case-controlled studies the risk of development of adenomas has been shown to increase with the estrogen strength of the OCs and duration of use; in women who have been taking OCs over 7 years the relative risk is 500 times that for matched control nonusers. The vascular complications of OC therapy include Budd-Chiari syndrome, peliosis hepatis, and periportal sinusoidal dilatation. The patient in this case was diagnosed to have periportal and midzonal hepatic sinusoidal dilatation association with OC medication. She underwent an operation on her liver which proved to be successful combined with cessation of OC use. The mechanism by which OCs cause these lesions is not known. In 5 of 13 cases similar to the one described here clinical and biochemical abnormalities resolved and 1 patient had a follow-up liver biopsy that revealed normal findings 10 months after cessation of OC therapy; there is no evidence to suggest that sinusoidal dilatation is irreversible.
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PMID:Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 40-1982. Tender hepatomegaly in a 29-year-old woman. 711 Feb 74

A study of the clinical profile of 59 patients who presented with hepatitis A virus infection showed that dark urine, fatigue, gastrointestinal complaints, and fever were the most common presenting symptoms. The most frequent physical findings were hepatomegaly and jaundice. The mean presenting laboratory tests included total bilirubin of 5 mg/dL, alkaline phosphatase of 269 units/L, and serum aspartate aminotransferase and alanine aminotransferase levels of 1442 mIU/mL and 1952 mIU/mL, respectively. Atypical manifestations included relapse, cholestasis, rash, and arthralgia. Two patients presented with hepatitis A and concomitant type I autoimmune chronic hepatitis, and both required immunosuppressive therapy. Five patients who presented with hepatitis A were pregnant, and during follow-up, none of their infants developed elevated serum transaminase values or had detectable IgM anti-HAV antibody. All 59 patients experienced complete clinical and biochemical recovery within 6 months after onset of illness.
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PMID:Clinical manifestations of hepatitis A: recent experience in a community teaching hospital. 787 41

A 66 year-old obese woman with arthrosis, self-medicated with oral nimesulide, 200 mg daily. After 6 weeks she developed nausea, jaundice and dark urine. Two weeks later she had recurrent hematemesis and was hospitalized. Besides obesity and anemia her physical examination was unremarkable. An upper GI endoscopy revealed 3 acute gastric ulcers and a 4th one in the pyloric channel. Abdominal ultrasonogram showed a slightly enlarged liver with diffuse reduction in ecogenicity; the gallbladder and biliary tract were normal. Blood tests demonstrated a conjugated hyperbilirubinemia (maximal total value: 18.4 mg/dl), ALAT 960 U/l, ASAT 850 U/l, GGT 420 U/l, alkaline phosphatases mildly elevated, pro-time 49% and albumin 2.7 mg/dl. Serum markers for hepatitis A, B and C viruses were negative. ANA, AMA, anti-SmA, were negative. Ceruloplasmin was normal. A liver biopsy showed bridging necrosis and other signs of acute toxic liver damage. Gastric ulcers healed after conventional treatment and hepatitis subsided after 2 months leaving no signs of chronic liver damage. The diagnosis of toxic hepatitis due to nimesulide was supported by the time-course of drug usage, sex, age, absence of other causes of liver disease, a compatible liver biopsy and the improvement after drug withdrawal. Peptic ulcers or toxic hepatitis have been previously described as independent adverse reactions in patients taking nimesulide or other NSAIDs but their simultaneous occurrence in a single patient is a unique event that deserves to be reported.
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PMID:[Bleeding gastric ulcers and acute hepatitis: 2 simultaneous adverse reactions due to nimesulide in a case]. 1122 44

Ultrasonography is the first line imaging investigation in patients with jaundice, right upper quadrant pain, or hepatomegaly. Most patients with jaundice have parenchymal or obstructive jaundice. A 56-year old man was admitted to the Institute of Digestive Diseases, Belgrade, with severe pains in the epigastrium, vomiting, icteric coloration of sclera, white stools and dark urine. The symptoms had developed 5 days after a Billroth II resection. The functional liver test indicated a pronounced cholestasis. Real-time ultrasonography showed in the projection of the pancreas head, a clear bordered unechogenic oval formation, with a size of 40 x 35 mm. This finding indicated a possibility of an afferent loop obstruction, accompanied by consecutive obstructive icterus due to compression on the common bile duct. Ultrasonographic examination was followed by surgical reintervention. With the development of noninvasive imaging, transcutaneous ultrasonography, computed tomography and magnetic resonance imaging, the diagnosis of pancreatic and other cysts in upper abdomen is usually straightforward. The important ultrasonographic characteristic of empty organs, compared to cysts and pseudocyts, is a change in the morphology and size of organs after a specific time interval. Air bubbles in the organs lumen are like mobile reflectors, and they are an important sign in identifying segments of the gastrointestinal tract.
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PMID:Jaundice after Billroth II resection. A case report. 1236 42

Ranitidine may cause liver injuries ranging from transient, subclinical serum transaminases increase every 100-1,000 treated patients to cholestatic hepatitis in less than 1/100,000. Other H2-receptor antagonists are more dangerous: 11 toxic hepatitis cases have been reported as adverse effect after 1 year of marketed ebrotidine. A 75-year-old male with ischemic cardiopathy history was started on an 8 days treatment of oral ranitidine due to pirosis, without any other changes of therapy; 48 h after drug withdrawal, light-coloured stools, dark urine and icteric scleras developed. On hospital admission, 10 days later, physical examination showed slight hepatomegaly and severe jaundice with skin excoriations followed by serum mixed bilirubin further increase and aminotransferases activities mild rise. Total bilirubin peaked at 381.33 mmol/l (5.1-17.1) and progressively returned to normal, after discharge home, in 3 months and now, 1 year later, there is no sign of liver disease. Ultrasonographic biliary anomalies and the most frequent causes of liver damage were excluded. Liver biopsy confirmed ranitidine as the most likely cause of liver toxicity since histological and ultramicroscopical study revealed a drug-induced picture. We report a rare case of intrahepatic cholestasis jaundice related to ranitidine, a widely used drug. Diagnosis would need an ethically unacceptable rechallange test.
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PMID:Intrahepatic cholestatic jaundice related to administration of ranitidine. A case report with histologic and ultramicroscopic study. 1578 90

Viral infection is one of the postulated causes of neonatal cholestasis. In addition to earlier reports on the association of viral infection and intrahepatic cholestasis (IH), recent studies have suggested a similar link to extra hepatic biliary atresia (EHBA). The aim of this work was to evaluate the role of some viral infections in neonates presenting with cholestasis to the Neonatology Ward of Zagazig University Hospitals. Sixty-two neonates were included in the study (44 cholestatic neonates and 18 apparently healthy neonates as the control group). All neonates were subjected to full history taking and complete physical examination. Laboratory investigations included CBC, liver function tests, bleeding profile, blood cultures, abdominal ultrasound and detection of HBsAg and serum IgM antibodies against certain viruses (CMV, Reovirus III, HSV I, HSV II, Rubella virus) using ELISA. Radionuclide cholescintigraphy was performed for patients only. The study revealed that cholestatic neonates were significantly associated with dark urine, pale stool and hepatomegaly compared with the control (P<0.004, P<0.001, P<0.008, respectively). Quantitation of IgM antibody titre using ELISA revealed significantly higher levels of serum anti-CMV IgM and anti-Reovirus III IgM in cholestatic than in the control groups. No significant differences were found in levels of anti-HSV I, anti-HSV II or anti-rubella antibodies between cholestatic and control groups. HBsAg was negative for all neonates; cholestatic and control. Lastly, no significant differences were found between neonates with EHBA (7 cases) and Intrahepatic cholestasis (37 cases) regarding anti -CMV IgM or anti -Reo III IgM. It can be concluded that CMV and Reovirus type 3 infections of the neonates are associated with the development of cholestatic disorder, not only due to IH cholestasis but also due to the production of EHBA.
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PMID:Role of some viral infections in neonatal cholestasis. 1673 27

Patients with long-chain 3-hydroxyacyl coenzyme A dehydrogenase (LCHAD) deficiency manifest hypoketotic hypoglycemia, hepatomegaly, hypotonia, lactic acidemia, acute renal failure, cardiomyopathy, and sudden death. We describe four novel mutations of the alpha- and beta-subunits of the mitochondrial trifunctional protein in four patients from three unrelated families. Their plasma acylcarnitine profiles suggested the presence of LCHAD deficiency by demonstrating highly elevated 3-hydroxyacyl carnitines by tandem mass spectrometry (MS/MS). Patients 1 and 2 had siblings who had died of lactic acidemia during the neonatal period. These patients also manifested lactic acidemia and died in the neonatal period. Patient 3 had a family history of Reye-like syndrome. She exhibited acute renal failure, rhabdomyolysis, pericardial effusion, and myopathy at the age of 12 years. DNA analysis of patients 1 and 2 revealed homozygosity for a c.1689+2T>G mutation of the HADHA gene, resulting in the skipping of exon 16 with an in-frame 69-bp deletion. Patient 3 was a compound heterozygosity of the HADHB gene, N307D/N389D. Patient 4, a 25-month-old baby, manifested recurrent episodes of lethargy, metabolic acidosis, elevated liver enzymes, and dark urine from the age of 10 months. Mutation analysis of the HADHB gene of patient 4 identified compound heterozygosity of N114D/N307D.
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PMID:Identification of novel mutations of the HADHA and HADHB genes in patients with mitochondrial trifunctional protein deficiency. 1714 51

Although an estimated 1 million persons in the United States are chronically infected with hepatitis B virus, the prevalence of hepatitis B has declined since the implementation of a national vaccination program. Hepatitis B virus is transmitted in blood and secretions. Acute infection may cause nonspecific symptoms, such as fatigue, poor appetite, nausea, vomiting, abdominal pain, low-grade fever, jaundice, and dark urine; and clinical signs, such as hepatomegaly and splenomegaly. Fewer than 5 percent of adults acutely infected with hepatitis B virus progress to chronic infection. The diagnosis of hepatitis B virus infection requires the evaluation of the patient's blood for hepatitis B surface antigen, hepatitis B surface antibody, and hepatitis B core antibody. The goals of treatment for chronic hepatitis B virus infection are to reduce inflammation of the liver and to prevent complications by suppressing viral replication. Treatment options include pegylated interferon alfa-2a administered subcutaneously or oral antiviral agents (nucleotide reverse transcriptase inhibitors). Persons with chronic hepatitis B virus infection should be monitored for disease activity with liver enzyme tests and hepatitis B virus DNA levels; considered for liver biopsy; and entered into a surveillance program for hepatocellular carcinoma.
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PMID:Hepatitis B: diagnosis and treatment. 2038 72


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