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

Amiodarone, a commonly used antiarrhythmic agent, has numerous adverse effects. The purpose of this case report is to highlight its hepatotoxicity, an unusual complication of long term amiodarone therapy. Our patient is a 76-year-old man with underlying ischaemic heart disease and recurrent ventricular tachycardia. Eleven months after commencing amiodarone, he developed asymptomatic raised aminotransferases which resolved following drug withdrawal. Amiodarone was then reintroduced and four years later, the patient developed hepatomegaly, worsening liver biochemistry and histopathological changes consistent with early cirrhosis. His symptoms improved following discontinuation of amiodarone. However, hepatomegaly and a low serum albumin still persist four years later.
 ...
PMID:Hepatotoxicity of amiodarone. 129 29

Perinatal transmission of human immunodeficiency virus is thought to occur in 25% to 50% of the offspring of infected women. Standard diagnostic methods do not permit identification of the infected newborns. To assess diagnostic methods and document the natural history of perinatal human immunodeficiency virus infection, 20 children born to human immunodeficiency virus-infected women were followed prospectively for 18 months by measuring antibody titer, Western blot profiles, and antigenemia, and the results were compared with clinical outcome. Endogenous synthesis of anti-human immunodeficiency virus IgG was demonstrated in 6 of the 8 infected children. Four children synthesized IgM against human immunodeficiency virus. Five had demonstrable p24 antigenemia. No significant differences between infected and noninfected children were noted at birth except drug withdrawal, which occurred more frequently in noninfected infants. The incidence of adenopathy, hepatomegaly, and neurologic and immunologic abnormalities in the infected children were compared with noninfected children. The distinguishing illnesses were the opportunistic infections, lobar pneumonia, and failure to thrive. Seven of the 8 infected children had human immunodeficiency virus-mediated disease by 1 year of age (Centers for Disease Control [Atlanta, Ga] P2 classification), and four had acquired immunodeficiency syndrome (Centers for Disease Control P2D). These studies offer an approach to diagnosis of human immunodeficiency virus infection in infants and document the natural history and possible outcomes of infected children.
 ...
PMID:Natural history and serologic diagnosis of infants born to human immunodeficiency virus-infected women. 280 55

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.
 ...
PMID:[Bleeding gastric ulcers and acute hepatitis: 2 simultaneous adverse reactions due to nimesulide in a case]. 1122 44

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.
 ...
PMID:Intrahepatic cholestatic jaundice related to administration of ranitidine. A case report with histologic and ultramicroscopic study. 1578 90