Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After undergoing withdrawal treatment for alcoholism as an in-patient for one year a 49-year-old woman was started on disulfiram, 250 mg daily, her liver function tests being normal. Except for vitamin B1 she received no further medication. Jaundice developed 13 days after onset of treatment and acute liver failure was diagnosed on the 18th day after a total disulfiram dose of 4.5 g (Quick value < 10%; bilirubin 460 mumol/l; GPT 5099 U/l; GOT 4142 U/l), as well as early renal failure (creatinine 300 mumol/l). An acute viral infection, autoimmune hepatitis and a metabolic liver disease were excluded by biochemical, serological and molecular biology tests. All toxicological tests were negative. The patient died 25 days after the onset of disulfiram treatment in hepatic coma due to a fulminant hepatitis with hepatorenal syndrome. Both a liver biopsy and the autopsy showed the signs of an acute hepatic dystrophy without cirrhosis. The temporal relationship between the disulfiram intake and onset of the illness, the exclusion of other causes of the fulminant hepatitis and the liver histology, which was compatible with a chemical-toxic hepatitis, indicate that this was a case of disulfiram-induced hepatitis. The hepatotoxicity of disulfiram is a very rare idiosyncratic reaction which is often fatal. Disulfiram administration must be discontinued at once if there is a rise in liver enzyme activity or jaundice occurs.
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PMID:[Fulminant hepatitis caused by disulfiram]. 840 76

Hepatitis, A is usually a mild and self-limiting infection of the liver. Whereas the clinical course is usually benign in children, complications such as prolonged cholestasis and fulminant liver failure have been reported in adults. Acute functional renal failure is an uncommon event in the absence of fulminating liver disease. So far, only cases of acute hepatitis A with biopsy-proven interstitial renal disease or tubular necrosis have been reported [Geltner et al. 1992. Kramer et al. 1986]. We present the case of a 35-year-old, previously healthy male with non-fulminant cholestatic viral hepatitis A, who developed progressive oliguric renal failure requiring dialysis therapy. Kidney biopsy ruled out glomerular disease and tubular necrosis. In the absence of bleeding and other causes of fluid depletion this case may be another variant of hepatorenal syndrome whose etiopathogenesis is only poorly understood.
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PMID:Acute renal failure complicating non-fulminant hepatitis A. 879 33

32 cases (21 acute severe malaria and 11 chronic malaria syndrome), who developed unusual complications and/or manifestations are reported. The acute manifestations were unexplained tachypnoea 4, pulmonary oedema 5 and shock due to multiple organ dysfunction syndrome 3, melena 2 and E coli septicaemia in one. The other features were concomitant salmonellosis 2, meningitis 1, renal failure 3, hepatorenal syndrome 2, hepatitis like illness 7, neck stiffness with normal CSF 3, urticaria and subconiunctival haemorrhage 2 each, apyrexial spell with anaemia 4, thromocytopenia 3, and hypoglycaemia 3 (two pretreatment and one while on quinine in 5% glucose drip). The chronic syndrome noted were hyperreactive malaria syndrome (Tropical splenomegaly) 3, repeated haemolysis 2, chronic simple malaria with positive parasitaemia and normal Igm levels 4, and cerebellar ataxia with tremors 3. Bone marrow in these cases was hypercullular with increase plasma cells. Liver biopsy revealed lymphocytic infiltration. There was no case with permanent neurogical deficit. All patients with pulmonary oedema and multiple organ dysfunction died but chronic syndrome patients recovered fully. Early recoginition of atypical manifestation and prompt treatment will decrease the mortality and morbidity due to malaria.
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PMID:Unusual acute and chronic complications of malaria. 928 1

Misoprostol, a prostaglandin E1 analog, is a racemate of four stereoisomers. On administration it rapidly de-esterifies to its active form, misoprostolic acid. Misoprostolic acid is 85% albumin bound and has a half-life of approximately 30 minutes. It is excreted in urine as inactive metabolites. No significant drug interactions have been reported. Besides its gastrointestinal protective and uterotonic activities, misoprostol regulates various immunologic cascades. It inhibits platelet-activating factor and leukocyte adherence, and modulates adhesion molecule expression. It protects against gut irradiation injury, experimental gastric cancer, enteropathy, and constipation. It improves nutrient absorption in cystic fibrosis. Misoprostol has utility in acetaminophen and ethanol hepatotoxicity, hepatitis, and fibrosis. It is effective in asthmatics and aspirin-sensitive asthmatic and allergic patients. It lowers cholesterol and severity of peripheral vascular diseases, prolongs survival of cardiac and kidney transplantation, synergizes cyclosporine, and protects against cyclosporine-induced renal damage. It works against drug-induced renal damage, interstitial cystitis, lupus nephritis, and hepatorenal syndrome. It is useful in periodontal disease and dental repair. Misoprostol enhances glycosoaminoglycan synthesis in cartilage after injury. It prevents ultraviolet-induced cataracts and reduces intraocular pressure in glaucoma and ocular hypertension. It synergizes antiinflammatory and analgesic effects of diclofenac or colchicine and has been administered to treat trigeminal neuralgic pain. It reduces chemotherapy-induced hair loss and recovery time from burn injury, and is effective in treating sepsis, multiple sclerosis, and pancreatitis.
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PMID:Misoprostol therapeutics revisited. 1119 38

A 65-year-old HBsAg positive man developed progressive cholestatic liver enzyme abnormalities with histopathological portoportal septum formation, cholestasis, limited mixed infiltrate and hepatocellular ballooning with a ground glass aspect after renal transplantation. Both clinical and pathological features were characteristic of fibrosing cholestatic hepatitis (FCH), a histological variant of hepatitis-B-virus (HBV) infection with a high mortality rate which affects immunocompromised patients. The diagnosis was made about 9 months after transplantation, after retrospective analysis had shown a postoperative increase in HBV replication. Discontinuation of prednisone treatment and starting antiviral lamivudine therapy reduced HBV DNA load immediately. However due to renal failure caused by hepatorenal syndrome, lamivudine therapy had to be interrupted. The patient died following subacute liver failure with progressive FCH. This case illustrates the importance of early diagnosis and treatment with reduction of immunosuppression and institution of antiviral therapy to prevent progression of FCH in immunocompromised HBsAg positive patients.
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PMID:[Fatal fibrosing cholestatic hepatitis following renal transplantation]. 1216 78

The shortage of cadaveric donor organs has led to the use of living donors and marginal cadaveric donors. To date, there have been only 2 reports on the use of hepatitis B surface antigen (HBsAg)-positive liver grafts. Here we describe the 5-yr posttransplantation sequence of a hepatitis B virus (HBV)-positive recipient who received an HBsAg-positive living donor liver graft. A 43-yr-old HBV-positive patient with hepatorenal syndrome received a living donor liver graft in October 2000 from a 27-yr-old HBsAg-positive carrier with no clinical evidence of HBV infection other than the serologic markers. The recipient recovered slowly after liver transplantation (LT). Recipient serum HBsAg was continuously positive despite anti-HBV therapy with high-dose hepatitis B immunoglobulin (HBIG) and lamivudine. The patient was also treated with famciclovir and interferon; to date, a final regimen of lamivudine and adefovir has kept liver function stable for 20 months. The recipient has lived for 64 months after transplantation. The donor has not revealed any clinical evidence of active hepatitis during follow-up. In conclusion, our result implicates that a recipient of liver graft from an HBsAg-positive carrier may survive for a long period following antiviral therapy with lamivudine and adefovir. Considering this living donor case and previously reported cases, the use of an HBsAg-positive cadaveric liver graft may deserve attention when no other donor is available.
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PMID:Five-year follow-up of a hepatitis B virus-positive recipient of hepatitis B surface antigen-positive living donor liver graft. 2174 46

Hepatitis E previously known as enterically transmitted non-A, non-B hepatitis, is a self limiting infectious viral disease of developing countries. Various issues regarding the pathogenesis of liver injury and its natural history remain unanswered after two decades of its discovery. A small proportion of patients develop fulminant hepatic failure. Mortality is very high if it is associated with pregnancy, especially during third trimester. After establishment of hepatitis A virus as a cause of decompensation of chronic liver disease, now there are reports that hepatitis E viruses also does the same. Acute hepatitis E in these patients has a protracted course with high morbidity and mortality. Many patients develop hepatorenal syndrome, hepatic encephalopathy and even liver failure after co-infection with hepatitis E virus. Now time has come to institute hepatitis E virus superinfection as one of the cause of acute on chronic liver failure. Hepatitis E is a problem of developing countries and Nepal is in the endemic zone. Sudden decompensation in chronic liver disease patient, who were otherwise stable and under regular follow up, should be carefully dealt with. Patient statistics at our unit shows that 7 cases of chronic liver diseases with superinfection with hepatitis E virus were dealt from April 2004 to August 2005. Two patients (29%) died and 5 recovered. In patients with recovery, there was deterioration of Child-Pugh grading and the duration of hospital stay was longer. Thus, hepatitis E in diagnosed chronic liver disease case should be taken apprehensively. Similarly patients of chronic liver disease traveling to endemic zone should take precaution. If vaccine against hepatitis E virus is developed, chronic liver disease patient would be the eligible candidate for vaccination beside pregnant ladies.
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PMID:Hepatitis E virus infection in chronic liver disease causes rapid decompensation. 1716 Jan

Primary biliary cirrhosis (PBC) is an autoimmune, slowly progressive, cholestatic, liver disease characterized by a triad of chronic cholestasis, circulating anti-mitochondrial antibodies (AMA), and characteristic liver biopsy findings of nonsuppurative destructive cholangitis and interlobular bile duct destruction. About 10% of PBC patients, however, lack AMA. A variant, called PBC-autoimmune hepatitis (AIH) overlap, is characterized by the above findings of PBC together with findings of elevated serum alanine aminotransferase, elevated serum immunoglobulin G, and circulating anti-smooth muscle antibodies, with liver biopsy demonstrating periportal or periseptal, lymphocytic, piecemeal necrosis. PBC is hypothesized to be related to environmental exposure in genetically vulnerable individuals. It typically occurs in middle-aged females. Prominent clinical features include fatigue, pruritis, jaundice, xanthomas, osteoporosis, and dyslipidemia. The Mayo Risk score is the most widely used and best prognostic system. Ursodeoxycholic acid is the primary therapy. It works partly by reducing the concentration and injury from relatively toxic bile acids. PBC-AIH overlap syndrome is treated with ursodeoxycholic acid and corticosteroids, especially budesonide. Obeticholic acid and fibrate are promising new, but incompletely tested, therapies. Liver transplantation is the definitive therapy for advanced disease, with about 70% 10-year survival after transplantation. Management of pruritis includes local skin care, dermatologist referral, avoiding potential pruritogens, cholestyramine, and possibly opioid antagonists, sertraline, or rifaximin. Management of osteoporosis includes life-style modifications, administration of calcium and vitamin D, and alendronate. Statins are relatively safe to treat the osteopenia associated with PBC. Associated Sjogren's syndrome is treated by artificial tears, cyclosporine ophthalmic emulsion to stimulate tear production; and saliva substitutes, cholinergic agents, and scrupulous oral and dental care. Complications of cirrhosis from advanced PBC include esophageal varices, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatoma formation.
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PMID:Primary biliary cirrhosis: Pathophysiology, clinical presentation and therapy. 2595 76

We report a case of lethal hepatorenal insufficiency in a 52-year-old man who received successful simultaneous hepatorenal transplantation from a deceased donor. The patient had undergone live-donor liver transplantation for type-C hepatitis and liver cirrhosis 11 years before he developed graft liver dysfunction due to recurrent viral hepatitis and cirrhosis. At that instance, he also developed end-stage renal dysfunction due to calcineurin inhibitor nephropathy and hepatorenal syndrome. Although he needed three open hemostases and abundant blood transfusion, he was withdrawn from continuous hemodiafiltration on the 55th day and discharged from the hospital on the 272nd day postoperatively. Simultaneous hepatorenal transplantation was reported to be associated with more favorable outcomes of graft function, lower rejection rates, but higher perioperative complication rates compared with liver transplantation alone in patients on hemodialysis. Particularly, close attention should be paid for hemostasis since patients have a hemorrhagic tendency until the recovery of graft liver function.
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PMID:[Simultaneous Hepatorenal Transplantation from a Brain-Dead Donor for Graft Dysfunction and Renal Insufficiency in a Liver Transplant Recipient : A Case Report]. 2888 15

Decompensated cirrhosis is a common reason for admission to the acute medical unit, and such patients typically have complex medical needs and are at high risk of in-hospital death. It is therefore vital that these patients receive appropriate investigations and management as early as possible in their patient journey. Typical presenting clinical features include jaundice, ascites, hepatic encephalopathy, hepato-renal syndrome or variceal haemorrhage. A careful history, examination and investigations can help identify the precipitating cause (infections, gastrointestinal bleeding, high alcohol intake / alcohol-related hepatitis or drug-induced liver injury), so appropriate treatment can be given. A 'care bundle' that has been endorsed by the British Society of Gastroenterology is available to help guide the management of patients with decompensated cirrhosis for the first 24 hours and ensure all aspects are addressed. Specific management of complications, such as infections, gastrointestinal bleeding, hepatic encephalopathy and hepatorenal syndrome, are discussed.
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PMID:Management of decompensated cirrhosis. 2970 95


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