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)

The etiology of 72 episodes of liver disease that developed in 62 of 162 renal-transplant recipients was evaluated. Infection with hepatitis B virus was a minor problem, and none of our patients had evidence of infection with hepatitis A. Cytomegalovirus infection was ubiquitous in the population and probably accounted for many episodes of acute liver disease. This agent's role in causing chronic hepatitis is less secure. Infections with other viruses including Epstein-Barr virus, adenovirus, and the herpes viruses were only rarely associated with hepatic disease. Azathioprine was responsible for some episodes of acute cholestasis but could not be incriminated as a direct cause of chronic disease. A cause could be identified for the majority of episodes of acute hepatic dysfunction, but the cause of most of the chronic hepatitis remains undetermined. It is likely that infection with non-A, non-B hepatitis virus accounts for much of this serious, often fatal, complication of renal transplantation.
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PMID:Etiology of liver disease in renal-transplant patients. 22 42

Hepatitis is a frequent complication of dialysis and renal transplantation; therefore, the occurrence of drug hepatotoxicity is an additional important consideration in renal allograft recipients. Azathioprine, needed for immunosuppression, and isoniazid, used for antituberculous chemoprophylaxis, are both potentially hepatotoxic. A retrospective study of 119 patients who received 126 renal allografts was done to estimate the probable incidence of isoniazid-related hepatic dysfunction. All patients in this series were administered isoniazid chemoprophylaxis. Posttransplantation hepatitis developed in 13 patients. Circumstantial evidence supported a presumptive diagnosis of isoniazid hepatotoxicity in three recipients. We concluded that routine isoniazid chemoprophylaxis is not justified in renal allograft recipients based on the probability of hepatotoxicity as contrasted to the infrequent occurrence of tuberculosis.
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PMID:Hepatic dysfunction during isoniazid chemoprophylaxis in renal allograft recipients. 37 76

By andrological and internal investigations in men with chronic aggressive hepatitis the problem is discussed, whether the therapy with Azathioprin can cause damage of the exogenous function of the testes. It would be demonstrated that within an observation time of 1720 days there have not been determined alterations of consistency and volume of the testes, sperm density and motility of spermatozoa, when the maximum of the daily dose was not more than 150 mg. Depending on the individual dose the morphology shows more pathological spermatozoa, but a direct and regular dependence could not be found. The density of spermatozoa did never decrease below values of 40 mill./ml. These results do not allow the suggestion that this cytostaticum is absolutely harmless. The main duty will always be to observe each patient currently and during a long period.
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PMID:[Andrologic study in immunosuppressive treatment of chronic aggressive hepatitis]. 71 16

Severe cholestatic jaundice occurred in two patients receiving prednisolone and azathioprine, one for chronic progressive hepatitis, the other for Wegener's granulomatosis. Reversible abnormal liver function, involving both elimination and synthesis, was in the foreground clinically. Signs of parenchymal-cell damage were only moderately severe. When azathioprine had been discontinued all previously abnormal values returned to normal within six to eight weeks. Azathioprine is an indirect optional hepatotoxin. If given over long periods there should be regular controls of blood count and liver functions.
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PMID:[Cholestatic jaundice after azathioprine treatment (author's transl)]. 94 26

In a randomised, controlled study, the efficacy and safety of an indigenously developed azathioprine formulation, Azoran/1000 (Searle), was compared with an imported formulation Imuran, as an immunosuppressive agent in fresh cases of renal transplantation. All 14 patients enrolled into the trial completed the study period were analysed. There were 8 episodes of rejection, 4 in each group. All these cases responded to pulse steroids. There was no instance of severe bone marrow suppression or hepatitis in either group and none of the patients had any drug related adverse effects. The results of this study show that Azoran is equiefficacious and safe as an immunosuppressive drug in renal transplants and compares satisfactorily in all respects with the imported formulation Imuran and has the added advantage of being easily available and less costly.
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PMID:Evaluation of the efficacy and safety of azathioprine (Azoran), in fresh cases of renal homotransplantation. 181 2

DST provides excellent graft survival in one- and zero-haplotype-matched donor-recipient pairs as well as a trend towards improving graft survival in HLA-identical matches; serum creatinine levels are good in functioning grafts; Imuran coverage does appear to decrease DST sensitization to the blood donor in nonsensitized patients undergoing a first transplant, which encourages early DST and transplantation in this group; flow cytometry has been extremely helpful in excluding subliminal anti-class 1 antigen activity in patients with positive B warm crossmatches alone; DST, in itself, does not appear to preclude subsequent cadaveric transplantation in patients sensitized to their blood donor; and the family history of the blood donor is known, with essentially no risk to the recipients of hepatitis, AIDS, etc. In regards to the issue of whether DST or Cs is better, both have merits, and one must be aware of the circumstances that relate to the optimum application of each therapy. Only a prospective study of DST- and Cs-treated patients with a long-term follow-up will probably resolve the issue of the optimum regimen for one-haplotype-matched living related donor-recipient pairs. The ultimate strategy may involve the selective use of each regimen for the most appropriate circumstances.
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PMID:Donor-specific blood transfusions versus cyclosporine--the DST story. 354 13

The effect of Silymarin (Legalon) upon liver lesions was investigated using four experimental models: In acute galactosamine-hepatitis, Silymarin administration achieved protection of the liver structure (electron-microscopy included), liver cell glycogen, RNA and enzymatic activity, Galactosamine-depressed gluconeogenesis in the isolated perfused rat liver was significantly preserved by Silymarin treatment. In lead and cadmium poisoning the structural damage and histochemical and histoenzymatic changes were partly but significantly prevented. The complex noxious effects of Imuran overdoses were favourably influenced by Silymarin, without diminishing the cytostatic-immunosuppressive action of Imuran.
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PMID:Effect of silymarin on experimental liver lesions. 733 95

Azathioprine can cause severe myelosuppression. The inherited activity of the enzyme thiopurine methyltransferase has been recently recognised as a major factor in the susceptibility to myelosuppression. Thiopurine methyltransferase deficiency occurs at a frequency of one in 300 and is associated with profound myelosuppression after a short course of azathioprine. Very low thiopurine methyltransferase activity represents the TPMTL/TPMTL genotype, and can be detected before therapy with azathioprine is started. We describe the first documented case of azathioprine-induced severe myelosuppression due to thiopurine methyltransferase deficiency in autoimmune liver disease. The azathioprine dose was low (1 mg/kg) and pancytopenia occurred after 56 days therapy. It would be advisable to measure thiopurine methyltransferase activity before patients with autoimmune hepatitis are exposed to azathioprine.
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PMID:Azathioprine-induced myelosuppression due to thiopurine methyltransferase deficiency in a patient with autoimmune hepatitis. 855 Oct 1

Influence of viral liver diseases on the occurrence of azathioprine hepatitis was evaluated in 21 kidney transplant recipients. Diagnosis of azathioprine hepatitis was always based on jaundice, which disappeared after azathioprine withdrawal in 18 patients and after azathioprine dose reduction in 3 patients. Histopathological diagnosis of azathioprine toxicity was ascertained in 14 patients. Rechallenge with azathioprine performed in 4 patients, within 2-4 months after the first jaundice episode, resulted in relapse of jaundice in all cases. Viral hepatitis B virus and hepatitis C markers were present in all 20 tested patients (serum hepatitis B surface antigen in 6 patients and anti-HCV antibodies in 17 patients). Biopsy-proven chronic hepatitis was observed in 18 patients, including 14 chronic active hepatitis, 3 chronic persistent hepatitis and cirrhosis in 1. In kidney transplant recipients, azathioprine hepatitis seems to be facilitated or induced by hepatitis B virus or hepatitis C virus chronic hepatitis. Azathioprine reduction or withdrawal should therefore be combined with the diagnostic evaluation and the treatment of viral liver diseases.
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PMID:Azathioprine hepatitis in kidney transplant recipients. A predisposing role of chronic viral hepatitis. 868 59

A 24-year-old woman was followed for about ten months with oral administration of prednisolone (22.5-35 mg/d) for autoimmune hepatitis. In June 1995, she noticed fatigue and appetite loss and blood chemistry revealed markedly deteriorated liver function. She was admitted to our hospital. The daily dose of prednisolone was increased to 60 mg. Her elevated levels of transaminases decreased gradually. Administration of azathioprine (100 mg/d) was started with tapering of prednisolone on August 18th. Ten days later, tender cervical lymphadenopathy and high fever occurred. Azathioprine administration was stopped immediately and intravenous antibiotics were given. On September 5th, 50 mg of azathioprine was administered again. Two hours later, the patient complained of intolerable pain from the lumbar region to the knee joints, which subsided following two injections of analgesics within a few hours. However, chills, high fever and hypotension (86/30 mmHg) subsequently developed. No bacterial growth was detected in blood culture. She was discharged on September 12th. On October 4th, she visited our out-patient clinic. The next day, she took one tablet (50 mg) of azathioprine at 10 o'clock. She noted intense pain from the thighs to the knees and calves around noon again. Her home doctor found that she exhibited shock (BP 67/?). She was immediately taken to our department. The same symptoms and signs as the above-mentioned occurred. Azathioprine was considered responsible for these two adverse reactions (shock) as an allergen. Later, systemic lupus eythematosus was diagnosed in 1996. And she died to pulmonary hypertension in May 1999. Physicians should be aware of the potential adverse effect of azathioprine administered in order to manage the patients with autoimmune disorders.
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PMID:[Autoimmune hepatitis complicated by intolerable pain of lower extremities and shock due to azathioprine]. 1086 28


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