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)

Soluble interleukin 2 receptors (sIL 2R) in the sera of patients with viral liver diseases were quantified with a solid-phase enzyme immunoassay using two monoclonal antibodies against the receptors. The sIL 2R levels in patients with acute hepatitis, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma were significantly higher than those in control subjects. In acute hepatitis patients, the high levels of sIL 2R observed during the florid stage returned to normal during remission. Levels in patients with chronic active hepatitis were significantly higher than in those with chronic persistent and lobular hepatitis, and levels observed during the exacerbation phase of chronic hepatitis were higher than they were during remission. Thus, in chronic hepatitis, sIL 2R levels increased in proportion to the inflammatory activity, and correlated well with serum transaminase (glutamic oxaloacetic transaminase: SGOT, glutamic pyruvic transaminase: SGPT) activities, but not with blood urea nitrogen or creatinine concentrations. In patients with a high degree of focal and piecemeal necrosis, serum sIL 2R levels increased further during recombinant interleukin 2 therapy. In post-hepatitic liver cirrhosis and hepatocellular carcinoma, sIL 2R levels correlated with serum cholinesterase and creatinine concentrations, but not with transaminase activities. Measurement of serum sIL 2R levels in patients with liver disease but without renal injury, may help in the diagnosis of inflammation in hepatitis, a process in which interleukin 2 may participate.
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PMID:Increased serum soluble interleukin 2 receptor levels in patients with viral liver diseases. 306 11

A multicenter prospective randomized trial of four versus six weeks of amphotericin B, 0.3 mg/kg per day, plus flucytosine, 150 mg/kg per day, was performed with 194 patients with cryptococcal meningitis. One or more toxic drug reactions developed in 103 patients: azotemia (51), renal tubular acidosis (two), leukopenia (30), thrombocytopenia (22), diarrhea (26), nausea/vomiting (10), and hepatitis (13). The four- and six-week regimens were complicated by toxicity in 44 percent and 43 percent of cases, respectively. Toxicity appeared during the first two weeks of therapy in 56 percent and during the first four weeks in 87 percent. Azotemia did not occur more frequently in renal transplant recipients or diabetic patients. Cytopenias did not appear more often in patients with hematologic malignancies or those receiving immunosuppressive therapies. Toxic reactions that contributed to death developed in five patients (two with azotemia, one with pancytopenia, one with hepatitis, one with ileus). Amphotericin B-induced azotemia was not a significant risk factor for the subsequent development of bone marrow, gastrointestinal, or hepatic toxicity attributable to flucytosine. Flucytosine toxicity was associated with peak serum flucytosine levels of 100 micrograms/ml or more during two or more weeks of therapy (p = 0.005). Peak 5-fluorouracil levels were not predictive of toxicity. An initial dose of flucytosine is recommended based on the creatinine clearance: 150 mg/kg per day at a creatinine clearance above 50 ml/minute, 75 mg/kg per day at a creatinine clearance of 26 to 50 ml/minute, and 37 mg/kg per day at a creatinine clearance of 13 to 25 ml/minute. The serum creatinine level should be monitored twice weekly and the creatinine clearance weekly during therapy in order to anticipate changes in serum flucytosine concentration. In addition, it is recommended that the serum flucytosine level be determined two hours after an oral dose once a week, and that the dose be adjusted to maintain a level of 50 to 100 micrograms/ml.
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PMID:Toxicity of amphotericin B plus flucytosine in 194 patients with cryptococcal meningitis. 330 26

For five years, eight patients had abnormally low serum concentrations of creatinine. All patients presented with severe hepatic failure, which was due to fulminant hepatitis in seven patients and to advanced primary biliary cirrhosis in one patients. The serum urate (as uric acid) concentration was also low in seven patients. Endogenous creatinine clearance was increased in all patients (2.38 to 14.75 mL/s [143 to 885 mL/min]). However, inulin clearance measured in four patients was reduced (25 to 32 mL/min) and the creatinine-to-inulin clearance ratio ranged from 4.5 to 9.9. This range can be explained largely by an increased tubular secretion of creatinine related to body fluid expansion caused by a large fluid infusion. Renal function would be extremely overestimated when assessed from serum concentrations or clearance of creatinine in such patients.
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PMID:Low serum creatinine levels in severe hepatic disease. 337 14

The pharmacokinetics of the antikaliuretic amiloride has been studied in healthy controls and in patients with chronic renal failure or hepatitis. It was 40% bound to protein. In healthy volunteers 49% of an oral dose was recovered unchanged in the urine. The renal clearance of amiloride was about 3 times the creatinine clearance, which means that it was predominantly excreted via tubular secretion. Renal impairment reduced the clearance of amiloride, causing a prolongation of the t1/2 and drug accumulation in plasma. In hepatitis the t1/2 of amiloride was prolonged and the AUC increased. Urinary recovery (Ae) of amiloride was greater in hepatitis patients than in controls.
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PMID:Pharmacokinetics of amiloride in renal and hepatic disease. 342 42

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

Alcohol, hepatitis B, and Non A Non B hepatitis were the main aetiologies of 124 patients with hepatic encephalopathy (HE) due to histologically proven liver cirrhosis. All had severe portal hypertension (PH) and usually increased inflammatory activity of the liver. In stage I (n = 27) 7.4% died, in stage II (n = 28) 14.3%, in stage III (n = 32) 50% and in stage IV (n = 37) 94.6%. Even in cirrhotics without PH, serum albumin, cholinesterase activity and prothrombin time (PT) were significantly decreased. But only in the case of PT did the magnitude of the decrease parallel the stage of HE. Hyperammonaemia and serum creatinine were increased in parallel with the stage of HE. Therefore, in liver cirrhosis a quotient derived from decreased PT and increased serum creatinine has a good prognostic value. Early diagnosis of HE is possible on the basis of writing tests and the determination of free or toxic ammonia.
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PMID:The role of protein metabolism in 204 liver cirrhotics with and without hepatic encephalopathy. I. Clinical and general biochemical findings. 372 88

Although a large number of patients are maintained on chronic dialysis, there is little information regarding the medical care rendered to these patients. We therefore obtained information on health care maintenance policies from 90 dialysis centers (8,104 patients) selected from each End-Stage Renal Disease (ESRD) Network. All centers except one obtained BUN, creatinine, electrolytes, calcium, and phosphorus at intervals of 1 month or less; 85% of centers obtained a multiple-test laboratory panel at monthly intervals. Annual physical examination, ECG, and chest x-ray were performed in 80% or more of the centers. Immunization policies varied with 88%, 64%, and 17% of centers offering influenza, pneumococcal, and hepatitis B vaccine, respectively. Patterns of surveillance for anemia, osteodystrophy, and hepatitis were variable. In view of the high frequency and cost of testing, prospective studies to determine optimal methods of health care maintenance in the chronic dialysis center are indicated.
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PMID:Selected health care maintenance policies in chronic dialysis centers. 405 Jul 81

A 34-year-old male presented with fulminant hepatitis A associated with acute renal failure. The patient was admitted four days after flu-like symptoms developed. Physical examination was unremarkable except for icteric sclerae. Laboratory studies showed SGOT 10719 U/l, SGPT 5780 U/l, prothrombin time 22%, BUN 25.5 mg/dl, and creatinine 2 mg/dl. Serum complements were within normal ranges, and circulating immune complexes were not detected. Anti-HAV IgM was positive. He developed hepatic coma on the fourth hospital day, and his renal function deteriorated progressively. He was treated with hemodialysis, but there was no improvement in consciousness. Although acute liver failure improved, he died on the 74th hospital day of subendocardial infarction. Autopsy examination showed acute renal tubular necrosis. The liver was enlarged and was in the residual stage of acute hepatitis without submassive necrosis. The development of fulminant hepatitis in hepatitis A has been rare, but in recent years acute renal failure in hepatitis A has been reported. Although the mechanisms responsible for renal failure in liver diseases are uncertain but could be multifactorial, immune complex-mediated nephritis and/or endotoxemia have been considered.
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PMID:Report of a case with fulminant hepatitis A associated with acute renal failure. 407 29

The knowledge about the pharmacokinetics of triamterene (TA) was limited until recently. The metabolic pathway of TA is the formation of p-hydroxytriamterene (OH-TA), which is subsequently conjugated with active sulfate to form p-hydroxytriamterene sulfuric acid ester (OH-TA-ester). The phase-II-metabolite is surprisingly pharmacologically active. TA and its metabolites were measured concomitantly by a specific and sensitive tlc-method. The i.v. kinetics of TA were determined after application of a newly developed lactic acid solution of the drug. Comparing these data with results after oral application of TA the bioavailability of TA was 52% and the extent of absorption 83%. The bioavailability of different dosage forms was correlated with in vitro-tests. In liver disease the pharmacokinetics of TA are markedly altered. While in cirrhosis the hydroxylation of TA was decreased, the biliary excretion of this agent was strongly reduced in hepatitis. In renal disease the excretion of TA and OH-TA-ester was reduced proportional to the reduction of endogenous creatinine clearance. In older patients the elimination of TA was impaired.
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PMID:[Pharmacokinetics of triamterene in healthy subjects and patients with liver and kidney function disorders]. 663 29

A life-threatening toxicity syndrome consisting of an erythematous, desquamative skin rash, fever, hepatitis, eosinophilia, and worsening renal function in 78 patients receiving allopurinol is described. In a majority of cases, the development of this syndrome was associated with the use of standard (200 to 400 mg per day) doses of allopurinol in patients with renal insufficiency. In pharmacologic studies, it was demonstrated that the renal clearance of the major metabolite of allopurinol, oxipurinol, is directly proportional to the renal clearance of creatinine (oxipurinol clearance = 0.22 X creatinine clearance -2.87). An inverse linear relation was noted between the serum oxipurinol half-life and the renal creatinine clearance [( serum oxipurinol half-life in hours]-1 = 0.00034 X creatinine clearance in milliliters per minute + 0.0045). Long-term use of 300 mg per day of allopurinol was found to result in elevated steady-state serum oxipurinol concentrations in patients with renal insufficiency (serum oxipurinol concentration in micromoles per liter = -2.5 X creatinine clearance in milliliters per minute + 326). Avoidance of allopurinol or use of reduced doses in patients with renal insufficiency according to proposed guidelines should be adequate to inhibit uric acid production in most patients and may reduce the incidence of life-threatening allopurinol toxicity.
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PMID:Severe allopurinol toxicity. Description and guidelines for prevention in patients with renal insufficiency. 669 61


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