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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Renal disorders complicating liver disease are a frequent finding. Extrahepatic causes like intoxications and circulatory dysfunction or diseases that simultaneously affect both the liver and the kidney, like multisystem or viral diseases (hepatitis B) have to be differentiated from clinical entities in which, like in liver cirrhosis or in fulminant hepatitis, the manifestation of renal disease has to be understood as a consequence of the hepatic disorders. Functional disturbances like the increases in tubular sodium reabsorption or the hepatorenal syndrome have been thoroughly investigate because of their clinical importance. Substantial research dealing with the consequences of the increased intrahepatic vascular resistance on systemic and renal hemodynamics and with vasoactive substances, either arising from the liver or accumulating due to poor inactivation by the liver, have led - in the last years - to a better understanding of the pathophysiology of renal involvement in liver disease. However, the exact pathophysiologic role of factors like the effective blood volume, the sympathoadrenergic tonus, the activation of the renin-angiotensin-aldosterone system, changes of kinin activity or in prostaglandin release and the accumulation of "false" neurotransmitters and endotoxins still remains to be established.
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PMID:[Kidney involvement in liver diseases. Pathophysiology and clinical course]. 664 4

The call for 'triage' as a specific policy for the selection of patients presenting with chronic renal failure, in the light of increasingly limited resources prompted us to question nephrologist on their bases for selection. We discovered no absolute criteria for rejection, but a consensus of opinion against those with additional and complicating factors to their renal disease such as age, hepatitis carriers and mental illness-a bias seen throughout the National Health Service. In this paper we discuss the validity of such criteria, the implications of the currently pragmatic and often covert practice of selection, and in this potentially finite area of demand we question the rationale for the limitation of resources.
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PMID:Triage and the patient with renal failure. 678 Jun 91

Twenty cases of sonographically visualized thickening of the gallbladder wall were reviewed and the clinical diagnoses compiled. In only eight of these patients was cholecystitis considered responsible for the finding. The rest had hepatitis, alcoholic liver disease with hypoproteinemia, heart failure, renal disease, and multiple myeloma; however, all lacked clinical evidence of gallbladder disease. Because of these findings, caution is urged in making the diagnosis of cholecystitis on the basis of wall thickening alone.
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PMID:Sonography of the thickened gallbladder wall: a nonspecific finding. 678 Dec 56

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 by a specific and sensitive tlc-method concomitantly. 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 according to endogenous creatinine clearance. In older patients the elimination of TA was impaired.
 ...
PMID:Pharmacokinetics of triamterene. 683 48

A 24-year old female patient developed extramembranous glomerulonephritis 8 months after acute hepatitis-B with virus antigen persisting in the serum. Two years later, the glomerular lesions were found to be clinically and histologically cured, with parallel disappearance of the antigen from the serum. Although the presence of HBsAg in the glomeruli could not be demonstrated, it is likely from the sequence of events that hepatitis-B virus was responsible for the renal disease.
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PMID:[Extramembranous glomerulonephritis following hepatitis-B. Simultaneous disappearance of serum virus antigen and glomerular lesions (author's transl)]. 742 18

Vascular access thrombosis (VAT) is frequent in some hemodialysis patients. Antiphospholipid antibodies (APL) have been involved in thrombosis, and have been reported to be present in a high proportion of patients with chronic renal failure. We studied the relationship between APL and thrombosis in 97 hemodialysis patients (HD). Lupus anticoagulant (LA) was assessed by activated partial thromboplastin time (APTT) and by tissue thromboplastin inhibition assay (TTI). IgG-anticardiolipin (ACA) was measured by a solid phase ELISA. The prevalence of APL was 31%; LA was found in 16.5% and was detected in all cases by TTI. Only one patient was positive for APTT. ACA was found in 15.5%. Only one patient was positive for LA and ACA. We found no relation between APL and age, length of time on dialysis, sex, type of dialysis membrane, drugs, and chronic B and C hepatitis. A high prevalence of APL was found in patients with undetermined nephropathy. When histories of thrombosis were examined, VAT was found to be significantly more frequent in patients with LA than in patients without LA (62% vs. 26%; P = 0.01). This relation was not present with ACA. Since VAT is one of the most frequent causes of morbidity for HD, diagnostic evaluation of VAT in HD should now include assay for LA.
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PMID:Antiphospholipids in hemodialysis patients: relationship between lupus anticoagulant and thrombosis. 747 66

Hepatitis C virus (HCV) infection is the leading cause of post-transplant non-A, non-B hepatitis. Although many end-stage renal disease patients present for transplantation already infected with HCV, some recipients acquire the infection by transmission from the donor organ. We have detected serological evidence for HCV infection in 6.8% of our organ donors using second-generation anti-HCV assays. Approximately one-third of the patients who received an organ from a HCV carrier donor developed chronic transaminasemia and 8 of 14 (56%) patients converted from HCV RNA negative to positive in the posttransplant period. Demonstration of the course of viremia and transaminasemia is presented for 2 patients in whom transmission of HCV occurred. Using pulsatile machine perfusion, we were able to demonstrate that a standard perfusion of 20 h reduced the viral load in the kidney by 75%, additional flushes and a subsequent perfusion reduced the total viral titer by more than 99%. Thus, although transmission of HCV does occur with solid-organ transplantation, differences in the incidence of transmission between centers may be related to techniques of organ preservation.
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PMID:Transmission of hepatitis C virus by kidney transplantation: impact of perfusion techniques and course of viremia post transplant. 749 83

Hepatitis C virus (HCV) is the leading cause of non-A, non-B hepatitis among renal allograft recipients. We sought to identify and describe a proteinuric renal disease occurring in our HCV-infected renal transplant patients. Patients with proteinuria exceeding 1 g/day were identified from a cohort of 98 HCV-infected kidney recipients. Qualitative and quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and restriction fragment-length polymorphism of the amplified RT-PCR product was performed to detect circulating HCV RNA, viral titer, and strain type, respectively. An immune complex nephritis (ICN) of the membranoproliferative pattern (MPGN) was found on five of eight biopsies. Two patients infected with the Hutch strain-type developed nephrotic-range proteinuria within three months posttransplant while the remaining three MPGN patients had been transplanted greater than 5 years prior to the onset of proteinuria. Testing for rheumatoid factors, cryoglobulins, hypocomplementemia, and circulating immune complexes failed to show a consistent pattern. Sucrose density gradient (SDG) equilibrium centrifugation was used to determine the buoyant-density of HCV virions from control (HCV-infected nonproteinuric recipients; n = 5) and nephrotic patients (n = 5). Whereas HCV virions from the control patients had a low buoyant density on sucrose gradients, a substantial percentage of the circulating HCV RNA from the MPGN patients was present in the high-density fractions in association with IgM and IgG. Treatment of the pooled high-density layers with NP40 followed by recentrifugation resulted in a shift of the HCV RNA to the medium-density layers. In conclusion, MPGN developed in five HCV-infected kidney recipients despite pharmacologic immunosuppression. Both the physicochemical properties of the HCV virions on SDG and their association with IgG and IgM in the high-density layers provide indirect evidence for the presence of circulating complexes of anti-HCV antibody and HCV antigen(s).
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PMID:De novo membranoproliferative glomerulonephritis in hepatitis C virus-infected renal allograft recipients. 754 75

With the introduction of interferon therapy for liver disease due to chronic viral hepatitis, it has become important to test individuals thought to have hepatitis C virus disease for the presence of the virus. Moreover, the current goal of therapy for hepatitis C virus-positive liver disease is to render the individual patient HCV-RNA negative. Recently, it has been reported that as many as one-third of the patients with hepatitis C virus liver disease test positive for the presence of mixed cryoglobulins. Few of these cryoglobulin-positive patients have overt disease manifestations of cryoglobulinemia, such as nephropathy, peripheral neuropathy and vasculitis. Because the cryoglobulins in patients with hepatitis C virus-positive disease are directed at hepatitis C virus epitopes, the precipitation of cryoglobulins from serum samples also effectively removes virus. When the viral carriage rate is low in terms of the number of genomes/unit serum, as occurs in cases that are partially treated, the serum can test negative for hepatitis C virus even by polymerase chain reaction, despite the presence of persistent viremia, if precautions preventing the precipitation of cryoglobulins prior to the removal of the sample for polymerase chain reaction testing are taken. From a group of 75 patients with hepatitis C virus-positive hepatitis seen at our institution in the last year (all HCV-RNA positive), 35% were found to test positive for the presence of cryoglobulins. Importantly, in all cases, the cryoglobulins collected tested strongly positive for HCV-RNA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cryoglobulinemia: a cause for false negative polymerase chain reaction results in patients with hepatitis C virus positive chronic liver disease. 766 64


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