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

An acute type rejection episode occurred in one of two patients treated with Interferon alpha (IFN alpha) for type C hepatitis (CHC). Histopathological examination of the graft kidney revealed focal cellular infiltration and chronic transplant glomerulopathy which showed acute or chronic type rejection. In spite of bolus administration of methyl-prednisolone, the elevation of serum creatinine level continued. After administration of anti-human lymphocyte globulin (AHLG), renal function improved, but urinary protein was still positive. Another patient had no episode of rejection during or after IFN alpha therapy.
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PMID:Interferon alpha therapy for chronic active hepatitis type C after renal transplantation and allograft rejection. 858 24

In order to determine the criteria in selecting candidates for orthotopic liver transplantation (OLT), we assessed the aetiology and prognostic indicators in 61 patients with fulminant or subfulminant hepatitis during the past 13 years. Several previously reported models of high risk predictors were not suitable for a large portion of our patients with different aetiological and ethnic backgrounds. In the present study, serological markers of various hepatitis viruses were tested and clinical parameters were compared between survivors and non-survivors. Multiple virus infection and multifactorial causes were important in the pathogenesis (48%) of acute liver failure. Among the 13 clinical parameters, six were considered significant on univariate analysis: prothrombin time prolongation (P < 0.001), total bilirubin, creatinine and alpha-fetoprotein (P < 0.01), age and cholesterol (P < 0.05). With stepwise logistic regression using most discriminatory cut-off values, an age of > 43 years (P = 0.0001), total bilirubin levels of > 23 mg/dL (P < 0.005) and prothrombin time prolongation > 19 s (P < 0.0001) were independent predictors of non-survival. When applied to determine the index of poor prognosis, the sensitivity, specificity, positive predictive value, negative predictive value and predictive accuracy were 100, 67, 95, 100 and 95%, respectively, in the presence of any one of these prognostic factors. We conclude that these indicators may be useful for selecting patients with acute liver failure indicated for OLT.
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PMID:Prognostic factor analysis of fulminant and subfulminant hepatic failure in an area endemic for hepatitis B. 879 11

In this clinicopathological study, we have examined the prevalence of biochemical and histological graft abnormalities in 116 patients who have lived for longer than five years since orthotopic liver transplantation (mean, 8.4 years [range, 5.2-19.5 years]). In each patient, the protocol biopsy was carried out in addition to full clinical, biochemical, and immunological evaluation. The renal function was preserved in most patients (mean creatinine, 86 micromol/L [0.95 mg%]) with only 35% showing any degree of impairment, and only one patient with pretransplant renal failure required dialysis. Forty one (35%) of the patients had normal biochemical liver function tests (LFTs); 19 of these patients had histologic abnormalities. Of the remaining 75 patients with abnormal LFTs, 65 were found to have histological abnormalities on liver biopsy. Some of the 84 patients with an abnormal histology had more than one finding but were placed into 6 categories according to the main change as follows: chronic hepatitis in 27; primary biliary cirrhosis-like changes in 8; cholangitis in 15; structural anomalies in 26; chronic rejection in 2; mild acute cellular rejection in 1; and miscellaneous in 5. The recurrence of B, C, or autoimmune hepatitis accounted for 14 cases of chronic hepatitis, whereas, in 13 cases, no cause could be detected. The latter cases included 8 patients who had liver transplants for primary biliary cirrhosis (PBC), leaving suboptimally treated rejection or disease recurrence as possible causes. Characteristic histological features of PBC were observed in 8 additional cases that had liver transplantations for this disease. Of the 26 cases with structural anomalies, various types of occlusive vasculopathy were detected during pre- or posttransplantation in 12 cases. All but one of these were maintained on azathioprine, the only possible etiological factor in the 14 other cases, 5 of whom showed stabilization or clinical and histological improvement following withdrawal of the drug. De-novo malignancy was seen in 3.4% of cases, causing mortality in only one patient to date. This study demonstrates an unexpectedly high prevalence of histological abnormalities that is found often in the presence of normal biochemical liver-function in liver grafts of long-term survivors. Although graft loss at this time is rare, protocol liver biopsies at 5 years, and thereafter at 2-year intervals, may allow for earlier beneficial therapeutic intervention.
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PMID:Graft and systemic disease in long-term survivors of liver transplantation. 898 90

Dimethyl sulfoxide (DMSO) can protect the liver from injury produced by a variety of hepatotoxicants when administered prior to or concomitant with the toxicants. This protective action has previously been attributed to DMSO-induced inhibition of bioactivation of the compounds to toxic intermediates. In these studies, the ability of DMSO to provide protection when administered 10 hr after a toxicant was evaluated in several animal models of xenobiotic-induced liver and kidney injury. In the guinea pig model of halothane-associated hepatotoxicity, male outbred Hartley guinea pigs received 2 ml/kg DMSO 10 hr after an inhalation exposure to 1.0% halothane, 40% O2 for 4 hr. DMSO decreased the extent of liver necrosis as indicated by a threefold decrease in plasma alanine aminotransferase activity 48 hr after exposure and a reduction in the incidence and extent of zone 3 necrosis. These results do not appear to be due to alterations in halothane biotransformation since DMSO administered at 10 hr after halothane had no affect on plasma concentrations of the halothane metabolite tritluoroacetic acid or covalent binding by reactive halothane biotransformation intermediates to hepatic protein. In addition, administration of the structurally analogous biotransformation inhibitor diallyl sulfide at 10 hr after halothane also had no affect on biotransformation or covalent binding but provided no protection from liver injury. Hepatic glutathione concentrations in the guinea pigs 24 hr after halothane exposure were also unaffected by late treatment with DMSO. Further studies in male Sprague-Dawley rats demonstrated the ability of DMSO to decrease the hepatic injury resulting from oral administration of 1.0 ml/kg chloroform or 0.5 ml/kg bromobenzene when administered 10 hr after either toxicant. The chloroform-treated rats also developed renal tubular necrosis with large increases in plasma creatinine and urea nitrogen, which were completely ameliorated by DMSO. Elucidating the mechanism(s) of this protective action of late DMSO administration should provide insight into the cascade of events that lead to liver and kidney injury from toxicants and, hopefully, therapeutic modalities for individuals suffering from acute, progressing, xenobiotic-induced hepatitis.
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PMID:Late dimethyl sulfoxide administration provides a protective action against chemically induced injury in both the liver and the kidney. 900 50

Interferon (IFN) therapy is of proven efficacy in chronic hepatitis C, but it is not universally effective and is often limited by side effects. Cyclosporine A (CsA) is a potent immunosuppressant widely used in organ transplantation. We conducted a pilot study to determine whether CsA therapy could affect aminotransferase activity and hepatitis C virus RNA levels in patients with chronic hepatitis C. Cyclosporine A was administered to 10 patients (mean age of 59 years; male:female = 9:1) who did not respond to IFN therapy previously and who had elevated serum alanine aminotransferase (ALT) values for at least 6 months. All patients were positive for HCV-RNA by RT-PCR with genotype 1b. Their mean duration of hepatitis was 15 years. Oral CsA was given for 3 months in a dose that was increased at 1 month intervals from 1.5-2.0 to 2.0-3.0 and 3.0-4.0 mg/kg per day. All patients completed the treatment schedule, although two patients developed mild non-symptomatic hypertension. Serum ALT levels gradually decreased in all but one patient. The mean percentage decrease was 59.5% at the end of therapy (from 153 +/- 82 to 62 +/- 48 IU/L; P < 0.02). The ALT levels fell to the normal range in five patients, although once therapy was discontinued the enzyme levels tended to return to pretreatment levels. Serum aspartate aminotransferase and g-glutamyl transpeptidase levels similarly decreased. The serum HCV-RNA titre, determined by competitive RT-PCR, did not change in any patient throughout the study period. There were no appreciable alterations in other laboratory tests, such as serum creatinine levels and lymphocyte subsets, except for an increase in serum alkaline phosphatase levels. These findings suggest that CsA, even in a relatively low dose, reduces serum aminotransferase levels without serious side effects in patients with chronic hepatitis C, although an antiviral effect was not noted.
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PMID:Cyclosporine therapy affects aminotransferase activity but not hepatitis C virus RNA levels in chronic hepatitis C. 907 26

Invasive fungal infections and their risk factors were prospectively assessed in 130 consecutive liver transplant recipients receiving tacrolimus as the primary immunosuppressive agent. Eleven percent (14) of the 130 patients had 17 episodes of invasive fungal infections. These included candidiasis (5%; 6 patients), cryptococcosis (5%; 6), aspergillosis (3%; 4), and chromomycosis (1%; 1). An elevated pretransplantation creatinine level, requirement of dialysis (pretransplantation or posttransplantation), duration of intensive care unit stay after transplantation surgery, and antibiotic use (other than for prophylaxis) within 4 weeks of transplantation were significant risk factors for fungal infections occurring within 100 days of transplantation. For fungal infections occurring after 100 days, persistence of renal dysfunction (serum creatinine level of >2.5 mg/dL at 3 months), dialysis, and histopathologically documented recurrence of hepatitis C virus hepatitis were significant risk factors. Mortality was significantly higher among patients with fungal infections than among all other patients (57% vs. 15%; P = .0009). Our study identified specific risk factors for invasive fungal infections in liver transplant recipients receiving tacrolimus; strategies to prevent fungal infections or to initiate early antifungal therapy might be most effectively targeted at these patients.
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PMID:Invasive fungal infections in liver transplant recipients receiving tacrolimus as the primary immunosuppressive agent. 911 44

Glomerular abnormalities are frequent in patients undergoing liver transplantation; however, renal dysfunction following transplantation is mainly attributed to cyclosporine toxicity. Membranoproliferative glomerulonephritis (MPGN) is seen in patients infected with hepatitis C virus (HCV), the virus responsible for 30% of the end-stage liver disease leading to liver transplantation. To determine the incidence of renal abnormalities in liver transplant recipients and the association with HCV, we undertook a longitudinal study in HCV-positive (n=91) and HCV-negative (n=106) liver transplant recipients. Mean creatinine clearance before transplantation was 94 ml/min/1.73 m2 in HCV+ patients and 88 ml/min/1.73 m2 in HCV- patients. By 3 months after transplantation, the mean creatinine clearance decreased by approximately one third in both groups. A greater proportion of HCV+ patients excreted >2 g protein/day after transplantation (P=0.05) and had renal biopsies showing MPGN than did HCV- recipients (4/10 HCV+ patients vs. 0/7 HCV- patients; P=0.1). In the HCV+ group, proteinuria was not associated with recurrent HCV hepatitis, DQ matching, posttransplant diabetes, or hypertension. Treatment of HCV-related MPGN with interferon-alpha2b appeared to stabilize proteinuria and renal function but did not reverse renal dysfunction nor cause liver allograft rejection. After transplantation, HCV+ patients had similar renal function over 3 years after transplantation, compared with HCV- patients, but they had an increased risk of proteinuria and occurrence of MPGN that was only partially responsive to interferon.
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PMID:Renal disease in hepatitis C-positive liver transplant recipients. 915 23

Anaemia is an almost invariable sign of chronic renal failure [1]. Although many factors have been implicated as causes of this anaemia, it seems probable that deficiency of erythropoietin is the main cause for most patients [2]. Institution of chronic dialysis can improve anaemia in end-stage kidney disease, continuous ambulatory peritoneal dialysis being reported as more successful [3]. The aim of this study was to investigate the influence of haemodialysis and continuous ambulatory peritoneal dialysis on anaemia during the first six months of treatment. We examined 21 persons (14 males and 7 females, aged from 18 to 78 years) on haemodialysis treatment and 13 persons (6 males and 7 females aged from 22 to 64 years) on continuous ambulatory peritoneal dialysis (Table 1). Standard procedures were used for measuring biochemical parameters. Urea and creatinine levels were high, almost incompatible with life, in all tested persons before dialysis treatment. During the first three months of both dialysis techniques urea and creatinine were significantly (p < 0.01) corrected, but remained above the normal ranges (Table 2). Patients on continuous ambulatory peritoneal dialysis have shown significantly (p < 0.01) lower urea and creatinine values compared to patients on haemodialysis (Graph 1). These data suggest better preservation of renal function and better control of the internal environment during continuous ambulatory peritoneal dialysis [6]. All tested patients were severely anaemic before the beginning of dialysis. During the first six months of haemodialysis erythrocyte count, haematocrit and haemoglobin levels were unchanged (Table 3). Transfusions and hepatitis episodes only temporary improved anaemia. Patients on continuous ambulatory peritoneal dialysis exhibited significant correction of anaemia already during the first three months of treatment (Graph 2). Though less significantly, haemoglobin values continued to rise even during the next three months. The reached haemoglobin levels were lower than normal, but significantly higher than values in patients on haemodialysis (p < 0.01), suggesting better control of anaemia during continuous ambulatory peritoneal dialysis. Transfusion requirement was irrelevant, and hepatitis was not noticed, so they cannot be held responsible for the improvement of anaemia. Greater iron consumption, illustrated by higher transferrin saturation, also confirmed increased erythopoitesis in patients undergoing continuous ambulatory peritoneal dialysis. They also had lower blood iron level than those on haemodialysis (who had) numerous blood transfusions. The improvement of anaemia during continuous ambulatory peritoneal dialysis may be the result of reduction in plasma volume [7] as well as an increase in red cell mass and a better clearance of middle molecules in comparison to patients on haemodialysis. The main cause is higher erythropoietin level [8]. All tested patients had low folic acid level. Patients who corrected anaemia showed fall in folat level. This was statistically remarkable during the first three months of continuous ambulatory peritoneal dialysis-from 3.64 ng/ml to 2.09 ng/ml. All these data suggest that both dialysis modalities are effective in the control of protein waste products level, but continuous ambulatory peritoneal dialysis has better influence on the improvement of anaemia that haemodialysis. This can be attributed to better removal of uremic toxins, improved protein metabolism, lower parathyroid hormone level and higher erythropoietin value due to peritoneal macrophage production.
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PMID:[The effect of hemodialysis and continuous ambulatory peritoneal dialysis on renal anemia]. 926 38

The serum concentrations of CA19-9 and carcinoembryonic antigen (CEA) were measured in 150 consecutive patients with histologically proven liver disease admitted to a liver unit for transplant assessment. A significant proportion of the cases studied had a CA19-9 above the upper limit of the reference range (35 kU/L): alcoholic liver disease (73%), primary sclerosing cholangitis (61%), primary biliary cirrhosis (60%), chronic hepatitis B (71%), chronic hepatitis C (84%), autoimmune hepatitis (36%) and hepatocellular carcinoma (54%). CEA was only elevated in a small proportion of the patients with benign liver disease and the degree of elevation was small (15-37 micrograms/L). Significantly raised CEA was observed in two patients (15%) with hepatocellular carcinoma. Statistically significant correlations were observed between the serum CA19-9 concentration and standard parameters of liver dysfunction: positive correlations with aspartate aminotransferase, alkaline phosphatase and bilirubin and negative correlations with albumin and gamma-glutamyltransferase. Positive relationships were also observed between CA19-9 and both CEA and creatinine. Both increased production of CA19-9 from biliary epithelial cells and decreased clearance due to cholestasis may be contributing to the elevation of CA19-9 in the bloodstream. Our data indicate that caution is needed in the interpretation of CA19-9 results in the presence of liver dysfunction.
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PMID:The effect of benign and malignant liver disease on the tumour markers CA19-9 and CEA. 946 46

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
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PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78


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