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Biomedical subjects

R H Wiesner

Publications and source records attributed to R H Wiesner.

At least 181 records · Page 10Linked to original sources
PubMed1993

Ulcerative colitis disease activity following treatment of associated primary sclerosing cholangitis with cyclosporin.

Thirty five adult patients with precirrhotic primary sclerosing cholangitis were randomly allocated to treatment for at least one year with low dose (4.1 mg/kg/day) cyclosporin or placebo in a double blind trial. Thirty patients had coexisting ulcerative colitis, including three who had previously undergone colectomy and one who discontinued treatment after three months. Of the remaining 26 patients, 16 received cyclosporin and 10 received placebo. Endoscopy was performed at entry to confirm the diagnosis of inflammatory bowel disease. The ulcerative colitis disease activity was prospectively classified annually as remission/mild, moderate, or severe using the Truelove and Witt's criteria. Before treatment there were no differences between the cyclosporin and placebo groups in the number of patients with remission/mild colitis, 14/16 (88%) v 9/10 (90%), and moderate colitis, 2/16 (12%) v 1/10 (10%). During treatment, a remission/mild disease course was present in 15/16 (94%) v 6/10 (60%), p = 0.05 and a moderate disease course in 1/16 (6%) v 4/10 (40%), p = 0.05. It is concluded that patients treated with cyclosporin for primary sclerosing cholangitis who have coexisting ulcerative colitis have a more benign course of colitis resulting both from improvement of moderately active colitis and from fewer flares of remission/mildly active colitis. These findings suggest that cyclosporin may be of benefit to the colon in patients with ulcerative colitis who are being treated with cyclosporin for primary sclerosing cholangitis.

Adult↗
PubMed1993

Use of Prograf (FK 506) as rescue therapy for refractory rejection after liver transplantation. US Multicenter FK 506 Liver Study Group.

This report describes the clinical characteristics and demographics of patients enrolled into this rescue trial for patients experiencing refractory rejection after liver transplantation. Actuarial graft and patient survival at 12 months postconversion was 50% and 72%, respectively. Actual treatment success at 3 months postconversion was 70%. Karnofsky scores and liver function tests were significantly improved for patients continuing on therapy indicating clinical benefit in these patients. The safety profile of FK 506 is acceptable for such a high-risk group of patients. These preliminary clinical results support the conclusion that FK 506 can effectively control and reverse refractory rejection in a majority of liver transplantation patients.

Acute Disease↗
PubMed1993

[Complications and risk factors of ileo-anal anastomosis with reservoir for ulcero-hemorrhagic rectocolitis associated with primary sclerosing cholangitis].

The study determined predictive factors for postoperative complications and outcome after ileal pouch-anal anastomosis in patients with ulcerative colitis and primary sclerosing cholangitis. Patients with ulcerative colitis and primary sclerosing cholangitis treated by colectomy and ileostomy are at high risk of troublesome bleeding from peristomal varices. Postoperative complications and outcome were assessed in 40 patients with ulcerative colitis and sclerosing cholangitis who received in ileal pouch-anal anastomosis between January 1981 and February 1990. Immediate postoperative and remote ileoanal anastomosis-related complications were high but related directly to the severity of liver disease. No patient had perianastomotic and bleeding. In patients with both ulcerative colitis and primary sclerosing cholangitis, ileal pouch-anal anastomosis is safe and is not associated with perianastomotic bleeding.

Adolescent↗
PubMed1993

Histological evidence for recurrence of primary biliary cirrhosis after liver transplantation.

Whether primary biliary cirrhosis recurs after orthotopic liver transplantation remains a controversial issue. Sixty consecutive patients with primary biliary cirrhosis with at least 1 yr of follow-up after liver transplantation were studied. All patients were treated with triple-drug immunosuppression (cyclosporine, prednisone, azathioprine). Hepatic biochemical parameters and protocol liver biopsy specimens were evaluated 1 wk, 3 wk, 4 mo and yearly after orthotopic liver transplantation and at times of liver dysfunction. Antimitochondrial antibody titers and IgM levels were determined at 4 mo and yearly. At the time of last follow-up, all patients had marked symptomatic improvement compared with their pretransplant condition, and 91% of the patients had normal hepatic biochemical parameters, including serum levels of alkaline phosphatase, bilirubin, ALT and IgM. In addition, all patients had significant decreases in antimitochondrial antibody titer (p = 0.0001) and significant decreases in serum levels of IgM (p = 0.0001). Forty-one of the 60 patients had near-normal liver histological appearance. Of those with abnormal histological appearance, five patients, 2 to 6 yr after orthotopic liver transplantation, had histological features typical of a florid duct lesion, suggesting recurrent primary biliary cirrhosis. All five patients with portal granulomas had normal hepatic biochemical values and were clinically asymptomatic. Two of the five patients had persistent antimitochondrial antibody titers. We consider the documented histological changes highly suggestive of recurrence of primary biliary cirrhosis after liver transplantation but, so far, have no evidence that the condition in these patients is progressive.

Adult↗
PubMed1993

Advances in the diagnosis, treatment, and prevention of cytomegalovirus infections after liver transplantation.

CMV is one of the most frequent viral infections after orthotopic liver transplantation. Thus, there should be a high index of clinical suspicion, particularly in liver transplant recipients who have risk factors for the development of CMV disease, including donor CMV seropositivity, the use of antilymphocyte preparations, and retransplantation. The availability of effective antiviral therapy to treat CMV disease has emphasized the importance of an aggressive approach to the early diagnosis and treatment of this viral infection. Ganciclovir has been a major advancement in the treatment of severe CMV disease and has had a major impact on reducing the incidence and severity of CMV disease and its complications in the liver transplant recipient. Furthermore, these antiviral agents are now being evaluated for their prophylactic potential. Indeed, a number of these agents or combinations of these agents have been shown to be effective in reducing the incidence and severity of CMV disease, particularly in the CMV-seropositive transplant recipient; however, the cost-effectiveness of such therapy and its overall impact on long-term graft and patient outcome remain poorly defined at this time. Further investigations will be needed to define the role and importance of prophylactic therapy for the prevention of CMV infection and disease in the liver transplant recipient.

Cytomegalovirus Infections↗
PubMed1992

Diagnosis of chronic hepatitis C after liver transplantation by the detection of viral sequences with polymerase chain reaction.

Chronic hepatitis frequently occurs after liver transplantation. The role of hepatitis C virus infection in patients after liver transplantation is unknown, although antibodies to HCV are detected in some of these cases. The use of polymerase chain reaction techniques for the detection of hepatitis C virus RNA should improve sensitivity and specificity, particularly in these immunosuppressed patients. Our goal was to further clarify the role of hepatitis C virus infection in chronic hepatitis occurring after liver transplantation. Patients with chronic hepatitis of uncertain origin after transplantation were identified. Serum samples taken at the time of the most recent liver biopsy that showed chronic hepatitis were tested for anti-hepatitis C virus using enzyme-linked immunoassay and supplemented by recombinant immunoblot assay (recombinant immunoblot assay I and recombinant immunoblot assay II). The samples were also tested for the presence of hepatitis C virus RNA using polymerase chain reaction. Of the 25 patients with chronic hepatitis, 15 (60%) had hepatitis C virus RNA present. Only seven (47%) of these 15 patients had anti-hepatitis C virus detected. Hepatitis C virus is a major cause of chronic hepatitis occurring after liver transplantation. The magnitude of hepatitis C virus infection will be underestimated if only currently available assays for anti-hepatitis C virus are used.

Base Sequence↗
PubMed1992

Prognostic features and role of liver transplantation in severe corticosteroid-treated autoimmune chronic active hepatitis.

To identify prognostic features and to define the role of liver transplantation in severe autoimmune chronic active hepatitis, findings before and after corticosteroid therapy in 111 patients were correlated with outcome and compared with the findings in 24 patients who had been selected independently for liver transplantation. Patients whose condition deteriorated during corticosteroid treatment were younger (32 +/- 3 yr vs. 43 +/- 2 yr; p less than 0.02) than those who experienced remission, but no individual features predicted outcome. Patients in whom therapy failed required longer durations of continuous treatment than did those who experienced remission (60 +/- 14 mo vs. 20 +/- 12 mo; p = 0.001). Of 13 patients who did not experience remission within 4 yr, 9 (69%) ultimately deteriorated. Ascites developed more often in those patients whose therapy failed and who died of liver failure than in counterparts who survived (86% vs. 33%). Patients undergoing transplantation were similar to those whose treatment failed, but they died less frequently (8% vs. 56%, p less than 0.01). Indeed, the 5-yr survival rate after transplantation was comparable to that of patients who had entered remission (92% vs. 100%). Successive biopsy samples failed to disclose recurrent autoimmune hepatitis after transplantation. Human leukocyte antigens A1, B8 occurred more commonly in patients in whom treatment failed or who underwent transplantation (70% vs. 41%, p less than 0.05). We conclude that failure to achieve remission within 4 yr and the human leukocyte antigen A1, B8 phenotype are associated with poor prognosis. Manifestations of liver decompensation, such as ascites, in patients who have been unable to experience remission justify consideration of transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗
PubMed1992

Hepatic allograft cyclosporine concentration is independent of the route of cyclosporine administration and correlates with the occurrence of early cellular rejection.

This study compares the hepatic-tissue cyclosporine concentrations in liver biopsy specimens from patients with and without cellular rejection after orthotopic liver transplantation. Nine patients without cellular rejection were studied, including five patients receiving intravenous cyclosporine who had biopsies on posttransplant day 7 and four patients receiving oral cyclosporine who had biopsies on day 21. In these patients no significant differences were seen in blood cyclosporine concentrations (mean +/- S.D.) (310 +/- 162 vs. 273 +/- 310 ng/ml) and hepatic-tissue cyclosporine concentrations (3,451 +/- 1,262 vs. 3,545 +/- 456 ng/gm). These nine patients without cellular rejection were then compared with eight patients with cellular rejection who were receiving intravenous cyclosporine, including seven patients who had biopsies on post-transplant day 7 and one patient who had a biopsy on day 14. In patients with and without cellular rejection blood cyclosporine concentrations were 330 +/- 64 vs. 294 +/- 146 ng/ml, and hepatic-tissue cyclosporine concentrations were 1,879 +/- 998 vs. 3,493 +/- 936 ng/gm, p less than 0.01. We conclude that hepatic-tissue cyclosporine concentrations are independent of the route of cyclosporine administration and that low hepatic-tissue cyclosporine concentrations correlate with early cellular rejection after orthotopic liver transplantation.

Administration, Oral↗
PubMed1992

Ischemic-type biliary complications after orthotopic liver transplantation.

Nonanastomotic biliary strictures that involve only the biliary tree of the graft occur after orthotopic liver transplantation in patients with hepatic artery thrombosis, chronic ductopenic rejection and ABO blood group incompatibility. This complication may also occur in the absence of these known risk factors. The major focus of our study was to evaluate the risk factors for nonanastomotic biliary stricturing of unknown cause after orthotopic liver transplantation. Results demonstrate that the development of biliary strictures is strongly associated with the duration of cold ischemic storage of allografts in both Euro-Collins solution and University of Wisconsin solution. Results also demonstrate that strictures are not associated with the type of biliary reconstruction, the primary liver disease, cytomegalovirus infection, allograft rejection or the presence of a positive lymphocytotoxic crossmatch. More recently, we have markedly reduced the occurrence of nonanastomotic biliary stricturing by decreasing the ischemia time of our allografts. Thus nonanastomotic biliary strictures appear to be the result of the ischemia/reperfusion-induced tissue injury associated with the harvest and implantation of allografts.

Adenosine↗
PubMed1992

Lack of association between cytomegalovirus infection, HLA matching and the vanishing bile duct syndrome after liver transplantation.

In this study we evaluated the association between cytomegalovirus infection alone or in relation to human leukocyte antigen matching and the development of vanishing bile duct syndrome, a form of chronic hepatic allograft rejection. A total of 81 consecutive liver transplant recipients were studied. Cytomegalovirus infection developed in 46 recipients (57%), and vanishing bile duct syndrome occurred in 9 recipients (11%). Cytomegalovirus infection developed in only five of the nine patients with vanishing bile duct syndrome. Univariate analysis of pretransplant recipient/donor cytomegalovirus serological tests and human leukocyte antigen typing showed they were not significant risk factors for the development of vanishing bile duct syndrome. Time-dependent analysis of cytomegalovirus infection after transplantation as a risk factor for vanishing bile duct syndrome, in a multivariate analysis with human leukocyte antigen match, showed no statistical significance. In our study, no association was found between cytomegalovirus infection alone or in relation to class I or II human leukocyte antigen match and the subsequent development of vanishing bile duct syndrome.

Acyclovir↗
PubMed1992

Papillary bile duct dysplasia in primary sclerosing cholangitis.

A 62-year-old man with a 20-year history of chronic ulcerative colitis and a 9-year history of primary sclerosing cholangitis (PSC) underwent orthotopic liver transplantation because of symptoms related to PSC and cholangiographic features compatible with a biliary neoplasm. Study of the excised liver revealed papillary mucosal lesions in the common hepatic duct and the right and left hepatic ducts as well as cholangiectases and other features typically associated with PSC. The papillary lesions consisted of abundant fibrovascular stroma covered by biliary epithelium with low-grade and high-grade dysplasia. Some periductal glands were also dysplastic. These features distinguished papillary dysplasia from classic biliary papillomatosis. Only one focus of microinvasion was found; there were no metastases. Among 60 cases of PSC in whom the entire liver could be studied after orthotopic liver transplantation, this was the only instance of unequivocal dysplasia. However, in one specimen, papillary hyperplasia was found. Detailed macroscopic and microscopic rereview of 23 livers from our patients with the longest history of PSC (range, 5-24 years) failed to reveal any additional cases with dysplasia. It is concluded that (a) papillary mucosal lesions in PSC may represent papillary dysplasia without invasion; (b) these lesions may evolve from papillary hyperplasia; (c) the process may be largely, if not entirely, in situ; and (d) the prevalence of dysplasia and carcinoma of bile ducts may be less than the 7%-9% reported in the literature for malignancies associated with PSC.

Bile Ducts↗