Search PubMed⌕ Search

Biomedical subjects

R H Wiesner

Publications and source records attributed to R H Wiesner.

At least 271 records · Page 15Linked to original sources
PubMed1987

Lymphocyte subsets in primary sclerosing cholangitis.

As an initial step in testing the hypothesis that immunoregulatory abnormalities are important in the pathogenesis of primary sclerosing cholangitis, we determined the number and percentage of lymphocyte subsets in the peripheral blood of 33 patients with primary sclerosing cholangitis. In these patients, when compared with normal and diseased controls, there was a significant reduction in the total number of circulating T cells because of a disproportionate decrease in Leu-2a (suppressor/cytotoxic) cells. This decrease resulted in a significantly increased ratio of Leu-3a to Leu-2a cells. Patients with cirrhosis had significantly higher Leu-3a/Leu-2a (helper/suppressor) ratios than did noncirrhotic patients; both disease groups, however, had ratios that were significantly higher than controls. The number and percentage of B cells were significantly increased. Alterations in the percentage of B cells correlated significantly with histologic stage and concentrations of gamma globulin, serum IgG, and bilirubin. We conclude that these abnormalities are suggestive of a defect in immunoregulation in primary sclerosing cholangitis, which is not secondary to advanced liver disease alone and appears to be independent of chronic ulcerative colitis or obstructive jaundice.

Adult↗
PubMed1987

Hemostatic evaluation of patients undergoing liver transplantation.

A detailed coagulation and thromboelastographic study was done on the first 50 liver transplantation procedures performed at the Mayo Clinic between March 1985 and June 1986. Most of the patients suffered from primary sclerosing cholangitis, primary biliary cirrhosis, or chronic active hepatitis. Seven patients required a second liver transplantation, and six patients died, none intraoperatively. Most of the patients had distorted hemostatic mechanisms preoperatively, as would be expected because the liver generates most of the clotting factors. The outstanding exception was factor VIII, which was usually in the high-normal range or even more elevated. Substantial deterioration of coagulation factors occurred regularly during reperfusion of the donor liver. In some instances, this trend was corrected within 1 hour, but platelet counts continued to decrease, and some coagulation factors rebounded only partially. Because thromboelastographic tracings are quickly available to the liver transplant team and because they tend to forewarn of impending hemostatic problems, we believe that thromboelastography is a reasonably effective procedure for monitoring coagulation during liver transplantation.

Blood Coagulation Factors↗
PubMed1987

Immunohistologic labeling as an indicator of liver allograft rejection.

Monoclonal antibodies were used to identify T-helper cells (TH) and T-suppressor/cytotoxic cells (TS/C) in biopsy specimens obtained 7, 21, 90, 180, and 365 days postoperatively, and during episodes of graft dysfunction, from 34 consecutive liver transplant patients treated with cyclosporine and steroids. Rejection was diagnosed by the presence of appropriate laboratory and light microscopic findings and at least 8 weeks of follow-up to exclude other causes of graft dysfunction. Four immunohistologic patterns were seen--no labeled cells (No), only lobular TS/C, only portal TH, and a portal mixture of TH and TS/C (mix). Of 36 specimens with the No or only lobular TS/C pattern, 29 were not associated with rejection. Of the 39 specimens with the portal TH or portal Mix pattern, 33 were associated with a rejection episode. In addition, in nine specimens from patients with no biochemical or routine histologic evidence of rejection, the presence of portal TH or a portal mix indicated immunologic rejection 5 days to 5 weeks before biochemical and routine histologic evidence of it was manifested. Immunohistologic labeling appears to be an early indicator of liver allograft rejection.

Antibodies, Monoclonal↗
PubMed1987

Human liver and conjugation of catecholamines.

To investigate the role of the liver in conjugation of catecholamines we measured the concentrations of free and conjugated norepinephrine, epinephrine, and dopamine in plasma of patients with severe liver disease who were undergoing liver transplantation. Comparisons were made with catecholamine levels in plasma of euhepatic patients who were undergoing abdominal aortic aneurysmectomy. We were also able to determine the importance of the liver in conjugation of exogenous dopamine because this compound was given to both groups of patients. The concentrations of conjugated amines were within the normal range in the patients undergoing liver transplantation, and administered dopamine was conjugated to a similar extent in the two groups of patients. The data suggest that the liver is not indispensable for the conjugation of circulating catecholamines.

Adult↗
PubMed1987

Serial determinations of the amino-terminal peptide of type III procollagen in severe chronic active hepatitis.

To evaluate the diagnostic significance of the amino-terminal propeptide of procollagen type III (P-III-P) in monitoring chronic liver disease, serum P-III-P concentrations were measured in 46 patients with severe chronic active hepatitis (CAH) at entry and at remission during a therapeutic clinical trial. Coded sera were analyzed for P-III-P concentrations by both a standard radioimmunoassay and a recently developed and potentially more precise radioimmunoassay that uses Fab fragments rather than intact antibodies for binding antigen. As compared with conditions in 22 normal controls, P-III-P concentrations were elevated in 98% and 72% of patients with CAH by use of the standard and Fab radioimmunoassays, respectively. With treatment, P-III-P levels fell at remission to levels that were not significantly different from control values, as measured by both assays. The Fab radioimmunoassay, either alone or combined with the standard radioimmunoassay, provided no advantage over the standard radioimmunoassay alone. Serum P-III-P levels, as measured by either assay, correlated poorly or not at all with standard liver function tests and with histologic grade of disease. These data suggest that P-III-P serum levels are abnormal in severe CAH but normalize when remission of disease has been achieved. Consequently, serum P-III-P levels may be a diagnostic aid in the sequential evaluation of patients with severe CAH requiring treatment, and this test deserves further investigation. In this regard, the standard P-III-P assay has greater diagnostic accuracy than the Fab assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Peristomal varices after proctocolectomy in patients with primary sclerosing cholangitis.

Primary sclerosing cholangitis is a chronic cholestatic liver disease that is commonly associated with chronic ulcerative colitis. We observed the development of varices in the abdominal wall surrounding the ileostomy stoma of patients with primary sclerosing cholangitis who underwent proctocolectomy and ileostomy for chronic ulcerative colitis. In 10 of 19 patients, the development of peristomal varices was documented 12-133 mo after operation. Risk factors for the development of peristomal varices included splenomegaly, esophageal varices, advanced histologic stage at liver biopsy, low serum albumin, thrombocytopenia, and an increased prothrombin time. Recurrent bleeding from peristomal varices was a major problem; 7 of 10 patients required repeated blood transfusions. The only therapy of long-term benefit was surgical decompression of the portal venous system in 1 patient and liver transplantation in a second patient. In contrast, there was no perirectal bleeding in 4 patients with primary sclerosing cholangitis who underwent proctocolectomy with an ileoanal anastomosis.

Abdominal Muscles↗
PubMed1986

Does propranolol precipitate hepatic encephalopathy?

A 52-year-old woman with primary biliary cirrhosis who had never had hepatic coma developed it while taking propranolol. The coma receded when the propranolol was stopped and 2 days later gastrointestinal bleeding did not precipitate hepatic coma. This raises the question whether propranolol and other beta blockers lead to hepatic encephalopathy.

Esophageal and Gastric Varices↗