PubMed Health⌕ Search

Biomedical subjects

T M Worner

Publications and source records attributed to T M Worner.

48 records · Page 3Linked to original sources
PubMed1983

Comparison of animal and vegetable protein sources in the dietary management of hepatic encephalopathy.

Theoretical considerations based on amino acid metabolism in patients with hepatic encephalopathy as well as some limited patient studies had led to the proposal that dietary protein derived from a vegetable source may be better tolerated and more efficacious in such patients. However, studies in normal humans have revealed that vegetable protein is not as nitrogen sparing as animal protein. This prompted us to study under metabolic ward conditions the effects of vegetable and animal protein sources in patients with hepatic encephalopathy with respect to mental status, nitrogen balance, and plasma amino acids. No significant differences regarding any of the parameters studied was observed in relationship to the source of dietary protein, but compliance to the regimen was more difficult with the vegetable protein diet.

Amino Acids↗
PubMed1982

Perivenular fibrosis in alcoholic liver injury: ultrastructure and histologic progression.

Twenty alcoholic patients underwent sequential biopsy of the liver as part of their medical evaluation. Of the 10 patients with simple fatty liver, 9 showed no progression of the histologic lesion after 1-2 yr. By contrast, of 10 patients with perivenular fibrosis, of the 9 who continued to drink all showed progression. Laboratory parameters did not distinguish between these two groups at the time of initial biopsy. The ultrastructure of the perivenular lesion was evaluated in 11 patients. The thickness of the perivenular rim was variable, but there was a good correlation between the thickness of the perivenular rim and the number of mesenchymal cells surrounding the venules (correlation coefficient r = 0.7634, p less than 0.001). Myofibroblasts represented the most common cell type but there was also infiltration with other mononuclear cells. Collagen fibers surrounding myofibroblasts were observed in the perivenular fibrotic area. Thus, in the group of alcoholics who were investigated in this study, myofibroblast proliferation and collagen deposition around the terminal hepatic venule represent the first apparent lesions in the sequence of events leading to alcoholic cirrhosis.

Fatty Liver, Alcoholic↗
PubMed1980

Plasma glutamate dehydrogenase: clinical application in patients with alcoholic liver disease.

The time course of plasma glutamate dehydrogenase (GDH) elevation was studied in 42 male alcoholics admitted for alcohol detoxification or for the treatment of medical complications of alcoholism and in 2 volunteers consuming 2 g/kg/day of ethanol under metabolic ward conditions. GDH values were usually highest during or immediately after cessation of drinking; thereafter, they fell rapidly toward the normal range. Early GDH values correlated well with liver histology in 37 patients who subsequently underwent diagnostic liver biopsy.

Enzymes↗
PubMed1979

Detection of alcoholism relapse: comparative diagnostic value of MCV, GGTP, and AANB.

Mean red blood cell volume (MCV), plasma gamma glutamyl transpeptidase (GGTP), and plasma alpha amino-n-butyric acid (AANB) were measured in 245 patients undergoing treatment for alcoholism at the V.A. Medical Center, Bronx, N.Y. and Raleigh Hills Hospitals, Denver, Colo. AANB and GGTP, but not MCV, decreased following withdrawal from alcohol and during a period of abstinence. Among patients who relapsed, AANB and GGTP, but not MCV, increased in a majority of subjects. The combined use of AANB and GGTP identified 28/33 heavy drinkers, while 4/33 patients in remission had positive tests. In conclusion, measurement of AANB and GGTP are useful in documenting the success of treatment for alcoholism and in identifying patients who relapse following treatment for alcoholism.

Alcoholism↗
PubMed1979

Alcohol-related diseases and carcinogenesis.

Possible mechanisms whereby alcohol abuse and alcohol-related diseases may promote the development of cancer are analyzed. The mechanisms discussed include: (a) contact-related local effects on the upper gastrointestinal tract; (b) the presence of low levels of carcinogens in alcoholic beverages; (c) induction of microsomal enzymes involved in carcinogen metabolism; (d) various types of cellular injury produced by ethanol and its metabolites and their relationship to cancer, particularly in the liver; (e) the nutritional disturbances frequently associated with alcohol abuse. The relationship between alcohol-induced cirrhosis and hepatocellular carcinoma is also discussed, and case histories of patients seen at the Bronx Veterans Administration Medical Center with hepatocellular carcinoma in the absence of cirrhosis are reviewed. Data are presented demonstrating the induction, by chronic ethanol consumption, of microsomal enzymes which convert procarcinogens to carcinogens. These data were derived from experiments in which the ability of microsomes isolated from liver, intestine, and lung tissues of ethanol-fed and control rats to activate several test carcinogens was examined in the Ames Salmonella-mutagenicity test. The hypothesis is presented that ethanol-mediated induction of enzyme systems which activate procarcinogens to carcinogens in various tissues contributes to the enhanced incidence of cancer in the alcoholic.

Alcoholism↗
PubMedDate not supplied

Frequency of hyperprolinemia in alcoholic liver cirrhosis: relationship to blood lactate.

In alcohol-induced liver injury, hyperprolinemia has been proposed as a marker of fibrogenesis probably secondary to hyperlactacidemia. However, some studies of plasma proline in alcoholics with cirrhosis have reported normal rather than increased levels. In order to evaluate the frequency of hyperprolinemia in alcoholic liver disease and its relationship to blood lactate, we measured plasma proline levels in 145 subjects including 91 alcoholics with a spectrum of liver disease as well as 22 nonalcoholics with liver injury unrelated to alcohol. We also studied baboons fed alcohol as 50% of total calories for 1 to 4 years. Among alcoholics only 21/91 had elevated proline values. Elevations were most frequent among patients with severe hepatic decompensation (3/8), in patients with alcoholic hepatitis on liver biopsy (5/17), and in those with acute alcohol-related withdrawal, with alcohol still present in the blood (4/9). Patients with liver disease unrelated to alcohol but severe in nature also has elevations in proline (3/3). Only 4/28 patients with cirrhosis due to alcohol had elevated values, and none of the baboons fed alcohol had hyperprolinemia whether withdrawn from alcohol or not. Hyperlactacidemia was associated with hyperprolinemia, but so were depressed serum albumin values and prolongations of the prothrombin time, suggesting a general association with severe liver disease. These results reveal that hyperprolinemia occurs infrequently in patients with alcohol-induced cirrhosis and therefore does not appear to be a sensitive marker of hepatic fibrosis in these patients.

Animals↗
PubMedDate not supplied

The role of alcoholism and liver disease in the appearance of serum antibodies against acetaldehyde adducts.

We recently presented preliminary data indicating the presence of antibodies against acetaldehyde adducts in sera of over 70% of alcoholic patients. To assess the respective roles of liver disease and alcohol consumption as well as the specificity of this immune response, 141 patients in various stages of alcoholic and nonalcoholic liver diseases were tested by a hemagglutination assay. Sixty-three (73%) of 86 alcoholics had antibody titers above control levels (p less than 0.0001). Alcohol consumption of these individuals was significantly higher (p less than 0.001) than that of those alcoholics with normal titers. Twenty-two patients (39%) with nonalcoholic liver diseases also had elevated levels of antibodies against acetaldehyde adducts (p less than 0.0005); of these, 8 had primary biliary cirrhosis (7 in Stages III and IV), 9 had chronic active hepatitis (6 with cirrhosis) and 5 had acute (virus- or drug-induced) hepatitis. Antibody titers did not correlate with levels of transaminase or alkaline phosphatase activity, nor with bilirubin, and albumin. However, in 52 alcoholics and in nonalcoholic patients with biopsy-confirmed liver disease, the highest titers were seen in the more advanced stages of liver damage. Thus, in addition to alcohol consumption, severity of liver disease may play a role in the appearance of circulating antibodies against acetaldehyde adducts.

Acetaldehyde↗
PubMedDate not supplied

Peripheral neuropathy after disulfiram administration: reversibility despite continued therapy.

The clinical history of an abstinent alcoholic developing paresthesias after one year's treatment with disulfiram (250 mg daily) is presented. Despite continued disulfiram in decreased dosage (125 mg daily), associated with multivitamin supplementation, marked improvement in symptoms and signs was noted, contrary to previous case reports. The peripheral sensorimotor neuropathy associated with disulfiram administration has been well described [1 - 8]. From those reports, it appears that symptoms may appear from several weeks to several months after the drug has been administered. Although the etiology of this neuropathy remains speculative, the usual treatment is to discontinue disulfiram once the toxicity develops. Presented here is the clinical course of a subject, whose neuropathic symptoms resolved with continued disulfiram administration at a lower daily dosage in conjunction with multivitamin therapy.

Adult↗