PubMed Health⌕ Search

Biomedical subjects

L Van Waes

Publications and source records attributed to L Van Waes.

At least 19 recordsLinked to original sources
PubMed1978

Alcoholism and alcoholic liver injury: new diagnostic and prognostic tests.

Recently developed tests that measure levels of alpha-amino-n-butyric acid (AANB) and serum glutamic dehydrogenase (GDH) may improve screening for early detection of heavy drinking and liver injury, respectively. With these tests, a "three-level" approach to the problem is now possible: (1) detection of heavy drinking on the basis of a biochemical marker (such as AANB); (2) detection of liver injury (necrosis and inflammation) on the basis of serum liver tests (such as GDH); and (3) detection of alcoholics in whom cirrhosis is prone to develop by the screening of liver biopsy specimens for precirrhotic lesions (such as pericentral sclerosis).

Alcoholism↗
PubMed1977

Glutamate dehydrogenase: a reliable marker of liver cell necrosis in the alcoholic.

The usefulness of blood enzyme determinations as markers of liver necrosis was tested in 100 alcoholics who underwent biopsy during clinical investigation. Mean values of glutamate dehydrogenase (GDH), serum aspartate and alanine transferase (SGOT and SGPT), ornithine carbamoyltransferase (OCT), and gamma-glutamyltranspeptidase (gamma-GTP) tended to rise with increasing liver cell necrosis, though values of SGOT, SGPT, OCT, and gamma-GTP showed considerable overlap between the 32 patients with histologically proved hepatitis and the 68 without. By contrast, GDH values showed virtually no overlap between patients with and without hepatitis, and a value of two and a half times the normal value discriminated between the two groups. Because of its easy determination and its reliable reflection of liver cell necrosis the GDH concentration should be estimated routinely in alcoholic patients.

Alcoholism↗
PubMed1977

Early perivenular sclerosis in alcoholic fatty liver: an index of progressive liver injury.

Alcoholic steatosis was associated with sclerosis around the terminal hepatic venules in liver biopsies of 40% of chronic alcoholics but not in those of moderate drinkers. To determine whether this sclerosis could be a precursor lesion of cirrhosis, controlled studies were performed in animal models. In the alcohol-fed baboons that developed fibrosis or cirrhosis, progressive perivenular sclerosis invariably started at the fatty liver stage before or even more commonly in the absence of alcoholic hepatitis. No sclerosis occurred in controls or in alcohol-fed baboons and rats that did not progress beyond the fatty liver stage. The clinical and experimental data indicate that sclerosis around the terminal venules, a common but often overlooked complication of alcoholic fatty liver, reflects heavy prolonged drinking, and may identify those patients who are susceptible to develop the more advanced lesions of alcoholic liver injury upon continued drinking.

Adult↗
PubMed1977

Carcinoma of the pancreas presenting as relapsing pancreatitis.

A case is reported of a 32-year old man, in which relapsing pancreatitis was the presenting symptom of an underlying carcinoma of the body of the pancreas. The rare association of clinically manifest pancreatitis and pancreatic carcinoma is reviewed and a possible pathogenetic mechanism is proposed in this case. It is suggested that pancreatic carcinoma should be suspected in patients with relapsing so-called idiopathic pancreatitis.

Acute Disease↗
PubMed1974

Chronic liver disease and hepatitis-B antigen: a prospective study.

A long-term follow-up of 45 patients with chronic hepatitis and 41 with cirrhosis is reported. Hepatitis-B antigen (HBAg) was present in 19 (42%) of the chronic hepatitis patients and in 20 (49%) of those with cirrhosis. The clinical course and biochemical and histological findings in the HBAg-positive and the HBAg-negative cases were similar, suggesting that HBAg-positive chronic liver disease is not a distinct clinical entity. The presence of antigen and autoantibodies was not found to be mutually exclusive. In HBAg-positive cases antigen tended to persist for months and years. When no irreversible lesions exist disappearance of the antigen may be a sign that the liver disease will resolve.

Adult↗