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Biomedical subjects

J Ludwig

Publications and source records attributed to J Ludwig.

At least 253 records · Page 14Linked to original sources

Drug effects on the liver. An updated tabular compilation of drugs and drug-related hepatic diseases.

Generic and chemical names of drugs and the possible adverse effects of these drugs on the human liver are tabulated. Most drugs compiled in these tables have been approved by the Federal Drug Administration. They are currently available in the United States, and they are listed in the 1983 Physicians' Desk Reference. Some important investigational drugs are listed also. The tables include: (1) generic names of drugs that have caused a characteristic morphologic change, such as granulomatous hepatitis; (2) morphologic diagnoses that have been documented after administration of each drug; and (3) references that can be matched to each drug and to its effects on the liver.

Carcinoma, Hepatocellular↗

Primary sclerosing cholangitis: findings on cholangiography and pancreatography.

Cholangiograms of 86 patients with primary sclerosing cholangitis (PSC) were compared with those of 82 patients with primary bile duct carcinoma and 16 with primary biliary cirrhosis. Multifocal strictures involving both intra- and extra-hepatic bile ducts were most common in PSC; they were diffusely distributed, short, and annular, alternating with normal or slightly dilated segments to produce a "beaded" appearance. Very short, band-like strictures occurred in 18 patients; 9 also had diverticulum-like out-pouchings. Fourteen patients had "diverticula" without band strictures. Both findings appear to be specific for PSC. Inflammatory bowel disease was seen in 57 patients (66%), who could not be distinguished cholangiographically from other PSC patients. Of 40 patients with adequate retrograde pancreatograms, 3 had abnormalities of the pancreatic ducts.

Adolescent↗

Autoimmune features as determinants of prognosis in steroid-treated chronic active hepatitis of uncertain etiology.

To determine if autoimmune features influence the prognosis of severe sporadic chronic active hepatitis of uncertain etiology, 126 corticosteroid-treated patients who had been screened to exclude active hepatitis B infection and possible drug effects or transfusion-related disease were categorized according to the presence of the lupus erythematosus cell, antinuclear antibody, smooth muscle antibody, and coexistent autoimmune diseases. Patients with autoimmune markers had findings similar to those without these features and responses to therapy were comparable. Remission (77% vs. 68%), treatment failure (16% vs. 14%), progression to cirrhosis (31% vs. 39%), and death from hepatic failure (4% vs. 12%) occurred with similar frequency in patients with and without the lupus erythematosus cell or antinuclear antibody. Although patients with the lupus erythematosus cell or antinuclear antibody tended to relapse less frequently than others, 5-yr survival was not increased (92% vs. 87%). Autoimmune diseases occurred as commonly in patients without the lupus erythematosus cell or antinuclear antibody as in those with these findings (16% vs. 17%), and the presence of these conditions did not identify patients with a different clinical behavior. In severe sporadic chronic active hepatitis of uncertain etiology, a clinically and prognostically distinct subgroup reflective of a possible autoimmune disorder cannot be defined.

Adolescent↗

Familial occurrence of primary sclerosing cholangitis and ulcerative colitis.

Members of three families had primary sclerosing cholangitis and chronic ulcerative colitis. In each family, two siblings were affected; in one instance, they were twin brothers. All six individuals had primary sclerosing cholangitis and five also had ulcerative colitis. These cases represent the first reported instances of the familial occurrence of both primary sclerosing cholangitis and chronic ulcerative colitis; illustrate the typical clinical, laboratory, radiologic, and pathological features of primary sclerosing cholangitis; and support the hypothesis that genetic factors may play a role in the etiology of this obscure disorder.

Adolescent↗

Diagnosis of Wilson's disease presenting as fulminant hepatic failure.

The clinical course, results of standard laboratory tests, parameters of copper metabolism, and hepatic morphology in 9 cases (3 of our own and 6 from the literature) of Wilson's disease presenting as fulminant hepatic failure were compared with the findings in 5 cases of idiopathic fulminant hepatic failure. Patients with Wilson's disease were usually younger, and 7 of the 9 patients had Kayser-Fleischer rings. Patients with idiopathic fulminant hepatic failure had elevated 24-h urinary copper, decreased ceruloplasmin, and low or normal serum copper. Fulminant hepatic failure with Wilson's disease differed from idiopathic fulminant hepatic failure by the following biochemical findings: (a) higher copper levels in serum, urine and liver; (b) less pronounced elevations of transaminase levels; (c) higher concentrations of total bilirubin; and (d) lower hemoglobin values. Serum copper was the most useful biochemical test in diagnosing Wilson's disease before death. At autopsy, only hepatic copper concentrations clearly separated the two groups. Serial serum copper levels (antemortem) and quantitative analysis of hepatic copper (after recovery or postmortem) in patients with fulminant hepatic failure should help to exclude Wilson's disease.

Adolescent↗

Xanthomatous neuropathy of liver.

A 36-year-old man with juvenile-onset diabetes mellitus developed cholestatic hepatitis of unknown cause, possibly drug-induced. He remained jaundiced for four months, until he died unexpectedly. At autopsy, severe and macroscopically identifiable xanthomatous neuropathy was found in the liver; it involved the unmyelinated nerves in the hilus and in all portal tracts examined. Microscopic evidence of minimal extrahepatic involvement of unmyelinated nerves was also found. Somatic nerves were affected by diabetic neuropathy but not by xanthomatous neuropathy. The condition seems to be a rare complication of diseases that are characterized by accumulations of lipids.

Adult↗

Accumulation of radionuclide-labeled platelets and fibrinogen in paraquat-damaged rat lungs.

After intraperitoneal injection of paraquat, rats showed evidence of neurologic and respiratory damage and had a mortality rate of 41% in 3 days. The lungs quadrupled in weight between the third and the fifth day. Pulmonary edema and extravascular fibrin and platelets were identified by light and transmission electron microscopy. As early as 4 h after injection of the paraquat, 51Cr from labeled platelets began accumulating in the lungs. The peak was reached by 48 h; 125I from labeled fibrinogen also concentrated in the lungs of treated rats. Total complement was unchanged. The paraquat-treated rat is a suitable model for study of the behavior of fibrin and platelets in permeability pulmonary edema. Disturbances of copper metabolism deserve further investigation.

Animals↗

Corticosteroid-treated chronic active hepatitis in remission: uncertain prognosis of chronic persistent hepatitis.

To assess the prognosis of patients with severe chronic hepatitis after histologic examination had shown an improvement to chronic persistent hepatitis, we followed 52 such patients regularly for 54 +/- 4 months after the cessation of corticosteroid therapy. In 24 patients, the condition deteriorated 7 +/- 1 months after therapy and required further treatment with prednisone. Histologic features of chronic active hepatitis, including bridging and multilobular necrosis, were documented in all 14 patients in whom biopsies were performed. In 20 of 24 patients, the disease responded to retreatment, but 13 again had relapses, and cirrhosis developed in two. Of 28 patients who remained asymptomatic for 48 +/- 6 months, 17 retained features of chronic persistent hepatitis, and nine had improvement to normal histologic features. Cirrhosis developed in two patients without clinical manifestations of active inflammation. Findings before and after treatment did not predict outcome. We conclude that severe chronic active hepatitis that has been treated with prednisone and converted to chronic persistent hepatitis will often and unpredictably deteriorate after treatment has been stopped. Cirrhosis develops rarely but may occur with or without clinically overt chronic active hepatitis.

Adolescent↗