Odd Dietrichson

Human Leucocyte Antigens in Patients with Alcoholic Liver Cirrhosis

No significant differences in the frequencies of HLA-B8, -B40, and other HLA-A, -B, and -C phenotypes were found among patients with histologically verified alcoholic cirrhosis compared with normal controls when the p values were multiplied by the number of comparisons. This was found both in the present study of 45 patients and in the combined data of this and three other similar studies. However, these findings do not rule out that alcoholic cirrhosis might be associated with HLA factors (for example. HLA-D/DR antigens) controlling immune responses.

Morphological Changes in Liver Biopsies from Patients with Rheumatoid Arthritis

Oxphenisatin is known to induce liver damage and is suspected to cause or perpetuate chronic liver disease. In order to evaluate the hepatotoxic effect of long-term therapy with oxyphenisatin 26 consecutive patients with rheumatoid arthritis were investigated for the presence of liver disease. In all cases, liver biopsy, biochemical liver function tests and determination of Hepatitis-B antigen were performed. Ten patients showed no pathological changes in the liver biopsy and a further 2 had only non-specific changes. Seven patients had fatty liver, 5 passive congestion, one haemosiderosis and only one had cirrhosis of the liver. No correlation was found between the activity of rheumatoid arthritis, and duration of the disease, the drug therapy given, and the liver damage.

Long-term Follow-up of e-Antigen (HBeAg)-positive Acute Viral Hepatitis

Eighteen consecutive patients with HBeAg in serum and histologically verified acute viral hepatitis were included in a follow-up study of the natural course of the disease. Five patients were followed up for from 2 to 6 months. Two of these healed clinically and cleared both HBeAg and HBsAg, while three were positive for HBeAg and HBsAg at the last control. Thirteen patients with a follow-up of from 27 to 102 months became HBeAg-negative during the time of observation. In all but one, progression of the liver disease stopped when HBeAg was cleared. The results further indicate a close association between the duration of HBe antigenemia and the severity of the liver disease.

The Role of Acute Hepatitis Type A, B, and Non-A Non-B in the Development of Chronic Active Liver Disease

In 19 patients followed from biopsy-verified acute viral hepatitis to chronic active liver disease and 74 patients followed to complete resolution verified by a normal liver biopsy, sera from the acute phase were studied for serologic evidence of hepatitis type A and B. Eleven of the 19 patients who developed chronic active liver disease progressed from acute hepatitis type B and 7 from acute hepatitis type non-A non-B. One patient could not be classified because the sera were exhausted. None had serological markers of actual hepatitis type A infection. Of the 74 patients with a histologically complete resolution, the acute episode could be classified as type B hepatitis in 47 and type A hepatitis in 13 patients. The remaining 14 patients were classified as having acute viral hepatitis type non-A non-B. Our findings confirm that type B and non-A non-B hepatitis may give rise to chronic liver disease, whereas type A hepatitis so far has not been demonstrated to initiate a chronic liver disease.

The prognosis of chronic aggressive hepatitis. A clinical and morphological follow-up study.

In a follow-up study of 85 patients with chronic aggressive (active) hepatitis (CAH) repeated liver biopsies and/or autopsy liver sections were available in 74 cases. The median time of observation was 45 months. Cirrhosis was demonstrated in 38 patients, and cirrhosis was suspected in a further five cases. Fifteen patients showed convincing histological improvement; and the remaining 16 still had chronic hepatitis. Twenty-six patients died during the observation period, seven of these of liver failure after development of cirrhosis. The clinical follow-up of the 59 survivors (median observation time 69 months) showed biochemically active liver disease in 11 cases, all having cirrhosis or chronic aggressive hepatitis in the last biopsy. The clinical findings were correlated with the morphological follow-up diagnosis and the immunosuppressive treatment. Comparison of the initial histological, clinical, and serological variables was made in two well-defined follow-up groups. There were more females, and marked portal inflammation, abnormal bile duct epithelium, and circulating autoantibodies occurred more frequently in the group with later development of cirrhosis than among the patients with subsequent morphological improvement. The results thus suggest candidates for thorough follow-up and more intensive immunosupressive or other treatment.