[Temporal arteritis without histological changes]. / Arteritis temporalis uden histologiske forandringer.

A patient with severe giant cell arteritis with involvement of both eyes is presented. The symptoms were partly reversible by treatment with high doses of prednison. Three months previously (having symptoms of polymyalgia rheumatica) she had started treatment with a low dosage of prednison. Biopsies of both temporal arteries showed no signs of giant cell arteritis at that time, and the results of eye examinations were normal. The importance of follow-up on patients with symptoms of polymyalgia rheumatica, even if biopsies of the temporal arteries show no histological changes, is emphasised.

Chronic persistent hepatitis. A clinical, serological, and prognostic study.

The diagnosis of chronic persistent hepatitis is based on a combination of clinical and morphological data. During a 7-year period 26 cases were diagnosed in 3 medical departments in Copenhagen. In 22 patients the disease was considered to be a sequela to acute viral hepatitis, and 12 had Australia antigen in serum. Only few patients had circulating auto-antibodies. The clinical and biochemical activity at the time of diagnosis was usually slight. A morphological and clinical follow-up study revealed that the course of the disease was generally benign. However, in 3 patients the last repeat biopsy showed progression to cirrhosis, severe portal fibrosis, and chronic aggressive hepatitis. Such exceptions may represent a sampling error in the interpretation of the first needle biopsy, or the correct diagnosis may have been chronic aggressive (active) hepatitis at a stage with slight activity. Clinical and biochemical observation is recommended in chronic persistent hepatitis, and in some patients serial needle biopsies are necessary to reveal the few exceptional cases which progress to an active chronic liver disease.

Chronic active hepatitis. Aetiological considerations based on clinical and serological studies.

The diagnosis of chronic active (aggressive) hepatitis is based mainly on characteristic morphological changes. During a 7-year period, 85 cases were diagnosed in three medical departments in Copenhagen. This material is presented by clinical, biochemical, and serological variables at the time of diagnosis. None of the patients had simultaneously occurring Australia antigen and circulating autoantibodies. A comparison between two serologically homogeneous groups revealed significant differences in sex and age distribution onset of disease, and biochemical activity. The investigation suggests the existence of aetiologically different forms of chronic active hepatitis. Some cases are apparently caused by a persistent viral infection, while others may be due to a primary autoimmune mechanism. A considerable number of the patients stated that they had had prolonged intake of the potentially hepatotoxic laxative, oxyphenisatin. Nineteen patients were challenged with the drug and eight reacted with an increased biochemical activity in the liver disease. All these patients belonged to the group with circulating autoantibodies. It is possible that oxyphenisatin may be the primary cause of the chronic liver damage in some cases.

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.

Serological evidence of hepatitis B infection in patients with chronic liver diseases: radioimmunoassay of HBsAg and anti-HBs.

The prevalence of hepatitis B surface antigen (HBsAg) and anti-HBs was determined by a sensitive double-antibody radio-immunoassay technique in a series of patients with chronic liver diseases. HBsAg was demonstrated in 37 out of 98 consecutive patients with chronic hepatitis (38%) and in 14 out of 108 patients with non-alcoholic cirrhosis (13%). HBsAg was not found in any of the patients with steatosis, alcoholic cirrhosis, or primary biliary cirrhosis. In the patients with chronic hepatitis HBsAg or anti-HBs was demonstrated in 83% of the patients below 40 years of age in contrast to 48% of the patients more than 40 years of age. It is concluded that a substantial part of the patients with chronic hepatitis has serological evidence of actual or past hepatitis B virus infection. This is in contrast to the groups of patients with other chronic liver diseases.

The accuracy of the clinical diagnosis in acute hepatitis and alcoholic liver disease. Clinical versus morphological diagnosis.

Microfilms were prepared from the case histories of 357 consecutive patients submitted to liver biopsy for the first time so that all information after the time of the liver biopsy was erased. The microfilms were assessed by four clinicians, and the pre-biopsy diagnostic proposals were graded according to the degree of certainty and were compared with the results of the liver biopsies. Out of 357 patients, 200 had a history of alcoholism, of whom 172 had alcohol-induced changes in the liver biopsies: 80 cases of alcoholic cirrhosis, 84 cases of steatosis, and 8 cases of alcoholic hepatitis without cirrhosis. In 65 of the 80 patients with biopsy-verified alcoholic cirrhosis the clinical pre-biopsy diagnosis was in agreement with the histological findings. In 51 cases in which the clinical diagnosis of alcoholic cirrhosis was given as moderately certain or very certain, 4 clinically incorrect diagnoses occurred. No incorrect diagnoses occurred in the 35 cases in which the clinicians claimed the greatest diagnostic accuracy. In the 84 patients with steatosis in the liver biopsies the clinicians felt uncertain or moderately certain about all but 2 patients, and 14 incorrect diagnoses occurred. In none of the 8 patients with histological alcoholic hepatitis without cirrhosis was a correct clinical diagnosis made. The clinical pre-biopsy diagnosis of acute hepatitis was in agreement with the results of the liver biopsies in 52 out of 57 patients. In 51 cases in which the clinical diagnosis of acute hepatitis was given as moderately certain or very certain, 1 clinically incorrect diagnosis occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Circulating T and B lymphocytes and immunoglobulin containing cells in the liver in chronic active liver disease.

The number of circulating T and B lymphocytes was estimated in 25 patients with biopsy-verified chronic non alcoholic liver disease. Fifteen of these had circulating HBSAg and/or anti-HBSAg and 10 were without these markers of HB virus infection. In both groups of patients a significant decrease of T cells and a parallel significant increase in null cells was found, but any difference with respect to T and null cells in patients in the two groups was not observed. Liver biopsies from five of the patients with and four without HBSAg and/or anti-HBSAg were studied for the presence of immunoglobulin bearing cells. In three out of five liver biopsies from the HBSAg and/or Ab positive patients and in two out of the four liver biopsies from the HBSAg and anti-HBSAg negative patients, a heavy periportal infiltration with plasma cells was found. However, the number and classes of the immunoglobulin containing cells could not be correlated either to the histological evaluation of the stage of activity of the liver disease or to the markers for HB virus infection. The immunological findings in the two groups of patients with chronic liver disease seem to be of the same nature and are most likely a consequence of the liver disease and not the cause of it.