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Summary The proportion of human peripheral blood CD8+ T cells that are CD57+ CD28– is low at birth but increases with age and in individuals infected with human cytomegalovirus (HCMV) or human immunodeficiency virus (HIV). These CD57+ CD28– CD8+ T cells contain large oligoclonal T‐cell expansions whose antigen specificity is unknown. We identified clonal expansions of virus‐specific memory cytotoxic T‐lymphocyte precursors (CTLp) in both healthy carriers of HCMV and in asymptomatic HIV‐infected subjects. In each subject, from the T‐cell receptor (TCR) β‐chain hypervariable sequence of each immunodominant CTL clone, we designed complementary oligonucleotide probes to quantify the size and phenotypic segregation of individual virus‐specific CTL clones in highly purified populations of peripheral blood CD8+ T cells. We found large clonal expansions of virus‐specific CTL clonotypes in CD57+ CD28– CD8+ T cells. Using limiting dilution analysis, we found functional peptide‐specific CTLp at high frequency in CD57+ CD28– cells. Thus, memory CTL specific for persistent viruses account for many oligoclonal expansions within CD57+ CD28– CD8+ T cells. [ABSTRACT FROM AUTHOR]

Three cases of hypophosphataemic osteomalacia presenting in adult life, in which a myopathy was a prominent presenting feature, are described. In one, a nasopharyngeal haemangioma was also present. Possible mechanisms underlying the myopathy are discussed briefly. [ABSTRACT FROM AUTHOR]

The intestinal absorption of (3H)cholecalciferol was studied in five patients with alcoholic liver disease, six patients with primary biliary cirrhosis, and 15 healthy subjects. The rate of appearance in plasma of (3H)cholecalciferol after oral ingestion and the subsequent appearance of (3H) polar metabolites in the alcoholic subjects were similar to those in the healthy subjects. In subjects with primary biliary cirrhosis the rate of appearance in plasma of (3H)cholecalciferol was significantly reduced. The rate of appearance of labelled polar metabolites of cholecalciferol was also lower in this group, suggesting that increased removal of labelled vitamin by conversion into more polar metabolites could not account for the reduced plasma (3H)cholecalciferol response. It is suggested that intestinal absorption of cholecalciferol is usually normal in alcoholic liver disease but impaired in primary biliary cirrhosis. Hepatic 25-hydroxylation is normal in alcoholic liver disease but may be defective in primary biliary cirrhosis. [ABSTRACT FROM PUBLISHER]

Serum immunoreactive prolactin was measured in 150 patients with liver disease of varying aetiology and severity and in 45 control subjects. The upper limit of the reference range for serum prolactin was 331 mU/l. Eighteen patients with liver disease (12%) had unexplained hyperprolactinaemia. No relationship existed between the prolactin value and the sex of the patient, the aetiology of the liver disease, the severity of the liver disease, or the presence of gynaecomastia. The cause of the hyperprolactinaemia in patients with liver disease and its clinical implications need further investigation. [ABSTRACT FROM PUBLISHER]

Twenty of 32 patients with either chronic cholestatic or hepatocellular liver disease had bone pain or recent fractures. On bone biopsy five patients had normal bone, 15 had osteomalacia, five had osteoporosis, and seven had a combination of osteomalacia and osteoporosis. In the presence of osteoporosis, osteomalacia was minimal or absent. There was no biochemical, radiological, or histological evidence of excess parathyroid activity. No significant correlations were demonstrated between the plasma and urinary biochemical findings and the presence of either osteoporosis or osteomalacia and bone biopsy was essential for correct diagnosis. There was no statistical relationship between low serum 25-hydroxy vitamin D values and the presence of osteomalacia. Bone disease was not prevented by regular intramuscular vitamin D2, although biochemical changes were improved. Drugs such as corticosteroids and cholestyramine may be important aetiological factors in hepatic osteodystrophy. [ABSTRACT FROM PUBLISHER]