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Biomedical subjects

S Sherlock

Publications and source records attributed to S Sherlock.

At least 379 records · Page 21Linked to original sources
PubMed1972

Cell-mediated immunity in patients positive for hepatitis-associated antigen.

Cell-mediated immunity to antigens prepared from both serum and liver of patients positive for hepatitis-associated antigen (H.A.A.) was measured by using the leucocyte migration test. Altogether, 43 patients with H.A.A.-positive acute and chronic liver disease, eight with serum antibody to H.A.A., and 13 controls were studied. The cell-mediated immunity detected was specific for H.A.A. or other antigenic determinants of the associated infective agent and could be found only in patients with evidence of previous contact with H.A.A.Cell-mediated immunity to the H.A.A.-positive test antigens was found in all but one of the patients with acute hepatitis, in about half of the patients with chronic aggressive hepatitis or cirrhosis, rarely in those with chronic persistent hepatitis, and in none of the apparently healthy carriers.Our results support the hypothesis that the cellular immune response plays an important part in the clearance of the infective agent from H.A.A.-positive patients and in the pathogenesis of the associated liver cell injury.

Acute Disease↗
PubMed1972

Chronic liver disease and mitochondrial antibodies: a family study.

Two sisters had primary biliary disease and associated autoimmune thyroiditis with high titres of mitochondrial and other autoantibodies. Their deceased mother possibly suffered from similar disorders. In the same family two brothers had multiple autoimmune reactions, including mitochondrial antibodies, but liver function tests gave normal results. Ten other close relatives were investigated. Australia antigen was not found in the proband or her relatives.

Adult↗
PubMed1972

Renal and intrarenal blood flow in non-cirrhotic portal hypertension.

The effect of portal hypertension or the consequent portal circulatory changes on renal haemodynamics was studied using the (133)xenon washout technique. Renal blood flow was reduced in nine of 11 patients with non-cirrhotic portal hypertension and this was accompanied by a redistribution of intrarenal blood flow, the distribution to and flow rate through the outer cortex being reduced while juxtamedullary and medullary flow was maintained. With slight or moderate decreases in cortical flow glomerular filtration was normal but poor cortical perfusion was associated with low creatinine clearances. These findings raise the possibility that portal hypertension or portal circulatory changes may play a role in the pathogenesis of the renal haemodynamic changes and functional renal failure which frequently complicate advanced hepatic cirrhosis.

Adolescent↗
PubMed1972

Immunosuppressive activity in patients with active chronic hepatitis and primary biliary cirrhosis treated with azathioprine.

The rosette inhibition test was used to measure serum immunosuppressive activity after azathioprine (1.5 mg/kg) in 20 patients with liver disease (10 with active chronic hepatitis, six with primary biliary cirrhosis, and four with miscellaneous hepatic disorders) and in nine healthy normal volunteers. Where possible testing was repeated after one week and after at least two months of treatment. The titre of immunosuppression was related to the degree of impairment of hepatic function, and was found to be low in those with severe and normal in those with mild disturbance of hepatic function. Titres were unrelated to the presence of immunological abnormalities such as smooth muscle antibodies. In patients treated for at least two months there was no relationship between the initial titre of immunosuppressive activity and the response to treatment. Thus some patients improved despite failure to develop immunosuppressive activity, while others deteriorated even though immunosuppressive activity was normal when first studied. The development of immunosuppressive activity after azathioprine seems to be dependent on adequate hepatic function and the favourable response of some patients with liver disease to the drug may not be due entirely to immunosuppression.

Adolescent↗
PubMed1972

The effect of octapressin on renal and intrarenal blood flow in cirrhosis of the liver.

The effect of octapressin (2-phenylalanine-8-lysine vasopressin) on renal and intrarenal blood flow was studied in 11 normotensive cirrhotic patients with abnormal renal perfusion. Renal haemodynamic changes were assessed with the (133)Xenon washout technique. Of the six patients given suppressor doses of octapressin intravenously renal blood flow improved in one only. A further three patients responded to the drug in a dose which increased the mean arterial pressure by 5 or more mm Hg. The increase in mean renal blood flow was accompanied by an improvement in renal cortical perfusion. In two patients renal blood flow decreased after the administration of octapressin. These findings, in conjunction with previous reports, suggest that octapressin will only consistently improve renal perfusion in cirrhotic subjects who are hypotensive and in whom the mean arterial blood pressure is raised by the drug, but do not exclude the possibility that octapressin may have a direct renal circulatory effect in some patients.

Adult↗
PubMed1972

Renal blood flow in malignant disease of the liver.

Although functional renal failure has been reported in patients with malignant disease of the liver, renal haemodynamics and function have not been investigated. Renal and intrarenal blood flow was measured using the (133)Xenon washout technique and creatinine clearances by the standard method in 14 patients with a variety of primary and secondary tumours of the liver in the absence of cirrhosis and without evidence of renal disease. In 11 patients renal and outer cortical blood flow was reduced and this was sometimes accompanied by a reduction in glomerular filtration rate. The pattern of renal circulatory changes was similar to that seen in renal dysfunction associated with hepatic cirrhosis. Possible causes of these disturbances and their significance in relation to the aetiology of functional renal failure in liver disease are discussed.

Adult↗