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Biomedical subjects

S Sherlock

Publications and source records attributed to S Sherlock.

At least 343 records · Page 19Linked to original sources
PubMed1974

ABO blood groups, Rhesus negativity, and primary biliary cirrhosis.

The distribution of blood groups and Rhesus negativity in 91 British patients with primary biliary cirrhosis was compared with a sample of registered blood donors. There were no significant differences from the expected proportions calculated from the control groups. Although the number of cases studied is small the analysis does not confirm previous reports of an excess of A group in the disease. If a genetic basis exists for primary biliary cirrhosis alternative markers must be found.

ABO Blood-Group System↗
PubMed1974

Treatment of chronic hepatic encephalopathy with levodopa.

Three of six patients with chronic hepatic encephalopathy treated with levodopa showed a significant improvement. One patient was probably improved whilst the remaining two patients failed to show any benefit. Serial electroencephalography did not demonstrate significant changes. Treatment with levodopa was associated with an improvement in ;speed-based' tasks as assessed by computerized psychometry. A significant rise in cerebral oxygen consumption was found during levodopa therapy. Gastrointestinal side effects were dose limiting. It is concluded that a therapeutic trial of levodopa in patients with chronic hepatic encephalopathy is indicated when the response to conventional therapy has been poor.

Adult↗
PubMed1974

The epidemiological importance of 'ay' and 'ad' subtypes of the HB-Ag.

The distribution of the subtypes ;ay' and ;ad' has been assessed in 159 hepatitis B antigen (HB-Ag) positive subjects with a variety of associated hepatic conditions. A specific subtype could not be correlated with any particular hepatic pathology when the whole group was considered. However, the distribution of these two subtypes did vary according to the geographical origin of the subject or infection, or the presumed route of infection, so that there was an apparent association of one subtype with a certain disease state. Subtyping performed on 10 HB-Ag-positive households showed the subtype to be the same within nine, emphasizing the epidemiological rather than the pathological importance of the ;ay' and ;ad' subtypes of the HB-Ag.

Carrier State↗
PubMed1973

Diagnosis of Gilbert's syndrome: role of reduced caloric intake test.

Reduction in caloric intake to 400 a day for 72 hours resulted in a significant increase in the plasma bilirubin concentration in patients with Gilbert's syndrome and in normal subjects. This was due to an increase in unconjugated pigment. There was no significant increase in the bilirubin concentration in patients with liver disease or haemolytic anaemia.The increase in unconjugated bilirubin was signficantly greater in Gilbert's syndrome than in normals but only when the initial bilirubin concentration was raised. It was usually seen within 24 hours of reducing the caloric intake. An increase of 100% or more suggests that unconjugated hyperbilirubinaemia is due to Gilbert's syndrome. In the normal subjects the unconjugated bilirubin level did not exceed 1.0 mg/100 ml.The increase in unconjugated bilirubin concentration on reducing the caloric intake may be due to decreased hepatic bilirubin uridine diphosphate glucuronyl transferase activity, which was shown to be present in seven rats starved for 72 hours. The effect of a 400 calorie diet for 24 hours on the unconjugated bilirubin level may distinguish Gilbert's syndrome from other causes of unconjugated hyperbilirubinaemia.

Anemia, Hemolytic↗