Biomedical subjects
Publications and source records attributed to M C Kew.
A nursing sister developed Australia-antigen-positive hepatitis 101 days after the blood of an Australia-antigen-positive patient was accidentally introduced into her eye. There may be important implications for those caring for patients with Australia-antigenemia or undertaking laboratory investigations on their blood.
Serum alpha-fetoprotein levels were measured serially by radioimmunoassay in 32 patients with acute viral hepatitis. With one exception, the levels were increased during the course of the illness. Raised concentrations of the protein occurred almost equally in patients with and without the hepatitis-B antigen. In the majority of patients the rise was modest but in seven levels were reached at which alpha-fetoprotein could be detected by immunodiffusion. Very high levels were more likely to occur in children. In eight patients the concentration increased as the serum glutamic pyruvic transaminase (SGPT) level, used as an index of hepatocyte damage, was returning to normal, a pattern which favoured increased synthesis of the protein during hepatocellular regeneration. In the remainder, the alpha-fetoprotein level paralleled that of SGPT, suggesting rather an acutephase reaction to liver injury.
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.
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.
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.
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The diagnosis of primary cancer of the liver was reviewed in 75 patients. A definitive diagnosis was made during life in 63% and in a further 20% this condition was suspected though histological confirmation was obtained only at necropsy. The most common presenting complaints were abdominal pain and weight loss and the most frequent findings hepatomegaly and ascites. Less than one-half of the patients were jaundiced and when present it was usually mild. An arterial bruit was heard over the liver in 25% of the patients. A sudden and unexplained deterioration in a patient known to have cirrhosis or haemochromatosis should raise the possibility of a primary hepatic tumour; this occurred in 24% of our patients.Alpha-fetoprotein was found in the serum of 11 out of 18 cases. The presence of a mass in the liver was frequently confirmed by liver scan, portal venography, or hepatic arteriography, but these showed no features diagnostic of a primary tumour. Liver scan also proved useful in localizing the lesion for biopsy purposes. Definitive diagnosis is dependent on the histological demonstration of the features of the tumour. This can frequently be achieved by percutaneous needle biopsy, which was positive in 38 out of 57 patients. Wedge biopsies were positive in a further nine patients.
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Evidence of portal hypertension was found in 50 out of 109 patients (47%) with primary biliary cirrhosis, and of these 32 bled from oesophageal varices. In four patients portal hypertension was the initial manifestation of the disease and this complication was recognized in a further 17 within two years of the first symptom of primary biliary cirrhosis. The development of portal hypertension was associated with a poor prognosis and death could frequently be attributed to variceal bleeding; the mean duration of survival from the time that portal hypertension was recognized was 14.9 months. Portal decompression operations may have improved the immediate prognosis in some patients but did not otherwise influence the progression of the disease. In 47 patients the histological findings in wedge biopsy or necropsy material were correlated with the presence or absence of varices. An association between nodular regeneration of the liver and varices was confirmed, but, in the absence of nodules, no other histological cause for portal venous obstruction could be found.
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