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Biomedical subjects

S Sherlock

Publications and source records attributed to S Sherlock.

At least 325 records · Page 18Linked to original sources
PubMed1975

Halothane-related hepatitis. A clinical study of twenty-six cases.

Twenty-six patients are described who had otherwise unexplained hepatitis after halothane anaesthesia. Twenty-four (92 per cent) had multiple exposures, and 11 (42 per cent) died. In eight patients a characteristic pattern of delayed postoperative pyrexia has been found. Obesity was common, but the clinical features and complications were those of any severe hepatitis. Obesity, early onset of jaundice after anaesthesia, and low thrombotest, were associated with a fatal outcome. None of those who were followed up after recovery developed clinical or biochemical evidence of chronic liver disease. The differential diagnosis of postoperative jaundice is discussed, and it is shown that halothane patients with hepatic encephalopathy are significantly older (25.4 plus or minus 11.6 years) than those referred to this unit with viral hepatitis of equal severity (34.1 plus or minus 16.4 years). Unexplained jaundice or delayed pyrexia after a previous administration of halothane should be a contraindication to its further use.

Adult↗
PubMed1975

Effects of clofibrate in primary biliary cirrhosis hypercholesterolemia and gallstones.

A patient with primary biliary cirrhosis is reported in whom the administration of clofibrate in a dose of 1 g per day for 2 months resulted in a marked increase in hypercholesterolemia, and endoscopic retrograde cholangiography showed multiple intrahepatic gallstones. The stones disappeared 3 months after stopping clofibrate and starting chenodeoxycholic acid in a dose of 125 mg daily. These observations are discussed in relation to the known effects of clofibrate on bile composition.

Chenodeoxycholic Acid↗
PubMed1975

Viral hepatitis and cirrhosis.

Most of the knowledge of post-hepatitic cirrhosis comes from studies performed in the last five years on the hepatitis B antigen-related variety. The position of other types of hepatitis (particularly type A) as an aetiological factor in cirrhosis remains conjectural. In general, the post-hepatitic cirrhosis develops insidiously after a mild or unrecognised acute episode of hepatitis. General progress is slow. Early deaths are due to liver failure. Later, primary hepatocellular carcinoma assumes increasing importance. Needle biopsy of the liver is usually necessary to confirm the diagnosis of cirrhosis and to estimate the degree of activity. Sampling errors when such a small specimen of liver is obtained must be taken into account, when formulating a diagnosis and prognosis. Prednisolone therapy is usually given if the patient is symptomatic, biochemical tests are abnormal and the liver biopsy confirms active chronic hepatitis with or without cirrhosis. The evidence of benefit is not so strong as for other forms of active hepatitis and cirrhosis such as the lupoid type. The management of the cirrhosis is otherwise along orthodox lines.

Acute Disease↗
PubMed1975

Prolonged survival in three brothers with severe type 2 Crigler-Najjar syndrome. Ultrastructural and metabolic studies.

Three brothers with severe type 2 Crigler-Najjar syndrome for over 50 years have been studied. Although the plasma unconjugated bilirubin (UCB) concentrations were in excess of 19 mg per 100 ml, no abnormal neurological signs were evident. Prolonged exposure to severe unconjugated hyperbilirubinemia does not therefore necessarily increase morbidity. Electron microscopy of liver tissue obtained from 2 patients before phenobarbital therapy showed hypertrophy and hyperplasia of smooth endoplasmic reticulum with unusual prominence of the Golgi apparatus and focal modification of the cell surface membranes. These changes may reflect the reactive state of the hepatocyte to high levels of unconjugated bilirubin. Phenobarbital therapy resulted in a marked reduction in UCB concentration and was accompanied by further hypertrophy of the smooth endoplasmic reticulum and minor changes in bile canaliculi. Dietary restriction to 400 cal daily for 3 days produced a dramatic increase in UCB. The addition of 2400 cal by the intravenous administration of 50% dextrose did not reduce the elevated UCB. In contrast, 2400 cal fed as a normal diet rapidly returned the UCB to basal levels. While on phenobarbital therapy, a similar response to caloric withdrawal and parenteral feeding was observed. These findings indicate that the hyperbilirubinemia of fasting does not depend on caloric deficiency per se, and suggest that either the route of caloric administration or the type of nutrient may influence the level of unconjugated hyperbilirubinemia.

Bile Acids and Salts↗
PubMed1974

Studies in alcoholic liver disease in Britain. I. Clinical and pathological patterns related to natural history.

A group of 258 patients with various forms of alcoholic liver disease-steatosis, mild and severe hepatitis, and cirrhosis-has been studied. Severity of disease as judged histologically did not correlate very well with clinical presentation although signs of hepatocellular failure were certainly commoner in severe hepatitis and cirrhosis. Fever, pigmentation, and clubbing were also pointers to these two conditions. Alcoholic hepatitis is probably precirrhotic and carries a poor prognosis and the best laboratory indicators of this are moderate elevation of white cell count and bilirubin. Prognosis in alcoholic liver disease is significantly improved by abstinence from alcohol.

Adult↗
PubMed1974

The relief of bone pain in primary biliary cirrhosis with calcium infusions.

Intravenous calcium infusions produced subjective relief of bone pain in 14 patients with primary biliary cirrhosis. The bone pain had developed despite long-term parenteral vitamin D therapy. The pain returned after two to three months, but a subsequent course of infusions again brought relief. Before treatment satisfactory iliac crest bone biopsies were obtained in 11 of the patients and were normal in seven; two patients had biopsies indicating osteomalacia and two osteoporosis. After treatment a repeat biopsy in one of the patients with osteomalacia showed marked reduction in osteoid. The infusion treatment produced no change in plasma calcium concentration, serum phosphate, or serum alkaline phosphatase. Absorption of oral calcium was also unchanged.

Arm↗
PubMed1974

Use of bumetanide in the treatment of ascites due to liver disease.

Bumetanide is an effective diuretic for the treatment of ascites. Fifteen out of 17 patients with chronic liver disease responded satisfactorily and the incidence of hepatic encephalopathy and electrolyte disturbances was similar to that previously observed with frusemide. Colicky abdominal pain was reported in three patients but no other adverse effects were noted. An unexpected response was obtained in two patients who had diuresis without natriuresis.

Adolescent↗
PubMed1974

Significance of intravascular coagulation and fibrinolysis in acute hepatic failure.

Twenty-two patients with acute hepatic failure were studied to determine the incidence and magnitude of intravascular coagulation and fibrinolysis and their relation to the severity of bleeding and prognosis. The mean platelet count, Thrombotest, plasminogen activator, and plasminogen were reduced; the reduction in fibrinogen was not statistically significant. Fibrin/fibrinogen degradation products were only moderately increased. Hepatic fibrin deposition was not extensive, being present in 11 of 22 hepatic sections, more in areas of confluent necrosis than in the sinusoids. The combination of increased fibrin/fibrinogen degradation products with decreased plasminogen activator, plasminogen, and thrombocytopenia is consistent with a diagnosis of intravascular coagulation and secondary local fibrinolysis. However, neither of these processes was severe. Severity of bleeding was related only to plasminogen levels and prognosis only to Thrombotest levels. There was no relation between hepatic histological and haematological findings. Heparin therapy is not indicated in the routine management of acute hepatic failure, as intravascular coagulation is not severe and heparin may itself cause massive bleeding.

Acute Disease↗
PubMed1974

The epidemiology of primary biliary cirrhosis: a survey of mortality in England and Wales.

Primary biliary cirrhosis is a rare disease in the general population. Estimates of its true incidence are difficult but since survival time is unaffected by treatment, mortality may reflect important regional and other variations. One hundred and sixty-five death certificates collected in England and Wales over the five-year period 1967-1971 were inspected and confirmed an overwhelming predilection for females. Deaths rose sharply at ages 50-54 in the latter with a peak of 4.1 million(-1) year(-1), with perhaps a secondary peak at ages 70-74. No relation of mortality with climate, altitude, soil type, annual temperature range, or occupation was found, although outside the UK a broad correlation exists with total cirrhosis deaths. There was a suggestive excess of deaths among married women. The greater frequency of deaths in the London area, a rise in mortality from country to urban areas, a fall-off in deaths from primary biliary cirrhosis in old age, and predominance for social class I suggest a simple relationship with standards of medical care or diagnosis. An ;epidemic' of deaths in 1971 is attributed to greater availability of the mitochondrial antibody test in the regions. The importance of familial primary biliary cirrhosis and various models of pathogenesis are discussed. Both constitutional and environmental factors producing the disease must be widely distributed in the population of this country.

Age Factors↗