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Biomedical subjects

S Sherlock

Publications and source records attributed to S Sherlock.

At least 271 records · Page 15Linked to original sources

Pre-eclampsia presenting with deep jaundice.

Pre-eclampsia complicated by deep jaundice occurred in a previously healthy primigravida. The main aetiological factor was disseminated intravascular coagulation; this caused both haemolysis and liver cell necrosis. Liver biopsy showed fibrin thrombi in the capillaries with microhaemorrhages and loss of periportal liver cells. The jaundice was attributed to both haemolytic and hepatocellular processes. Organs other than the liver were relatively unaffected.

Adult↗

Serum alpha-fetoprotein levels in patients with acute and chronic liver disease. Relation to hepatocellular regeneration and development of primary liver cell carcinoma.

Using a radioimmunoassay technique serum alpha-fetoprotein could be detected in healthy adults in concentrations of less than 20 microgram/l. Of patients with acute, viral hepatitis 43% exhibited a transient rise of serum alpha-fetoprotein, the peak occurring eight to nine days after the maximum recorded serum aspartate transaminase activity. Patients with hepatic damage due to paracetamol poisoning were also shown to have transiently raised levels, the peak occurring earlier than in subjects with viral hepatitis. Six subjects with fatal fulminant hepatitis were studied; the three with the more protracted illness were noted to have increased levels before death. Twenty of 163 cases of chronic liver disease also had raised serum alpha-fetoprotein concentrations. In four, primary liver cell cancer developed; in two of these the serum alpha-fetoprotein levels rose progressively, and in two it remained raised but at low levels.

Acetaminophen↗

Percutaneous transhepatic cholangiography using the "Chiba" needle--80 cases.

Using the Chiba needle for percutaneous transhepatic cholangiography, bile ducts have been visualized radiographically in 80% of 80 patients with cholestatic jaundice. The success rate was 94.4% in the 54 patients with dilated bile ducts due to an extrahepatic bilary obstruction, and 50% of the 20 patients with undilated ducts. Four patients developed ascending cholangitis with septicaemia on the same day as the procedure, and early surgery after visualization of obstructed bile ducts is recommended. The technique was successful in three of five patients with sclerosing cholangitis. Percutaneous cholangiography using the Chiba needle is a convenient method of opacifying the biliary system in patients with severe large bile duct obstruction.

Cholangiography↗

Kayser-Fleischer-like rings in patients without Wilson's disease.

Three patients, one with cryptogenic cirrhosis, one with active chronic hepatitis and one with neonatal hepatitis, were found to have corneal pigmentation rings indistinguishable from early Kayser-Fleischer rings on slit lamp examination. They did not have the clinical features of Wilson's disease and their serum copper and ceruloplasmin concentrations were normal. Urinary copper excretion rates and hepatic concentrations were only slightly raised but were below the range found in symptomatic Wilson's disease. It is concluded that the Kayser-Fleischer ring would no longer be considered as pathognomonic of Wilson's disease.

Adult↗

Transfer factor in the attempted treatment of patients with HBsAg-positive chronic liver disease.

Six patients with hepatitis B surface antigen-positive (HBsAg-pos) chronic liver disease have been treated with transfer factor (TF) prepared from leucocytes of normal blood donors with no history of hepatitis, and with TF from subjects recently recovered from type B hepatitis. In three patients there were transient elevations of aspartate transaminase (AsT) after 'specific' TF, representing damage or destruction of hepatocytes, and in two of these patients there was coincidental complement consumption, suggesting that TF had stimulated production of antibody. In one other patient there was an increase in E-rosetting lymphocyte (ERL) concentration representing a change in T-lymphocyte reactivity. One of the two patients who had no measured response to TF had a primary liver cell carcinoma and was receiving prednisolone therapy. TF prepared from subjects who have recently recovered from type B hepatitis may have temporarily altered the immunological status of patients with HBsAg-pos chronic liver disease, but it did not have a beneficial therapeutic effect.

Adult↗

Presentation and course of asymptomatic primary biliary cirrhosis.

Twenty patients without symptoms of hepatobiliary disease were diagnosed as having asymptomatic primary biliary cirrhosis. In every patient liver histology was diagnostic of, suggestive of, or compatible with the diagnosis. Eighteen had a positive serum mitochondrial antibody, 18 had raised serum immunoglobulin M, and 17 had markedly raised serum alkaline phosphatase values. A mean of 4.5 years after diagnosis, 10 of the patients had not developed hepatobiliary symtoms; 4 of these 10 patients have survived 6 to 10 years. Ten patients developed symptoms after a mean of 2.2 years from initial diagnosis; 7 are still alive but 3 have died of liver failure. The development of symptoms could not be predicted by either serum biochemical tests or hepatic histology. It is concluded that the diagnosis of asymptomatic primary biliary cirrhosis is compatible with 10 or more asymptomatic years.

Adult↗

Intrahepatic cholestasis in childhood.

The apparent well-being of some children who as neonates were believed to have obstructive jaundice prompted us to study the clinical course, histologic features and possible etiologic factors in 17 children with cholestasis in the neonatal period. During a follow-up period of five months to 22 years, all had signs of chronic cholestasis, but only four died (two from nonhepatic causes); the others live remarkably normal lives. Serial hepatic biopsies in 11 showed a variety of initial lesions, which progressed to hypoplasia of the intrahepatic bile ducts, increasing portal fibrosis and eventual cirrhosis. Although evidence of possible viral infection was found in only 10 cases, a hepatitis, beginning either before or after birth, appears to be a likely original cause. The histologic changes seen may represent different stages of one process, starting as cholestasis with or without evidence of hepatitis and progressing to obliteration or failure of normal growth of the intrahepatic bile ducts.

Adolescent↗

Serum-25-hydroxy-vitamin-D in untreated parenchymal and cholestatic liver disease.

Serum-25-hydroxy-vitamin-D (25 OHD) concentration has been measured in 106 patients with untreated parenchymal and cholestatic liver disease. Low mean values were found in groups of patients with alcoholic hepatitis and cirrhosis, non-cirrhotic active chronic hepatitis, lupoid and cryptogenic cirrhosis, symptomatic primary biliary cirrhosis, and acute and chronic biliary disease. In a group of patients with presymptomatic biliary cirrhosis the mean value was not significantly different from normal. It is concluded that in the presence of significant parenchymal or cholestatic liver disease serum-25-OHD concentrations are usually low. The mechanisms for the reduction remain to be clarified, but low serum-25-OHD values may play a contributory role in the aetiology of osteomalacia in chronic liver disease.

Acute Disease↗

Percutaneous transhepatic obliteration of gastro-oesophageal varices.

Percutaneous transhepatic portal-vein catheterisation was attempted to obliterate the major variceal venous supply in 13 decompensated cirrhotic patients, who continued to bleed after conservative therapy. Obliteration was achieved and bleeding stopped in 7 patients. In 5 patients obliteration was technically unsuccessful. The remaining patient had an unsuspected portal-vein block diagnosed by the transhepatic technique. 1 patient with successfully obliterated varices died after a haemothorax and haemorperitoneum developed. Follow-up splenic venography at three to six months in the 6 successfully thrombosed patients showed that 4 had persistent obliteration and had not re-bled. 2 patients re-bled from incompletely obliterated varices. It is concluded that selective obliteration of the major variceal supply is effective in stopping acute gastro-oesophageal variceal bleeding, but that greater experience is necessary before the long-term effectiveness of the procedure can be determined.

Adult↗

Primary liver cell carcinoma in the presence or absence of hepatitis B antigen.

The clinical course and pathological patterns of a group of 13 patients with both primary liver cell carcinoma and Hepatitis B surface antigen (HBsAg) are described and contrasted with those of 43 patients with primary liver cell carcinoma but without HBsAg. HBsAg-positive carcinoma patients demonstrated a higher incidence of splenomegaly, transudative ascites, and the presence of alpha-fetoprotein, although none of these reached statistical significance. Serum bilirubin was significantly higher in patients with HBsAg. HBsAg-positive carcinoma patients most frequently originated from countries where the presence of HBsAg is high in the general population. Survival time from the diagnosis of primary liver cell carcinoma was shorter in patients with HBsAg.

Adolescent↗

Ascorbic acid deficiency in liver disease.

Leucocyte ascorbic acid (LAA) levels were measured in 138 patients with liver disease. Significantly reduced levels were found in 37 patients with alcoholic liver disease (P less than 0-01) and 25 patients with primary biliary cirrhosis (P less than 0-05). In the primary biliary cirrhosis patients, cholestyramine therapy was associated with significantly lower levels of the vitamin (P less than 0-05). Liver ascorbic acid measured in Menghini needle biopsies in 20 patients was significantly correlated with LAA (r=0-807, P less than 0-001). No significant correlation was found between LAA and haematological indices, conventional liver function tests, or cholesterol levels in any group of patients. Patients with LAA levels below 100 nM/10(8) WBC had significantly higher antipyrine half-lives (mean=28-3 h) than patients with LAA levels above this level (mean=18-6 h) (P less than 0-05). Delayed drug metabolism related to low LAA should be considered when drugs metabolised by the liver are prescribed for patients with alcoholic liver disease or primary biliary cirrhosis.

Alcoholism↗