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Biomedical subjects

S Sherlock

Publications and source records attributed to S Sherlock.

At least 127 records · Page 7Linked to original sources
PubMed1983

A giant cystic mesenchymal hamartoma of the liver: diagnosis, management, and study of cyst fluid.

A 21-yr-old West Indian woman with a giant hepatic cyst is reported. Preoperative investigations revealed that it was not a simple congenital cyst but that it was highly vascular. Studies of the cyst fluid obtained by percutaneous catheter drainage suggested that the epithelial lining was of bile duct origin. Fluid output was increased by secretin administration, but remained unchanged after amiloride. Bromsulphthalein did not enter the cyst fluid after intravenous injection. A hemihepatectomy was performed and the histologic appearances of the lesion were consistent with cystic mesenchymal hamartoma, a rare lesion in this age group. The patient is well 4.5 yr later.

Adult↗
PubMed1982

Radiological patterns of cortical bone modelling in women with chronic liver disease.

The pattern of cortical bone modelling in healthy and diseased populations can be derived from simple measurements taken from radiographs of tubular bones. To determine the pattern of bone modelling in women with chronic cholestatic and parenchymal liver diseases, these parameters have been measured in 83 women with primary biliary cirrhosis (PBC), 34 with steroid-treated chronic active hepatitis (CAH) and 27 with parenchymal liver disease (PLD) not treated with corticosteroids. Bone modelling profiles have been compared in these groups with expected pattern in healthy females. Abnormal bone modelling occurs in all three groups. In PBC, cortical thinning is progressive from the fourth decade onwards. In steroid-treated CAH, an initial increase in cortical thickness is observed in the third and fourth decades, after which cortical thinning occurs. In the PLD group, progressive loss of bone cortex is present from the fourth decade onwards. In all forms of liver disease, cortical thinning results from widening of the medullary cavity rather than resorption of the cortical surface.

Bone Diseases↗
PubMed1982

Patterns of hepatocyte injury in man.

Three patterns of hepatocyte injury in man, direct, immunological, and cholestatic, are described. The characteristics of the direct pattern are predominantly mitochondrial damage, central (zone 3) necrosis, and, usually, fatty change. It can be subdivided into the alcohol type (also seen with obesity, in diabetes, as a reaction to perhexiline, in Wilson's disease, and in Indian childhood cirrhosis) and the Reye's syndrome type (also seen with tetracycline toxicity, fatty liver of pregnancy, and cytotoxic drugs). Reactive drug metabolites, metal poisoning, and anoxia are also associated with the direct pattern of hepatocyte injury. The immunological pattern is characterised by damage to cell membranes with piecemeal necrosis of periportal (zone 1) hepatocytes and mononuclear-cell infiltration. Examples include chronic active hepatitis, primary biliary cirrhosis, and drug reactions such as those to halothane. In the cholestatic pattern there is disturbance of the bile-secretory mechanism with retention of bile within the hepatocytes. Cholestatic liver injury may be intrahepatic, as in sex-hormone cholestasis, or extrahepatic, as in choledocholithiasis or carcinoma of the bile ducts. Identification of the type of hepatocyte injury is valuable in diagnosis, in assessing prognosis, and in selecting treatment.

Cholestasis, Intrahepatic↗
PubMed1982

Hepatic iron stores and markers of iron overload in alcoholics and patients with idiopathic hemochromatosis.

Liver iron concentrations were determined in 60 alcoholics with liver disease of varying severity, 15 patients with untreated idiopathic hemochromatosis, and 16 control subjects with biliary tract disease. Mean liver iron concentrations (microgram/100 mg dry weight) were significantly greater in the alcoholics (156.4 +/- 7.8 (SEM); P less than 0.05) and in patients with idiopathic hemochromatosis (2094.5 +/- 230.7; P less than 0.01) than in control subjects (53.0 +/- 7.0). Liver iron concentrations of greater than 140 micrograms/100 were found in 17 alcoholics (29%) and in all 15 patients with idiopathic hemochromatosis. Liver iron concentrations greater than 1000 micrograms/100 mg were found in all patients with idiopathic hemochromatosis but in none of the alcoholics. In the alcoholics no relationship existed between liver iron concentrations and the amount of alcohol consumed daily, the length of the drinking history, the amount of beverage iron consumed daily, or the severity of the liver disease. Serum ferritin concentrations reflected iron stores in patients with hemochromatosis and in alcoholics with minimal liver disease. However, in alcoholics with significant liver disease serum ferritin concentrations did not reflect iron stores accurately, although with normal values iron overload is unlikely. Serum iron concentration and percentage saturation of total iron-binding capacity were of little value in assessing iron status in either alcoholics or patients with hemochromatosis. Measurement of the liver iron concentration clearly differentiates between alcoholics with significant siderosis and patients with idiopathic hemochromatosis.

Alcoholism↗
PubMed1982

Noncirrhotic extrahepatic and intrahepatic portal hypertension.

A variety of conditions may lead to the development of portal hypertension in the absence of cirrhosis. In virtually all cases, increased resistance to flow at the level of the portal vein, sinusoids, or hepatic vein is the major contributing factor to the elevated portal pressure, although increased flow may be a contributor in certain instances. Variceal hemorrhage is the major complication of these disorders, but is better tolerated than in cirrhosis because of better hepatocellular function. Therapy should in general be conservative and directed toward any underlying pathology, where such can be identified.

Adolescent↗
PubMed1982

Vitamin D, hydroxyapatite, and calcium gluconate in treatment of cortical bone thinning in postmenopausal women with primary biliary cirrhosis.

Women with primary biliary cirrhosis malabsorb calcium, phosphate and vitamin D, and develop accelerated cortical bone thinning. We have assessed the value of parenteral vitamin D, oral hydroxyapatite (HA), and calcium gluconate (CG) in the treatment of cortical bone thinning in primary biliary cirrhosis. Sixty-four postmenopausal women with primary biliary cirrhosis were assigned randomly into three groups: one group receiving no mineral supplements (control), one group receiving HA, and one group receiving CG. All patients received parenteral vitamin D2 (100,000 IU monthly). Eleven patients withdrew from the study and 10 withdrew due to poor compliance (six HA, four CG). Over a 14-month follow-up period, none of the groups showed a significant change in serum calcium or inorganic phosphate levels. Pre- and posttreatment hand radiographs were used to assess changes in metacarpal cortical thickness using the technique of caliper radiogrammetry. Cortical bone loss occurred in the control group (p less than 0.01). The HA group showed a significant gain in cortical bone thickness (p less than 0.01), while no significant change occurred in the CG group. This study indicated that vitamin D2 does not halt metacarpal cortical bone thinning in primary biliary cirrhosis. The addition of CG prevents bone thinning, and HA promotes positive cortical bone balance.

Bone Diseases, Metabolic↗
PubMed1982

Lichen planus and primary biliary cirrhosis.

The association of lichen planus and primary biliary cirrhosis in five patients is reported. The coexistence of the two diseases is probably more than coincidental and may be due to the fact that both conditions are based on an alteration of mechanisms. There is great similarity between primary biliary cirrhosis and chronic graft-versus-host disease and a common pathogenesis for the two entities has been postulated. Since lichen planus is one of the most common manifestations of graft-versus-host disease, its association with primary biliary cirrhosis is of significance, although not unexpected.

Adult↗
PubMed1982

The pathology of hepatitis A in man.

Liver biopsies from 17 patients with serologically established hepatitis A were examined by light microscopy. Biopsies were taken from 2 to 27 weeks after onset of symptoms. All showed acute hepatitis, usually with centrilobular lesions but also commonly with a striking portal and periportal inflammatory reaction, resembling that seen in chronic active hepatitis. The infiltrate was rich in plasma cells. Centrilobular cholestasis was common and occasionally severe. Neither cholestasis nor the periportal lesion appeared to be related to patient age or to the timing of liver biopsy. All patients made a full recovery and none developed chronic liver disease. The histological changes differed from those reported in children and in chimpanzees in the presence of centrilobular lesions, but resembled them in that the latter two groups also had periportal lesions. These lesions may lead to a false impression of impending chronicity if the aetiology of the hepatitis is not known at the time of liver biopsy.

Adult↗
PubMed1982

Immunocytochemical identification of caeruloplasmin in hepatocytes of patients with Wilson's disease.

Decreased serum caeruloplasmin levels in patients with Wilson's disease have been attributed to decreased caeruloplasmin synthesis in the hepatocyte. An immunoperoxidase procedure was used to identify caeruloplasmin in liver biopsies. The pattern of staining in biopsies from patients with Wilson's disease did not differ from the pattern seen in normal adult or neonatal liver. This indicates that immunoreactive caeruloplasmin is synthesized by the liver cell in Wilson's disease. Low serum levels of caeruloplasmin may reflect an abnormality of copper incorporation into the apoprotein or an abnormality of holocaeruloplasmin export.

Adolescent↗
PubMed1982

Treatment of alcohol-related liver disease with thioctic acid: a six month randomised double-blind trial.

A randomised double-blind trial of thioctic acid (alpha-lipoic acid), 300 mg/day versus placebo was carried out in 40 patients with pre-cirrhotic alcohol-related liver disease over a six month period. Twenty patients received the active drug and 20 placebo. Twenty-two of the 40 patients (55%) abstained from alcohol and showed significant improvements (p less than 0.01) in mean values for serum aspartate transaminase, serum glutamyl transpeptidase, and mean corpuscular volume. Seventeen of the 22 (77%) showed overall histological improvement on liver biopsy. The remaining 18 patients (45%) continued to drink but significantly reduced their mean daily alcohol intake (p less than 0.001). No significant changes occurred in their laboratory indices, but five of the 18 (28%) showed overall histological improvement. Changes occurred irrespective of treatment with thioctic acid, which suggested that, over six months, this drug did not influence the course of alcohol-related liver disease.

Adult↗
PubMed1982

Plasma amino-acid patterns in liver disease.

Plasma amino-acid concentrations were measured in 167 patients with liver disease of varying aetiology and severity, all free of encephalopathy, and the results compared with those in 57 control subjects matched for age and sex. In the four groups of patients with chronic liver disease (26 patients with chronic active hepatitis, 23 with primary biliary cirrhosis, 11 with cryptogenic cirrhosis, and 48 with alcoholic hepatitis +/- cirrhosis) plasma concentrations of methionine were significantly increased, while concentrations of the three branched chain amino-acids were significantly reduced. In the first three groups of patients plasma concentrations of aspartate, serine, and one or both of the aromatic amino-acids tyrosine and phenylalanine were also significantly increased, while in the patients with alcoholic hepatitis +/- cirrhosis plasma concentrations of glycine, alanine, and phenylalanine were significantly reduced. In the three groups of patients with minimal, potentially reversible liver disease (31 patients with alcoholic fatty liver, 10 with viral hepatitis, and 18 with biliary disease) plasma concentrations of proline and the three branched chain amino-acids were significantly reduced. Patients with alcoholic fatty liver also showed significantly reduced plasma phenylalanine values. Most changes in plasma amino-acid concentrations in patients with chronic liver disease may be explained on the basis of impaired hepatic function, portal-systemic shunting of blood, and hyperinsulinaemia and hyperglucagonaemia. The changes in patients with minimal liver disease are less easily explained.

Adolescent↗