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Biomedical subjects

S Sherlock

Publications and source records attributed to S Sherlock.

At least 415 records · Page 23Linked to original sources

47 Calcium abosrption in parenchymatous and biliary liver disease.

As measured by whole body retention of isotopic calcium given in milk, absorption of calcium was impaired in 10 patients with chronic parenchymal non-biliary liver disease who were icteric. Mean absorption was normal in 15 patients with parenchymal liver disease who were anicteric although some individual patients absorbed less than any of the controls. Depressed absorption of calcium was seen in 10 patients with primary biliary cirrhosis and seven patients with intra- or extra-hepatic biliary obstructive disease. The most likely cause for this malabsorption is reduced bile salt secretion into the intestinal lumen which impairs vitamin D and fat absorption. The finding that parenteral vitamin D increased calcium absorption to normal levels in five patients with primary biliary cirrhosis suggests that deficiency of this vitamin is a major and correctable factor leading to calcium malabsorption in such patients. Precipitation of calcium salts by excess intraluminal fat appears to be a further possible factor reducing calcium absorption in these patients. These findings emphasize the importance of parenteral vitamin D therapy in patients with chronic obstructive biliary diseases. They also suggest that certain patients with chronic parenchymatous liver disease, particularly those who are icteric, may also occasionally require therapy with vitamin D.

Animals↗

Copper kinetics in liver disease.

The plasma clearance and the liver uptake of intravenously administered (64)Cu were significantly impaired in four patients with Wilson's disease. These defects were unlikely to be simply expressions of the high liver copper concentration as the plasma clearance and hepatic uptake of (64)Cu were normal in four patients with primary biliary cirrhosis, in whom the liver copper concentration was raised to a degree comparable to that in Wilson's disease. The normal liver uptake and plasma clearance of (64)Cu in three patients with other forms of hepatocellular disease suggest that impaired liver cell function does not have a significant effect. The precise nature of the defect in copper transport in Wilson's disease remains to be elucidated; it is possible that delayed uptake of copper by the hepatic lysosomes may account for the toxic effects of the metal.

Adult↗

The serum concentration of the third component of complement beta-1C-beta-1A in liver disease.

Serum C(3) (beta(1C)/beta(1A)) has been measured in normal individuals and the range found is in agreement with findings of other authors (85-370 mg/100 ml). In 18 patients with acute hepatitis and massive necrosis serum C(3) was consistently reduced to below 50% of normal. In other patients with acute hepatitis the serum C(3) concentration was normal. In the majority of the 150 patients with chronic liver disease serum C(3) concentration was normal. However, 10 patients (six with active chronic hepatitis, four with cryptogenic cirrhosis) had hypocomplementaemia. The reason for the depression is not clear but could reflect either decreased synthesis or increased consumption, or a combination of the two.

Acute Disease↗

Jaundice due to iprindole.

Twenty-one patients treated for depression with iprindole developed evidence of liver damage: 15 were jaundiced, five had bilirubinuria, and one had pruritus. These complications occurred between four and 21 days after initial exposure to the drug. All patients recovered. Light and electron microscopic findings in liver biopsies of one of these patients were those of cholestasis without inflammation.

Adult↗

Quantitative measurement of iron stores with diethylenetriamine penta-acetic acid.

The use of the chelating agent diethylenetriamine penta-acetic acid (DTPA) for measuring body storage iron was investigated in patients with iron excess whose stores could be determined by venesection. Iron excretion after DTPA bore a close semi-logarithmic relationship to body iron stores when these were increased. The excretion of DTPA-bound (59)Fe was similarly related to the size of the stores, indicating that the increased iron excretion produced by DTPA in iron overload states reflects both increased tissue iron available for chelation and greater stability of the iron-chelate complex. Evidence was obtained that injected (59)Fe-DTPA could be used as a marker for chelated tissue iron enabling the DTPA-chelatable body iron pool to be calculated. There was a highly significant correlation between DTPA-chelatable iron and body storage iron. The regression intercept approximated to the origin, implying a specific relation between the DTPA effect and storage iron. The SE of the mean estimate for storage iron on DTPA-chelatable iron was 0.25 g (5.6%). Mean storage iron values of 392 mg for males and 243 mg for females were predicted from the findings in control subjects.

Adult↗