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Results for “Jaundice, Obstructive”

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At least 199 records · Page 11Linked to original sources
PubMed1990

Pancreatic hormone changes in infantile obstructive jaundice.

Metabolic disturbances of pancreatic hormones in obstructive jaundice in infancy were evaluated experimentally and clinically. In our experimental study, using young rats, the level of plasma insulin (IRI) gradually increased after ligation of the common bile duct. These levels were a little lower than those in the non-treated controls. The level of plasma glucagon (IRG) increased remarkably 4 weeks after ligation of the common bile duct. Clinically, there were no significant differences in the levels of IRI and IRG among normal controls and cases of neonatal hepatitis and congenital biliary atresia (CBA). In CBA patients, these levels can be correlated with the progression of hepatic fibrosis; an increase in IRG and a decrease in the IRI/IRG mol ratio was noticed in patients with grade III of hepatic fibrosis. These results indicate that, in obstructive jaundice in infancy, the more severe the hepatic damage due to obstructive jaundice, the higher the level of plasma glucagon concentration will rise.

Animals↗
PubMed2001

[Red blood cell's deformability in obstructive jaundice].

UNLABELLED: Several factors with well known haemorheological consequences are identified in obstructive jaundice e.g.: hyperlipidemia, endotoxemia, changes in oxidant-antioxidant status. Previous investigations have shown the decrease of red blood cell deformability. They have been assessed by filtration technique in obstructive jaundice without the exclusion of patients with systemic inflammatory response syndrome. The aim of this study is the examination of red blood cell deformability by laser diffractometry in patients with obstructive jaundice. Seven patients with obstructive jaundice (total serum bilirubin 163 +/- 69 mmol/l) without systemic inflammatory response syndrome and 24 healthy adults underwent red blood cell deformability measurement by laser diffractometer Rheodyn SSD. Significant increase of elongation indexes of erythrocytes in all coagulation tensions has been observed. CONCLUSION: In obstructive jaundice the increase of erythrocyte deformability has been detected.

Aged↗
PubMed1982

Endotoxin, prostaglandins and renal fibrin deposition in obstructive jaundice.

The delayed clearance of endotoxins in obstructive jaundice may cause renal impairment by inducing renal vasoconstriction and glomerular fibrin deposition as a consequence of intravascular coagulation. As endotoxins activate arachidonic acid metabolism we have examined the effects of selective inhibitors on mortality, plasma TXB2 and 6-oxo-PGF1 alpha production and renal fibrin deposition in rats with obstructive jaundice following endotoxin administration. Jaundiced rats had a high mortality following endotoxin--58 per cent at 4 h and 83 per cent at 24 h. Pretreatment with indomethacin 3 mg/kg i.p., dazoxiben 3 mg i.p. or prostacyclin 300 ng/kg i.v. produced significant improvements in survival. Endotoxaemia was associated with significant elevations of plasma TXB2 and early inhibition of plasma 6-oxo-PGF1 alpha generation. Renal fibrin deposition, assessed using indirect immunofluorescence and a 125I-labelled fibrinogen uptake ratio, occurred in jaundiced kidneys following endotoxin and could be prevented using indomethacin, dazoxiben and prostacylin. These results suggest that endotoxin-induced TXA2 production can cause renal fibrin deposition in obstructive jaundice, thus contributing in the pathogenesis of the renal impairment.

6-Ketoprostaglandin F1 alpha↗