Blood coagulation and fibrinolytic activity in Indian childhood cirrhosis.
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Biomedical subjects
Publications and source records attributed to B Dube.
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Coagulation studies were made on 22 pregnant women with acute infective hepatitis and on 15 normal control pregnant women in third trimester. Fourteen hapatitis patients had clinical evidence of liver failure and all of them had a haemorrhagic diathesis; none of the patients without liver failure showed clinical evidence of haemostatic defects. Coagulopathy was present in most patients, its severity being greater in those with hepatic failure. Significant alterations were observed in bleeding time, whole blood clotting time, prothrombin time, thrombin time, plasma fibrinogen and serum levels of fibrinogen degradation products. The last three disturbances were most frequent in patients with liver failure. Increased fibrinolysis and disseminated intravascular coagulation also appeared to play a contributory role, particularly in patients with hepatic failure.
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Investigations on 114 anaemic pregnant women revealed that megaloblastosis occurred in more than half. A therapeutic follow-up approach clearly indicated that vitamin B12-deficiency was fairly common in such patients; the need of iron supplementation in many of them for achieving complete remission emphasized the poor status of iron stores. All patients with normoblastic marrow achieved full remission with iron therapy alone. The deficiency of haematinic factors appears to be largely due to poor nutrition.
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Coagulation studies were performed in 61 patients of acute infective hepatitis. 18 with clinical signs of liver failure had bleeding and all succumbed. The 47 patients without liver failure showed no haemorrhagic diathesis and all of them had uneventful recovery. Though coagulopathy was present in most of the patients, the severity and frequency of coagulation defects were more in those with signs of hepatic failure. Hypofibrinogenemia, elevated serum fibrinogen degradation products and accelerated euglobulin lysis were conspicuous in patients with hepatic failure. It appears that while diminished synthesis of coagulation factors is the main basis for coagulopathy in patients without hepatic failure, additional factors like local or disseminated intravascular coagulation and increased fibrinolysis also contribute significantly to the coagulopathy in cases of liver failure.
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Twelve Indian patients with pre-eclampsia, 15 with eclampsia and 15 with normal pregnancy in the third trimester were investigated. A systemic bleeding diathesis was encountered in two patients with eclampsia and in none with pre-eclampsia; two patients with pre-eclampsia, however, had excessive uterine haemorrhage. Coagulation studies showed statistically significant prolongation of thrombin time, elevation of serum fibrinogen degradation products (FDP) and hypofibrinogenaemia in patients with pre-eclampsia as well as eclampsia. In patients with eclampsia, significant thrombocytopenia also occurred. Euglobulin lysis time showed no significant change in patients with pre-eclampsia and eclampsia. There was no significant difference in the coagulation profile between patients with eclampsia and pre-eclampsia, except for more hypofibrinogenaemia in the former. The laboratory findings suggest the occurrence of intravascular coagulation in patients with pre-eclampsia and eclampsia.