[Erythrocyte dehydrogenase glucose-6-phosphate deficiency and selective IgA deficiency: a familial study].
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Biomedical subjects
Publications and source records attributed to J Núñez Carril.
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Antithrombin III (AT III) levels in 37 healthy people and in 103 patients diagnosed of hepatic cirrhosis (75 due to ethylism, 26 cryptogenic and 7 post-hepatitis) have been studied. Forty seven patients presented a compensation in their cirrhosis and 56 an unbalance. AT III concentration was decreased in cirrhotic patients (14.9 + 1.09 mg/dl), being p less than 0.0005 in relation to healthy patients (24.3 + 0.87 mg/dl). Concentration resulted lesser in patients with unbalance (13.9 + 1.8 mg/dl) than in patients with compensation (18.1 + 1.6 mg/dl). Moreover, statistical study between them showed significant results. AT III, though is a protein whose hepatic synthesis is not clear, decreases in diffuse hepatic disease and so much as more severe is the hepatic damage. Cirrhotic patients did not present thromboembolic phenomena, perhaps because of depression of coagulation factors.
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Activity of serum C3 and C4 fractions have been measured in 35 individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency and various clinical manifestations. Determination of serum complement was carried out in six cases during an abrupt hemolytic phase; the remaining 29 patients were asymptomatic at the time of laboratory test, but the past history revealed acute hemolytic syndroe in 11 cases. There were no statistical significant differences between C3 and C4 fraction levels of patients with G6PD deficiency and those corresponding to a group of 30 normal controls. Immunoallergic theories causing hemolytic episodes in patients with G6PD deficiency are discussed.
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