Comparison of conventional high dose insulin therapy with small dose intramuscular insulin therapy in diabetic ketoacidosis

[No abstract available

The effect of phenobarbital upon the prolonged prothrombin time in parenchymal liver disease

Eight patients with parenchymal liver disease who had prolonged prothrombin time unresponsive to vitamin K1 were given phenobarbital 60 to 100 mg daily. Prothrombin time decreased in 6 to 19 days to near normal or normal values. In four patients liver biopsies were done without incident. The effect of phenobarbital probably is related to hepatic microsomal enzyme induction

The coincidence of glucose-6-phosphate dehydrogenase deficiency and hemoglobin s gene in çuxurova province, Turkey

PubMedID: 3953546A total of 1,582 subjects from 10 villages of different ethnic populations were screened for glucose-6-phosphate dehydrogenase (G5PD deficiency (GdB-, Mediterranean variant) and hemoglobin S gene, and the coincidence of both abnormalities was determined. Although the prevalence of both abnormalities was found to be highest in an Eti-Turk group living in the Tarsus area, coincidence was not significant. In a single village of Adana Eti-Turks, however, coincidence was found to be significant, although neither the frequency of G5PD deficiency nor the existence of hemoglobin S gene was highest in that village. © 1986 by 1986 The Johns Hopkins University School of Hygiene and Public Health.Received for publication Match 19, 1985, and in final form August 8, 1985. Abbreviations: G»PD, glucose-6-phosphate dehydrogenase; Hb, hemoglobin. 1Cukurova University, Medical Faculty, Department of Hematology, Adana, Turkey. (Reprint requests to Dr. Tevfik Akoglu.) 'Cukurova University, Medical Faculty, Department of Nephrology, Adana, Turkey. This work was supported by Grant TAG-427 from the Scientific and Technical Research Council of Turkey

Erythrocyte membrane ATPase activity of G6PD-deficient individuals and the effect of primaquine metabolite(s) on membrane ATPase enzymes

PubMedID: 6152296Erythrocyte membrane Na+/K+, Ca2+/Mg2+ and Mg2+ ATPase activities in addition to the calmodulin-activated Ca2+/Mg2+ ATPase enzyme were measured in both G6PD-deficient and normal individuals. Although all three membrane ATPase activities were somewhat higher in the G6PD-deficient erythrocytes, only activated Ca2+/Mg2+ ATPase activity was significantly increased. The effect of primaquine on the membrane ATPases was also compared with other ATPase inhibitors. Primaquine was ineffective on erythrocyte membrane ATPase in vitro. However, sera containing primaquine metabolite(s) were inhibitory to Ca2+/Mg2+ and Mg2+ ATPase systems of only G6PD-deficient erythrocytes. Other ATPase inhibitors showed a similar inhibitory effect in G6PD-deficient and normal erythrocytes, indicating a specific influence of primaquine on ATPase system in G6PD-deficiency. It is suggested that this effect of primaquine may be an additional factor for haemolysis observed in the people with GdB- type of G6PD-deficiency among the Mediterranean populations

Genetic linkage study of familial Mediterranean fever (FMF) to 16p13.3 and evidence for genetic heterogeneity in the Turkish population.

Familial Mediterranean fever (FMF) is an autosomal recessive condition that is almost entirely restricted to the non-Askhenazi Jews, Arabs, Armenians, and Turks. Genetic linkage study of a large group of non-Turkish families has previously mapped the FMF locus to the 16p13.3 region and shown that this locus resides 0.305 cM distal to D16S246. Furthermore, allelic association has also been shown with D16S3070 (75%) and D16S3275 (66%). However, no genetic heterogeneity has been described for any of the three major reported groups of FMF families. Here, we describe the genetic linkage relationship of the fourth major group of Turkish families and report the first evidence for genetic heterogeneity of this condition. Two point linkage analysis and haplotype inspection of 15 DNA markers from the reported region of the FMF locus identified tight linkage in a group of six Turkish FMF families. A maximum lod score of 9.115 at theta = 0.00 was observed for D16S3024. Nine other DNA markers provided similar evidence of linkage with lod score values of above 5.21. However, two other FMF families were completely unlinked to this region of chromosome 16. Haplotype construction of DNA markers in five consanguineous linked families showed that a segment of homozygosity has been conserved for D16S3070 and D16S2617. No other DNA markers showed any such conservation. Therefore, we suggested that these two markers reside in close proximity to the FMF locus. Furthermore, we observed 80% allelic association with D16S2617 but no association with D16S3070 or any other DNA markers from the FMF critical region. In summary, we conclude that our Turkish families are also linked to the reported FMF locus at 16p13.3, there is a genetic heterogeneity for this condition at least in our group of Turkish families, and D16S2617 is in linkage disequilibrium in the Turkish FMF families. Combination of this study with previously published observations suggests that the FMF locus resides between D16S246 and D16S3070/D16S2617 and within a region of about 250-300 kb