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Background: Hemoglobin disorders are the leading health concern in the world including India. There is a paucity of literature on the spectrum of hemoglobin disorders in southern districts of Odisha state. This study was undertaken to elucidate the occurrence of different hemoglobin disorders in a tertiary health care facility of Odisha state, India. Methods: The study cases were suspected patients of all age groups advised for screening of different hemoglobin disorders. Hemoglobin disorders were screened by sickling slide test and high-performance liquid chromatography (HPLC) using the Variant-II hemoglobin testing system as per the manufacturer's guidelines. Results: Over 2 years, 2332 blood samples (including 1102 pediatric and 1230 adult cases) were investigated, out of which, 1380 (59.2%) of cases had abnormal hemoglobin disorders. The most common was sickle cell disorders (48.67%, 1135/2332) followed by β-thalassemia (11.32%, 264/2332). Some rare variants were detected as hemoglobin D -Punjab , hemoglobin E, hemoglobin Lepore, hereditary persistence of fetal hemoglobin, hemoglobin with high P2 window, hemoglobin with high P3 window etc, Among the cases with abnormal hemoglobin disorders, 744 (53.9%), 545 (39.5%) and, 91 (6.6%) cases were found to have the heterozygous, homozygous and, double heterozygous state. Of the 188 ante-natal cases screened, 31.4% of cases had abnormal hemoglobin variants with sickle cell disorders being the most prevalent one. Conclusion: Along with the high occurrence of sickle cell disorders in the study area, some other rare hemoglobin disorders are also prevalent which calls for a large community-based cohort study.
Background: Hemoglobin disorders are the leading health concern in the world including India. There is a paucity of literature on the spectrum of hemoglobin disorders in southern districts of Odisha state. This study was undertaken to elucidate the occurrence of different hemoglobin disorders in a tertiary health care facility of Odisha state, India. Methods: The study cases were suspected patients of all age groups advised for screening of different hemoglobin disorders. Hemoglobin disorders were screened by sickling slide test and high-performance liquid chromatography (HPLC) using the Variant-II hemoglobin testing system as per the manufacturer's guidelines. Results: Over 2 years, 2332 blood samples (including 1102 pediatric and 1230 adult cases) were investigated, out of which, 1380 (59.2%) of cases had abnormal hemoglobin disorders. The most common was sickle cell disorders (48.67%, 1135/2332) followed by β-thalassemia (11.32%, 264/2332). Some rare variants were detected as hemoglobin D -Punjab , hemoglobin E, hemoglobin Lepore, hereditary persistence of fetal hemoglobin, hemoglobin with high P2 window, hemoglobin with high P3 window etc, Among the cases with abnormal hemoglobin disorders, 744 (53.9%), 545 (39.5%) and, 91 (6.6%) cases were found to have the heterozygous, homozygous and, double heterozygous state. Of the 188 ante-natal cases screened, 31.4% of cases had abnormal hemoglobin variants with sickle cell disorders being the most prevalent one. Conclusion: Along with the high occurrence of sickle cell disorders in the study area, some other rare hemoglobin disorders are also prevalent which calls for a large community-based cohort study.
Recently, it was demonstrated that prolonged hyperinsulinism associated with hypoglycemia, both in vivo and in vitro, caused covalent glycoinositolphospholipid (GPI) binding to the C termini of both hemoglobin b-chains, which resulted in the formation of a novel, hitherto unrecognized, minor hemoglobin fraction (GPI-Hb) (Niketi} et al., Biochem. Biophys. Res. Commun. 239 (1997) 435). In this study it was demonstrated that exposure of erythrocyte membranes to insulin causes the activation of membrane protease as well as that the formation of GPI-Hb parallels its activity. It is suggested that the insulin-activated protease is able to catalyze, albeit slowly, the transpeptidation, i.e., the replacement of the carboxy-terminal amino acid(s) residues of the Hb b-chains with GPI as an exogenous nucleophile. To our knowledge the present results show for the first time that insulin stimulates protease activity in erythrocyte membranes, as well as that insulin-activated protease may be involved in post-translational GPI binding to proteins.
Atherosclerosis is a major complication of diabetes, increasing the risk of cardiovascular related morbidities and mortalities. The hallmark of diabetes is hyperglycemia which duration is best predicted by elevated glycated haemoglobin A1C (HbA1C) levels. Diabetic complications are usually attributed to oxidative stress associated with glycation of major structural and functional proteins. This non-enzymatic glycation of long lived proteins such as collagen, albumin, fibrinogen, liver enzymes and globulins result in the formation of early and advanced glycation end products (AGEs) associated with the production of myriads of free radicles and oxidants that have detrimental effects leading to diabetic complications. AGEs have been extensively discussed in the literature as etiological factors in the advancement of atherogenic events. Mechanisms described include the effects of glycation on protein structure and function that lead to defective receptor binding, impairment of immune system and enzyme function and alteration of basement membrane structural integrity. Hemoglobin (Hb) is a major circulating protein susceptible to glycation. Glycated Hb, namely HbA1C is used as a useful tool in the diagnosis of diabetes progression. Many studies have shown strong positive associations between elevated HbA1C levels and existing cardiovascular disease and major risk factors. Also, several studies presented HbA1C as an independent predictor of cardiovascular risk. In spite of extensive reports on positive associations, limited evidence is available considering the role of glycated Hb in the etiology of atherosclerosis. This editorial highlights potential mechanisms by which glycated hemoglobin may contribute, as a causative factor, to the progression of atherosclerosis in diabetics.
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