Abstract

Background: Endocrine action is integrative and an endocrine dysfunction of one gland is known to affect other endocrine glands. Parathyroid glands are associated with the beta cell function. Thus, insulin resistance observed in type 2 diabetes mellitus (T2DM) may be associated with alterations of parathyroid hormones and their metabolic pathways. These have been reported to have a genetic root, postulated to be aberrant haemoglobin gene resulting in haemoglobin variants. This has not been fully explored in sub-Saharan Africa, which has significant population of haemoglobin variants. Aim: The aim of this study was to evaluate the status of parathyroid dysfunction and its association with haemoglobinopathies among Sub-Saharan Africans with type 2 diabetes mellitus. Method: A total of 204 individuals aged 25 – 80 years which comprised 100 T2DM and 104 Controls without T2DM were enrolled from a tertiary hospital, in Ibadan, Nigeria and environs.10mL intravenous blood was obtained from each participant. Parathyroid Hormone (PTH) was measured using enzyme linked immunosorbent assay (ELISA). Calcium, Phosphate, Albumin and Fasting Plasma Glucose (FPG) were analysed spectrophotometrically. Haemoglobin A2 (HbA2), Haemoglobin A (HbA), Haemoglobin C (HbC) and Haemoglobin S (HbS) and Glycated haemoglobin (HbA1c) were determined by High Performance Liquid Chromatography (HPLC) method using Variant Haemoglobin Testing System (Bio-Rad Variant II). Data analysed using appropriate statistical analysis were significant at p<0.05. Results: Normal parathyroid function, hyperparathyroidism and hypoparathyroidism were present in 93% vs 96%, 3% vs 0.96% and 4% vs 6.73% in T2DM and controls respectively. T2DM and controls with AA and Non AA had 62% vs 31% normoparathyroidism, 3% vs 0% hyperparathyroidism and 2% vs 2% hypoparathyroidism respectively. The association between parathyroid gland disorder in T2DM and controls with the various haemoglobin variants was not significant (p>0.05) but the difference between parathyroid function in the control group with and without Beta Thalassaemia Trait was significant (p<0.05). Conclusion: Hypoparathyroidism and hyperparathyroidism were revealed in Type 2 Diabetes Mellitus and control individuals with haemoglobin genotype AA (HbAA). Hypoparathyroidism was also found among controls with Beta Thalassaemia Trait. Timely identification of these disorders may be helpful in appropriate therapeutic regimen to facilitate bone growth, prevent fractures and complications of parathyroid gland in these individuals. KEYWORDS: Haemoglobin Variants, Parathyroid Dysfunction, Type 2 Diabetes Mellitus (T2DM).

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