Abstract
A defective synthesis of vitamin D contributes to alterations in calcium homeostasis due to chronic endocrinopathies, leading to metabolic bone diseases. This study aimed to ascertain the levels of calcium, vitamin D, and parathyroid hormone (PTH) in children with β-thalassemia. In this case-control study, 36 children with major β-thalassemia receiving iron chelation therapy were included. For the control group, 36 cases matched for age and sex were selected. The packed cell volume (PCV) requirements varied among the thalassemic children, with an average PCV requirement of 78.57±49.07. The study was conducted for six months in the Department of Pediatrics at the Government Medical College, Nagpur, India. Serum PTH levels were determined by immunoassay, and serum vitamin D levels were assessed using electrochemiluminescence technique. Additional tests looked at liver function, serum ferritin, calcium, phosphorus, and complete blood count. The student's t-test, Mann-Whitney, and chi-square tests were used for statistical analysis. In comparison to the control group (10.4±1.21 g/dL), the case group's mean hemoglobin level was considerably lower (5.62±1.9 g/dL) (p<0.001). The mean serum ferritin level in the cases was notably higher (3073±1262.24 ng/mL) compared to the control group's level (58.37±29.67 ng/mL) (p<0.001). A total of 80.6% of cases compared to 5.6% of controls had vitamin D deficiency, and 72.2% of cases compared to 2.8% of controls had PTH deficit, both of which showed statistically significant differences (p<0.001). Significant differences were observed between the case and control groups for the mean levels of total serum calcium (8.51±0.84 mg/dL), vitamin D (15.23±10.07 ng/mL), and PTH (14.66±19.86 pg/mL) (9.13±0.6 mg/dL, p=0.05; 34.94±9.57 ng/mL, p<0.001; 32.08±12.42 pg/mL, p<0.001; respectively). Growth failure may result from the markedly reduced serum calcium, vitamin D, and PTH levelsin children with β-thalassemia. The relevance of treatment approaches is highlighted by the possibility that these anomalies are caused by excessive iron and inadequate nutritional support.
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