Endocrine Abstracts

Introduction: Calcium ions (Ca²⁺) play an essential role in process of correct β-cell insulin secretion. Hypocalcemia impairs insulin secretion leading to glucose metabolism disorders and insulin resistance.

Case study: 62 -year old female patient with 18 years history of type 2 diabetes, treated with insulin, suspected of hypoparathyroidism, was admitted to the Department and Clinic of Endocrinology, Medical University of Lublin because of hypocalcaemia. She was experiencing latent tetany signs like muscle tremors, paresthesia and an unpleasant tingling sensation in her hands, additionally persistent dry cough. Clinical observation and laboratory findings with classic constellation of symptoms (hypocalcemia, hyperphosphatemia, undetectable concentrations of parathyroid hormone (PTH), latent tetany signs, history of nephrolithiasis and of subcortical nuclei calcifications) have confirmed the diagnosis of late onset primary hypoparathyroidism. Significant clinical improvement following introduction of calcium and active form of vitamin D supplementation were achieved. Based on normal blood glucose levels with relatively low daily insulin requirement an attempt at discontinuing insulin therapy was made. In spite of hypoglycemic therapy cessation, patient’s glucose levels remained in the normal range. For the purpose of diagnosis verification oral glucose tolerance test (OGTT) was performed, and did not reveal any glucose metabolism disorders. These observations led us to conclude that recognized hyperglycemia was secondary to prolonged hypocalcemia.

Conclusions: The optimal concentrations of organism’s cytosolic Ca²⁺ are required for appropriate β-cell insulin release. Hypocalcemia is regarded as a factor implicated in pathogenesis of glucose metabolism disorders thus normalizing serum calcium levels allows for restoration of adequate insulin secretion.