Endocrine Abstracts

Introduction: Graves’ disease (GD) is often treated with radioiodine therapy for cure. While, post external irradiation and post-radioiodine therapy (RAI) induced hyperparathyroidism after many years of latency is a well known phenomenon, there are only anectodal reports of post-radioiodine hypocalcemia. The factors contributing to this are poorly understood. In this context, we evaluated our own series to look deeper in to this issue.

Material and methods: This retrospective study was conducted on 65 surgically managed GD patients. Diagnosis of GD was based on clinical picture, thyroid function tests, radionuclide scanning and histopathology. Exclusion criteria were subjects with vitamin D deficiency (20 ng/dl), chronic renal, hepatic or inflammatory disease or drugs interfering with calcium metabolism. All subjects were normocalcemic preoperatively (8.5–10 mg/dl). Hypocalcemia was treated with calcium supplements and vitamin D. Parameters such as severity of Graves’ disease, Statistical analysis was performed by SPSS 20.0 version. Descriptive statistics, t test and Chi-square tests were performed.

Results: 6/65 patients (9.3%) developed hypocalcemia. Average follow-up duration of subjects was 18.4±4.5 months (14–24). Average onset of clinical and/or biochemical hypocalcemia was at 4.2±1.5 months (2–7). Serum calcium level during first detection of hypocalcemia was 6.9±1.5 mg/dl (5.6–8.2). Corresponding serum parathyroid hormone level was 35±14 pg/ml (25–65). Hypocalcemia resolved after treatment for 2 months on an average. No further hypocalcemic episodes during follow-up period. Range of RAI dosage was 7–12 mCi. None of factors such as severity of hyperthyroidism, duration of hyperthyroidism, goiter size, age of patient, serum parathyroid hormone level and sex had statistically significant influence on occurrence of hypocalcemia on correlation and multivariate analysis.

Conclusions: Our study shows that post RAI hypocalcemia is a frequent morbidity. Further it is independent of any physiological or disease related factors. The exact cause of this curious phenomenon appears to be enigmatic, but we hypothesize that collateral damage caused by radiation causes temporary parathyroid stunning. More studies are needed to unravel this mystery, but active watch at followup post RAI therapy is recommended in routine management of GD.

Keywords: Graves’ disease, Parathyroid hormone, hypocalcemia, Thyroidectomy, Radioiodine, Hypoparathyroidism