title: Hypoparathyroidism in transfusion-dependent patients with beta-thalassemia.
abstract: Hypoparathyroidism is thought to be a rare consequence of iron overload seen in beta-thalassemic transfused patients. This study was conducted to determine the prevalence of hypoparathyroidism in a large number of beta-thalassemic patients, and its potential correlation with the presence of other endocrinopathies caused by iron overload. Serum and urine biochemical parameters were measured in 243 thalassemic patients (136 females and 107 males) in order to determine the prevalence of hypoparathyroidism and evaluate bone turnover. The patients were divided into two groups according to the presence of hypoparathyroidism. We compared the prevalence of other endocrinopathies and disease complications in the two groups. Hypoparathyroidism was detected in 13.5% of the patients (33 subjects; 17 males and 16 females). Serum-intact parathyroid hormone, and total and ionized calcium were significantly lower, while phosphorus was significantly higher in thalassemic patients with hypoparathyroidism. The reduction in BMD was more prominent in normal thalassemic patients (Z score = -2.246 +/- 0.97) compared with those with hypoparathyroidism (Z score = -1.975 +/- 0.89), although the difference was not statistically significant. Disturbed glucose metabolism was more common in patients with hypoparathyroidism (P < 0.05). In addition, heart dysfunction was statistically more frequent in this group (odds ratio = 2.51, P < 0.05). Hypoparathyroidism is a not infrequently observed complication in thalassemic patients. Since the concentration of ferritin is not a valuable tool in the prediction of the development of hypoparathyroidism, parathyroid function should be tested periodically, particularly when other iron overload-associated complications occur.
authors.affiliation: Division of Endocrinology and Metabolism, "Hippokrateion" Hospital of Athens, 108 Vassilisis Sofias Avenue, 115 27, Athens, Greece. drangelnick@hotmail.com
authors.forename: Nicholas G
authors.initials: NG
authors.lastname: Angelopoulos
authors.forename: Anastasia
authors.initials: A
authors.lastname: Goula
authors.forename: Grigorios
authors.initials: G
authors.lastname: Rombopoulos
authors.forename: Victoria
authors.initials: V
authors.lastname: Kaltzidou
authors.forename: Eugenia
authors.initials: E
authors.lastname: Katounda
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Kaltsas
authors.forename: George
authors.initials: G
authors.lastname: Tolis
mesh_terms: D000328:Adult; D000367:Age Factors; D001669:Biochemical Phenomena; D001671:Biochemistry; D001803:Blood Transfusion; D015519:Bone Density; D001842:Bone and Bones / Q000378:metabolism; D002614:Chelating Agents / Q000494:pharmacology; D004703:Endocrine System / Q000378:metabolism / Q000473:pathology; D005260:Female; D005293:Ferritins / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007011:Hypoparathyroidism / Q000378:metabolism / Q000473:pathology*; D007501:Iron / Q000378:metabolism; D007502:Iron Chelating Agents / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D015233:Models, Statistical; D010280:Parathyroid Glands / Q000378:metabolism; D010281:Parathyroid Hormone / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism; D013789:Thalassemia / Q000378:metabolism; D017086:beta-Thalassemia / Q000378:metabolism*
chemical_list: D002614:Chelating Agents; D007502:Iron Chelating Agents; D010281:Parathyroid Hormone; D010758:Phosphorus; D005293:Ferritins; D007501:Iron; D005947:Glucose