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Hypoparathyroidism in a Case of Transfusion Dependent Thalassemia

Repeated blood transfusions in transfusion dependent thalassemia (TDT) leads to iron overload-related endocrine complications. Hypoparathyroidism (HPT) with severe signs of hypocalcemia is a recognized complication among these patients. A 14-year-old thalassaemic boy, on regular transfusion and on a...

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Autores principales: Majumder, Anirban, Basu, Sagar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Journal of the ASEAN Federation of Endocrine Societies 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7784244/
https://www.ncbi.nlm.nih.gov/pubmed/33442182
http://dx.doi.org/10.15605/jafes.035.01.23
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author Majumder, Anirban
Basu, Sagar
author_facet Majumder, Anirban
Basu, Sagar
author_sort Majumder, Anirban
collection PubMed
description Repeated blood transfusions in transfusion dependent thalassemia (TDT) leads to iron overload-related endocrine complications. Hypoparathyroidism (HPT) with severe signs of hypocalcemia is a recognized complication among these patients. A 14-year-old thalassaemic boy, on regular transfusion and on anticonvulsant therapy with a presumptive diagnosis of epilepsy for the last 1 year, was admitted with high fever and severe muscle cramps with positive Trousseau’s sign. He was diagnosed as a case of primary HPT and magnesium deficiency on the basis of low serum calcium, high phosphate, normal alkaline phosphates, very low intact parathyroid hormone (iPTH), normal serum vitamin D and very low serum magnesium level. His calcium, magnesium and phosphate level normalised following treatment with intravenous magnesium and calcium. His iPTH improved but remained at low normal. He was discharged from hospital with oral calcium, calcitriol, and magnesium supplementation. The anticonvulsant (Phenobarbitone) was successfully withdrawn gradually over the next six months without any recurrence of seizure in the subsequent 3 years of follow up. Acquired HPT (apparently from hemosiderosis) is a common cause of hypocalcemia; and magnesium depletion further complicated the situation leading to severe hypocalcemia with recurrent episodes of convulsion. Magnesium replacement improved the parathyroid hormone (PTH) value proving its role in acquired HPT. Very high phosphate level on admission and poor PTH response with respect to the low serum calcium, indicates intrinsic parathyroid pathology. Metabolic abnormalities should always be evaluated in thalassaemic subject with seizure disorder and it appears that the initial convulsive episodes were due to hypocalcemia. Muscle pain, cramps or convulsion may occur from HPT and simultaneous magnesium deficiency in transfusion dependent thalassaemic subjects. Metabolic correction is more important than anticonvulsant medication. Calcium and magnesium should both be assessed routinely in transfusion dependent thalassemic patients.
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spelling pubmed-77842442021-01-12 Hypoparathyroidism in a Case of Transfusion Dependent Thalassemia Majumder, Anirban Basu, Sagar J ASEAN Fed Endocr Soc Case Report Repeated blood transfusions in transfusion dependent thalassemia (TDT) leads to iron overload-related endocrine complications. Hypoparathyroidism (HPT) with severe signs of hypocalcemia is a recognized complication among these patients. A 14-year-old thalassaemic boy, on regular transfusion and on anticonvulsant therapy with a presumptive diagnosis of epilepsy for the last 1 year, was admitted with high fever and severe muscle cramps with positive Trousseau’s sign. He was diagnosed as a case of primary HPT and magnesium deficiency on the basis of low serum calcium, high phosphate, normal alkaline phosphates, very low intact parathyroid hormone (iPTH), normal serum vitamin D and very low serum magnesium level. His calcium, magnesium and phosphate level normalised following treatment with intravenous magnesium and calcium. His iPTH improved but remained at low normal. He was discharged from hospital with oral calcium, calcitriol, and magnesium supplementation. The anticonvulsant (Phenobarbitone) was successfully withdrawn gradually over the next six months without any recurrence of seizure in the subsequent 3 years of follow up. Acquired HPT (apparently from hemosiderosis) is a common cause of hypocalcemia; and magnesium depletion further complicated the situation leading to severe hypocalcemia with recurrent episodes of convulsion. Magnesium replacement improved the parathyroid hormone (PTH) value proving its role in acquired HPT. Very high phosphate level on admission and poor PTH response with respect to the low serum calcium, indicates intrinsic parathyroid pathology. Metabolic abnormalities should always be evaluated in thalassaemic subject with seizure disorder and it appears that the initial convulsive episodes were due to hypocalcemia. Muscle pain, cramps or convulsion may occur from HPT and simultaneous magnesium deficiency in transfusion dependent thalassaemic subjects. Metabolic correction is more important than anticonvulsant medication. Calcium and magnesium should both be assessed routinely in transfusion dependent thalassemic patients. Journal of the ASEAN Federation of Endocrine Societies 2020-04-28 2020 /pmc/articles/PMC7784244/ /pubmed/33442182 http://dx.doi.org/10.15605/jafes.035.01.23 Text en © 2020 Journal of the ASEAN Federation of Endocrine Societies https://creativecommons.org/licenses/by-nc/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International.
spellingShingle Case Report
Majumder, Anirban
Basu, Sagar
Hypoparathyroidism in a Case of Transfusion Dependent Thalassemia
title Hypoparathyroidism in a Case of Transfusion Dependent Thalassemia
title_full Hypoparathyroidism in a Case of Transfusion Dependent Thalassemia
title_fullStr Hypoparathyroidism in a Case of Transfusion Dependent Thalassemia
title_full_unstemmed Hypoparathyroidism in a Case of Transfusion Dependent Thalassemia
title_short Hypoparathyroidism in a Case of Transfusion Dependent Thalassemia
title_sort hypoparathyroidism in a case of transfusion dependent thalassemia
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7784244/
https://www.ncbi.nlm.nih.gov/pubmed/33442182
http://dx.doi.org/10.15605/jafes.035.01.23
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