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FRI698 Hypoparathyroidism Secondary To Covid-19
Disclosure: M. Hussain: None. T.K. Reddy: None. A. Mohiuddin: None. D. Lovre: None. R. Galagan: None. Introduction: New onset adult hypoparathyroidism is most often caused by thyroid surgery or autoimmune illness. To date, little is known about the effect of the novel coronavirus (SARS-CoV-2) on par...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Oxford University Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10554655/ http://dx.doi.org/10.1210/jendso/bvad114.466 |
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author | Hussain, Mariam Reddy, Tina K Mohiuddin, Arianna Lovre, Dragana Galagan, Robert |
author_facet | Hussain, Mariam Reddy, Tina K Mohiuddin, Arianna Lovre, Dragana Galagan, Robert |
author_sort | Hussain, Mariam |
collection | PubMed |
description | Disclosure: M. Hussain: None. T.K. Reddy: None. A. Mohiuddin: None. D. Lovre: None. R. Galagan: None. Introduction: New onset adult hypoparathyroidism is most often caused by thyroid surgery or autoimmune illness. To date, little is known about the effect of the novel coronavirus (SARS-CoV-2) on parathyroid glands. Most recent hypotheses are that Covid-19 might affect the parathyroid glands directly through invasion of parathyroid gland tissues by SARS-CoV-2 virus or indirectly secondary to respiratory failure and chronic respiratory alkalosis. Case Report: We report the case of a 32-year-old male with post-viral hypoparathyroidism secondary to COVID-19.Only a few cases of COVID-19 induced hypoparathyroidism have been reported in the literature. Our patient was admitted to the hospital for severe and symptomatic hypocalcemia three weeks after a viral-like upper respiratory tract infection and diarrhea. He complained of paresthesias, muscle cramps and muscle weakness. He had no autoimmune or neck surgical history. Initial lab test results revealed a corrected calcium of 4.5 mg/dL (8.4-10.3 mg/dL), ionized calcium 2.4 mg/dL (4.5-5.3 mg/dL), PTH < 1.0 pg/mL (12-65 pg/mL), phosphorus 6.2 mg/dL (2.5-4.7 mg/dL), magnesium 1.6 mg/dL (1.5-2.6 mg/dL), Vit D, 25-hydroxy 17.3 ng/mL (30-100 ng/mL), and creatinine 1.13 mg/dL (0.7-1.4 mg/dL), consistent with hypoparathyroidism. An ECG showed QTc prolongation to 506 msec. SARS-coV-2/flu/RSV cepheid multiplex was negative, SARS-CoV-2 Spike Ab was positive. He had never received a COVID vaccine. The patient was admitted to ICU for IV calcium drip, oral calcium and calcitriol supplementation. He was transitioned to a medical ward when his severe hypocalcemia was corrected and he was ultimately discharged on oral calcitriol 1 mcg BID and calcium carbonate 1000 mg po TID. A thorough workup for a cause of the hypoparathyroidism was performed, including anti-PTH antibody, 21-hydroxylase antibody, TSI, and TPO antibody, all of which were negative. Genetic testing was performed, including CASR gene sequencing analysis and AIRE DNA sequencing, both of which were negative. After other causes of hypoparathyroidism were excluded, COVID-19 was reasoned to be the etiology of this patient’s hypoparathyroidism. Our case highlights a post-viral hypoparathyroidism secondary to COVID-19. Further studies are needed to elucidate the mechanistic relationship between COVID-19 and hypoparathyroidism. Presentation: Friday, June 16, 2023 |
format | Online Article Text |
id | pubmed-10554655 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-105546552023-10-06 FRI698 Hypoparathyroidism Secondary To Covid-19 Hussain, Mariam Reddy, Tina K Mohiuddin, Arianna Lovre, Dragana Galagan, Robert J Endocr Soc Bone And Mineral Metabolism Disclosure: M. Hussain: None. T.K. Reddy: None. A. Mohiuddin: None. D. Lovre: None. R. Galagan: None. Introduction: New onset adult hypoparathyroidism is most often caused by thyroid surgery or autoimmune illness. To date, little is known about the effect of the novel coronavirus (SARS-CoV-2) on parathyroid glands. Most recent hypotheses are that Covid-19 might affect the parathyroid glands directly through invasion of parathyroid gland tissues by SARS-CoV-2 virus or indirectly secondary to respiratory failure and chronic respiratory alkalosis. Case Report: We report the case of a 32-year-old male with post-viral hypoparathyroidism secondary to COVID-19.Only a few cases of COVID-19 induced hypoparathyroidism have been reported in the literature. Our patient was admitted to the hospital for severe and symptomatic hypocalcemia three weeks after a viral-like upper respiratory tract infection and diarrhea. He complained of paresthesias, muscle cramps and muscle weakness. He had no autoimmune or neck surgical history. Initial lab test results revealed a corrected calcium of 4.5 mg/dL (8.4-10.3 mg/dL), ionized calcium 2.4 mg/dL (4.5-5.3 mg/dL), PTH < 1.0 pg/mL (12-65 pg/mL), phosphorus 6.2 mg/dL (2.5-4.7 mg/dL), magnesium 1.6 mg/dL (1.5-2.6 mg/dL), Vit D, 25-hydroxy 17.3 ng/mL (30-100 ng/mL), and creatinine 1.13 mg/dL (0.7-1.4 mg/dL), consistent with hypoparathyroidism. An ECG showed QTc prolongation to 506 msec. SARS-coV-2/flu/RSV cepheid multiplex was negative, SARS-CoV-2 Spike Ab was positive. He had never received a COVID vaccine. The patient was admitted to ICU for IV calcium drip, oral calcium and calcitriol supplementation. He was transitioned to a medical ward when his severe hypocalcemia was corrected and he was ultimately discharged on oral calcitriol 1 mcg BID and calcium carbonate 1000 mg po TID. A thorough workup for a cause of the hypoparathyroidism was performed, including anti-PTH antibody, 21-hydroxylase antibody, TSI, and TPO antibody, all of which were negative. Genetic testing was performed, including CASR gene sequencing analysis and AIRE DNA sequencing, both of which were negative. After other causes of hypoparathyroidism were excluded, COVID-19 was reasoned to be the etiology of this patient’s hypoparathyroidism. Our case highlights a post-viral hypoparathyroidism secondary to COVID-19. Further studies are needed to elucidate the mechanistic relationship between COVID-19 and hypoparathyroidism. Presentation: Friday, June 16, 2023 Oxford University Press 2023-10-05 /pmc/articles/PMC10554655/ http://dx.doi.org/10.1210/jendso/bvad114.466 Text en © The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Bone And Mineral Metabolism Hussain, Mariam Reddy, Tina K Mohiuddin, Arianna Lovre, Dragana Galagan, Robert FRI698 Hypoparathyroidism Secondary To Covid-19 |
title | FRI698 Hypoparathyroidism Secondary To Covid-19 |
title_full | FRI698 Hypoparathyroidism Secondary To Covid-19 |
title_fullStr | FRI698 Hypoparathyroidism Secondary To Covid-19 |
title_full_unstemmed | FRI698 Hypoparathyroidism Secondary To Covid-19 |
title_short | FRI698 Hypoparathyroidism Secondary To Covid-19 |
title_sort | fri698 hypoparathyroidism secondary to covid-19 |
topic | Bone And Mineral Metabolism |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10554655/ http://dx.doi.org/10.1210/jendso/bvad114.466 |
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