{"title":"Primary hypoparathyroidism associated with catatonia in a patient with bipolar affective disorder: A case report","authors":"Tulasi Sindhuja , Akash Kumar , Gurveen Bhatia , Snehil Gupta , Ashok Kumar","doi":"10.1016/j.psycr.2023.100196","DOIUrl":null,"url":null,"abstract":"<div><p>Primary hypoparathyroidism is caused by parathyroid hormone (PTH) deficiency and characterized by hypocalcemia. Psychiatric manifestations such as mood disorders, however, are uncommon in primary hypoparathyroidism; therefore, neuro-psychiatric manifestations, including mood disorders, in the latter condition can pose a significant diagnostic challenge. Furthermore, co-morbid psychiatric disorders, metabolic conditions, and concurrent (psychotropic) medications can complicate the clinical picture of either of the conditions, including posing substantial diagnostic and management challenges. In this paper, we report a case of primary hypoparathyroidism with catatonia in a patient with a pre-existing bipolar affective disorder (BPAD) with poor response to mood stabilizers and antipsychotic medication for two years.</p><p>The girl, of age 18 years presented to the emergency department in a catatonic state characterized by mutism, posturing, stupor, negativism, waxy flexibility, and echolalia (Bush-Francis Catatonia Rating Scale (BFCRS) score was 16). Her symptoms responded poorly to psychotropic medications, moreover, she was overly sensitive to adverse effects of various medication (e.g., very prolonged QTc interval). Laboratory investigations showed that she had severe hypocalcemia, hypomagnesemia, hyperphosphatemia, and alkalosis. Her PTH levels were significantly low. Upon correction of dyselectrolytaemia (through calcium and magnesium supplements) and concurrent intake of tab. Olanzapine, a significant improvement in her symptoms was noticed. After excluding all causes of acquired hypoparathyroidism, we concluded it as primary hypoparathyroidism. The case highlights the importance of having a comprehensive and wider assessment of such atypical presentations of catatonia, especially if it responds poorly to conventional treatments.</p></div>","PeriodicalId":74594,"journal":{"name":"Psychiatry research case reports","volume":"3 1","pages":"Article 100196"},"PeriodicalIF":0.0000,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773021223000949/pdfft?md5=c71394053e1ab1f547ed7be238134814&pid=1-s2.0-S2773021223000949-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Psychiatry research case reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2773021223000949","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Primary hypoparathyroidism is caused by parathyroid hormone (PTH) deficiency and characterized by hypocalcemia. Psychiatric manifestations such as mood disorders, however, are uncommon in primary hypoparathyroidism; therefore, neuro-psychiatric manifestations, including mood disorders, in the latter condition can pose a significant diagnostic challenge. Furthermore, co-morbid psychiatric disorders, metabolic conditions, and concurrent (psychotropic) medications can complicate the clinical picture of either of the conditions, including posing substantial diagnostic and management challenges. In this paper, we report a case of primary hypoparathyroidism with catatonia in a patient with a pre-existing bipolar affective disorder (BPAD) with poor response to mood stabilizers and antipsychotic medication for two years.
The girl, of age 18 years presented to the emergency department in a catatonic state characterized by mutism, posturing, stupor, negativism, waxy flexibility, and echolalia (Bush-Francis Catatonia Rating Scale (BFCRS) score was 16). Her symptoms responded poorly to psychotropic medications, moreover, she was overly sensitive to adverse effects of various medication (e.g., very prolonged QTc interval). Laboratory investigations showed that she had severe hypocalcemia, hypomagnesemia, hyperphosphatemia, and alkalosis. Her PTH levels were significantly low. Upon correction of dyselectrolytaemia (through calcium and magnesium supplements) and concurrent intake of tab. Olanzapine, a significant improvement in her symptoms was noticed. After excluding all causes of acquired hypoparathyroidism, we concluded it as primary hypoparathyroidism. The case highlights the importance of having a comprehensive and wider assessment of such atypical presentations of catatonia, especially if it responds poorly to conventional treatments.