Severe Hypercalcemia Caused by Calcium-Alkali Syndrome after 15 Years of Postoperative Hypoparathyroidism in a Patient with Undiagnosed Hyperaldosteronism.

IF 0.9 Q4 ENDOCRINOLOGY & METABOLISM
Case Reports in Endocrinology Pub Date : 2024-02-16 eCollection Date: 2024-01-01 DOI:10.1155/2024/3067354
Natália Diel Boufleuer, Dimitris V Rados, Tatiana Zambonato, Clara K Maraschin, Beatriz D Schaan
{"title":"Severe Hypercalcemia Caused by Calcium-Alkali Syndrome after 15 Years of Postoperative Hypoparathyroidism in a Patient with Undiagnosed Hyperaldosteronism.","authors":"Natália Diel Boufleuer, Dimitris V Rados, Tatiana Zambonato, Clara K Maraschin, Beatriz D Schaan","doi":"10.1155/2024/3067354","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The triad of hypercalcemia, metabolic alkalosis, and acute kidney injury associated with ingesting high doses of calcium and absorbable bases characterizes the calcium-alkali syndrome. <i>Clinical Case</i>. We report the case of a patient with postthyroidectomy hypoparathyroidism 15 years ago due to differentiated thyroid cancer who presented with severe hypercalcemia. He had adequate control of calcemia for many years on treatment with calcitriol and calcium carbonate and hypertension treated with amlodipine, losartan, and hydrochlorothiazide. After a period of loss to follow-up, he suddenly presents with severe hypercalcemia, metabolic alkalosis, and loss of renal function. Upon hydration and withdrawal of calcitriol and calcium replacements, hypercalcemia resolved. The etiological investigation identified no granulomatous or neoplastic diseases, but an aldosterone-producing adrenal incidentaloma was found. The cause of hypercalcemia in this patient was calcium-alkali syndrome due to calcium carbonate replacement potentiated by hydrochlorothiazide and primary aldosteronism. Six months after the hospitalization and suspension of calcium and vitamin D, the patient returned to hypocalcemia, reinforcing the diagnosis.</p><p><strong>Conclusion: </strong>Although seldom described, the calcium-alkali syndrome is an expected complication for individuals with postoperative hypoparathyroidism, as they require lifelong calcium and vitamin D supplementation. This case also shows the importance of hydrochlorothiazide use and primary aldosteronism as possible triggers of life-threatening hypercalcemia.</p>","PeriodicalId":9621,"journal":{"name":"Case Reports in Endocrinology","volume":"2024 ","pages":"3067354"},"PeriodicalIF":0.9000,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10890900/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Case Reports in Endocrinology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/2024/3067354","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction: The triad of hypercalcemia, metabolic alkalosis, and acute kidney injury associated with ingesting high doses of calcium and absorbable bases characterizes the calcium-alkali syndrome. Clinical Case. We report the case of a patient with postthyroidectomy hypoparathyroidism 15 years ago due to differentiated thyroid cancer who presented with severe hypercalcemia. He had adequate control of calcemia for many years on treatment with calcitriol and calcium carbonate and hypertension treated with amlodipine, losartan, and hydrochlorothiazide. After a period of loss to follow-up, he suddenly presents with severe hypercalcemia, metabolic alkalosis, and loss of renal function. Upon hydration and withdrawal of calcitriol and calcium replacements, hypercalcemia resolved. The etiological investigation identified no granulomatous or neoplastic diseases, but an aldosterone-producing adrenal incidentaloma was found. The cause of hypercalcemia in this patient was calcium-alkali syndrome due to calcium carbonate replacement potentiated by hydrochlorothiazide and primary aldosteronism. Six months after the hospitalization and suspension of calcium and vitamin D, the patient returned to hypocalcemia, reinforcing the diagnosis.

Conclusion: Although seldom described, the calcium-alkali syndrome is an expected complication for individuals with postoperative hypoparathyroidism, as they require lifelong calcium and vitamin D supplementation. This case also shows the importance of hydrochlorothiazide use and primary aldosteronism as possible triggers of life-threatening hypercalcemia.

一名未确诊的高醛固酮症患者术后甲状旁腺功能减退 15 年后因钙-碱综合征引发的严重高钙血症
简介高钙血症、代谢性碱中毒和急性肾损伤是钙-碱综合征的三重特征,与摄入高剂量的钙和可吸收碱有关。临床病例。我们报告了一例 15 年前因分化型甲状腺癌导致甲状腺切除术后甲状旁腺功能减退的患者,他出现了严重的高钙血症。多年来,他使用降钙素三醇和碳酸钙治疗,血钙得到了充分控制,并使用氨氯地平、洛沙坦和氢氯噻嗪治疗高血压。经过一段时间的随访,他突然出现严重的高钙血症、代谢性碱中毒和肾功能丧失。在补充水分、停用降钙三醇和钙替代品后,高钙血症缓解。病因调查未发现肉芽肿或肿瘤性疾病,但发现了一个产生醛固酮的肾上腺偶发瘤。该患者高钙血症的病因是碳酸钙替代和原发性醛固酮增多引起的钙碱综合征。在住院并暂停服用钙剂和维生素 D 6 个月后,患者再次出现低钙血症,从而强化了诊断:钙-碱综合征虽然很少被描述,但却是术后甲状旁腺功能减退症患者的预期并发症,因为他们需要终身补充钙和维生素D。本病例还显示了使用氢氯噻嗪和原发性醛固酮增多症作为可能引发危及生命的高钙血症的诱因的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Case Reports in Endocrinology
Case Reports in Endocrinology ENDOCRINOLOGY & METABOLISM-
CiteScore
2.10
自引率
0.00%
发文量
45
审稿时长
13 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信