Tselovalnikova Tatiana, Jadhav Kavita, Foxworth John, Cabandugama Peminda K, Galustian Sophia, Drees Betty M
Department of Internal Medicine, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
Associate Dean Academic Enrichment, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
AACE Clin Case Rep. 2024 May 3;10(4):156-159. doi: 10.1016/j.aace.2024.04.007. eCollection 2024 Jul-Aug.
BACKGROUND/OBJECTIVE: Severe hypocalcemia is common in critically ill patients. There are different mechanisms. To our knowledge, there are no data about the acute presentation of hypocalcemia at the time of diagnosis of aplastic anemia (AA). The objective of this case report was to describe the case of hypoparathyroidism with severe hypocalcemia in a critically ill patient with AA.
A 60-year-old man presented with severe hypocalcemia with a calcium level of 6.1 mg/dL (reference range, 8.6-10.3 mg/dL) and hypoparathyroidism with a parathyroid hormone level of 11 pg/mL (reference range, 12-88 pg/mL). He developed a critical state caused by newly diagnosed AA and its complications, such as an acute decrease in the platelet value to a critically low level of 2 × 10/cmm, complicated by neutropenic fever and lower gastrointestinal bleeding. After the initiation of immunosuppressive therapy for AA, his parathyroid hormone-calcium metabolism improved and remained stable but did not normalize completely.
In our patient, hypoparathyroidism with hypocalcemia may have been caused by cytokine-related upregulation of the calcium-sensing receptor in the setting of AA. On the other hand, given the severity of the initial hypocalcemia and only partial improvement in calcium homeostasis with residual mild hypocalcemia after treatment initiation for AA, autoimmune causes cannot be entirely ruled out, nor could a combination of cytokine-mediated and autoimmune causes.
It is essential to treat the underlying causes of hypocalcemia, which, in this case, were AA and hypoparathyroidism.
背景/目的：严重低钙血症在危重症患者中很常见，其机制多样。据我们所知，目前尚无关于再生障碍性贫血（AA）诊断时低钙血症急性表现的数据。本病例报告的目的是描述一名患有AA的危重症患者发生甲状旁腺功能减退伴严重低钙血症的病例。
一名60岁男性，血钙水平为6.1mg/dL（参考范围8.6 - 10.3mg/dL），诊断为严重低钙血症，甲状旁腺激素水平为11pg/mL（参考范围12 - 88pg/mL），诊断为甲状旁腺功能减退。他因新诊断的AA及其并发症而处于危急状态，如血小板值急剧下降至极低水平2×10/cmm，并伴有中性粒细胞减少性发热和下消化道出血。在开始针对AA的免疫抑制治疗后，他的甲状旁腺激素 - 钙代谢有所改善并保持稳定，但未完全恢复正常。
在我们的患者中，甲状旁腺功能减退伴低钙血症可能是由AA情况下细胞因子相关的钙敏感受体上调引起的。另一方面，鉴于初始低钙血症的严重程度以及在开始针对AA治疗后钙稳态仅部分改善且仍残留轻度低钙血症，自身免疫性病因不能完全排除，细胞因子介导和自身免疫性病因的组合也不能排除。
治疗低钙血症的根本原因至关重要，在本病例中，根本原因是AA和甲状旁腺功能减退。
