与危重病和再生障碍性贫血有关的低钙血症和甲状旁腺功能减退症

Q3 Medicine

AACE Clinical Case Reports Pub Date : 2024-07-01 DOI:10.1016/j.aace.2024.04.007

Tatiana Tselovalnikova MD, PhD , Kavita Jadhav MD, FACP , John Foxworth PharmD , Peminda K. Cabandugama MD, DABOM , Sophia Galustian MD , Betty M. Drees MD, FACP, FACE

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引用次数: 0

摘要

背景/目的严重低钙血症在重症患者中很常见。其发病机制各不相同。据我们所知，目前还没有关于再生障碍性贫血（AA）诊断时出现急性低钙血症的数据。病例报告一名60岁的男性患者出现严重低钙血症，血钙水平为6.1毫克/分升（参考范围：8.6-10.3毫克/分升），甲状旁腺功能减退，甲状旁腺激素水平为11皮克/毫升（参考范围：12-88皮克/毫升）。新确诊的 AA 及其并发症导致他病情危重，如血小板值急剧下降至 2 × 103/cmm 的极低水平，并伴有中性粒细胞减少性发热和下消化道出血。在开始对AA进行免疫抑制治疗后，他的甲状旁腺激素-钙代谢情况有所改善并保持稳定，但并未完全恢复正常。另一方面，鉴于最初低钙血症的严重程度，以及在开始治疗AA后，钙稳态仅得到部分改善，但仍存在轻度低钙血症，因此不能完全排除自身免疫原因，也不能排除细胞因子介导的原因和自身免疫原因的结合。

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Hypocalcemia and Hypoparathyroidism Associated With Critical Illness and Aplastic Anemia

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.

Case Report

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 × 10³/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.

Discussion

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.