PDF(Pubmed)
Abstract：
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: It is essential to treat the underlying causes of hypocalcemia, which, in this case, were AA and hypoparathyroidism.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: It is essential to treat the underlying causes of hypocalcemia, which, in this case, were AA and hypoparathyroidism.
摘要：
■严重的低钙血症在危重患者中很常见。有不同的机制。据我们所知,没有关于在诊断再生障碍性贫血(AA)时急性出现低钙血症的数据.本病例报告的目的是描述危重AA患者的甲状旁腺功能减退伴严重低钙血症的病例。
■一名60岁男子出现严重的低钙血症，钙水平为6.1mg/dL（参考范围，8.6-10.3mg/dL）和甲状旁腺功能减退，甲状旁腺激素水平为11pg/mL（参考范围，12-88pg/mL)。他发展了由新诊断的AA及其并发症引起的危急状态，例如血小板值急性下降到2×103/cmm的极低水平，并发中性粒细胞减少性发热和下消化道出血。AA开始免疫抑制治疗后，他的甲状旁腺激素-钙代谢改善并保持稳定,但未完全恢复正常.
■在我们的病人中，甲状旁腺功能减退症伴低钙血症可能是由AA患者中细胞因子相关的钙敏感受体上调引起的。另一方面,考虑到初始低钙血症的严重程度，并且在AA治疗开始后钙稳态仅有部分改善，伴有残留的轻度低钙血症，自身免疫性原因不能完全排除,细胞因子介导的和自身免疫原因的组合也不可能。
■治疗低钙血症的根本原因至关重要，which,在这种情况下,是AA和甲状旁腺功能减退。
■一名60岁男子出现严重的低钙血症，钙水平为6.1mg/dL（参考范围，8.6-10.3mg/dL）和甲状旁腺功能减退，甲状旁腺激素水平为11pg/mL（参考范围，12-88pg/mL)。他发展了由新诊断的AA及其并发症引起的危急状态，例如血小板值急性下降到2×103/cmm的极低水平，并发中性粒细胞减少性发热和下消化道出血。AA开始免疫抑制治疗后，他的甲状旁腺激素-钙代谢改善并保持稳定,但未完全恢复正常.
■在我们的病人中，甲状旁腺功能减退症伴低钙血症可能是由AA患者中细胞因子相关的钙敏感受体上调引起的。另一方面,考虑到初始低钙血症的严重程度，并且在AA治疗开始后钙稳态仅有部分改善，伴有残留的轻度低钙血症，自身免疫性原因不能完全排除,细胞因子介导的和自身免疫原因的组合也不可能。
■治疗低钙血症的根本原因至关重要，which,在这种情况下,是AA和甲状旁腺功能减退。
