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Hypocalcemia and Hypoparathyroidism Associated With Critical Illness and Aplastic Anemia.
Tselovalnikova, Tatiana; Jadhav, Kavita; Foxworth, John; Cabandugama, Peminda K; Galustian, Sophia; Drees, Betty M.
Afiliación
  • Tselovalnikova T; Department of Internal Medicine, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
  • Jadhav K; Department of Internal Medicine, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
  • Foxworth J; Associate Dean Academic Enrichment, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
  • Cabandugama PK; Associate Program Director for Research, Internal Medicine Residency Program, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
  • Galustian S; Clinical Pharmacology Section, Department of Internal Medicine, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri.
  • Drees BM; Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic, Cleveland, Ohio.
AACE Clin Case Rep ; 10(4): 156-159, 2024.
Article en En | MEDLINE | ID: mdl-39100634
ABSTRACT
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.

Conclusion:

It is essential to treat the underlying causes of hypocalcemia, which, in this case, were AA and hypoparathyroidism.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: AACE Clin Case Rep Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: AACE Clin Case Rep Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos