title: Sleeping parathyroid tumor: rapid hyperfunction after removal of the dominant tumor.
abstract: BACKGROUND
  Due to frequent multiplicity of tumors in multiple endocrine neoplasia type 1, it may be difficult to decide when to stop a parathyroid exploration. A fall of intraoperative serum PTH by a certain percentage during parathyroid surgery is often used as one criterion for ending the operation.
  
  
  RESULTS
  We report two patients with primary hyperparathyroidism due to multiple endocrine neoplasia type 1 who had their first parathyroidectomy at the National Institutes of Health. In both cases, two and a half glands were removed, an extensive search was done for an occult parathyroid tumor, and intraoperative PTH decreased markedly to the lower limits of normal, suggesting a successful operation. Despite this, both patients became hypercalcemic within 3 d after the operation and showed persistent primary hyperparathyroidism. Detailed findings suggest the following course: chronic hypercalcemia had caused near total suppression of PTH secretion by an undiscovered parathyroid tumor (sleeping parathyroid tumor). When the hypercalcemia decreased after surgery due to the removal of the dominant parathyroid tumor(s), the abnormal yet previously suppressed tumor rapidly began to oversecrete PTH and thus caused postoperative hypercalcemia.
  
  
  CONCLUSIONS
  Even a fall of the intraoperative PTH to the lower limits of the normal range cannot guarantee that removal of all parathyroid tumors has been complete in cases with multiple tumors. These findings likely reflect strikingly differing PTH secretory functions among distinct tumors in the same patient, with hypercalcemia at least from a dominant tumor suppressing PTH secretion by one or more other parathyroid tumors.
authors.affiliation: Diabetes, Endocrine and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. sahzene.yavuz@nih.gov
authors.forename: Sahzene
authors.initials: S
authors.lastname: Yavuz
authors.forename: William F
authors.initials: WF
authors.lastname: Simonds
authors.forename: Lee S
authors.initials: LS
authors.lastname: Weinstein
authors.forename: Michael T
authors.initials: MT
authors.lastname: Collins
authors.forename: Electron
authors.initials: E
authors.lastname: Kebebew
authors.forename: Naris
authors.initials: N
authors.lastname: Nilubol
authors.forename: Giao Q
authors.initials: GQ
authors.lastname: Phan
authors.forename: Steven K
authors.initials: SK
authors.lastname: Libutti
authors.forename: Alan T
authors.initials: AT
authors.lastname: Remaley
authors.forename: Manuel
authors.initials: M
authors.lastname: Van Deventer
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Marx
mesh_terms: D000293:Adolescent; D005189:False Positive Reactions; D006801:Humans; D006934:Hypercalcemia / Q000097:blood / Q000503:physiopathology; D049950:Hyperparathyroidism, Primary / Q000097:blood / Q000503:physiopathology / Q000601:surgery; D008297:Male; D018761:Multiple Endocrine Neoplasia Type 1 / Q000097:blood / Q000503:physiopathology / Q000601:surgery*; D010281:Parathyroid Hormone / Q000097:blood; D010282:Parathyroid Neoplasms / Q000097:blood / Q000503:physiopathology / Q000601:surgery*; D016105:Parathyroidectomy / Q000009:adverse effects*; D011183:Postoperative Complications / Q000097:blood / Q000503:physiopathology*; D055815:Young Adult
chemical_list: D010281:Parathyroid Hormone