Suppressibility of parathyroid hormone in primary hyperparathyroidism.
OBJECTIVE
To describe an unusual case of pathologically confirmed primary hyperparathyroidism in a patient presenting with severe hypercalcemia and an undetectable parathyroid hormone (PTH) level.


METHODS
We present a detailed case report and outline the serial laboratory findings. In addition, the possible causes of low serum PTH levels in the setting of primary hyperparathyroidism are discussed.


RESULTS
A 16-year-old female patient presented with severe epigastric pain, found to be attributable to acute pancreatitis. At hospital admission, her serum calcium concentration was high (14.0 mg/dL); the patient also had a normal serum phosphorus level of 3.6 mg/dL and an undetectable PTH level (<0.2 pmol/L). An evaluation for non-PTH-mediated causes of hypercalcemia revealed a partially suppressed thyroid-stimulating hormone concentration and a below normal 1,25-dihydroxyvitamin D level, consistent with her suppressed PTH. One week after the patient was dismissed from the hospital, repeated laboratory studies showed a serum calcium value of 11.1 mg/dL, a serum phosphorus level of 2.8 mg/dL, and an elevated PTH concentration of 11.0 pmol/L, consistent with primary hyperparathyroidism. A repeated 1,25-dihydroxyvitamin D measurement was elevated. A parathyroid scan showed a parathyroid adenoma in the left lower neck area, and she subsequently underwent successful surgical resection of a pathologically confirmed parathyroid adenoma.


CONCLUSIONS
This case demonstrates that the serum PTH level can be suppressed in patients with primary hyperparathyroidism. Moreover, it emphasizes the need for careful evaluation of the clinical context in which the PTH measurement is determined. Consideration should be given to repeating measurement of PTH and serum calcium levels when the initial laboratory evaluation of hypercalcemia is unclear because dynamic changes in calcium metabolism may occur in the presence of secondary contributing factors.
Khoo
Teck-Kim
TK
Department of Internal Medicine and the Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic College of Medicine, Mayo Clinic Rochester, Rochester, Minnesota 55905, USA.
Baker
Claire H
CH
Abu-Lebdeh
Haitham S
HS
Wermers
Robert A
RA
D015746:Abdominal Pain; D000208:Acute Disease; D000236:Adenoma / Q000150:complications / Q000601:surgery; D000293:Adolescent; D000681:Amylases / Q000097:blood; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000097:blood / Q000209:etiology; D049950:Hyperparathyroidism, Primary / Q000097:blood / Q000175:diagnosis* / Q000209:etiology; D008049:Lipase / Q000097:blood; D009325:Nausea; D010195:Pancreatitis / Q000150:complications / Q000201:enzymology; D010281:Parathyroid Hormone / Q000097:blood*; D010282:Parathyroid Neoplasms / Q000150:complications / Q000601:surgery; D010758:Phosphorus / Q000097:blood; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood; D014839:Vomiting
D010281:Parathyroid Hormone; D014284:Triiodothyronine; D014807:Vitamin D; D010758:Phosphorus; C097949:1,25-dihydroxyvitamin D; D013972:Thyrotropin; D008049:Lipase; D000681:Amylases; D013974:Thyroxine