12597 Undetectable Intact Pth - Can It Still Be Due To Primary Hyperparathyroidism?

Abstract Disclosure: S.S. Bantu: None. R.S. Rosenthal: None. Introduction: Primary hyperparathyroidism (PHPT) is the most common cause of hypercalcemia. It is caused by increased levels of parathyroid hormone (PTH) from the parathyroid glands. There is a shift in the clinical presentation of PHPT from symptomatic disease to asymptomatic presentation, due to the inclusion of calcium in basic metabolic panel. We present a patient who had hypercalcemia with undetectable PTH due to PHPT caused by parathyroid adenoma. PTH levels were detectable with resolution of hypercalcemia and improvement in symptoms after the parathyroidectomy. Very few case reports have been reported of PHPT with low or suppressed intact PTH. Case: 66-year-old female with history of hyperlipidemia, hypothyroidism, hypertension, obstructive sleep apnea who was referred for evaluation of hypercalcemia noted on basic metabolic panel. She complained of fatigue, body aches, insomnia and denied any calcium supplements. Calcium 11.1mg/dl, albumin 4.2gm/dl, PTH <1pg/ml, vitamin D 39ng/ml, ionized calcium 1.46 mMol/L, phosphorus 2.6mg/dl, magnesium 2.3mg/dl, PTHrP 0.7pMol/L. After ruling out other causes of hypercalcemia, parathyroid ultrasound showed 1.8 x 1.3 x 1.1cm right inferior parathyroid adenoma. Sestamibi scan showed an approximately 1.5x 1cm lesion in the right inferior parathyroid region confirming the adenoma. A trial of calcitonin was done to make sure it is PHPT to which she responded. Surgery was done with removal of the right inferior parathyroid gland. Intraoperative PTH was done at 5, 10, 15 mins after the removal of the gland which was still undetectable at 1pg/ml. Pathology showed hypercellular parathyroid of 1927mg. Post operatively her symptoms improved with resolution of hypercalcemia and her PTH was detectable at 15.8pg/ml. Discussion: This patient presented as a diagnostic challenge with hypercalcemia, undetectable PTH and parathyroid adenoma. Serial dilutions of the intact PTH were done which didn’t show the hook effect. Undetectable PTH in our case could be explained by the secretion of a mutated form of the intact PTH molecule by the parathyroid adenoma suggesting post-translational change in the molecule that is not measurable by the current assays but still it exerts it effect on the PTH receptor. Our report highlights that PHPT should be considered even in the setting of undetectable serum PTH. More research is needed to study the identification and measurement of the post-translational changes in the intact molecule of the PTH. Presentation: 6/2/2024