Normocalcemic primary hyperparathyroidism in a patient with severe osteoporosis receiving teriparatide
A 61-year-old, married lady, was referred to our Endocrine Clinic by a general practitioner, with a background of hypertension (untreated, since four years) and right hemi-thyroidectomy (performed 15 years ago for multinodular goiter), with complaints of persistent lower backache (non-radicular) and generalized severe body ache that had worsened after she was put on teriparatide (since four months). The teriparatide was started by the primary care physician for severe osteoporosis that was thought to be due to premature menopause (achieved at the age of 35 years). She was a vegetarian, non-smoker, non-ethanolic without any significant family history or drug history.\nExamination revealed a lady withdrawn in pain, weighing 61 kg, with a body mass index of 27.5 kg/m2. The blood pressure was 160/92 mm of Hg supine and 170/106 mm of Hg when sitting, without any postural fall. The proximal muscle weakness was 4/5 in all four limbs. General and systemic examination was otherwise normal.\nBiochemistry was unremarkable, except for mild hyponatremia (sodium 130 mmol/L) and elevated alkaline phosphatase 140 IU/L (50-136), which was associated with a corrected calcium of 9.7 mg/dl (calcium 10.1 mg/dL, albumin 4.5 gm %) and normal liver function. Although teriparatide therapy could possibly have accounted for these changes, we chose to look at her previous results, with a suspicion of a possible secondary cause for the elevated high alkaline phosphatase on the background of worsening symptoms.\nIt was noted that she had corrected calcium as high as 10.3 mg% on review of her previous results, which we thought was significantly elevated, especially as her diet was poor in calcium. Further enquiry suggested large volumes of fluid intake (free water) approximately 4-5 liters/day, which the patient put down to persistent thirst, which we considered to be secondary to polydipsia. The adrenal and thyroid screen (TSH: 1.14 mIU/ml) screen was normal\nSubsequent specialized testing revealed an elevated parathormone 166 pg/mL (11-54), insufficient vitamin D3 27 ng/L (11-42), and hypercalciurea (24-hour urine calcium 624 mg % (50-300 mg%)), and thus a PTH-dependant etiology for hypercalcemia was considered.\nPlain x-ray of the chest was normal. A s keletal survey revealed spondylolisthesis of L4 over L5, without any obvious fractures. Dual Energy X-Ray Absorptiometry (DEXA) densitometry showed a worsening T-score at the spine (T-scores, hip — 2.3, spine — 3.9, forearm — 4.5), compared to the previous results. The echocardiogram was consistent with evidence of systemic hypertension showing diastolic dysfunction with mild concentric left ventricular hypertrophy. A fundoscopy revealed evidence of early hypertensive changes.\nSpecialized imaging in the form of Doppler ultrasound of the neck suggested a mass at the inferior pole of the right lobe of the thyroid gland (most likely a parathyroid adenoma). The SESTAMIBI scan confirmed the presence of a right inferior parathyroid adenoma as localized by ultrasonography.\nA minimal invasive parathyroidectomy was undertaken. A mass 1.5 × 1.0 cm was removed that was consistent with parathyroid adenoma. Microscopy showed an encapsulated lesion composed of a diffuse proliferation of chief cells with surrounding delicate capillary network []. The patient continued to remain well with corrected calcium of 9.3 mg%, with a plan of yearly zolendronic acid infusions for a total of five infusions