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Endocrine Abstracts (2020) 70 EP61 | DOI: 10.1530/endoabs.70.EP61

ECE2020 ePoster Presentations Bone and Calcium (65 abstracts)

A case of primary hyperparathyroidism presenting with acute pancreatitis

Bengur Taskiran 1 , ertaç berker 1 , Dilek Beypinar 2 , Mehmet Fatih Ekici 3 , Sami Evirgen 4 & Kevser Onbasi 1


1Endocrinology, Kutahya University of Health Sciences, Kutahya, Turkey; 2Pathology, Eskisehir Osmangazi University, Eskisehir, Turkey; 3General Surgery, Kutahya University of Health Sciences, Kutahya, Turkey; 4Gastroenterology, Kutahya University of Health Sciences, Kutahya, Turkey


A 42 year old male patient was admitted to the gastroenterology unit in due to severe abdominal pain and vomiting. He denied any chronic illness and drug usage. His family history was nonsignificant for any endocrine disease. Based on biochemical studies (lipase 2280 U/l, calcium 15.0 mg/dl, phosphorus 1.7 mg/dl amylase 631 U/l, creatinine 1.16 mg/dl, ALP 735 U/l) severe hypercalcemia induced acute pancreatitis was the diagnosis. 25 OH vitamin D was 5 ng/ml and parathyroid hormone level was 2496 pg/ml, Electrolytes, liver function tests, billlirubin, CBC differential, lipid profile, Calcitonin, and TSH level were in the normal range. A left-sided atypical mass (10 mm; 17 HU on non-contrast series, 45 HU on early and 82 HU on delayed contrast enhanced series) and renal stones were detected on abdominal CT. Mild osteopenia was evident on DEXA. Neck ultrasound revealed a heterogenous hypoechoic mass with increased vascularity and measuring 34×20 mm in size in the right parathyroid lodge. Calcium level normalized after zoledronic acid administration. Calcitonin was unavailable. When diagnostic work-up was underway, severe hypercalcemia ensued again. It could not be controlled with hydration and 160 mg/day furosemide, so a second dose of zoledronic acid was administered. Mildly elevated (<x1.5 UNL) urinary catecholamine levels in 7.5 l 24 h urine was at first attributed to polyuria. Polyuria was resulted from nephrogenic diabetes insipidus induced by hypercalcemia, hydration, and forced diuresis. However since an atypical adrenal mass was present and severe hypercalcemia ensued shortly after zoledronic acid therapy, we could not spend any time for repeating catecholamine tests or performing scintigraphy such as DOTATE/MIBG. Such a small lesion (10 mm) might have been invisible on scintigraphy. We diagnosed pheochromocytoma unless proven otherwise and alpha blocker therapy was commenced. The patient underwent parathyroidectomy and unilateral adrenalectomy at the same session without any peri- and post-operative complication. Following parathyroidectomy, calcium and parathyroid hormone reached a nadir of 7.5 mg/dl and 14 pg/ml, respectively (albumin 3.6 g/dl, phosphorus 2.2 mg/dl, magnesium 1.5 mg/dl). The final pathological report whether the adrenal lesion was a pheochromocytoma and the parathyroidal lesion was an atypical parathyroid adenoma or carcinoma are pending. Genetic tests for MEN are planned. Our case was challenging in terms of timing and decision of operation. Relatively young age and absence of any accompanying chronic disease probably helped to tackle potential complications including severe hypercalcemia, acute pancreatitits, and simultaneous extraction of adrenal mass and parathyroid adenoma.

Volume 70

22nd European Congress of Endocrinology

Online
05 Sep 2020 - 09 Sep 2020

European Society of Endocrinology 

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