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Case Report: Unusual electrolyte changes in primary hyperparathyroidism-a call to suspect underlying Gitelman
Dasili Wickramasinghe Aruna Shantha1, Sasmitha Ravindu Waidyatilleke1, Kanishka Piumi Senevirathne1
1Department of Medicine, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka.
Background:
Primary hyperparathyroidism (PHPT) is commonly associated with hypercalcemia, hypophosphatemia, and hypercalciuria. Hypokalemia and hypomagnesemia are rare and indicate a complicated etiology.
Case Presentation:
We describe a 74-year-old woman who presented with metabolic encephalopathy and moderate dehydration. Biochemical examinations revealed a parathyroid crisis with severe hypercalcemia (4.18 mmol/L), hypophosphatemia, hypokalemic (2.5 mmol/L) metabolic alkalosis, severe hypomagnesemia (0.23 mmol/L), and a high level of intact parathyroid hormone (243.0 pg/mL). The electrolyte imbalances were resistant to proper hydration and electrolyte replacement. Markedly, urine analysis showed renal potassium and magnesium wasting and severe hypocalciuria (calcium-to-creatinine clearance ratio, 0.0093). The presence of this paradoxical hypocalciuria despite PHPT brought into question the possibility of an underlying renal tubulopathy or accompanying vitamin D deficiency. Vitamin D assay showed deficiency with a level of 14.2 ng/mL. Ultrasound neck and contrast-enhanced computed tomography of the neck showed a right thyroid lesion for which the patient underwent right hemithyroidectomy and parathyroidectomy. Histopathological examination revealed a parathyroid adenoma. Although the patient's hypercalcemia settled postoperatively, hypomagnesemia persisted despite vitamin D supplementation, which indicates the presence of underlying renal tubulopathy, likely Gitelman syndrome.
Conclusion:
This case emphasizes that persistent hypokalemia, hypomagnesemia, and unexpected hypocalciuria in patients with PHPT should prompt clinicians to suspect concurrent renal tubulopathies such as Gitelman syndrome.
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