AACE clinical case reports · 2020
HYPERCALCEMIC PATIENT DIAGNOSED WITH PRIMARY HYPERPARATHYROIDISM AFTER DAPAGLIFLOZIN TREATMENT.
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Akhanlı Pınar, Hepsen Sema, Ucan Bekir, Saylam Güleser, Cakal Erman
Аннотация
OBJECTIVE: Hypercalcemia associated with the use of sodium-glucose transporter-2 (SGLT-2) inhibitors is very rare. Only 2 cases have been reported in the current literature. In these cases hypercalcemia occurred with the use of SGLT-2 inhibitors taken with thiazides and excessive calcium salts. We present a case of hypercalcemia and primary hyperparathyroidism diagnosed after dapagliflozin treatment.
METHODS: We describe the medical history, laboratory test results, parathyroid ultrasound, 4-dimensional computed tomography-magnetic resonance imaging, and histopathology findings of the patient.
RESULTS: A 49-year-old man with 5-year history of type 2 diabetes mellitus was found to have hypercalcemia with corrected calcium of 11.28 mg/dL (reference range [RR] is 8.8 to 10.6 mg/dL) 6 months after starting dapagliflozin. Previous records showed normocalcemia for many years. Parathyroid hormone level was 70.8 pg/mL (RR is 15 to 65 pg/mL) and 24-hour urinary calcium excretion level was 492 mg/day (RR is 100 to 300 mg/day). On parathyroid ultrasound, a 4 × 9 × 14-mm hypoechoic lesion inferior to the right thyroid lobe was detected. A 15 × 10 × 9-mm oval lesion was observed in the right paratracheal area. A lesion at T1 vertebra level was also seen on 4-dimensional computed tomography-magnetic resonance imaging. The patient underwent lower right parathyroidectomy. Histopathology confirmed the diagnosis of parathyroid adenoma. The patient was asymptomatic 3 months after the operation with a normal corrected calcium level of 9.2 mg/dL.
CONCLUSIONS: SGLT-2 inhibitors could have unmasked an underlying mild hyperparathyroidism, as they can increase predisposition to hypercalcemia when used with medications causing it. Volume depletion caused by SGLT-2 inhibitors may also contribute to hypercalcemia. For these reasons, calcium levels should be monitored in patients taking SGLT-2 inhibitors.
METHODS: We describe the medical history, laboratory test results, parathyroid ultrasound, 4-dimensional computed tomography-magnetic resonance imaging, and histopathology findings of the patient.
RESULTS: A 49-year-old man with 5-year history of type 2 diabetes mellitus was found to have hypercalcemia with corrected calcium of 11.28 mg/dL (reference range [RR] is 8.8 to 10.6 mg/dL) 6 months after starting dapagliflozin. Previous records showed normocalcemia for many years. Parathyroid hormone level was 70.8 pg/mL (RR is 15 to 65 pg/mL) and 24-hour urinary calcium excretion level was 492 mg/day (RR is 100 to 300 mg/day). On parathyroid ultrasound, a 4 × 9 × 14-mm hypoechoic lesion inferior to the right thyroid lobe was detected. A 15 × 10 × 9-mm oval lesion was observed in the right paratracheal area. A lesion at T1 vertebra level was also seen on 4-dimensional computed tomography-magnetic resonance imaging. The patient underwent lower right parathyroidectomy. Histopathology confirmed the diagnosis of parathyroid adenoma. The patient was asymptomatic 3 months after the operation with a normal corrected calcium level of 9.2 mg/dL.
CONCLUSIONS: SGLT-2 inhibitors could have unmasked an underlying mild hyperparathyroidism, as they can increase predisposition to hypercalcemia when used with medications causing it. Volume depletion caused by SGLT-2 inhibitors may also contribute to hypercalcemia. For these reasons, calcium levels should be monitored in patients taking SGLT-2 inhibitors.