Case presentation
A 19-year-old woman was admitted with low-grade fever and myoclonus in February 2021. She had sought medical attention 40 days before her admission because of delayed menstruation treated with dydrogesterone. After two days, she experienced a diffuse erythematous rash on her face and was treated with an antihistamine. However, no improvement was observed, and she developed fever and myoclonic movements. On admission, she had an erythematous rash across the nose and cheek and myoclonic movements in the tongue and lower limbs. Their body temperature was 37.8˚C. Other vital signs were in the normal range. Trousseau’s and Chvostek’s signs were positive. She had no remarkable past medical and family history. Initial laboratory tests showed normochromic normocytic anemia, leukopenia, and hypocalcemia (Table 1). Electrocardiography revealed a prolonged QT interval. Treatment of hypocalcemia was started with calcium gluconate infusion and was continued with calcium carbonate (1200 mg elemental calcium daily) and calcitriol (1 microgram daily) orally. Serial serum calcium levels during treatment were: 5.5 (0.6), 5.5 (0.7), 7.8 (0.95), 7.9 (0.91), 8 (0.95), and 8.8 (1.01) mmol/L total (ionized calcium). The tests were requested with the possibility of hypoparathyroidism secondary to autoimmune diseases (Table 1). Thyroid ultrasound showed a large heterogeneous thyroid consisting of many hypoechoic nodules (Hashimoto type).
Brain magnetic resonance imaging was normal.SLE was diagnosed based on the malar rash, pancytopenia, positive anti-nuclear antibody (ANA), positive anti-dsDNA, and low serum complement levels. The patient was treated with prednisolone 30 mg/d and hydroxychloroquine 5 mg/kg/d. Due to severe hypocalcemia, average phosphorus, and low parathyroid hormone (PTH), hypoparathyroidism was diagnosed as the cause of the patient’s hypocalcemia. In our opinion, autoimmune damage to parathyroid glands was the best explanation for hypoparathyroidism in this patient, given no history of surgery or irradiation in the neck, negative family history, absence of other genetic disorders, and underlying SLE disease. According to high TSH level, standard T4 and T3, and high anti-thyroid peroxidase antibody (anti-TPO), the diagnosis of sub-clinical Hashimoto’s thyroiditis was also made.