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.