A 32 year old manual labourer who is not on long term treatment for any medical comorbidities, presented to our medical unit with fever, headache and arthralgia of 3 days duration. Towards the latter part of the third day he has noticed tetany/carpal spasms of both hands which brought him to the hospital. On inquiry he denied any perioral or fingertip paresthesia. He had no symptoms to suggest a respiratory, gastrointestinal or genitourinary focus of infection. There was no photo/phonophobia or history of seizures or muscle cramps.
He has undergone surgery for bilateral posterior subcapsular cataract at the age of 30 years for which the cause has not been previously evaluated. Although he had experienced several episodes of febrile illnesses during his lifetime, he has never experienced carpal spasms along with any febrile illness before. He did not give any past history of any neck or thyroid surgeries or irradiation. He was not on any long term medications and there was no significant history of familial illnesses.
On examination he was short with a height of 142 cm with normal upper and lower body proportions. He was febrile with a viral exanthem involving the upper trunk. He was not overtly anxious or hyperventilating. Notably he was having bilateral carpal spams with positive Chvostek sign. Trousseau sign was negative. His vitals including the blood pressure were stable. No other skeletal deformities such as scoliosis or short metacarpals were noted.
Cardiovascular, respiratory and abdominal examination revealed no abnormality. Fundal examination did not reveal papilloedema and there was no significant muscle weakness or hyper-reflexia on examination of the motor system.
With the ongoing dengue epidemic in Sri Lanka, dengue fever was suspected and an urgent full blood count and serum ionized calcium level were ordered on admission as the patient had carpal spasms.
The full blood count was suggestive of an ongoing viral illness with leucopenia (3.2 × 109/l) and thrombocytopenia (105 × 109/L) and thus he was tentatively diagnosed as a possible case of dengue fever. Serum ionized calcium level was 0.62 mmol/l, which was considerably below the reference level (1.05–1.30 mmol/L). Calcium was replaced urgently with intravenous 10% calcium gluconate which relieved the patient of his hypocalcemic symptoms. ECG obtained later did not show any rhythm abnormalities or hypocalcemic changes. He was given regular intravenous 10% calcium gluconate (six hourly) to keep the serum ionized calcium levels within normal limits during the acute illness and daily serum ionized calcium levels were monitored.
Further work up was done to evaluate his hypocalcaemia while the patient was monitored and managed as for dengue fever according to the national guidelines for dengue fever management. Twice daily full blood counts were carried out to monitor the course of dengue fever.
His baseline renal and liver functions tests were normal except for slightly raised aspartate aminotransferase (AST) (92 μ/l, range 10–40 μ/l) and alanine aminotransferase (ALT) (87 μ/l, range 7–56 μ/l) levels and was attributed to the ongoing viral illness, which later came down to the baseline normal levels. Serum magnesium (0.9 mmol/l, range 0.8–1.1 mmol/l), alkaline phosphatase (ALP) (109 U/l, range 100–360 U/l) and 25-hydroxy vitamin D level were within normal limits.
Serum inorganic phosphate level was slightly elevated (1.6 mmol/l, range 0.8–1.5 mmol/l) and at this point hypoparathyroidism or pseudohypoparathyroidism needed to be excluded and the intact PTH level was obtained which was significantly low/undetectable (< 2.5 pg/ml, range 14–72 pg/ml).
Non contrast computed tomography (NCCT) scan of the brain revealed multiple basal ganglia, subcortical and cerebellar calcifications (Fig. 1).
He did not demonstrate clinical or biochemical features of addison’s disease or mucocutaneous candidiasis to suggest that his hypoparathyroidism was part of an autoimmune polyglandular syndrome (Type 1) and there was no family history of conditions related to autoimmune polyglandular syndrome (Type 1). Nor did he demonstrate any specific syndromic features to suggest an underlying genetic disorder. Genetic analysis with regard to genetic hypoparathyroidism could not be carried out as facilities for such testing was not available in the country at the time of reporting.
Rest of the endocrine profile including thyroid stimulating hormone, free thyroxin, follicular stimulating hormone, luteinizing hormone and random 9 a.m. cortisol levels were normal.
His platelet count dropped to a minimum of 82 × 109/l on day 5 of his febrile illness after which defervescence occurred with rising platelet and white blood cell counts over the next few days. He made an uneventful recovery without any features of dengue fluid leakage and by day 8 of his acute illness his platelet count rose up to 162 × 109/l and had a normal serum ionized calcium level of 1.1 mmol/l. Dengue IgM/IgG serology done on day 8 of illness was positive which confirmed the initial diagnosis of dengue fever.
Following recovery from dengue fever he was started on regular oral calcium replacement therapy in the form of calcium carbonate along with one alfa cholecalciferol.
Patient was discharged from the hospital on oral calcium supplementation with the follow up plan of regular monitoring of serum calcium and 24 h urinary calcium excretion levels.
