Calcium
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Hypercalcaemia: case report A 14-year-old girl developed hypercalcaemia during treatment with calcium for hypoparathyroidism [dosages not stated]. The girl presented with recurrent panic attacks associated with poor school performance for about 8 weeks. The attacks occurred mainly at school and lasted up to 30 minutes with dyspnoea, intermittent eyes crossing and stiffening of primarily her right arm. Complete recovery took about 5 minutes. She also reported intermittent "bone aches" and bad headaches that worsened in the morning. Head MRI was normal. Her medical history was notable for poor tooth mineralisation and recurrent candida vaginitis. Menarche occurred at 12 years of age, with persistent irregular cycles. She reported no improvement in her panic attacks after 3 months psychiatry therapy, which included 2-week trial of oral paroxetine [Paxil] 10mg tablet every morning, as prescribed by her family physician off-label at that time for paediatric use. Her physical examination was grossly normal, except for eye twitching. As her family physician was about to adjust her paroxetine at the recommended 2-week interval, her blood tests revealed severe hypocalcemia. Her family physician discontinued paroxetine, and requested hospitalisation for further management. Workup was consistent with primary hypoparathyroidism. During hospitalisation, she responded to IV calcium, without complications and was transitioned to oral calcium along with concomitant calcitriol [Rocatrol]. She was diagnosed with an anxiety disorder, based on Diagnostic and Statistical Manual of Mental Disorders criteria prior to her hypoparathyroidism diagnosis. On discharge, serum calcium was 7.5 mg/dL. Her parathyroid-directed antibodies returned consistent with autoimmune hypoparathyroidism. The family was informed of rare possibility for additional autoimmune endocrine and immune system dysfunction. Following 4 months of hypoparathyroidism therapy, she presented with vomiting and dehydration. Laboratory work showed hypercalcaemia. Supplemental oral calcium was discontinued. However, over the next 4 weeks, the girl’s calcium continued to increase. She was re-hospitalised. Investigations confirmed underlying primary adrenal deficiency. Despite severe cortisol and mild aldosterone deficiencies, her electrolytes and blood glucose levels remained within normal limits, except for transient hypercalcaemia. Her GI complaints and hypercalcemia resolved within a few days with IV hydration and start of daily hydrocortisone [Cortef] and fludrocortisone [Florinef]. Oral calcium was re-initiated. The girl’s underlying triad of hypoparathyroidism, adrenal insufficiency and candidiasis were consistent with a genetic mutation subtype of autoimmune polyglandular syndrome (APS), likely type-1 (APS-1) or autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy. Blood sent for high-resolution genetic assessment, returned homozygous for known APS-1 deletion of nucleotides 1094-1106 on chromosome 21 at 21q22.3.7-9. Paediatric endocrine service followed her
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