Endocrine Abstracts

A 49-year-old lady was referred to the endocrine clinic for hypophosphataemia. Apart from tiredness, she had no other symptoms. Past medical history was significant for bronchiectasis, obstructive sleeps apnoea, caudaequina syndrome, migraine and anxiety. She had frequent hospitalisations due to bronchiectasis exacerbations requiring systemic steroids. Usual medications included azithromycin, gabapentin, omeprazole, antacids, laxatives, carbocisteine, fluoxetine, montelukast, propranolol and inhaled formoterol and budesonide. She drank at least 16 pints of milk every week, did not drink alcohol in excess and stopped smoking two years ago. Examination was unremarkable with negative Chvostek sign, no proximal myopathy and no evidence of endocrine disease. Body mass index was raised in the overweight range. Phosphate levels were persistently low for the last two years, with the lowest recorded at 0.15 mmol/l during hospital admissionrequiring intravenous phosphate replacement. Calcium and other bone biochemistry were normal. 25-hydroxy Vitamin D level was 61 nmol/l and she was commenced on oral cholecalciferol 1000 IU/day. Urine tests did not suggest renal potassium loss. She was maintained on oral phosphate replacement on outpatient basis as she was not keen to stop PPI and antacids. Phosphate is a molecular element critical to normal cellular function. Intestines, kidneys and bones are important in phosphate homoeostasis. Hypophosphataemia is caused by inadequate phosphate intake, reduced intestinal absorption, increased renal excretion, phosphate shift from extracellular to intracellular space or a combination of above mechanisms. In our case, hypophosphataemiawas thought to be caused by PPI and antacids, frequent use of steroids, frequent hospital admissions, and intermittent under-nutrition and feeding (‘fast and feast’). Severe and/or symptomatic cases need intravenous replacement as generalised muscular weakness, rhambdomyolysis and acute kidney injury are potential complications. Mild cases may not present with any symptoms but it is important to explore the cause and replace phosphate orally as prolonged hypophosphatemia can lead to osteoporosis or osteomalacia due to reduced bone mineralisation and there are no contraindications of oral phosphate replacement.