Multiple drugs interaction
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Acute hyperosmolar hyperglycaemic state: case report A 15-year-old boy developed acute hyperosmolar hyperglycaemic state (AHHS) following concomitant administration of itraconazole, prednisone, fluticasone-propionate, salmeterol/fluticasone-propionate and glucose [not all routes stated]. The boy, who had cystic fibrosis-related diabetes (CFRD), presented to the emergency department (ED) with a short history of lethargy, vomiting, nausea, hyperglycaemia and hyperosmolar without ketosis. Prior to the presentation, he was admitted at the age of 14.3 years, with a diagnosis of allergic bronchopulmonary aspergillosis (ABPA), and started receiving treatment with oral prednisone 40 mg/day, oral itraconazole 100 mg/day, fluticasone propionate [Flixotide] 125µg 2 puffs inhalation twice a day, salmeterol/fluticasone-propionate (25µg/125µg) [Seretide] and fluticasone-propionate [Flixonase] 50 µg/spray, 1 spray in each nostril twice a day. Concomitantly, he was receiving ceftazidime, tobramycin and other medications. During the admission, laboratory tests showed post-prandial hyperglycaemia at 17 mmol/L and glycosylated Hb (HbA1c) at 39 mmol/moL. He was discharged on insulin suspension isophane [isophane insulin]. On current presentation, he presented with a 24 hour history of lethargy, vomiting, nausea, headache and tremor. He reported 2 weeks of polyuria, polydipsia and nocturia. He had been drinking large volumes of an oral rehydration solution and high glucose drinks. Examination showed following: weight 49.2kg, mild dehydration, very irritable, Glasgow coma score 14/15, afebrile, HR 109 /minute, BP 135/90mm Hg, respiratory rate 24 /minute and oxygen saturations 99%. Investigations showed marked hyperglycaemia with serum glucose of 61 mmol/L and hyperosmolality at 339 mOsm/kg without significant ketosis or acidosis. He was diagnosed with AHHS, which was attributed to pharmacokinetic drug interaction between itraconazole, prednisone, fluticasone-propionate, salmeterol/fluticasone-propionate and glucose. Initially, the man’s dose of prednisone was decreased to 20 mg/day. IV fluid and insulin was administered with clinical and biochemical improvement. The dose of prednisone was further reduced to 10 mg/day, while itraconazole was continued. Insulin doses were steadily increased over the next 2 weeks. Subsequently, HbA1c increased to 84 mmol/moL. Afterwards, he was transferred to the tertiary hospital and doses of insulin were further increased. The dose of prednisone was reduced to 5 mg/day and itraconazole was discontinued. Thereafter, insulin sensitivity improved with frequent hypoglycaemia as well as serial reduction in insulin dose. Two months following discontinuation of itraconazole, blood glucose was well controlled. Two months later, a followup showed improvement in lung function. Forced expiratory volume (FEV1) and forced vital capacity (FVC) had increased. Bernhardt IT, et al. Acute hyperosmolar hyperglycaemic state in cystic fibrosis-related diabetes caused by glucocorticoid and itraconazole interaction. Jour
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