Summary
Inhaled corticosteroids (ICS) are established as a cornerstone of management for patients with bronchoconstrictive lung disease. However, systemic absorption may lead to suppression of the hypothalamic–pituitary–adrenal (HPA) axis in a significant minority of patients. This is more likely in ‘higher risk’ patients exposed to high cumulative ICS doses, and in those treated with frequent oral corticosteroids or drugs which inhibit cytochrome p450 3A4. Hypothalamic–pituitary–adrenal axis suppression is frequently unrecognized, such that some patients, notably children, only come to light when an adrenal crisis is precipitated by physical stress. To minimize this risk, ‘higher risk’ patients and those with previously identified suppressed cortisol responses to Synacthen testing should undergo an education programme to inform them about sick day rules. A review of ICS therapy should also be undertaken to ensure that the dose administered is the minimum required to control symptoms.
Background: Vitamin D deficiency is increasingly recognized in patients with primary hyperparathyroidism but some clinicians are reluctant to replace vitamin D due to concerns with aggravating hypercalcaemia. We investigated the impact of vitamin D repletion in asymptomatic patients with normocalcaemic and hypercalcaemic primary hyperparathyroidism. Methods: This is a retrospective analysis of 111 patients with elevated parathyroid hormone concentrations (>6.4 pmol/L) referred to our endocrine clinic between January and December 2012; we identified 39 patients with primary hyperparathyroidism and vitamin D deficiency, i.e. 25 hydroxy vitamin D <20 mg/L. Patients were categorized into normocalcaemic (n ¼ 23) and hypercalcaemic (n ¼ 16) groups and the impact on biochemical parameters was recorded after at least six months treatment with either 1600 or 3200 units daily of cholecalciferol. Results: Both normocalcaemic and hypercalcaemic groups showed a rise in 25 hydroxy vitamin D concentrations after replacement (p <0.0001). Parathyroid hormone concentrations fell in the normocalcaemic group (p ¼ 0.08) but individually, five patients showed a rise (8-38% of baseline). In the hypercalcaemic group, parathyroid hormone remained static but the adjusted calcium concentration fell significantly (p ¼ 0.006) except in two patients who showed mild rises (3 and 6%, respectively). There was no deterioration in renal function or calcium-related adverse events in any of the groups. Conclusions: Our study supports the safety of vitamin D replacement in patients with mild asymptomatic primary hyperparathyroidism and coexistent vitamin D deficiency. Repletion does not aggravate hypercalcaemia and may limit disease progression. Patients with normocalcaemic primary hyperparathyroidism need further characterization from longitudinal studies.
A day 1 post-operative early morning cortisol is a useful tool to predict adrenal reserve post-pituitary surgery, enabling clinicians to avoid unnecessary blanket glucocorticoid replacement.
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