Inhaled corticosteroids (ICS) are common medications, used in respiratory medicine for controlling conditions such as asthma and other obstructive airway diseases. The systemic effects of oral corticosteroids are well known and established; inhaled steroids have been known to cause relatively minor and localized adverse effects such as oral candidiasis. However, less attention has been paid to their systemic effects. Although currently there is a paucity of prospective studies demonstrating the systemic effects of inhaled corticosteroids, there are numerous retrospective studies adding evidence to this link. Inhaled corticosteroids can affect the hypothalamo-pituitary-adrenal axis, bone density and growth, eyes, skin and immunity including an increased risk of pneumonia. Clinicians are recommended to aim for the lowest possible dose to avoid these systemic side effects. Fluticasone is more likely to cause systemic effects compared to budesonide. Newer ICS molecules such as ciclesonide may be more beneficial in reducing such systemic complications on prolonged use. This paper provides an updated overview of the common systemic effects encountered with ICS treatment.

Prognosis and appropriate treatment goals for older adults with diabetes vary greatly according to frailty. It is now recognised that changes may be needed to diabetes management in some older people. Whilst there is clear guidance on the evaluation of frailty and subsequent target setting for people living with frailty, there remains a lack of formal guidance for healthcare professionals in how to achieve these targets.

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Diabetic ketoacidosis is usually associated with type 1 diabetes; however, it is increasingly being recognised in type 2 diabetes. The three main mechanisms suggested are: insulinopaenia, elevation in counter‐regulatory hormones as a stress response, and increase in free fatty acids. This review aims to highlight the mechanism of diabetic ketoacidosis in type 2 diabetes, the difference compared to its occurrence in type 1 diabetes, the main triggers and its management. The most common mechanism is relative insulin deficiency (insulinopaenia) and usual triggers are non‐concordance or infection. Treatment is exactly the same as in type 1 diabetes with intravenous fluid resuscitation and insulin, though the duration of treatment may not be as long. These patients are able to stop insulin following resolution of ketoacidosis and can be managed on oral hypoglycaemic agents. It is important for clinicians to be aware of this condition due to the increasing burden of type 2 diabetes and to avoid unnecessary treatment with insulin in the long term.