In addition to steroids, other major endocrine medicines associated with peripheral oedema are sex hormones and anti-diabetes drugs.⁵

Several increase sodium retention by acting on epithelial sodium channels (ENaCs) such as androgens (danazol, testosterone), aromatase inhibitors (anastrozole, letrozole, exemestane), and tamoxifen, which may also affect lymphatic system oestrogen receptors causing lymphoedema.^15,23

Antiandrogenic hormone therapy with gonadotrophin releasing hormones (GnRH) such as goserelin or leuprolide have effects both via ENaCs and changes in progesterone activity. Antiandrogens used in prostate cancer (eg abiraterone or enzalutamide) may have mineralocorticoid effects leading to sodium and water retention.^15,24

Insulin can increase capillary permeability, cause arteriole vasodilatation and increase sodium and water retention by RAAS stimulation. Insulin oedema syndrome is a rare feature of initiating or intensifying insulin therapy for people with poorly controlled diabetes. It appears to arise from rapidly correcting glycaemic level and is usually mild and affects the lower legs but can become more severe.^15,25

Use of pioglitazone with insulin can substantially increase the likelihood of oedema; glitziness can increase in oedema likelihood by 5% in monotherapy or 15% when used with insulin. A suggested mechanism is by increasing blood volume with a resulting leaky vasculature.^13,26,27