Q J Med 1994; 87: 437-441
© 1994 Association of Physicians
research-article |
Oedema in patients with Addison's disease on replacement therapy: glcocorticoid excess and mineralocorticoid deficiency?
Department of Vascular Medicine, Postgraduate Medical School, Royal Devon and Exeter Hospital Exeter, UK
Address correspondence to Dr M.D. Flynn, Consultant Physician, Prince Philip Hospital, Llanelli, Dyfed SA14 8QF
Received 18 March 1994 Accepted for publication 13 July 1994.
Steroid hormones influence mechanisms related to oedema formation, including postural vasocon-striction and vascular tone. We studied fifteen patients (7 male, 8 female) with primary adrenal failure on clinically optimal replacement therapy. Five patients, all female, had clinically detectable oedema. Patients with oedema had evidence of mineralocorticoid deficiency, with increased supine and erect plasma renin activity and greater postural fall in blood pressure. Mean morning plasma cortisol levels were significantly higher in the group with oedema, suggesting they were receiving insufficient mineralocorticoid and a possible relative excess of glucocorticoid. There were no significant differences between patients with and without oedema in lower-limb cutaneous blood flow or in postural vasocon strictor responses measured by laser Doppler flow-metry. The mechanism of oedema formation is unclear, but appears not to be modulated by haemo-dynamic mechanisms with expansion of intravascular volume or, in contrast to the known effects of sex hormones, by impairment of postural vasocon-striction. Theoretically, excess glucocorticoid replacement may result in oedema formation, by direct action on vascular tone, by altering capillary permeability, or by influencing other factors such as atrial natiuretic peptide. Measurement of plasma renin activity in conjunction with plasma cortisol profiles may be useful in adjusting replacement therapy in patients with Addison's disease and oedema.