Long-term steroid therapy can result in secondary adrenal insufficiency due to suppression of the hypothalamic-pituitaryadrenal axis. Systemic intercurrent illness can often precipitate adrenal crisis in such patients if steroid therapy is not increased temporarily to tide over the period of metabolic stress.The aetiology of adrenal insufficiency can be differentiated by checking serum ACTH which is high in Addison's disease and suppressed in secondary adrenal failure due to hypothalamic or pituitary causes. Adrenocortical autoantibodies to 21-hydroxylase are positive in 80% of patient's with Addison's disease. 4 Our patient had taken prednisolone for seven years and presented with incipient adrenal crisis six months after this was discontinued. Secondary adrenal failure due to long-term adrenal suppression was initially considered as the cause of adrenal failure but the generalised hyperpigmentation and positive adrenal antibodies suggest a diagnosis of autoimmune Addison's disease. Our patient was fortuitously being partially treated for Addison's disease while on prednisolone for presumed polymyalgia rheumatica, but developed overt adrenal insufficiency when this was discontinued. We are aware of at least one other case in which primary adrenocortical failure was masked by exogenous steroid administration. 5 Our patient subsequently developed primary autoimmune hypothyroidism and this, along with the history of pernicious anaemia, supports a common autoimmune aetiology.The ubiquitous long-term use of oral glucocorticoids to treat a variety of respiratory, rheumatological and haematological disorders carries the risk of causing adrenal insufficiency. Signs and symptoms of adrenal insufficiency in such patients should be anticipated and treated with 'crisis' dose steroid replacement during metabolic stress. Primary autoimmune Addison's disease often presents with non-specific symptoms and diagnosis is often delayed. A high index of suspicion remains the cornerstone of diagnosis. lesson of the month (2)Lesson A malnourished 82-year-old woman was referred to the emergency department with an extensive, painful rash. This had worsened despite two weeks treatment for herpes zoster. A month prior to admission she had undergone patellar surgery with a brief interruption of warfarin treatment. Warfarinisation had been commenced a year previously for a postoperative pulmonary embolus. Examination revealed extensive tender and malodorous erythematous plaques with a violacious hue. Central necrotic eschars and vesiculobullous changes were evident and there was involvement of the face, breasts, trunk and limbs (Fig 1). Warfarin-induced skin necrosis (WISN) was suspected necessitating the cessation of warfarin, and administration of vitamin K and low molecular weight heparin. Broad-spectrum antibiotics, enteral feeding and a three-day course of methylprednisolone, as vasculitis could not be excluded, were commenced. Biopsy of involved skin showed vascular thrombi, patchy necrosis and recent haemorrhage consistent with WI...
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