Mineralocorticoid adverse effects are manifested in the retention of sodium and water with edema and hypertension, and in the increased excretion of potassium with the possibility of hypokalemic alkalosis. In susceptible patients, cardiac failure may be induced.
Adverse glucocorticoid effects lead to mobilisation of calcium and phosphorus with osteoporosis and spontaneous fractures; muscle wasting and nitrogen depletion; and hyperglycemia with accentuation or precipitation of the diabetic state. The insulin requirements of diabetic patients are increased. Increased appetite is often reported.
Impaired tissue repair and immune function can lead to delayed wound healing and increased susceptibility to infection. Increased susceptibility to all kinds of infection, including septicemia, tuberculosis, fungal infections, and viral infections, has been reported in patients on corticosteroid therapy. Infections may also be masked by the anti-inflammatory, analgesic and antipyretic effects of glucocorticoids. The increased severity of varicella and measles may lead to a fatal outcome in a non-immune patients receiving systemic corticosteroid therapy.
Other adverse effects include menstrual irregularities, amenorrhea, hyperhidrosis, skin thinning, ocular changes including development of glaucoma and cataract, mental and neurological disturbances, benign intracranial hypertension, acute pancreatitis and avascular necrosis of bone. An increase in the coagulability of the blood may lead to thromboembolic complications. Peptic ulceration has been reported but reviews of the literature do not always agree that corticosteroids are responsible for an increased incidence. Adverse effects should be treated symptomatically, with the corticosteroid dosage reduced or slowly withdrawn where possible.
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