Although deleterious side effects of steroids are more common with prolonged administration 1), some can occur even with short treatment courses. Some evidence suggests that low-dose glucocorticoids (≤10mg/d of prednisolone or prednisone equivalent) for rheumatoid arthritis does not increase osteoporotic fractures, blood pressure, cardiovascular disease, or peptic ulcers 2), but weight gain and skin changes are common. Possible side effects include 3) 4):
● cardiovascular and renal
○ sodium and water retention
● CNS
○ progressive multifocal leukoencephalopathy (PML)
○ mental agitation or “steroid psychosis”
○ spinal cord compression from spinal epidural lipomatosis: rare
○ pseudotumor cerebri, or Idiopathic intracranial hypertension (IIH)
● endocrine
○ caution: because of the growth suppressant effect in children, daily glucocorticoid dosing over prolonged periods should be reserved for the most urgent indications
○ secondary amenorrhea
○ suppression of hypothalamic-pituitary-adrenal axis: reduces endogenous steroid production →
risk of adrenal insufficiency with steroid withdrawal
○ Cushingoid features with prolonged usage (iatrogenic Cushing’s syndrome): obesity, hypertension, hirsutism…
● GI: risk increased only with steroid therapy > 3 weeks duration and regimens of prednisone > 400–1000 mg/d or dexamethasone > 40 mg/d 5)
○ gastritis and steroid ulcers: incidence lowered with the use of antacids and/or H2 antagonists (e.g. cimetidine, ranitidine…)
○ pancreatitis
○ intestinal or sigmoid diverticular perforation 6): incidence ≈ 0.7%. Since steroids may mask signs of peritonitis, this should be considered in patients on steroids with abdominal discomfort, especially in the elderly and those with a history of diverticular disease. Abdominal X-ray usually shows free intraperitoneal air
● inhibition of fibroblasts ○ impaired wound healing or a wound breakdown ○ subcutaneous tissue atrophy
● metabolic ○ glucose intolerance (diabetes) and disturbance of nitrogen metabolism ○ hyperosmolar nonketotic coma ○ hyperlipidemia ○ tend to increase BUN as a result of protein catabolism
● ophthalmologic ○ posterior subcapsular cataracts ○ glaucoma
● musculoskeletal
○ avascular necrosis (AVN) of the hip or other bones: usually with prolonged administration →cushingoid habitus and increased marrow fat within the bone13 (prednisone 60 mg/d for several months is probably the minimum necessary dose, whereas 20 mg/d for several months will probably not producing AVN). Many cases blamed on steroids may instead be due to alcohol use, cigarette smoking, liver disease, underlying vascular inflammation…
○ osteoporosis: may predispose to vertebral compression fractures which occur in 30–50% of patients on prolonged glucocorticoids. Steroid-induced bone loss may be reversed with cyclical administration of etidronate in 4 cycles of 400 mg/d ✖ 14 days followed by 76 days of oral calcium supplements of 500 mg/d (not proven to reduce the rate of VB fractures)
○ muscle weakness (steroid myopathy): often worse in proximal muscles
● infectious
○ immunosuppression: with possible superinfection, especially fungal, parasitic
○ possible reactivation of TB, chickenpox
● hematologic
○ hypercoagulopathy from inhibition of tissue plasminogen activator
○ steroids cause emargination of white blood cells, which may artifactually elevate the WBC count even in the absence of infection
● miscellaneous
○ hiccups: may respond to chlorpromazine (Thorazine®) 25–50 mg PO TID-QID ✖ 2–3 days (if symptoms persist, give 25–50 mg IM)
○ steroids readily cross the placenta, and fetal adrenal hypoplasia may occur with the administration of large doses during pregnancy
DEXA, however, has many systemic side effects and may interact negatively with glioma therapy.
The long-term side effects of dexamethasone are well known, including Cushingnoid appearance, truncal obesity, lymphopenia, immunosuppression, hyperglycemia, steroid myopathy, fluid retention, visual blurring, tremor, mood/behavioral changes (including psychosis), osteoporosis, and cerebral atrophy 7).