====== Steroid side effects ======

Although deleterious [[side effect]]s of [[steroid]]s are more common with prolonged administration
((Marshall LF, King J, Langfitt TW. The Complication of High-Dose Corticosteroid Therapy in Neurosurgical Patients: A Prospective Study. Ann Neurol. 1977; 1:201–203)), some can occur even with short treatment courses. Some [[evidence]] suggests that low-dose [[glucocorticoid]]s (≤10mg/d of [[prednisolone]] or [[prednisone]] equivalent) for [[rheumatoid arthritis]] does not increase [[osteoporotic fracture]]s, [[blood pressure]], [[cardiovascular disease]], or [[peptic ulcer]]s
((Da Silva JA, Jacobs JW, Kirwan JR, et al. Safety of low
dose glucocorticoid treatment in rheumatoid
arthritis: published evidence and prospective trial data. Ann Rheum Dis. 2006; 65:285–293)),
but weight gain and skin changes are common. Possible side effects include
((Kountz DS. An Algorithm for Corticosteroid Withdrawal. Am Fam Physician. 1989; 39:250–254))
((Braughler JM, Hall ED. Current Application of "High-Dose" Steroid Therapy for CNS Injury: A Pharmacological Perspective. J Neurosurg. 1985;
62:806–810)):

● cardiovascular and renal

○ [[hypertension]]

○ [[sodium]] and water retention

○ [[hypokalemic alkalosis]]

● 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
((Lu WY, Rhoney DH, Boling WB, et al. A Review of
Stress Ulcer Prophylaxis in the Neurosurgical
Intensive Care Unit. Neurosurgery. 1997; 41:416–426))

○ 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
((Weiner HL, Rezai AR, Cooper PR. Sigmoid Diverticular Perforation in Neurosurgical Patients Receiving High-Dose Corticosteroids. Neurosurgery.
1993; 33:40–43)): 
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
((Dietrich J, Rao K, Pastorino S, et al. Corticosteroids in brain cancer patients: benefits and pitfalls. Expert Rev Clin Pharmacol. 2011;4(2):233–242. )).