Trabecular bone loss in the lumbar spine precedes cortical bone loss in the femoral neck. Exhaustive list
Allergic: allergic or hypersensitivity reactions, anaphylactoid reaction, anaphylaxis, and urticaria.Cardiovascular: hypertension, congestive heart failure in susceptible patients, premature atherosclerotic disease, arrhythmias, and possible hyperlipidemia.Dermatologic: impaired wound healing, petechiae and ecchymoses, thinning of the skin, facial erythema, and increased sweating.Endocrine: Cushingoid features, growth suppression in children, secondary adrenocortical and pituitary unresponsiveness, menstrual irregularities, decreased carbohydrate intolerance, and latent diabetes mellitus. In patients with diabetes, increased requirements of insulin or oral hypoglycemic agents.Fluid and electrolyte disturbances: sodium retention, fluid retention, potassium loss, hypokalemic alkalosis, or congestive heart failure in susceptible patients.Gastrointestinal: peptic ulcer, pancreatitis, abdominal distention, and ulcerative esophagitis.Metabolic: protein catabolism which causes negative nitrogen balance.Musculoskeletal: muscle weakness, loss of muscle mass, steroid myopathy, osteoporosis, tendon rupture (especially Achilles), vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fracture of long bones.Neurological: increased intracranial pressure with papilledema, convulsions, vertigo, and headache.Ophthalmic: posterior sub-capsular cataracts, increased intraocular pressure, glaucoma, and exophthalmos. Withdrawal
Feedback of the exogenous glucocorticoids at the hypothalamic–pituitary–adrenal (HPA) axis inhibits the secretion of the corticotropin-releasing hormone (CRH) and the adrenocorticotropic hormone (ATCH) at the hypothalamus and pituitary glands, respectively. Prolonged suppression leads to inadequate responses to physical and emotional stresses, such as illness and trauma. Suppression of ATCH may result in adrenal hypoplasia or secondary adrenal gland atrophy within 6 weeks of methylprednisolone therapy, leaving a patient at risk for developing life-threatening adrenal insufficiency crisis.
Contrary to the solubilities above, methylprednisolone sodium succinate is soluble in water and alcohol, slightly soluble in acetone and insoluble in chloroform

Chemical properties
Methylprednisolone, or 6α-methylprednisolone, also known as 11β,17,21-trihydroxy-6α-methylpregna-1,4-diene-3,20-dione, is a synthetic pregnane steroid and a derivative of hydrocortisone (11β,17α,21-trihydroxypregn-4-ene-3,20-dione) and prednisolone (11β,17α,21-trihydroxypregn-1,4-diene-3,20-dione). A variety of methylprednisolone esters with differing characteristics exist and have been marketed for medical use. They include methylprednisolone aceponate (Advantan), methylprednisolone acetate (Depo-Medrol), methylprednisolone succinate (Solu-Medrol), and methylprednisolone suleptanate (Medrosol, Promedrol). Synthesis
Synthetic steroids are synthesized from cholic acid and sapogenins obtained from cattle and plants, respectively. History, society and culture
Methylprednisolone was first synthesized and manufactured by The Upjohn Company (now Pfizer) and Food and Drug Administration (FDA) approved in the United States on 2 October 1957. The patent has since expired, and generics are now available. In 2021, it is ranked as the 153rd most commonly prescribed medication in the United States, with more than four million prescriptions. It has jumped four spots in the rankings from 2017. Methylprednisolone has been a prescribed therapy amidst the COVID-19 pandemic, but there is no evidence it is either safe or effective for this purpose. Research
Methylprednisolone has been a prescribed therapy amidst the COVID-19 pandemic, but there is no evidence it is either safe or effective for this purpose. References
External links
"Methylprednisolone". Drug Information Portal. U.S. National Library of Medicine.