HPA itself. Thus, the physiological range of GCs is monitored by the negative feedback loop GCs exert on any portion of the HPA. Methylprednisolone structurally and functionally mimics endogenous corticoids and will act upon the HPA in a similar fashion. Pharmacokinetics Methylprednisolone is approved for oral and parenteral administration. Methylprednisolone (Medrol) for oral administration is available in a tablet formulation in 2 mg, 4 mg, 8 mg, 16 mg or 32 mg strengths. Both methylprednisolone acetate (Depo-Medrol) and methylprednisolone succinate (Solu-Medrol) are approved for intramuscular injection. Depo-Medrol is additionally approved for intralesional, intra-articular, and soft tissue injections. Depo-Medrol is available as sterile aqueous solution in 20 mg/mL, 40 mg/mL, or 80 mg/mL strengths. Solu-Medrol is the only derivative of methylprednisolone that is approved for intravenous infusion, as the sterile powder is soluble in water and can be mixed with a diluent. Strengths vary from 40 mg to 2g. Synthetic glucocorticoids are similar to endogenous steroids in metabolism, but differ in affinity for glucocorticoid and mineralocorticoid receptors, affinity for protein-binding, rate of elimination, and metabolic products. Oral methylprednisolone is readily absorbed from the gastrointestinal tract with a bioavailability of 89.9%. In contrast to endogenous GCs, methylprednisolone does not bind to the glycoprotein transcortin (corticosteroid binding globulin, CBG) but does have moderate protein binding to albumin. Thus, pharmacokinetics of methylprednisolone is linear and show no dose dependency. Patients exhibiting low albumin concentrations are at risk for adverse effects during glucocorticoid therapy. Oral methylprednisolone has a moderate distribution into tissue at 1.38L/kg. Methylprednisolone is primarily eliminated by hepatic metabolism and renal excretion of metabolites; with renal excretion of unchanged methylprednisolone at only 1.3–9.2%. Methylprednisolone can be interconverted with methylprednisone. Hepatic metabolism is mediated by 11 beta-hydroxysteroid dehydrogenases (11[beta]-HSD) and 20-ketosteroid reductases. Methylprednisolone undergoes renal excretion of hydrophilic inactive metabolites, including 20-carboxymelthylprednisolone and 6[beta]-hydroxy-20[alpha]-hydroxymethylprednisolone. Medical uses As stated previously, the primary use of methylprednisolone is to suppress inflammatory and immune responses. Methylprednisolone achieves this primarily by regulating the number and function of leukocytes, cytokines and chemokines. Its widespread inflammatory control is conducive in use across multiple disorders regardless of pathology. Methylprednisolone is commonly prescribed as short-term therapy for acute flares, as seen with acute gouty arthritis. It can be prescribed during on-going therapy in lower doses contingent upon monitorization of adverse effects. Dosage strength and formulation are optimized per medical use. Asthma In 2001–2002, 11.4% of patients diagnosed with asthma and seen at an