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 outpatient visit were prescribed oral corticosteroids as a long-term control therapy. The National Asthma Education and Prevention Program (NAEPP) indicates systemic methylprednisolone in both short and long term therapies to quickly control and to suppress persistent asthma, respectively. For exacerbations that result in a visit to the Emergency Department (ED), oral methylprednisolone is preferred over intravenous administration, unless there are issues with adherence or vomiting. Oral methylprednisolone is less invasive and studies have shown that equivalent efficacy compared to intravenous methylprednisolone.
Those being treated for retinal neurocysticercosis can face retinal damage if they are not first checked for ocular cysticeri, since changes to existing lesions in the eye by albendazole can cause permanent blindness. Overdose
Because of its low solubility, albendazole often cannot be absorbed in high enough quantities to be toxic. The oral LD50 of albendazole in rats was found to be 2,500 mg/kg. It takes 20 times the normal dose to kill a sheep, and 30 times the normal dose to kill cattle. Overdose affects the liver, testicles, and GI tract the most. It can manifest with lethargy, loss of appetite, vomiting, diarrhea, intestinal cramps, dizziness, convulsions, and sleepiness. There is no specified antidote. Interactions
The antiepileptics carbamazepine, phenytoin, and phenobarbital lower the plasma concentration and the half life of albendazole sulfoxides R(+) enantiomer. The antacid cimetidine heightens serum albendazole concentrations, increases the half life of albendazole, and doubles albendazole sulfoxide levels in bile. It was originally thought to work by increasing albendazole bioavailability directly; however, it is now known that cimetidine inhibits the breakdown of albendazole sulfoxide by interfering with CYP3A4. The half-life of albendazole sulfoxide thus increases from 7.4 hours to 19 hours. This might be a helpful interaction on more severe cases, because it boosts the potency of albendazole. Paradoxically, cimetidine also inhibits the absorption of albendazole by reducing gastric acidity.Several other interactions exist. Corticosteroids increase the steady-state plasma concentration of albendazole sulfoxide; dexamethasone, for example, can increase the concentration by 56% by inhibiting the elimination of albendazole sulfoxide.