Interaction between Pyridostigmine and Hydrocortisone
Moderate Antagonism

ID DDInter1548 and DDInter885
Interaction Corticosteroids and adrenocorticotropic agents may diminish the therapeutic effects of acetylcholinesterase inhibitors in myasthenia gravis. The mechanism of interaction is unknown. Marked deterioration in muscle strength has been reported in patients with myasthenia gravis shortly after the initiation of corticosteroid therapy, particularly when high dosages were used.
arterial pressure NOS decreased icterus heart attack Neutropenia bone marrow failure Embolism pulmonary heart rate increased sinus tachycardia edema extremities respiratory failure
Management Corticosteroid therapy should be instituted at relatively low dosages (15 to 25 mg/day of prednisone or equivalent) and in a controlled setting in patients with myasthenia gravis. Respiratory support should be available, and the dosage should be increased stepwise as tolerated (approximately 5 mg/day of prednisone or equivalent at 2- to 3-day intervals until marked clinical improvement or a dosage of 50 mg/day is reached). Dose reductions of the acetylcholinesterase inhibitor may be required as symptoms improve, which often may be delayed and gradual.
References
Alternative for Pyridostigmine N07A
Alternative for Hydrocortisone S01C
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Potential Metabolism Interactions

Substrate-Substrate Interaction:If more than one drug is metabolized by the same CYP, it is possible that its metabolism is inhibited because of the competition between the drugs. That means, it can be useful to lower the dosage of the drugs in the drug-cocktail because they remain longer in the organism than in monotherapy.
Inhibitor-Inhibitor Interaction:Combining two or more inhibitors of one CYP, should be compensated by lowering the dosage of these drugs because the metabolism is reduced and the drugs remain longer in the organism than in monotherapy. Not adapting the dosage bears the risk of even more side effects.
Inhibitor-Substrate Interaction:Combining drugs that have inhibitory effect and are substrates of one particular CYP, should be compensated by lowering the dosage. They rest longer in the organism than in monotherapy. Not adapting the dosage bears the risk of even more side effects.