Erythromycin base, drug interactions

Erythromycin is a substrate for the cytochrome P450 (CYP 450) 3A4 isoenzyme. Once bound to CYP 3A, erythromycin stimulates its own metabolism via demethylation and oxidation to nitroalkane metabolites. These nitroalkane metabolites appear to form stable complexes with the iron of the CYP 3A4 isoenzyme, decreasing its functional capacity. Depending upon the erythromycin dose and duration of therapy, CYP 3A4 activity could be inhibited to undetectable activity and serves as the basis of erythromycin-associated metabolic-based drug-drug interactions. 

Secondary> hyperparathyroidism 30 mg PO daily Parathyroid carcinoma 30 mg PO bid titrate q2—4wk based on Ca PTH levels swallow whole take w/ food Caution [C, /—] w/ Szs Disp Tabs SE N/V/D, myalgia, dizziness, 4- Ca2+ Interactions T Effects W/ CYP3A4 inhibitors such as ketoconazole, itraconazole, erythromycin T effects OF drugs metabolized at CYP2D6 such as TCA, thioridazine, flecainide, vinblastine EMS Monitor ECG for signs of hypocalcemia (T QT interval) OD May cause severe hypocalcemia calcium salts can be given... 

The adverse effect profile of roflmnilast has been described previously. However, new data became available recently. A systematic review smnmarised the available data on adverse effects and drug reactions of roflmnilast. This systematic review was based on six clinical trials with a total population of 9102 COPD patients, with the study duration ranging between 24 and 52 weeks [89 ]. Roflmnilast is metabolised by CYP 3A4, CYP 2C19 and CYP 1A2. Inhibitors of these enzymes such as erythromycin or ketoconazole were shown to increase the activity and half-life of roflumilast. In contrast, drugs that induced these enzymes, like rifampicin, had the opposite effect, reducing the activity and half-life of roflumilast. Roflumilast did not significantly interact with montelukast, budesonide, or antacids. 

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