Cholemax Drug Interactions

Capsule: Antacids (Aluminum-containing): Decreased absorption of ursodeoxycholic acid.
Bile acid sequestrants: Decreased absorption of ursodeoxycholic acid. Administer bile acid sequestrants (cholestyramine, colestipol) at least 2 hours before or after ursodeoxycholic acid.
Clofibrate: Possible reduced efficacy of ursodeoxycholic acid because of increased hepatic cholesterol secretion caused by clofibrate (and possibly other antilipemic drugs).
Estrogen: Possible reduced efficacy of ursodeoxycholic acid because of increased hepatic cholesterol secretion caused by estrogen.
Hormonal contraceptives: Possible reduced efficacy of ursodeoxycholic acid because of increased hepatic cholesterol secretion caused by oral contraceptives.
Oral suspension: UDCA suspension should not be administered concomitantly with colestyramine, colestipol or antacids containing aluminium hydroxide and/or smectite (aluminium oxide), because these preparations bind UDCA in the intestine and thereby inhibit its absorption and efficacy. Should the use of a preparation containing one of these substances be necessary, it must be taken at least 2 hours before or after UDCA suspension.
UDCA suspension can affect the absorption of ciclosporin from the intestine. In patients receiving ciclosporin treatment, blood concentrations of this substance should therefore be checked by the physician and the ciclosporin dose adjusted if necessary.
In isolated cases, UDCA suspension can reduce the absorption of ciprofloxacin.
In a clinical study in healthy volunteers concomitant use of UDCA (500 mg/day) and rosuvastatin (20 mg/day) resulted in slightly elevated plasma levels of rosuvastatin. The clinical relevance of this interaction also with regard to other statins is unknown.
UDCA has been shown to reduce the peak plasma concentrations (Cmax) and area under the curve (AUC) of the calcium antagonist nitrendipine in healthy volunteers. Close monitoring of the outcome of concurrent use of nitrendipine and UDCA is recommended. An increase in the dose of nitrendipine may be necessary. An interaction with a reduction of the therapeutic effect of dapsone was also reported. These observations, together with in-vitro findings, could indicate a potential for UDCA to induce cytochrome P450 3A enzymes. Induction has, however, not been observed in a well-designed interaction study with budesonide, which is a known cytochrome P450 3A substrate.
Oestrogenic hormones and blood cholesterol lowering agents such as clofibrate increase hepatic cholesterol secretion and may therefore encourage biliary lithiasis, which is a countereffect to UDCA used for dissolution of gallstones.