Ropinirole is not an inhibitor or inducer of CYP1A2 or other CYP enzymes in vivo. Risk for gastrointestinal adverse events in the form of vomiting and nausea motivates vigilance against insufficient intake of food, especially of carbohydrate.

Ropinirole is indicated for the treatment of restless legs syndrome and Parkinsons. Very common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are vomiting and nausea. Other common side effects are abdominal pain, fatigue, syncope, somnolence and dizziness. In the low doses employed there are no side effects pointing to engagement of the stress-activated dopamine pathways that give rise to porphyrinogenic glucagon-signaling and cortisone-release.

Insignificant.

Ropinirole is metabolised mainly by CYP1A2 (Kaye 2000 and SPC) with minor contribution by CYP3A. Only 10% is excreted as unchanged drug (Kaye 2000). Half-life elimination is 6 hours. In vitro studies have shown that ropinirole is a potent inhibitor of CYP2D6 and a less potent inhibitor of CYP1A2 (Kvernmo 2006). However, in vitro data also indicate that ropinirole has low potential to inhibit CYP450 enzymes at therapeutic doses (SPC). Ropinirole did not change the pharmacokinetics of theophylline, a CYP1A2 substrate, when co-administrated (SPC and Thalamas 1999). This indicates that ropinirole is not an inhibitor or an inducer of CYP1A2. Plasma concentrations of ropinirole are unlikely to exceed 0.01 µM (Bloomer 1997 and Boothman 1990) which makes it unlikely that ropinirole will activate PXR and induce CYP enzymes.

Thunell, clinical observation (n=1): tolerated.

Uneventful use reported in 1 patient with acute porphyria.