A very common side effect of montelukast is upper respiratory tract infection. Since infections have a potential to trigger acute porphyric attacks vigilance is motivated regarding signs or symptoms of infection and/or possible symptoms of a porphyric attack.

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, nausea, diarrhoea and pyrexia.

Montelukast is listed as a moderate inducer of CYP1A2 in vivo. CYP1A2 amounts quantitatively to more than 10 % of the CYPs in the liver. A moderate induction of this CYP isoenzyme may possibly increase the activity of ALAS-1 to a level which is sufficient to precipitate an attack.

Leukotriene receptor antagonist containing functional groups like chloroquinoline, cyclopropan, aliphatic sulfide and acetic acid.

Montelukast is indicated for the treatment of asthma. It is administered orally.

Montelukast is metabolised mainly by CYP2C8, with contributions by CYP3A4 and CYP2C9 to a minor degree (Karonen 2012). In vitro data indicates that therapeutic plasma concentrations of montelukast do not inhibit CYP3A4, CYP2C9, CYP1A2, CYP2A6, CYP2C19 and CYP2D6 (SPC). In vitro studies in human liver microsomes found montelukast to be a selective competitive inhibitor of CYP2C8, but not to be a mechanism-based inhibitor (Walsky 2005). Despite being a CYP2C8 inhibitor in vitro, clinical drug-drug interaction studies with pioglizazone and rosiglitazone, CYP2C8 substrates, showed that montelukast does not inhibit CYP2C8 in vivo (Jaakkola 2006, Kim 2007). The concentrations of ethinyl estradiol and norethinedrone (substrates of CYP3A4) were unaffected when co-administrated with montelukast for 8 days (Jarvis 2000). This might indicate that montelukast is not an inhibitor or an inducer of CYP3A4, but it was not specified which pharmacokinetic parameters that were measured in the study. Montelukast demonstrated activity in an hPXR transactivation assay, but the clinical induction is predicted to be low (Sinz 2006). It is not known to inactivate any enzymes via mechanism-based inhibition in vitro (Obach 2007). Montelukast is listed as a moderate inducer of CYP1A2 in vivo (FDA). However, in a clinical dose (10 mg) study montelukast decreased the pharmacokinetics of theophylline (substrate of CYP1A2 and to a minor degree, CYP3A4) by 8% (Jarvis and Markham 2000), which indicates that montelukast is a weak inducer. Studies have shown that when co-administrated, montelukast do not have any significant effect on the AUC of warfarin (a CYP2C9 substrate) (Jarvis and Markham 2000 and Van Hecken 1999), which indicates that montelukast is not an inhibitor or an inducer of CYP2C9.

Uneventful use reported in 1 patient with acute porphyria.