Because of its ability to inhibit cytochrome P450 3A4 CC-3, caution should be used when considering interactions with other medications.Itraconazole is pharmacologically distinct from other azole antifungal agents in that it is the only inhibitor in this class that has been shown to inhibit both the hedgehog signaling pathway and angiogenesis. These distinct activities are unrelated to inhibition of the cytochrome P450 lanosterol 14 alpha-demethylase and the exact molecular targets responsible remain unidentified. Functionally, the antiangiogenic activity of itraconazole has been shown to be linked to inhibition of glycosylation, VEGFR2 phosphorylation, trafficking, and cholesterol biosynthesis pathways. Evidence suggests the structural determinants for inhibition of hedgehog signaling by itraconazole are recognizably different from those associated with antiangiogenic activity. Pharmacokinetics
Itraconazole, like cyclosporine, quinidine, and clarithromycin, can inhibit P-glycoprotein, causing drug interactions by reducing elimination and increasing absorption of organic cation drugs. With conventional itraconazole preparations serum levels can vary greatly between patients, often resulting in serum concentrations lower than the therapeutic index. It has therefore been conventionally advised that patients take itraconazole after a fatty meal rather than prior to eating.A product (Lozanoc) licensed through the European union decentralised procedure has increased bioavailability, decreased  sensitivity to co ingestion of food, and hence decreased variability of serum levels. Chemistry
The itraconazole molecule has three chiral carbons. The two chiral centers in the dioxolane ring are fixed in relation to one another, and the triazolomethylene and aryloxymethylene dioxolane-ring substituents are always cis to each other. The clinical formulation is a 1:1:1:1 mixture of four stereoisomers (two enantiomeric pairs).
Factitious disorder imposed on another (FDIA), also called Munchausen syndrome by proxy (MSbP), is a condition in which a caregiver creates the appearance of health problems in another person, typically their child. This may include injuring the child or altering test samples. The caregiver then presents the person as being sick or injured. Permanent injury or death of the victim may occur as a result of the disorder. The behaviour occurs without a specific benefit to the caregiver.The cause of FDIA is unknown. The primary motive may be to gain attention and manipulate physicians. Risk factors for FDIA include pregnancy related complications and a mother who was abused as a child or has factitious disorder imposed on self. Diagnosis is supported when removing the child from the caregiver results in improvement of symptoms or video surveillance without the knowledge of the caregiver finds concerns. Those affected by the disorder have been subjected to a form of physical abuse and medical neglect.Management of FDIA may require putting the child in foster care. It is not known how effective therapy is for FDIA; it is assumed it may work for those who admit they have a problem. The prevalence of FDIA is unknown, but it appears to be relatively rare. More than 95% of cases involve a persons mother.The prognosis for the caregiver is poor. However, there is a burgeoning literature on possible courses of therapy.The condition was first named, as "Munchausen syndrome by proxy", in 1977 by British pediatrician Roy Meadow.