Sertaconazole, sold under the brand name Ertaczo among others, is an antifungal medication of the Benzothiophene class. It is available as a cream to treat skin infections such as athletes foot. It is also available in a vaginal tablet form. The most popular of these is Gyno-Dermofix. Medical uses
In randomized, double-blind, multicentre trials of 3 to 6 weeks duration (n=127-383), a significantly greater number of patients with tinea of the glabrous skin and tinea pedis receiving a topical 2% sertaconazole cream once or twice daily achieved a successful mycological cure compared with recipients of a placebo cream. Side effects
Side effects were rarely reported with sertaconazole therapy, but may include contact dermatitis, burning on application site and skin dryness. Pharmacology
Pharmacodynamics
Sertaconazole has several known mechanisms of action. It is considered fungistatic, fungicidal, antibacterial, antiinflammatory, antitrichomonal, and antipruritic.Like other imidazole antifungals, sertaconazole blocks the synthesis of ergosterol by inhibiting the 14α-demethylase enzyme. Ergosterol is a critical component of the fungal cell membrane. Inhibition of ergosterol synthesis prevents fungal cells from multiplying and impairs hyphae growth. Chemically, sertaconazole contains a benzothiophene ring which makes it unique from other imidazole antifungals. A benzothiophene ring is a sulfur analogue of the indole ring found in the amino acid tryptophan. Tryptophan is found in the fungal membrane in addition to lipids such as ergosterol. The benzothiophene ring in sertaconazole mimics tryptophan and increases the drugs ability to form pores in the fungal cell membrane.
The protozoan is in the smaller of its two forms, called an amastigote, which is round, non-motile, and only 3–7 micrometers in diameter. Inside the stomach of the sandfly, the amastigotes quickly transform into elongated and motile forms called the promastigotes. Promastigote is spindle-shaped, triple the size of the amastigote, and has a single flagellum that allows mobility. The promastigotes live extracellularly in the alimentary canal, reproducing asexually, then migrate to the proximal end of the gut where they become poised for a regurgitational transmission. As the fly bites, the promastigotes are released from the proboscis and introduced locally at the bite site.Once inside the human host, promastigotes invade macrophages. Inside the cells they transform back into the smaller amastigote form. The amastigotes replicate in the most hostile part of the macrophage cell, inside the phagolysosome, whose normal defensive response they are able to prevent. After repeated multiplication, they break down their host cell by sheer pressure of mass, but there is some recent speculation that they are able to leave the cell by triggering the exocytosis response of the macrophage. The daughter cells protozoans then migrate to fresh cells or through the bloodstream to find new hosts. In this way the infection is progressive, spreading to the hosts mononuclear phagocyte system, particularly the spleen and liver. The free amastigotes in peripheral tissues are then ingested by sandfly to enter another cycle. Regulatory T and B cells
The cell-mediated immunity (CMI) that kills Leishmania also produces inflammation. If the inflammation is excessive, it can cause tissue damage.