PMID- 15050029 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20200929 IS - 1476-7961 (Print) IS - 1476-7961 (Electronic) IS - 1476-7961 (Linking) VI - 2 IP - 1 DP - 2004 Mar 29 TI - Dermatology for the practicing allergist: Tinea pedis and its complications. PG - 5 AB - Tinea pedis is a chronic fungal infection of the feet, very often observed in patients who are immuno-suppressed or have diabetes mellitus. The practicing allergist may be called upon to treat this disease for various reasons. Sometimes tinea infection may be mistaken for atopic dermatitis or allergic eczema. In other patients, tinea pedis may complicate allergy and asthma and may contribute to refractory atopic disease. Patients with recurrent cellulitis may be referred to the allergist/immunologist for an immune evaluation and discovered to have tinea pedis as a predisposing factor. From a molecular standpoint, superficial fungal infections may induce a type2 T helper cell response (Th2) that can aggravate atopy. Th2 cytokines may induce eosinophil recruitment and immunoglobulin E (IgE) class switching by B cells, thereby leading to exacerbation of atopic conditions. Three groups of fungal pathogens, referred to as dermatophytes, have been shown to cause tinea pedis: Trychophyton sp, Epidermophyton sp, and Microsporum sp. The disease manifests as a pruritic, erythematous, scaly eruption on the foot and depending on its location, three variants have been described: interdigital type, moccasin type, and vesiculobullous type. Tinea pedis may be associated with recurrent cellulitis, as the fungal pathogens provide a portal for bacterial invasion of subcutaneous tissues. In some cases of refractory asthma, treatment of the associated tinea pedis infection may induce remission in airway disease. Very often, protracted topical and/or oral antifungal agents are required to treat this often frustrating and morbid disease. An evaluation for underlying immuno-suppression or diabetes may be indicated in patients with refractory disease. FAU - Al Hasan, Muhannad AU - Al Hasan M AD - Department of Internal Medicine, James H, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA. krishnas@etsu.edu FAU - Fitzgerald, S Matthew AU - Fitzgerald SM FAU - Saoudian, Mahnaz AU - Saoudian M FAU - Krishnaswamy, Guha AU - Krishnaswamy G LA - eng PT - Journal Article DEP - 20040329 PL - England TA - Clin Mol Allergy JT - Clinical and molecular allergy : CMA JID - 101152195 PMC - PMC419368 EDAT- 2004/03/31 05:00 MHDA- 2004/03/31 05:01 PMCR- 2004/03/29 CRDT- 2004/03/31 05:00 PHST- 2003/11/25 00:00 [received] PHST- 2004/03/29 00:00 [accepted] PHST- 2004/03/31 05:00 [pubmed] PHST- 2004/03/31 05:01 [medline] PHST- 2004/03/31 05:00 [entrez] PHST- 2004/03/29 00:00 [pmc-release] AID - 1476-7961-2-5 [pii] AID - 10.1186/1476-7961-2-5 [doi] PST - epublish SO - Clin Mol Allergy. 2004 Mar 29;2(1):5. doi: 10.1186/1476-7961-2-5.