Dermatology for the Practicing Allergist: Tinea Pedis and Its Complications

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

:6; Personal non-commercial use only. The Journal of Rheumatology

ABSTRACT. Objective. To determine the extent to which cognitive dysfunction (CD) observed in patients with systemic lupus erythematosus (SLE) exceeds that seen in a matched control group of patients with rheumatoid arthritis (RA), and to estimate the prevalence of CD in SLE in a community-based sample. Methods. A random subsample of 31 patients with SLE was compared to patients with RA matched by age, sex, and race and derived from the same patient population. Cognitive function was assessed by the Automated Neuropsychological Assessment Metrics (ANAM). The primary outcome was the total throughput score (number of correct responses divided by the time taken for those responses averaged over all subtests), adjusted for premorbid intelligence, neuromuscular efficiency, disease activity, damage, depression, fatigue, and health-related quality of life. Results. There were no statistically significant differences in mean throughput scores between patients in the SLE and RA groups in any subtest of the ANAM or in the total throughput score. The frequency of CD, defined as either total scores > 1.5 SD below the mean of the RA population, or 4 or more ANAM subtests each > 1.5 SD below the RA mean, was similar in patients with SLE and in RA controls. Conclusion. We found no differences in cognitive function between patients with SLE and RA, suggesting that the CD found in some patients with SLE may represent the consequences of a chronic and/or inflammatory disease rather than SLE-related central nervous system damage. (First Releas