Chronic idiopathic erythroderma is an independent condition which is likely to occur in elderly men. Immunity is shifted to the Th2 type in CIE; however, the mechanism may differ from that of atopic dermatitis.

No abstract

The present authors have previously reported that chronic idiopathic erythroderma (CIE) that lasts for more than 3 months without specific causes occurs almost exclusively in older men. No standardized therapeutic treatments for the condition have been established to date. To assess the efficacies and safeties of current treatments for CIE, the present authors reviewed cases of CIE. Twenty cases were identified, of which CIE was treated with oral corticosteroids, oral cyclosporine A (CsA), ultraviolet therapy, or a combination of these therapies. CIE was cured in 8/20 (40%) of these cases, and the average time to cure was 19.3 months. Oral CsA was the most effective treatment at relatively low doses (50–100 mg/day), which resulted in cures in four cases. Ultraviolet therapy also effectively cured two subjects, and oral corticosteroids cured one patient. In patients that were treated with oral CsA or corticosteroids, the terminations of the treatments within 2 to 3 months resulted in relapses in multiple patients. The maintaining of the treatments for a certain period may be necessary in cases that involve treatments with these orally administered drugs. Although CIE is a chronic and potentially refractory disease, it can evidently be cured or well controlled via appropriate long‐term therapies.

Herpes simplex virus (HSV) periodically forms characteristic blisters in the perioral and genital areas in a subset of people. Because of the lack of accurate tests for this common virus, various types of perioral/anogenital lesions are often misdiagnosed as herpes. Also, though asymptomatic HSV‐positive people shed virus, the precise time course of symptoms and viral shedding is unclear. The loop‐mediated isothermal amplification (LAMP) method amplifies target DNA sequences without thermal cycles, simpler and faster than polymerase chain reaction (PCR). To investigate clinico‐laboratorial correlation and whether HSV can be detected in the oral cavity during symptom occurrence, we collected 445 specimens from 211 patients who visited our clinic with suspected herpetic lesions or non‐symptomatic volunteers. DNA was extracted from swabs simultaneously taken from lesions (n = 219) and seemingly asymptomatic oral mucosa (n = 226). HSV‐1 and HSV‐2 DNA sequences were amplified by LAMP and validated by quantitative real‐time PCR. The LAMP method detected HSV DNA almost as sensitively (97%) as PCR. Positivity for HSV DNA was found in 54% (40/74) of specimens from the perioral/oral area. Review of clinical images of recurrent herpes labialis revealed that HSV DNA was detected only from lesions located on the perioral skin and/or the dry, vermillion part of the lip; no HSV DNA was found in immunocompetent patients with lesions confined to the oral mucosa except primary infection. This observation may be an important principle for clinical diagnosis of recurrent herpes. HSV was detected in the oral mucosa in 2.7% (6/226) of samples; all of these patients had either primary infection or were immunosuppressed. Virus shedding in the mucosa was apparently tightly regulated by the immune system. Patients with suppressed or no immunity (naïve cases) did shed virus in the mucosa. LAMP is a simple method to reliably distinguish recurrent/primary herpes from other conditions.

No abstract