Atopic dermatitis (AD) is a multifactorial, chronically-relapsing, eczematous disease that usually manifests hyperimmunoglobulinemia E and eosinophilia. The significance of this IgE and eosinophilia still remains unclear. The Th1/Th2 balance theory can roughly outline the pathomechanisms of AD; however, the details remain largely unknown. Therapeutic guidelines are based on avoidance of exacerbating factors, skin care, and topical/oral medication. The recent development of topical calcineurin inhibitors has had a highly beneficial impact on the treatment of AD in combination with topical steroids.
The NC/Nga (NC) mouse, an animal model for human atopic dermatitis, develops eczematous lesions when raised in a conventional environment. In the present study, the therapeutic and prophylactic effects of emedastine difumarate, an anti-allergy drug, was examined using NC/Nga mice. The experimental mouse population was divided into those reared in a conventional environment, which had developed eczematous lesions, and those reared in a sterile environment and recently transferred to a conventional environment, which had not yet developed any symptoms. Emedastine difumarate was administered in water to both populations for 10 or 14 weeks in dosages of 1 mg/kg/day or 10 mg/kg/day, respectively, and the condition of these mice was compared with that of untreated controls. The effect of the drug was evaluated by scoring skin manifestations, such as erythema, edema, bleeding, erosion, hair loss, and dryness. The frequency of scratching during 30 min, plasma IgE level, and the number of mast cells and eosinophils in the skin tissue were also examined. Prophylactic administration of emedastine difumarate significantly suppressed the development of skin lesions and scratching at 1 mg/kg/day and more strongly at 10 mg/kg/day throughout the experiment for 14 weeks. Therapeutic administration of emedastine difumarate at 10 mg/kg/day significantly suppressed eczematous skin lesions and led to reduced scratching for 10 weeks. Administration of emedastine difumarate at 10 mg/kg/day to both mouse populations significantly suppressed the infiltration of mast cells and eosinophils into the skin but did not affect the plasma IgE level. These results indicate that the NC/Nga mouse is an excellent animal model for evaluating the effect of anti-allergy medications and that emedastine difumarate has significant therapeutic and prophylactic effects for eczematous skin lesions in NC/Nga mice.
We treated several skin diseases with narrowband UVB (NB-UVB) and UVA1. NB-UVB was used to treat patients with psoriasis, plaque type parapsoriasis, and vitiligo, and UVA1 was used to treat patients with atopic dermatitis and prurigo nodularis. We adopted 0.5 J/cm2 and 5.0 J/cm2 as starting doses for NB-UVB and UVA1, respectively. In order to avoid overdose, the increment of the doses were 0.1 J/cm2 for NB-UVB therapy and 1.0 J/cm2 for UVA1 therapy. Results were more successful when the treatment was administered twice a week. Positive effects (67–99% improvement) were achieved in 38.6% of psoriasis patients, in 100% of plaque type parapsoriasis patients, in 37.5% of vitiligo patients (NB-UVB), in 47.1% of atopic dermatitis patients, and in 71.5% of prurigo nodularis patients (UVA1). There were no severe side effects during these treatment periods.
Narrow-band UVB is a light source with a narrow wavelength and a peak at 311 nm. Therapy using this lamp has been introduced recently for the treatment of recalcitrant dermatoses in Europe and the United States, but there have only been a few reports in Japan. We investigated narrow-band UVB therapy on the base of narrow-band minimal erythema dose (nMED) for a 79-year-old Japanese male with recalcitrant generalized vitiligo vulgaris. Narrow-band UVB therapy was effective for his body and extremities, but not effective for the dorsa of his hands.
A 61-year-old Japanese man, who visited our clinic in April 4 2003, had suffered from occasional attacks of urticaria and anaphylactic shock associated with exercise after the ingestion of wheat for one year. Blood examination revealed that his total serum IgE was 44.5 IU/ml, RAST (Index) was 2.3 for wheat, and 2.3 for gluten. The challenge test with exercise following ingestion of wheat noodles (120 g) induced generalized urticaria and shock. The diagnosis of wheat-dependent exercise-induced anaphylaxis was made. A significant amount of gliadin was detected in his serum in parallel with symptoms during the challenge test of wheat noodles combined with exercise. However, serum gliadin was not detected after the ingestion wheat noodles alone. We concluded that the exercise induces the absorption of wheat allergen from the gut, resulting in the appearance of symptoms in the patient.
We investigated where the tracer should be injected in cases of sentinel lymph node biopsy of extensive extramammary Paget’s disease. It became clear that differences arose in the identification of the sentinel lymph node (SN) when changing the injection site of the blue dye and RI tracer. When the tracer was injected around the outermost circumference of the clinically invasive area of Paget’s disease, two or more SNs were widely identified in both sides of the inguinal region. However, when the tracer was injected only around the advanced area, one SN was detected in both inguinal regions. Considering the purpose of sentinel lymph node biopsy, it is optimal for the patient that the tracer should be injected in the advanced area of extramammary Paget’s disease when performing sentinel lymph node biopsy.