著者

Hidehisa Saeki

出版者

日本医科大学医学会

雑誌

Journal of Nippon Medical School (ISSN:13454676)

巻号頁・発行日

vol.84, no.1, pp.2-11, 2017-01-15 (Released:2017-03-22)

参考文献数

37

被引用文献数

15

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The guidelines for the treatment of atopic dermatitis (AD) issued by the Japanese Dermatological Association (JDA), which are basically designed for dermatologists, were first prepared in 2000 and revised in 2016. The guidelines for AD of the Japanese Society of Allergology (JSA), which are basically designed for allergologists, including internists, otorhinolaryngologists, ophthalmologists, and dermatologists, were first prepared in 2009 and revised in 2014. In this article, I review the definition, pathophysiology, etiology, epidemiology, diagnosis, severity classification, examination for diagnosis and severity assessment, and treatments for AD in Japan according to these two guidelines for AD (JDA and JSA). Based on the definition and diagnostic criteria for AD of the JDA, patients meeting three basic criteria, 1) pruritus, 2) typical morphology and distribution of the eczema, and 3) chronic or chronically relapsing course, are regarded as having AD. Treatment measures for AD basically consist of drug therapy, skin care, and elimination of exacerbating factors. Drugs that potently reduce AD-related inflammation in the skin are topical corticosteroids and tacrolimus. It is most important to promptly and accurately reduce inflammation related to AD by using these topical anti-inflammatory drugs. Proactive therapy refers to a treatment method in which, after inducing remission, a topical corticosteroid or tacrolimus ointment is intermittently applied to the skin in addition to skin care with moisturizers in order to maintain remission.

著者

Yuri Kinoshita Hidehisa Saeki

出版者

日本医科大学医学会

雑誌

Journal of Nippon Medical School (ISSN:13454676)

巻号頁・発行日

vol.84, no.3, pp.110-117, 2017-06-15 (Released:2017-07-19)

参考文献数

43

被引用文献数

9

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Toxic epidermal necrolysis (TEN) is a severe adverse drug reaction associated with the separation of skin and mucous membranes at the dermal-epidermal junction. Although it is rare, many treatments have been trialed because of its high mortality rate. Active interventions performed to date include the use of systemic corticosteroids, intravenous immunoglobulins (IVIg), cyclosporine, plasmapheresis, anti-tumor necrosis factor drugs and N-acetylcysteine, but none has been established as the most effective therapy. IVIg and short-term high-dose corticosteroids were regarded as the most promising treatments for TEN in a comprehensive review of all reported TEN cases from 1975-2003. When used with an appropriate dose and timing, the beneficial effects of IVIg can be maximized. Although no randomized controlled trials have been conducted, cyclosporine and plasmapheresis are considered to be beneficial. As no gold standard for active intervention for TEN has been established, the choice of treatment relies partly on the available guidelines and the experience of the dermatologist. There is still much to be investigated regarding the pathogenesis of TEN, and new findings may contribute to the identification of an effective active intervention strategy.

著者

Yuri Kinoshita Hidehisa Saeki

出版者

日本医科大学医学会

雑誌

Journal of Nippon Medical School (ISSN:13454676)

巻号頁・発行日

vol.83, no.6, pp.216-222, 2016-12-15 (Released:2017-01-27)

参考文献数

47

被引用文献数

18

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Toxic epidermal necrolysis (TEN) is a rare skin condition, most often drug-induced, known for its skin detachment and high mortality. In general, acute TEN is considered a T-cell mediated, type IV hypersensitivity disorder. It mostly results from a cumulative effect of risks from the drug structure, drug metabolism, HLA alleles and T cell clonotypes. However, the precise mechanism of TEN is still unknown. Apoptosis or necroptosis causes keratinocytes to lose their shape and adhesion, and necrosis predominates within a few days. Total epidermal necrosis separates the epidermis from the dermis. TEN is regarded as an immune reaction with predominantly CD8+ T lymphocytes, monocytes/macrophages, and natural killer cells. Impaired regulatory T-cells, T-helper 17 cells, cytotoxic granules such as perforin-granzyme and granulysin, tumor necrosis factor α, annexin, microRNA-18a-5p, and drug metabolites are all thought to be involved. From what is known, it can be assumed their mechanism is complex, and there is still much to be investigated. New findings will contribute to the identification of effective active methods of intervention.