Stevens-Johnson syndrome（SJS）and toxic epidermal necrolysis（TEN）are rare and life-threatening cutaneous adverse drug reactions with high mortality rates. While there is no established therapy for SJS/TEN, systemic corticosteroids, plasma exchange, and intravenous immunoglobulins（IVIG）have all been used to treat the condition. The inhibition of the activities of a variety of inflammatory cells and the products released by these activated cells is likely to be the major mechanism of efficacy of IVIG against SJS/TEN. Although the utility of IVIG for treating SJS/TEN is still controversial in SJS/TEN, this might be due to differences in the doses of IVIG administered and/or the timing of their administration, or the insufficient suppression of inflammation. Recently, clinical studies conducted in Japan and other countries have shown that IVIG are effective against early stage SJS/TEN when used together with steroids. Therefore, the administration of IVIG together with steroids should be considered as a treatment for patients with refractory SJS/TEN. Although the severity and rarity of SJS/TEN make it difficult to assess the efficacy of novel treatments in large clinical randomized controlled trials, further studies are needed to determine the therapeutic efficacy of IVIG.

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　Patch testing（PT）is useful for identifying the causes of dermatitis that is resistant to palliative treatment. However, PT of substances that are encountered in daily life sometimes produces false-negative results, which can cause dermatologists to overlook possible causes of dermatitis, even if they have conducted careful interviews with patients prior to PT. The Japanese standard allergens（JSA）are useful for identifying allergens among substances that produce false-negative results during PT and for drawing attention to unexpected causes of allergic reactions that might not be suspected before PT. When performing PT, the JSA should be used as much as possible. Since 2015, 22 standard allergens have been readily available in Japan. It is expected that more Japanese dermatologists will employ PT in daily clinical practice.

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　Recent clinical and experimental studies have provided insights into the pathological mechanisms of alopecia areata and revealed that it is an organ-specific and cell-mediated autoimmune disease.　Various triggers, such as viral infections, trauma, hormones, and emotional/physical stressors, can activate autoreactive cytotoxic T cells（CTL）, which produce interferon（IFN）-γ. IFN-γ abrogates the immune privilege of hair follicles（HF）, upregulates CXCL10 expression, and induces higher interleukin 15 expression in HF keratinocytes. HF autoantigens are subsequently recognized by CTL, which results in hair loss. During these immunological responses, cytokines and chemokines are regarded as key players that mediate autoimmune inflammation. Interestingly, JAK inhibitors have been found to produce dramatic improvements in alopecia areata in both humans and C3H/HeJ mice. This review suggests that therapies that target cytokines/chemokines could be useful for alopecia areata.

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　A 62-year-old garbage collector who had worked for 11 years in an off-set printing factory developed infiltrative erythematous dermatitis on her forearms. The patient was positive on patch testing with 2 components of the etching solution compounded in the fountain solution used for printing；component A contained 5-chloro-2-methyl-4-isochiazolin-3-one（MCI）and 2-methyl-4-isothiazolin-3-one（MI）, and component B contained MI and 2-n-octyl-4-isothiazolin-3-one（OIT）. She also reacted positive to Kathon CG（MCI/MI, 100ppm）, MI（0.1% aq）, OIT（0.1 and 0.01%pet）, and 1,2-benzisothiazoline-3-one（BIT, 0.5%pet）. The patient’s dermatitis developed 4-months after MCI had first been added to the etching solution, and it seemed that she had become sensitized to MCI, and that simultaneous or cross sensitization to MI, OIT and BIT had also occurred.

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　A 45-year-old woman with atopic dermatitis, who had eczema on her face and limbs, was topically treated with Locoid^® ointment and Lidomex^® cream. The following day, erythema and swelling developed, and she consulted our hospital. We suspected contact dermatitis caused by the topical ointments and performed patch tests. The patch tests produced positive reactions to Locoid^® ointment and Lidomex^® cream, and patch testing with the ingredients of these drugs detected positive reactions to the main ingredients; i.e., hydrocortisone butyrate and prednisolone valerate acetate. In addition, patch tests involving other topical corticosteroids produced a positive reaction to Almeta^® ointment, which had been used to treat the patient after she had visited our hospital. These results indicate that the patient had become sensitized to the abovementioned substances and that the Almeta^® ointment had also provoked symptoms because of its partial structural similarity with the structure of the steroid nucleus.

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　An 87-year-old woman developed warm, painful, and poorly demarcated erythema on both lower legs. The combination of these clinical manifestations, a slightly elevated serum C-reactive protein level, and leukocytosis led to a tentative diagnosis of cellulitis. However, the administration of antibiotics did not improve her symptoms. A histopathological analysis of a skin specimen taken from the erythematous lesion on her left leg revealed septal panniculitis and so we diagnosed the patient with erythema nodosum. Bed rest did not improve the patient’s symptoms, and her serum C-reactive protein levels continued to increase. A computed tomography scan revealed thickening of the gastric wall together with adenopathy of the perigastric and periaortic lymph nodes, and a gastric ulcer was found during endoscopy. A histopathological analysis of a biopsy specimen taken from the ulcer revealed diffuse large B-cell lymphoma. The final diagnosis in this case was erythema nodosum accompanied with Malignant Lymphoma. The possibility of a dermadrome involving an underlying malignancy should be considered in patients with persistent or refractory erythema nodosum, especially in elderly patients.

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　A 48-year-old woman developed photocontact dermatitis on her forearm due to sunscreen. The previous summer she had developed photocontact dermatitis on the dorsal side of her left foot after using a plaster containing ketoprofen. We subjected the sunscreen and the ingredients of the ketoprofen-containing plaster to patch and photopatch testing.
　The photopatch test produced a positive result for ketoprofen, and both the patch and photopatch tests produced positive reactions to the ultraviolet A absorbent avobenzone, which was present in both the sunscreen and plaster.
　We surmised that the patient’s most recent episode of photocontact dermatitis had been caused by the avobenzone in the sunscreen and advised the patient to avoid this substance. Thus, patients with a history of photocontact dermatitis caused by a ketoprofen-containing plaster should undergo patch and photopatch testing of all of the ingredients in such plasters and should be advised of the implications of any reactions they display to components that are used as ultraviolet absorbers.

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