Urticaria has long been known to be a reaction pattern of the skin which may be produced by a considerable number of individual causes. It is a vascular reaction pattern of the skin characterized by the appearace of transient erythematous or whitisch swelling in the skin. The study of the mechanism of the production of urticaria has been done and the following results were obtained.
1) Among the various chemical mediators histamine might be the most potent to cause the urticaria. It might released from the mast cells surrounding of the capillary bed in upper dermis and caused the urticaria by the vasodilation and the increase of capillary permeability. Most of histamine liberators which release the histamine from mast cell might thought to go through the vessels to dermis in urticaria.
2) Dermographism might caused by kinin rather than histamine.
3) The category of cholinergic urticaria may be necessary to discuss more in Japan.

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In oder to discuss the classification of drug eruptions, the definition of those must be clarified. Many authors had described various concepts about drug eruptions, but following definition considered to be more appropriate, i. e., drug eruptions are the all dermatologic disturbances which may be caused by internally absorbed and circulating drugs or those metabolites. According to the definition, the clinical types of those would be classified into three categolies as follows.
1. Original types: Urticaria, eczematous type, non-specific erythemas, erythema multiforme-like eruption, bullous type, fixed eruption, purpuras, pigment anomalies, enanthemas, acneiform eruptions, erythema nodosum-like, erythematodes-like, vasculitis-like, lichen planus-like, psoriasis vulgarislike parapsoriasis-like, pustular psoriasis-like eruptions and others.
2. Severe forms: Erythrodermia (exfoliative dermatitis), muco-cutaneous ocular syndrome and toxic epidermal necrolysis.
3. Iatrogenic skin disorders: Herpes zoster, warts, keratoma, cancer, furunculosis, candidiasis, candidiasis black hairy tongue, pellagra, porphyrinuria, alopecia, hypertrichosis, poliosis, hyperidrosis, chromoidrosis, atrophy and ulcer.
If the term of drug eruption would be used in a narrow sense, the last must be excluded.

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The pathogenesis of drug eruption was studied clinically and experimentally. While no direct evidence for the increased formation of antibodies in patient with drug eruption was obtained the patients with experimentally induced drug eruption were noted with remarkable alteration of immuno-globlin (γG, γA and γM) and the complements titer (C′H₅₀) after and before administration of the suspected drugs, and decrease in white blood corpsules and thrombocytes after causative drugs of hypersensitivity were given. Accordingly, the establishment of sensitizing state due to diathese would be of the first necessity. Among the factors which promote the onset of drug eruption include especially autonomous nerves specifically the parasympathic tension, which intensifies the tendency for exudative inflammation of the skin and scarring. Furthermore, primary and the sencodary liver dysfunction, and the decreased function in the ammonia diposal as well as paticipation of histamin as a chemical mediator which formulate circulus viciosus responsible for advancement in the process of the disease. Finally potentialities of abnormal production of antibody and the promoted reaction in the various organs including the skin play grate role in the pathogenesis of the drug eruption.

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The diagnosis of a drug eruption is sometimes easy and at other times almost impos sible to establish. When the clinical history is suggestive and the skin test are positive, the diagnosis is easily made. However, in the majority of the patients with drug eruptions, skin tests are negative in spite of an obvious history. Therefore, it is very important to have a reliable clinical or in vitro technique by which drug eruption may be diagnosed. The relations between the causative drugs, the forms of eruptions and skin tests were investigated from 120 patients for the past five years. Skin tests (patch and intradermal) were positive only in 30%. The polivalent and cross-sensitivity was discussed in view of skin tests in one patient who was thought to be sensitive to various drugs. We have applied lymphocytic transformation and the incorporation of tritiated thymidine of blood lymphocyte cultured in vitro in the presence of causative drugs. Lymphocye cultures from 25 patients who are sensitive to various drugs have been studied. The test have been positive only in 5 cases. Hence, it is concluded that, though a response is demonstrable in certain cases, this is not useful as a in vitro technique in drug eruptions.

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1) The principle of the therapy of drug eruption is the confirmation of the causative drug.
2) The first choice in the treatment of severe form is steroid hormone together with fluid supplement. Findings in blood, liver and kidney function should be given sufficient attention in the course of treatment. All the questionable drugs are discontinued.
3) Special treatment is seldom necessary in mild form. In order to avoid the repeated occurrence, the causative drugs should be confirmed.
4) An allergy card should be made and given to the patient to carry around.

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A man of 40 years, who worked at a coalmine in Fukuoka Prefeture in 1954, had a rash at his right scapula area. The rash spread gradually in his right upper arm and his back. Its color was red brown, it was struck with yellow white scales and its periphery rose. He visited our skin clinic at Kagoshima University Hospital and was diagnosed as Chromblastomycosis disease with Hormodendrum pedrosoi. He was cured by various treatments with intravenous dropping injection (total 1330 mg), intradermal injection (total 1429.5 mg), 3% ointment application ODT therapy of Amphotericin B or surgical excision in three years.

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