A new classification of lupus erythematosus was proposed. The new one is divided into four sections (Tab. 3) and, I hope, should be used by checking the concerned items in four sections. As compared with the previous ones (Tab. 1 and 2.), the new one will give some benefit to understand the present status of the patient with lupus erythematosus at each time when examinations were performed, and also will be of use for the treatment of the patients.

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Histological and histochemcal studies of systemic lupus erythematosus (SLE) were performed on 31 autopsy cases. Results obtained and brief comments on them were as follows. Hematoxylin bodies (HX bodies) and fibrinoid necrosis of the vascular system were the main pathologic condions in SLE. HX bodies were found in 16 cases, with regularity in areas of fibrinoid necrosis. They were considered to represent the in vivo counterpart of the in vitro LE phenomenon, even though some tinctorial characteristics were different. HX bodies were PAS positive, not metachromatic, and might show reduced Feulgen reaction. When some of HX bodies were ingested by polymorphonuclear luekocytes, LE cells could be detected in the tissue. Fibrinoid necrosis had occasionally been described in other conditions and considered not pathognomonic of SLE. However, in SLE vascular lesions were widespread, and so often took the form of fibrinoid necrosis. Not only Libman-Sacks endocarditis but also glomerular lesions called “wire loop” lesion and “hyaline thrombi” could be regarded as variants of fibrinoid necrosis. In this meaning, fibrinoid necrosis could be regarded as almost pathognomonic of SLE. Fibrinoid necrosis of small vessels was frequent and encountered in 16 cases. Severe necrotizing angiitis as seen in periarteritis nodosa was noted in 6 cases. Endocarditis occurred in 10 cases and fully developed lesions conforming to the description of Libman and Sacks were present in 5 cases. Fibrinoid necrosis of the cardiovascular system was a common site of HX bodies, and not infrequently had a diffuse hematoxyphilic tincture suggesting the deposition of the nuclear substance. Lupus nephritis characterized by pleomorphic and irregular glomerular damage was noted in 25 cases. The most distinctive features included necrosis (often fibrinoid necrosis), karyorrhexis, hyaline thrombi, wire loop lesion and HX bodies. The frequency of the latter three findings was 48%, 61% and 39%, respctively. Thickening of the basement membrane refered to as wire loop lesion was brightly eosinophilic and a hard refractile appearance. Hyaline thrombi were eosinophilic globules filling the lumen of capillaries and closely resembled wire loop lesions. Both lesions had similar staining properties as noted in the vascular fibrinoid and were frequent sites of HX bodies. They showed not rarely a rather diffuse hematoxyphilic tincture, where Feulgen reaction was weakly positive. Another important and the most frequent change in SLE was the concentric lamination of dense collagen fibers arround the central arterioles of the spleen. This change called onion skin lesion was noted in 29 cases. The most remarkable pulmonary change in SLE was a variety of the interstitial pneumonia. This lesion occurred in 11 cases and the most distinctive features included were alveolar exsudate containing fibrin, hyaline membrane, HX bodies, formation of Masson bodies, and fibrosis of alveolar septa. The majority of lesions in SLE might be induced by the immune complexes deposited in the affected vessels. The lesion is histologically characterized by changes in the vessel wall leading to fibrinoid necrosis and the basement membrane thickening, in which deposition of immunoglobulin, complement and fibrinogen are detected. The presence of hematoxyphilic substance with positive Feulgen reaction suggests the deposition of the nuclear substance. Actually DNA antigen has been demonstrated in the glomeruli and the acid eluate from affected glomeruli is said to be rich in antinuclear antibodies. When regard to the pathogeneis of SLE, simultaneous presence of DNA and anti-DNA antibodies in the lesion should raise attention to the role of immune complexes on the vascular system including renal glomeruli.

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Alteration in serum immunoglobulin levels (IgG, IgA and IgM) of patients with lupus erythematosus was studied. Sera were obtained from 25 patients with SLE, 14 patients with DLE, and 9 patients with chilblain lupus. There was significant tendency for elevation of IgG and IgA levels in exacerbation stage of SLE. In DLE, three immunoglobulin levels were slightly elevated, but there was no great difference between DLE and normal subjects. The sera of chilblain lupus showed high levels of immunoglobulins. K/L ratio of light chain was almost normal. IgG/IgA ratio covered a wide range in SLE and chiblain lupus. It was suggestible that there were some disorders in producing system of immunoglobulins (IgG and IgA) in SLE and chilblain lupus.

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Three studies were carried out on the lymphocytes of the patients with Lupus Erythematosus in order to: (1) look for chromosomal aberrations in peripheral lymphocytes; (2) examine the function of immunologically competent lymphoid cells (cellular antibody); (3) determine the presence or absence of immunoglobulin production by cultured peripheral lymphocytes. Various chromosomal aberrations were frequently observed in cultured lymphocytes from patients with SLE, but few in DLE. Significantly increased frequency of chromosomal aberrations in SLE, especially G group chromosomal abnormalities including G trisomy, suggests that there is an association between chromosomal abnormalities and autoimmune disease. The examination of delayed hypersensitivity indicated that there was a functional failure of immunologically competent lymphoid cells in SLE. The direct immunofluorescent staining showed that PHA stimulated lymphocytes from patients with SLE contain γ-globulin, IgG and IgM. It seems likely that these cells produce each immunoglobulin.

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To know the pathophysiology of erythematodes, the serum complement level (CH50), its diurnal changes, the titers of nine components of the complement and kinin-like substance were measured.
1) Normal level of CH50 was 37.7±5.8 u.
2) CH50 in various skin diseases was within 29 to 70 unit. There was no specificity on CH50 level in DLE, but CH50 in SLE was under 30 u. in almost cases.
3) Diurnal variation of CH50 assayed every 4 hours was no significant differences between normal control and SLE. It was round 6 u. in both.
4) An acute decrease of CH50, C1, C4, C2, C3, C5, C6, IA and kinin-like substance was observed before the clinical severe condition.

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A 21-year-old man with angiokeratoma corporis circumscriptum naeviforme was reported. Keratotic hemangiomatous lesions, which had been spread and enlarged very slowly since his birth, were systematically noted on the left side of buttocks and of lower limbs. Biopsy specimens revealed that a marked hyperkeratosis, without parakeratosis, an intensive dilatation of capillaries in the upper dermis just beiow the epidermis, and a distinct proliferatioln of immature endothelial cells of newly formed capillaries in the deeper dermis. The patient was successfully treated with a plastic surgery, i. e., resection of the lesions and skin grafts repeatedly carried out. Thirty-four cases with the disease reported in Japan, were reviewed. As the results, it was considered a marked hyperkeratosis of the lesions were caused with defects of nutrition and oxygen due to a disturbance of blood circulation in congenital hemangiomatous skin changes.

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We have observed 15-month-old infant who had primary herpetic infection of the right index finger. From the skin lesion herpes simplex virus was isolated in Vero cell culture and the identification was performed electronmicroscopically. The primary nature of the atack was proved by the demonstration of a marked rise in neutralizing antibodies from under 1: 2 to 1: 32 between the 4th day and 11th day.

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The effects of corticosteroids were studied on guinea pig DNCB dermatitis, using the following methods: hematoxylin-eosin, PAS, toluidine blue stains and succinic dehydrogenase, phosphorylase and alkaline phosphatase reactions. In allergic dermatitis, eczematous changes appeard on the epidermal follicles 3 hours after challenging. These changes extended gradually into the entire skin. On the contrary, prmary irritant dermatitis showed epidermal necrosis and subepidermal bullae reaching their peak 6∼12 hours after induction. Findings of improvement were observed 24 hours after induction. Triamcinolone acetonide, therefore, was injected intralesionally on test sites of the guinea pigs 1 hour prior to the challenging. Histochemical studies were made 6 hours and 48 hours after challenging. 48 hours after challenging, improvement of the epidermis was observed on the basal layer in the HE, toluidine blue stains and succinic dehydrogenase reaction.

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Vitamin A acid was applied to the dorsal aspects of guinea pig earlobes and psoriasiform tissue reaction was produced microscopically and the suppressive effects of corticosteroids on the epidermal proliferation were statistically analysed using ³H-thymidine autradiography. The results were as follows.
1) Vitamin A acid applications for successive 3 days produced epidermal cell proliferation. The degree of epidermal proliferation became more intense in the group of guinea pigs, to which, vitamin A acid was applied for 7 to 21 days. The epidermal proliferation continued at least for one week.
2) Epidermal proliferation was not suppressed in the group of combined vitamin A acid and corticosteroid administration and in the group of animals to which corticosteroid ointments were applied after the discontinuance of viamin A acid application.
However, subcutaneous injection of corticosteroids after the dicontinuance of vitamin A acid application was statistically found to suppress epidermal proliferation.

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As a result of the investigation made of the incidence of urticaria classed by age and sexuality, results of clinical biochemical tests, tabulation of the antihistaminic agents used, and results of the treatments with the antihistaminics on 277 patients with urticaria the authors have encountered in the last ten months, the following conclusion has been reached:
1. Results of clinical biochemical tests:
a. Hepatic function tests (S-GOT and S-GPT):
The S-GPT and the S-GOT have been fonud to be scarcely correlated with urticaria.
b. RA reaction, ALSO value, and peripheral white blood cell count: These test items have been found to scarcely vary with urticaria.
c. CRP:
The CRP has been found to fall along with improvements in the condition.
2. Incidence of urticaria classed by age and sexuality:
The incidence, when classed by age, has proved to be high in the age grades of teenage to 30′s, and when classed by sexuality, to be about two times higher in females.
3. Antihistaminic agents:
Homochlorcyclizine (Homoclomin) has been chiefly used, and a number of patients have been medicated with two different antihistaminic agents in conjunction.
4. The therapy with antihistaminic agents have cured almost all patients within 20 days.
The treatment with histaglobin has been suggested for patients who have not been improved in condition within 20 days.

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Ammonia metabolism in the human skin was studied by skin ammonia which was determined with Okuda’s method for direct quantitative colorimetry as well as column chromatography. The results are as follows.
1) The human skin of a whole leyer contained 3.3±1.3μg of ammonia per 100mg of the skin by wet weight.
2) The highest ammonia level was detarmined in the lower dermis portion.
3) Ammonia biosynthesis in the human skin was as potential as in the muscles, which amounted 2.7μg/100mg of the skin by wet weight after incubation for 90 minutes at 37°C. However a similar biosynthesis was not observed in the subcutaneous fat tissue. The skin ammonia was redeemed to be produced most preminently in the epidermis and the upperdermis.
4) The hnman skin ammonia was considered to be produced primarily from adenosine and a series of the nucleotides, i. e. ATP, ADP and AMP as well as amino acids.
5) Two principal biosynthetic pathways of the human skin ammonia are presumed to be one by which IMP and ammonia are produced through AMP deamination by AMP deaminase, and another, Inosine and ammonia produced through adenosine deamination by adenosine deaminase.

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Rinderon VA ointment (subsequently abbreviated as RD-VAO) was painted on the field of treatment before electron beam therapy for malignant tumors to attempt to alleviate the skin injury now accepted as unavoidable with this therapy. To evaluate the response, 18 postoperative cases of malignant goiter and one case of metastases to the cervical glands from a malignant mediastinal tumor, were used. The cases consisted of 16 females and 3 males. Among the total 19 cases, ED-VAO was painted onto the frontal region of the neck of 3 cases and RD-VAO base (vehicle) was applied to 3 cases. In another 3 cases the field size was divided into two and RD-VAO applied to one side and the base applied to the opposite side. The remaining 9 cases served as controls. Ten MeV electron beam therapy was carried out to the frontal regions of the neck. After 6000 rad, a total lesions dose, comparison studies were carried out on macroscopic skin changes and on microscopic, obtaining a skin slice from both sides of neck in one case where the field size was separated into two. As a result it was revealed that; (1) in cases painted with RD-VAO, the skin injury was markedly alleviated as compared with the control group, (2) the specimens painted RD-VAO showed milder histological changes as compared with specimens from areas painted only with RD-VAO base (vehicle), and (3) the part painted only with the base showed some decrease in skin injury.

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