Biomedical subjects
Publications and source records attributed to W Torinuki.
A 2.5-year-old boy presented with skin lesions consistent with Mucha-Habermann disease, which appeared about 5 days after an injection of freeze-dried live attenuated measles vaccine. He responded to both oral and topical corticosteroid therapy. To my knowledge, this represents the first such association of Mucha-Habermann disease with virus vaccination.
Two patients with solar urticaria are described. They complained of transient pruritic erythema, but not frank wheal, on sun-exposed areas. However, urticarial wheals were elicited by polychromatic radiation in the ultraviolet and visible light ranges; the action spectra for solar urticaria ranged from 400 to 550 nm in case 1 and from UVA to 550 nm in case 2. In patients manifesting only transient pruritic erythema on sun-exposed areas, phototests are essential for making a confident diagnosis of solar urticaria.
I report a case of photocontact dermatitis due to piroxicam gel, a nonsteroidal anti-inflammatory drug. A 62-year-old man developed pruritic eczematous lesions after applying the gel for 2 days. The patient reacted positively to photopatch testing with ultraviolet A and piroxicam (1% and 0.1% in petrolatum). In addition, the patient had positive patch tests to thimerosal, thiosalicylate, and in vitro-irradiated solution of piroxicam plus human serum albumin, but the tests with the mercurial compounds were negative. These results support the close relationship between sensitivity to thiosalicylate component of thimerosal and photosensitivity to piroxicam, as indicated recently.
In six Japanese patients with papulovesicular light eruption (PVLE), photoprovocative tests were performed by irradiating UVA or UVB on the skin of the back on three consecutive days. One patient developed the typical lesion of PVLE at the test site with two consecutive daily irradiations of UVA. The remaining 5 patients had no abnormal phototest reactions. It was obvious that UVA plays an etiological role in at least some cases of PVLE.
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To evaluate the possibility of ultraviolet (UV) rays as an aggravating factor of atopic dermatitis (AD), UV-B phototest was performed in patients with AD. Resulting, minimal erythema doses for UV-B were all within normal range and AD lesions were not reproduced by irradiation. UV-B may not be an important factor for skin aggravation in patients with AD.
We quantitated numbers of mast cells in the sclerotic skin noted on the dorsa of the hands of 10 patients with porphyria cutanea tarda (PCT), and compared them with those of diffuse scleroderma and healthy controls. Mast cell counts in sclerodermoid skin of PCT patients were significantly greater than those in involved skin of 9 patients with diffuse scleroderma in its late stage and also greater than those in normal skin of 8 controls. When mast cell density was analyzed according to the depth of the dermis, an 84% increase was noted in the uppermost layer (0-0.2 mm in depth) and a 150% increase in the second uppermost layer (0.2-0.4 mm in depth) in the patients with PCT when compared with those in the corresponding sites of the controls. These results suggest a possible role of mast cells in the pathogenesis of sclerodermoid skin of PCT.
By using single radial immunodiffusion, plasma levels of four complement-modulating proteins, i.e. C1 inhibitor (C1INH), C4-binding protein (C4bp), factor H and factor I were measured in 42 psoriatic patients and in 60 patients with other inflammatory skin diseases in comparison with 27 normal controls. In psoriatic patients and those with related pustular dermatoses, the levels of C4bp, factor H and factor I were significantly increased. They correlated well with both extent of skin changes and disease activity. In contrast, in nonpsoriatic inflammatory dermatoses only factor H values were significantly increased in toxic erythema and factor I in atopic dermatitis. These results offer additional support for the hypothesis that the complement system is involved in psoriasis and related sterile pustular dermatoses.
To determine the long-term cutaneous side effects of methoxsalen phototherapy (PUVA) and Goeckerman regimen, a total of 151 Japanese psoriatic patients treated with PUVA, Goeckerman regimen, or both therapies in our department from 1976 to 1986 were evaluated for skin cancers. Sixty-seven patients had been treated with PUVA, 43 with Goeckerman regimen, and 41 with both therapies. One patient alone (62-year-old man) developed squamous cell carcinoma on the leg with cumulative ultraviolet A (UVA) dose of only 51 joules/cm2, he had a history of treatment with superficial x-ray therapy to this area 30 years prior to PUVA. The cancer was detected after 1.4 years of PUVA treatment. However, other patients at follow-up, even those who had received a cumulative dose of UVA of more than 1000 joules/cm2, had no skin cancer after more than 2 years. This report in Japanese patients confirms that only previous exposure to other risk factors such as ionizing radiation appears to be a most important factor for skin cancer formation in PUVA-treated Japanese patients.
We found an increased amount of immunoreactive tyrosinase in human melanocytes after 6-d culturing with vitamin D3 (cholecalciferol). Most of these melanocytes became more dendritic and swollen in a fashion similar to that noted in the skin after ultraviolet irradiation. However, 7-dehydrocholesterol (pro-vitamin D3) or 1 alpha,25-dihydroxy-vitamin D3 (activated vitamin D3) were found to have little effect on the same system. Because vitamin D3 is known to be photochemically converted from pro-vitamin D3 in the skin by ultraviolet irradiation, the mechanism of human skin pigmentation after ultraviolet irradiation, thus far unknown, may be at least partly explained by this stimulating effect of vitamin D3 on melanocytes.
An unusual case of 'photosensitive psoriasis' is reported. This patient had experienced an exacerbation after sea-bathing, and psoriatic eruptions were observed on the sun-exposed areas of the body. Phototesting with ultraviolet-B (UV-B) revealed his minimal erythema dose to be within normal limits. Three to four weeks after phototesting, however, he developed a psoriatic macule on the area exposed to the suberythematous dose of UV-B. The histologic features of the skin lesion provoked by UV-B irradiation were similar to those of naturally occurring lesions on areas covered by clothes. Moreover, failure to reproduce skin lesions following tape-stripping ruled out a proneness of this patient to develop the Köbner phenomenon nonspecifically.
By using single radial immunodiffusion we measured the plasma levels of four complement modulating proteins, i.e., C1 inhibitor, C4-binding protein, factor H and factor I in 19 psoriatic patients in comparison with those of healthy controls. Except for C1 inhibitor which was only marginally elevated, they were found to be significantly increased in psoriatic patients. When psoriatic patients were classified into subgroups based on the clinical severity, the levels of factor H and those of factor I showed a close positive correlation with the activity and extent of the skin lesions, whereas such clear relationship could not be found with C1 inactivator or with C4-binding protein. These results offer additional support for the hypothesis that the complement system is involved in psoriasis.
To elucidate the pathomechanisms of irritant pustular dermatitis and to evaluate the role of leukocytes in pustulation induced by croton oil, we compared the skin responses in leukopenic-and decomplemented guinea pigs with those in control saline-injected animals, to 1% croton oil application. Both decomplemented and control animals responded similarly to croton oil, showing erythema and pustulation at 24 h after topical application; microscopically numerous mononuclear and polymorphonuclear cells infiltrated the skin. Meanwhile, the clinical and histopathological response of leukopenic animals to croton oil was significantly depressed. Time-course study of inflammatory infiltrate in the dermis of controls revealed that mononuclear cells preceded the infiltration of polymorphonuclears. Although leukocytes constitute an important component in croton oil dermatitis, our results suggest that unclarified chemical mediators, other than complement-derived chemotactic factors, play a crucial role as a primary chemoattractant in the production of pustulation at the croton oil-applied site.
We used patch testing to compare the ability to elicit contact sensitivity to dinitrochlorobenzene (DNCB) of uninvolved with vitiliginous skin of 31 patients with vitiligo. The induction of DNCB contact sensitivity was possible in the vitiliginous skin in the same way as in normal skin. The DNCB contact sensitivity reactions, however, were generally diminished in vitiliginous skin, although the number of cases showing similar DNCB contact reactivity between normal and vitiliginous skin increased when the sensitization procedure was performed in vitiliginous skin instead of normal skin. On the other hand, delayed skin reactions to intradermally injected Candida albicans antigen were not suppressed in vitiliginous skin. The number of Langerhans' cells was not decreased in vitiliginous skin as compared with that of normal skin. The epidermal cells derived from vitiliginous skin, however, tended to show a lower stimulatory effect in the allogeneic mixed skin cell lymphocyte culture reaction than those from normal skin. These results suggest a possibility of functional impairment of Langerhans' cells in vitiliginous skin.
Epidermal cysts are one of the most common tumors of the skin. Although asymptomatic ordinarily, they may sometimes become severely inflamed with massive invasion of polymorphonuclear leukocytes (PMN). We studied in vitro PMN chemotactic properties of the aqueous extract prepared from the horny material of epidermal cysts obtained from three patients. A crude aqueous extract of the horny content of the cysts showed PMN chemotactic activity, which, however, was less than that of a horny layer extract prepared from normal skin. Characterization of PMN chemotactic activity using a Sephadex G-75 column showed a peak in the low molecular weight fractions eluting between the vitamin B12 and phenol red markers, which corresponds with the peak of absorbance at 280 nm. The chemotactic substances withstood boiling and trypsin or protease digestion. Although the chemotactic activity was partially ether-extractable, the presence of leukotriene B4 was not demonstrated by radioimmunoassay. In addition to their own chemotactic activity, the horny extracts of epidermal cysts showed cytotaxigenic properties in the presence of fresh serum.
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Using OKT6 monoclonal antibody, we investigated the number of epidermal Langerhans' cells (LCs) in involved skin from patients with psoriasis, before and after mechlorethamine (HN2) or PUVA treatment. The number of LCs remained at about pretreatment number during three weeks of HN2 treatment alone, though they were reduced after 10 systemic PUVA treatments. Therefore, in contrast to PUVA which influences LCs, HN2 seems to have little effect on LCs. LCs in psoriatic plaques were, in number, 3-4 times less numerous than those in uninvolved, nontreated epidermis.
To evaluate the role of the complement system in inflammation induced by chlorpromazine (CPZ) and ultraviolet-A (UVA) irradiation, the phototoxic response in guinea pigs decomplemented by cobra venom factor was compared with that in saline-treated animals. Phototoxic lesions were induced in animals by intradermal injections of CPZ solution, followed by UVA irradiation. Clinically, the normal animals developed erythema and induration which showed a maximal response at 10 h with a mean value of 1.6 on a scale of 0 to 3+. The complement-depleted animals showed a weaker clinical response than the normal animals 6-24 h postirradiation (p less than 0.05). These clinical changes were associated with increased vascular permeability, as demonstrated by extravasation of i.v. injected Evans blue in saline-treated animals. In vitro UVA irradiation of serum containing CPZ resulted in a dose-dependent diminution of total complement activity. Such irradiated serum showed immunoelectrophoretic C3 conversion. These results suggest that the complement system is involved in the development of CPZ-induced phototoxic lesions.