Disseminated superficial actinic porokeratosis like drug eruption: a case report. (1/192)

We report a 54-year-old male patient who developed an unusual form of generalized drug eruption. He had pain and breathlessness on the left chest wall. He had history of taking several drugs at private clinics under a diagnosis of herpes zoster. Two weeks later he had a generalized skin eruption. Examination showed multiple variable sized, mild pruritic, erythematous macules and papules on the face and upper extremities. Skin lesions take the form of a clinically consistent with disseminated superficial actinic porokeratosis (DSAP). Methylprednisolone 16 mg, astemisole 10 mg, oxatomide 60 mg was prescribed. Topical corticosteroid cream was applied. Within two months, his eruption had cleared almost completely. The pathogenetic mechanisms of this case are unclear, but drug and UV light have been considered.  (+info)

Anti-elongation factor-1alpha autoantibody in adult atopic dermatitis patients. (2/192)

Adult atopic dermatitis (AD) patients develop severe facial lesions, which sometimes distribute in sun-exposed areas similar to the rash of systemic lupus erythematosus. To declare autoimmunity in the pathogenesis of AD, we investigated serum antinuclear antibody (ANA) in 256 adult AD patients and identified its ligands. A high titer of ANA was found in 31.3% of AD patients and 75% of the ANA showed a homogenous pattern. Sixty-five percent of ANA(+) sera reacted to a 52 kDa protein (p52) in HeLa cell immunoblots. By screening the HeLa cell cDNA expression library with anti-p52 sera, a clearly positive clone was isolated. The sequence of this cDNA was identical to human elongation factor (hEF)-1alpha. The eluate of IgG bound to hEF-1alpha-glutathione S-transferase (GST) fusion protein recognized a band at 52 kDa in a HeLa cell immunoblot, and stained Hep-2 cell nuclei and cytoplasma as reported in hEF-1alpha distribution. The anti-p52 AD sera recognized the hEF-1alpha-GST fusion protein. The anti-hEF-1alpha antibody-positive AD patients were characterized by higher facial involvement and lower white blood cell counts compared with antibody-negative patients. The present results suggest the possible involvement of autoimmunity in the pathogenesis of adult AD.  (+info)

A retarded rate of DNA chain growth in Bloom's syndrome. (3/192)

The cytogenetic observation that homologous chromatid interchange occurs in Bloom's syndrome more often than normal prompted an investigation of DNA replication in that rare genetic disorder. Using DNA fiber autoradiography, an estimation was made of the rate of one component of ongoing DNA replication, DNA chain growth. The rate in Bloom's syndrome dermal fibroblasts in tissue culture was found to be significantly slower than that in normal control cells. (The rate was found to be normal in Fanconi's anemia cells.) The explanation for the retarded chain growth may be either that an enzyme concerned directly with semiconservative DNA replication is defective or that a defective enzyme not itself concerned directly with replication results in disturbed cellular metabolism which in turn affects replication.  (+info)

Epidemiology of the incidence of oro-facial noma: a study of cases in Dakar, Senegal, 1981-1993. (4/192)

Oro-facial noma is an oral gangrene occurring in early childhood in extremely poor areas. As many as 70-90% of those with noma die, and to date, there is no satisfactory treatment to fight this disease. Within the context of the World Health Organization international program against noma, a 13-year retrospective study based on clinical records was carried out in Dakar, Senegal in an attempt to understand the epidemiology of noma. Between 1981 and 1993, 199 cases of noma were identified, among them; 36.7% were acute cases and 63.3% showed sequelae. Chronic sequelae of noma were seen in patients 2-41 years of age, but the acute phase of noma was found only in young children (77.7% in those 1-4 years of age, maximum age = 9 years, mean age +/- SD age = 3.4 +/- 1.9 years). A total of 73.1% of the cases with acute disease were reported in the Dakar, Diourbel and Kaolack regions during the dry season (57.0% of the cases). The lesions of progressive noma were localized mainly on the upper lip (42.4%) and the cheek (31.1%). A total of 96.9% of the patients with acute diseases were had poor general health with serious associated diseases; only 20.0% had a good vital prognosis. The development of epidemiologic surveillance programs for noma should be a public health priority in Senegal.  (+info)

Is demodex really non-pathogenic? (5/192)

Although usually considered a non-pathogenic parasite in parasitological textbooks, Demodex folliculorum has been implicated as a causative agent for some dermatological conditions, such as rosacea-like eruptions and some types of blepharitis. Several anecdotal reports have demonstrated unequivocal tissue damage directly related to the presence of the parasite. However, this seems to be exceedingly rare, in contrast with the marked prevalence of this infestation. We have had the opportunity to observe one of such cases. A 38-year-old woman presented with rosacea-like papular lesions in her right cheek. Histopathological examination revealed granulomatous dermal inflammation with a well-preserved mite phagocytized by a multinucleated giant cell. This finding may be taken as an evidence for the pathogenicity of the parasite, inasmuch as it does not explain how such a common parasite is able to produce such a rare disease.  (+info)

Elastin peptides induce migration and terminal differentiation of cultured keratinocytes via 67 kDa elastin receptor in vitro: 67 kDa elastin receptor is expressed in the keratinocytes eliminating elastic materials in elastosis perforans serpiginosa. (6/192)

To delineate the molecular mechanism of transepidermal elimination of dermal elastic materials in elastosis perforans serpiginosa, the interaction between elastin and cultured keratinocytes was studied in vitro. Synthetic elastin peptide VGVAPG elicited chemotactic responses to the cultured keratinocytes at the dose of 10-9 M. Treatment of keratinocytes with 10-6 or 10-5 M elastin peptides resulted in the suppression of cell growth and the increased expression of involucrin and transglutaminase-1, markers of terminal differentiation. When cultured keratinocytes were treated with the elastin peptides, the expression of 67 kDa elastin receptor was increased. The induction of terminal differentiation by elastin peptides was attenuated by the treatment with the combination of anti-67 kDa elastin receptor antibody. The results indicate that elastin is a potent inducer of migration and terminal differentiation of cultured keratinocytes, which is mediated by the 67 kDa elastin receptor. In the lesional skins of patients with elastosis perforans serpiginosa, the 67 kDa elastin receptor was specifically expressed in the epidermis immediately surrounding the elastic materials that were being eliminated. The elastin receptor may be involved in the interaction between keratinocytes and elastin in elastosis perforans serpiginosa.  (+info)

Effects of electric field reduction in visual display units on skin symptoms. (7/192)

OBJECTIVES: This study investigated the facial skin complaints of office workers before and after the static electric fields of a visual display unit were reduced. METHODS: On the basis of a screening survey of 4556 office workers in 11 companies, 120 of 227 subjects reporting facial skin complaints were randomly selected to this double blind intervention study. Antistatic measures were used to reduce the static electric fields of the visual display unit in the intervention group but not in the control group, which worked with a visual display unit resembling that of the intervention group. Electric fields, dust concentration, health complaints, and psychological behavior tests were recorded before and after the intervention. RESULTS: The intervention group reported statistically significantly fewer facial skin complaints than the control group. In the intervention group, among those with an office dust concentration of >58 microg/m3, a median reduction of 1.5 skin index points (scale 0-8) was achieved, whereas there was no change in the control group. In the regression model "group category" was still a significant variable after control for background factors. In addition, further linear regression analyses indicated that several static electric field parameters were predictors of the skin complaint reduction. CONCLUSIONS: This field trial indicates that removing static electric fields from visual display units can probably help reduce the facial skin complaints of workers in offices with high dust concentrations.  (+info)

Periorbital dermatitis as a side effect of topical dorzolamide. (8/192)

AIM: To report periorbital dermatitis as a late side effect of topical dorzolamide hydrochloride (Trusopt), a drug used to reduce intraocular pressure. METHODS: A retrospective study of 14 patients who developed periorbital dermatitis while using topical dorzolamide hydrochloride was undertaken. Six patients underwent patch testing for sensitivity to Trusopt, dorzolamide hydrochloride, and the preservative benzalkonium chloride. RESULTS: The periorbital dermatitis occurred after a mean period of 20.4 weeks of commencing dorzolamide hydrochloride therapy. 13 patients had used preserved topical beta blocker treatment for a mean period of 34.2 months without complication before the introduction of dorzolamide. In eight (57.1%) the dermatitis resolved completely after discontinuing dorzolamide but in six (42.9%) resolution of the dermatitis did not occur until the concomitant preserved beta blocker was stopped and substituted with preservative free drops. Patch testing for sensitivity to Trusopt, dorzolamide hydrochloride, and benzalkonium chloride was negative. CONCLUSION: These findings suggest that dorzolamide can cause severe periorbital dermatitis. Although the dermatitis may resolve when dorzolamide is discontinued, this does not always occur and in some patients all topical medication containing benzalkonium chloride needs to be stopped.  (+info)