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PubMed1977

The effects of indomethacin on long-wave ultraviolet-induced delayed erythema.

Indomethacin, a known inhibitor of prostaglandin synthesis, administered topically as a 2.5% solution, intradermally in 10 mug doses, and orally in a dose of 150 mg/day for 2 days did not diminish the delayed erythema produced a long-wave ultraviolet light (320-400 nm). The delayed phototoxic erythema produced by 8-methoxypsoralen and subsequent exposure the long-wave ultraviolet light was similarly unaffected. By comparison, topical and intradermal indomethacin treatment produced sustained decrease in the erythemal response to ultraviolet radiation in the UVB ranges (290-320 nm).

Administration, Oral↗
PubMed1983

Lymphocyte subsets and Langerhans cells/indeterminate cells in erythema multiforme.

A peroxidase-antiperoxidase study using monoclonal antibodies directed against T and B lymphocytes and Langerhans cells/indeterminate cells (LC/IC) was undertaken in order to understand more clearly the changes observed in erythema multiforme. At the various stages of development, from normal skin to target lesions, the quantity of inflammatory cells differed, but in each case the number of T8+ (cytotoxic/suppressor) cells was greater than the number of T4+ (helper/inducer) cells in the epidermis, whereas the latter exceeded the former in the dermis. Concomitant with the initial epidermis changes, there was an increase in the number of T6+ (LC/IC) cells in the upper and lower epidermis. With slight to moderate basal unit destruction, the number of LC/IC in the upper epidermis exceeded those in the lower epidermis. With severe basal unit destruction, there was a loss of LC/IC in the lower epidermis as detected by T6 reactivity. In fully formed blisters, the LC/IC in the upper half of the epidermis were decreased in parallel with the degree of epidermal necrosis. The character of the lymphocytic inflammatory infiltrate and redistribution in LC/IC are similar to those findings described in allergic contact dermatitis. The clinical, histologic, and immunopathologic changes in erythema multiforme appear to be due in part to cellular immune mechanisms with the lymphocyte as the predominant effector cell, and our data suggest a possible role for LC/IC in this disorder.

Erythema Multiforme↗
PubMed1983

Response of human skin to ultraviolet radiation: dissociation of erythema and metabolic changes following sunscreen protection.

After UV irradiation of human skin there is an increase in epidermal and stratum corneum thickness and an increase in the thymidine autoradiographic labeling index. Previously we have demonstrated that persistent exposure to ultraviolet radiation (UVR) alters the distribution and activities of glucose-6-phosphate dehydrogenase (G-6-PDH) and succinic dehydrogenase (SDH) within the epidermis; G-6-PDH activity is increased over the whole epidermis and SDH activity is diminished in the granular cell area but increased in the basal layer. When skin is protected by an efficient sunscreen and irradiated with UVB, there is almost complete inhibition of the erythema normally seen following UVR exposure. In this study we have investigated the cytochemical, cell kinetic, and histometric changes that take place in the epidermis after UVB irradiation, with and without two different types of sunscreen. Some of the histometric and metabolic changes associated with UVB exposure were still evident despite sunscreen protection and the successful blocking of the erythema response. The implications of these findings are discussed together with the use of sunscreens to prevent development of solar damage.

Adult↗
PubMed1983

Erythema multiforme: microvascular damage and infiltration of lymphocytes and basophils.

The sequence of alterations occurring in recurrent erythema multiforme was studied with clinical observations, 1-micrometer tissue sections, and immunofluorescence techniques. Lesions evolved through 3 stages: an initial red papule, a vesicle surmounting a red papule, and a target (iris) lesion. Focal endothelial cell swelling was present in clinically normal skin. In the red papule, endothelial cytoplasmic swelling, vacuolization, and nuclear hypertrophy with luminal obliteration of superficial venules developed. These venular alterations were more marked with endothelial cell necrosis, and involved deeper venules as well in vesicular and target lesions. Lymphocytes surrounded the venules and infiltrated the lower epidermis in the red papule and the vesicular lesions. Venular damage was correlated with the degree of infiltration by lymphocytes, apparently the primary effector cell, suggesting the venule as a primary target of injury. Hypogranulated basophils were noted around venules in vesicular and target lesions. Fibrin deposits were identified within and interstitially beneath the vesicles. The presence of lymphocytes, basophils, and interstitial fibrin deposition is similar to the changes of cutaneous delayed-type hypersensitivity and suggests a role for cell-mediated immunity in the pathogenesis of erythema multiforme.

Adolescent↗
PubMed1979

Ineffectiveness of aprotinin on psoralen-UVA-(PUVA)-induced erythema.

Because bradykinin constitutes a possible candidate for mediation of topical 8-methoxypsoralen-UVA-(PUVA)-induced erythema, aprotinin (Trasylol), inhibitor of kallikrein and interrupter of the cascade leading to kinin production was assessed in guinea pigs. Response was assessed at 24, 48, and 72 hr after topical PUVA and there was no significant difference between normal saline and aprotinin by intradermal or intraperitoneal routes of administration. The results of this study indicate that intradermal and intraperiotoneal aprotinin, in the dose and method tested, is not capable of significantly decreasing erythema induced by topical PUVA in guinea pigs.

Animals↗
PubMed1980

Erythema multiforme: direct immunofluorescence studies and detection of circulating immune complexes.

The immunologic parameters of 23 patients with erythema multiforme who were seen by us (17 patients) or who had biopsies sent for immunofluorescence testing (6 cases) are reviewed. Biopsy specimens were sectioned and tested with labeled antisera to human IgG, IgA, IgM, C3 and fibrin. Fourteen biopsies showed IgM deposits in the superficial blood vessels, 13 demonstrated C3, 15 showed fibrin deposition, and 1 biopsy showed IgA deposition. All biopsies were negative for IgG. Eight serum samples tested by indirect IF were negative for skin-reactive antibodies. In addition to IF testing, serum samples from 20 patients were tested for circulating immune complexes with a Clq binding radioassay and a monoclonal rheumatoid factor (mRF) inhibition assay. Immune complexes were not detected by the Clq binding assay, but 6 of 20 serum samples demonstrated low to moderate levels of immune complexes by the mRF inhibition assay. By sucrose density gradient ultracentrifugation in the mRF-reactive material in one serum sample sedimented in high molecular weight fractions and also demonstrated anticomplementary activity. These findings suggest that immune complex formation and subsequent deposition in the cutaneous microvasculature may play a role in the pathogenesis of erythema multiforme.

Antigen-Antibody Complex↗
PubMed1975

New observations in the histopathology of erythema nodosum.

Erythema nodosum presents variable clinical and histologic patterns of response in the vessels, septa, and fat lobules of the subcutaneous tissue. Acute or chronic phlebitis with hemorrhage may be commonly observed; acute panniculitis is observed in foci, but at time it may be the principal histologic feature; lymphocytic infiltration of fat lobules is often found, and lymphoid nodules are not infrequent; rarely, chronic granulomatous lesions involve septa or fat lobules; and proliferative lipocyte response may be observed. Because these variable histologic patterns may be coexistent, excision biopsy and multiple sections are necessary to recognize them. The variable histologic features correlate with the different clinical forms: acute nodular, chronic nodular, migrating plaque lesion, cellulitis, and the rate suppurative form. This variety of panniculus response in erythema nodosum can be explained on the basis of host-tissue response to a delayed hypersensitivity reaction to an antigenic stimulus.

Adipose Tissue↗
PubMed1990

Phototoxic erythema following PUVA treatment: independence of complement.

The effect of PUVA treatment on normal human serum (NHS), on isolated PMN, or on C3-deficient guinea pigs and congenic (C3-competent) control animals was tested. At a concentration of 0.1 or 1 mM/l 8-MOP and UVA doses of 5-30 J/cm2, PUVA failed to induce any detectable C3-cleavage in NHS. Furthermore, when the complement (C) activation in NHS had been induced before or after PUVA treatment by various methods. PUVA did not modulate the extent of C3-cleavage. PUVA did not affect the viability of isolated PMN, nor did it induce a release of LDH or elastase. No differences between C3-deficient and C-competent guinea pig skin exposed to PUVA were observed in erythema or histologic responses. Immunohistologic examination of specimens from normal guinea pigs revealed C3b and C3d deposits on necrotic keratinocytes, findings restricted to the PUVA-treated areas. Necrosis of keratinocytes was present in skin specimens of C3-deficient animals from PUVA-treated sites to a similar extent. However, deposits of C3-related antigens were completely absent there. From these observations, we suggest that the induction of phototoxic erythema following PUVA treatment is independent of complement.

Animals↗
PubMed2003

Topical tacrolimus 0.1% ointment (protopic) reverses nickel contact dermatitis elicited by allergen challenge to a similar degree to mometasone furoate 0.1% with greater suppression of late erythema.

The aim of this study was to evaluate the ability of topical tacrolimus 0.1% under occlusion for 48 h to suppress nickel-elicited allergic contact dermatitis in a randomized, petrolatum- and mometasone furoate 0.1% ointment-controlled double-blind, intra-individual study which included 28 women volunteers. 3 closed patch tests (Finn Chambers on Scanpor, Epitest Ltd Oy, Tuusula, Finland) containing 0.1 ml of 5% nickel sulfate in petrolatum were applied on day 0. After removal on day 2, the study compounds were applied under occlusion for 48 h. The eczema reaction and the degree of erythema were evaluated clinically and by reflectance spectrophotometry at days 4 and 7, respectively. Mean visual scores corresponding to petrolatum-treated sites were significantly higher than those corresponding to both mometasone furoate and tacrolimus at days 4 (P < 0.001) and 7 (P < 0.001). In both tacrolimus- and mometasone furoate-treated sites, there was a significant decrease in visual scores with time (P < 0.001) from day 2 to day 7, and the corresponding mean decreases in scores were 0.73 and 1.04, respectively. The difference between both was 0.30 in favour of tacrolimus (95% confidence intervals, -0.04 and 0.65), although this did not reach statistical significance (P = 0.084). Mean erythema index values were similar at day 2. Significant differences among treatment sites were seen at days 4 (P < 0.001) and 7 (P < 0.001). The decrease was significantly more pronounced on day 7 in patches where tacrolimus had been supplied (P < 0.5). This method might provide useful means to compare different concentrations and/or presentations of tacrolimus or other calcineurin inhibitors and topical anti-inflammatory agents.

Administration, Topical↗
PubMed2004

Vancomycin-induced linear IgA disease manifesting as bullous erythema multiforme.

BACKGROUND: Vancomycin-induced linear immunoglobulin A (IgA) disease, an autoimmune, blistering disease in response to vancomycin administration, is characterized by a subepidermal, vesiculobullous eruption and linear IgA deposition along the basement membrane zone on direct immunofluorescence. CASE REPORT: We report the case of an 81-year-old man treated with vancomycin who developed diffuse erythema multiforme and tense bullae involving the palmoplantar surfaces. Discontinuation of vancomycin therapy resulted in complete resolution of this patient's cutaneous eruption. RESULTS: Biopsy of a representative skin lesion demonstrated lichenoid interface dermatitis with focal subepidermal clefting, dyskeratosis, and prominent eosinophils. Direct immunofluorescence showed linear basement membrane staining with immunoreactants to IgA; indirect immunofluorescence demonstrated the presence of circulating IgG antibodies binding in an intercellular pattern. Immunoprecipitation studies using the patient's serum revealed 210, 130, and 83 kDa target antigens. CONCLUSIONS: Presenting with an initial clinical picture suggestive of bullous erythema multiforme, this patient's subsequent clinical course and direct immunofluorescence confirm the diagnosis of linear IgA bullous disease (LABD). His indirect immunofluorescence findings and immunoprecipitation results suggest that circulating non-IgA antibodies may represent a newly recognized immunopathologic feature of vancomycin-induced linear IgA disease, underscoring the variable and unpredictable manifestations of this drug-induced cutaneous disease.

Aged↗
PubMedDate not supplied

Erythema nodosum in association with celiac disease.

We present a 16-year-old girl with a 4-year history of chronic persistent erythema nodosum. Recurrently low serum iron values suggested the possibility of a malabsorption syndrome. The presence of antitransglutaminase and antiendomysium antibodies and the jejunal biopsy specimen findings showed an underlying celiac disease. On a strict gluten-free diet, the skin lesions resolved and the girl has since remained symptom free for 9 months. Thus celiac disease can be a triggering factor for erythema nodosum. In the chronic form of the skin lesions, serologic testing for this specific enteropathy may be justified.

Adolescent↗
PubMed1985

Effect of somatostatin in necrolytic migratory erythema of glucagonoma.

A 63-year-old woman with necrolytic migratory erythema associated with a glucagonoma in the pancreas is described. The diagnosis was suggested on the basis of a characteristic lesion in skin biopsy. Infusion of somatostatin (25 micrograms/h) for 48 hours was followed by a rapid and almost complete healing of the skin eruptions. Serum glucagon was depressed during infusion. No significant changes in plasma glucose were detected. As the patient experienced a cramp-like sensation after cessation of somatostatin infusion, a tail-off period in the infusion program is advocated. The pathogenesis of necrolytic erythema in glucagonoma is discussed.

Adenoma, Islet Cell↗
PubMed2004

Dermacentor-borne necrosis erythema and lymphadenopathy: clinical and epidemiological features of a new tick-borne disease.

This paper describes the epidemiological and clinical features of a tick-borne disease differing somewhat from other tick-borne diseases found previously in Spain. All patients were bitten by Dermacentor marginatus or a large tick. The clinical features include a crustaceous or necrotic lesion at the site of the tick's attachment, surrounded by an erythema (erythema migrans-like) and painful regional lymphadenopathies. The probable aetiological agent is Rickettsia slovaca. Similar cases have been reported in other European countries.

Adult↗
PubMed1992

Two patients with solar urticaria manifesting pruritic erythema.

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.

Adult↗
PubMed1993

A case of herpes-associated erythema multiforme in a Japanese child.

A case of a five-year-old Japanese boy with herpes-associated erythema multiforme (HAEM) was reported. The patient had eleven recurrences of herpes labiaris within one year; four of these recurrences were accompanied by erythema multiforme. A study of the human leukocyte antigens revealed the presence of HLA-DQW3, which has been reported to be significantly frequent in Caucasian patients with HAEM. Oral administration of acyclovir at the onset of herpes labialis was effective in preventing HAEM. Early administration of oral steroids at the onset of HAEM also prevented its exacerbation.

Acyclovir↗
PubMed1994

Erythema gyratum repens associated with hypereosinophilic syndrome.

We report a case of typical erythema gyratum repens lesions observed as a manifestation of idiopathic hypereosinophilic syndrome in a 63-year-old man. While erythema gyratum repens is usually associated with malignancy, an intensive search over a 30-month period failed to reveal any evidence of neoplasm. With administration of dapsone, the typical gyrate lesions disappeared as the subject's hypereosinophilia improved.

Erythema↗
PubMed1995

Three cases of chemotherapy-induced acral erythema.

Three cases of chemotherapy-induced acral erythema are reported. All the patients had received cyclophosphamide, vincristine, adriamycin, prednisolone, and granulocyte-colony stimulating factor (G-CSF) for the treatment of leukemia or malignant lymphoma. From 35 to 45 days after the start of chemotherapy, painful erythematous lesions developed on their palms, soles, fingers, and toes, resulting in blister formation and desquamation. The recent higher incidence of chemotherapy-induced acral erythema may be correlated with the popularity of G-CSF, which allows the use of higher doses of chemotherapeutic drugs.

Adult↗
PubMed1998

Drug eruption (erythema multiforme type) due to a digestive enzyme drug.

An 84-year-old Japanese male had pruritic indurated erythema on his upper limb and left lower abdomen, which had developed abruptly two months before visiting our hospital. Hematological examination showed eosinophilia, 550/mm3. Histopathological findings were suggestive of erythema multiforme in response to a drug. By means of patch tests and a p.o. challenge test, Aczym, a digestive enzyme drug, was shown to be the cause of his condition. Further study revealed that the specific ingredients involved were pancreatin and Taka-diastase. An eruption resulting from ingestion of a digestive enzyme drug has not previously been reported.

Aged↗