[Polymorphic light eruption: prophylaxis using a topical combination of antioxidants and UVA protection formulations]. / Lucite estivale bénigne: prévention par un topique associant des filtres anti-UVA et des antioxydants.

BACKGROUND: In a recent randomized, double-blind, placebo-controlled clinical study, the efficacy of a combination consisting of 0.25% alpha-glucosyl-rutin, 1% vitamin E and a broad-spectrum, highly UVA-protective sunscreen (sun protector factor 15 - persistent pigmentation darkening 6) regarding prevention of polymorphous light eruption was well demonstrated. We evaluated this combination under real solar exposure conditions. PATIENTS AND METHODS: Patients with three previous typical polymorphous light eruptions (including one in the last year) were included in an open prospective multicenter study. The preparation was applied every two hours after the first summer exposure. No topical or systemic treatments presumed to be effective against polymorphous light eruption were given concomitantly. Evaluation was performed after the summer by a dermatologist. RESULTS: Two of the 54 patients dropped out of the study, one for an adverse effect (contact dermatitis). At the end of the study following application of the test preparation, no eruption was seen for 35 patients (67%), with minor eruption for 10 patients (19%) and an marked eruption for 7 patients (13%). Pruritus (present in all patients the year before) was not seen in 36 patients (69%), was considered bearable for 36 patients and unbearable for only 3 patients compared to 27 before inclusion. For the dermatologists, efficacy was excellent for 35 patients and good for 7 patients, giving global efficacy of around 80%, with inadequate results in 10% of cases (5 patients). Concerning protection against erythema, the test product reduced sunburn by 60% compared with the previous year. DISCUSSION: Because of the high clinical efficacy of the product noted after UVA challenge tests and verified by this clinical study under actual conditions of exposure, it may be proposed as a new prophylactic treatment for polymorphous light eruption.

[Medical activity in a emergency outpatient department dermatology]. / Intérêt d'une consultation hospitalière d'urgences dermatologiques.

BACKGROUND: The aim of this study was to characterize the medical activity of a dermatology emergency room and to compare it with 1) outpatients, scheduled visits to the same department and 2) visits to community dermatologists in private practice. METHODS: All the 500 patients who attended the emergency room in one month and all the 411 patients with scheduled appointments during one week within the same period were included prospectively. The clinical diagnoses were recorded and compared between the two groups using chi square and linear correlation tests. Data on the diagnoses made by community dermatologists in private practice were obtained from another study. RESULTS: In the emergency room, 4 diagnoses accounted for 71.4 of all visits: infections (29 p. 100), dermatitis (23.8 p. 100), rashes (11 p. 100) and urticaria (7.6 p. 100). In scheduled visits the 4 leading diagnosis were cancer and precancerous lesions (28.7 p. 100), dermatitis (11.7 p. 100), fungal infections (8.3 p. 100) and acne (7.1 p. 100). There was no correlation (r=0.14; p=0.6) between the 16 more prevalent diagnoses in the emergency room and the prevalence of the same diagnoses in scheduled visits in the hospital department. The emergency diagnosis were also not correlated with those seen in private practice (r=0.21; p=0.4). Seven percent of emergency room consultants were hospitalized. COMMENTS: Skin disorders encountered in the dermatology emergency room differ from those seen both in the outpatient hospital department and in community private practice.

[Risk factors for cutaneous wart onset in transplant recipients]. / Facteurs associés à l'apparition de verrues chez les transplantés d'organe.

INTRODUCTION: Transplant recipients are at increased risk for cutaneous warts. We have investigated the delay of their onset warts and some possible risk factors for their occurrence. PATIENTS AND METHODS: Clinical data were summarized on a standard question and examination sheet. Warts were diagnosed on clinical grounds and course duration assessed on patients' report. Immunosuppressive therapy and HLA group were collected from clinical transplantation records. An actuarial curve was used to evaluate the delay of onset of warts. To compare associated risk factors among the two groups (patients with warts and patients without warts) at 1 year and 3 years following transplant, single variate analysis was performed. RESULTS: At the time of transplant, the prevalence of warts was 16 p. 100. It was increased with the duration of immunosuppression: 23 p. 100 at 1 year, 35 p. 100 at 3 years, 45 p. 100 at 5 years and 54 p. 100 at 7 years. Warts were multiple and principally localized on the hands. Transplant recipients without cutaneous warts 3 years after transplant had less intensive immunosuppressive therapy than the group with cutaneous warts. No association was found between age, sex, HLA markers, actinic keratosis and wart onset. DISCUSSION: The prevalence of warts increases with the duration of transplantation. Cutaneous warts are generally multiple and have a chronical course without spontaneous remission. More intensive immunosuppressive therapy increases their occurrence. This trial cannot evaluate the association between carcinoma and warts. On the basis of our study, there is no relationship between actinic keratosis and warts, nor HLA markers and warts.

Physiopathology and treatment of severe drug eruptions.

This review will focus on recent advances concerning the most severe cutaneous drug reactions: the Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reactions with eosinophilia and systemic symptoms. The most significant progress concerned the demonstration that drugs more often than reactive metabolites are immunogenic and induced several kinds of responses. These findings provided the rationale for using new therapeutic approaches, which will be discussed.

Il-4 and IFN-gamma mRNA induction in human peripheral lymphocytes specific for beta-lactam antibiotics in immediate or delayed hypersensitivity reactions.

Beta-lactam antibiotics elicit CD4+ and CD8+ T-cell-mediated immune responses that play a central role in allergic reactions. However, the involvement of a type 1- (Th1 or Tc1) or a type 2-like (Th2 or Tc2) differentiation in drug allergy remains unclear. We investigated the expression of interleukin 4 (IL-4) and interferon gamma (IFN-gamma) mRNA by quantitative reverse transcription and polymerase chain reaction (RT-PCR) in patient-derived peripheral blood lymphocytes following specific in vitro stimulation. Samples were collected from a total of 19 patients who had developed immediate or delayed clinical manifestations of hypersensitivity to beta-lactam and from 11 control subjects. Peripheral blood mononuclear cells (PBMCs) were stimulated with either free antibiotics or antibiotic-human serum albumin (HSA) conjugates. Specific induction of IFN-gamma mRNA expression was observed in 11 of 11 allergic patients with immediate reactions, in 6 of 8 patients with delayed reactions, and in 4 of 11 control subjects. IL-4 mRNA expression was induced in 5 of 11 allergic individuals with immediate reactions but in none of the 8 patients with delayed responses and none of the 11 control subjects. IL-4 mRNA expression was only induced following activation with free drugs, while IFN-gamma mRNA expression was predominantly induced in CD4+ T cells following stimulation with HSA-conjugated drugs. Immediate-type hypersensitivity to beta-lactams was not associated with a pure type 2-like response when PBMCs were specifically stimulated in vitro: Some patients with well-documented history of beta-lactam-induced immediate allergic reaction showed a high IFN-gamma response. Contact dermatitis involved Tc1 and Th1 cells and other delayed hypersensitivity reactions to beta-lactams were restricted to Th1 responses.

Mechanisms of drug-induced allergic contact dermatitis.

Allergic contact dermatitis is induced by a wide variety of drugs that trigger specific immune responses following topical exposure. Identified chemical structures involved in such reactions include the mercuric and thiosalicylic acid groups of thimerosal, the diphenylketone group of the anti-inflammatory drug ketoprofen, the amide or ester structure of local anesthetics, and the side-chain and thiazolidine ring of beta-lactams. The T cell responses to such compounds involve CD4+ and CD8+ alphabeta+ T lymphocytes and also CD4 /CD8 gammadelta+ T cells. Although "T helper 2" cytokine production by drug-specific human T cells from patients with allergic contact dermatitis has been described, T helper 1-like and T cytotoxic 1-like responses clearly play key roles in this cutaneous reaction.