BackgroundNeutrophils are generally considered less responsive to glucocorticoids compared to other inflammatory cells. The reported increase in human neutrophil survival mediated by these drugs partly supports this assertion. However, it was recently shown that dexamethasone exerts potent anti-inflammatory effects in equine peripheral blood neutrophils. Few comparative studies of glucocorticoid effects in neutrophils and other leukocytes have been reported and a relative insensitivity of neutrophils to these drugs could not be ruled out.ObjectiveWe assessed glucocorticoid-responsiveness in equine and human peripheral blood neutrophils and neutrophil-depleted leukocytes.MethodsBlood neutrophils and neutrophil-depleted leukocytes were isolated from 6 healthy horses and 4 human healthy subjects. Cells were incubated for 5 h with or without LPS (100 ng/mL) alone or combined with hydrocortisone, prednisolone or dexamethasone (10−8 M and 10−6 M). IL-1β, TNF-α, IL-8, glutamine synthetase and GR-α mRNA expression was quantified by qPCR. Equine neutrophils were also incubated for 20 h with or without the three glucocorticoids and cell survival was assessed by flow cytometry and light microscopy on cytospin preparations.ResultsWe found that glucocorticoids down-regulated LPS-induced pro-inflammatory mRNA expression in both cell populations and species. These drugs also significantly increased glutamine synthetase gene expression in both equine cell populations. The magnitude of glucocorticoid response between cell populations was generally similar in both species. We also showed that dexamethasone had a comparable inhibitory effect on pro-inflammatory gene expression in both human and equine neutrophils. As reported in other species, glucocorticoids significantly increase the survival in equine neutrophils.ConclusionsGlucocorticoids exert genomic effects of similar magnitude on neutrophils and on other blood leukocytes. We speculate that the poor response to glucocorticoids observed in some chronic neutrophilic diseases such as severe asthma or COPD is not explained by a relative lack of inhibition of these drugs on pro-inflammatory cytokines expression in neutrophils.

The use of RTX for many autoimmune diseases, especially pemphigus, is increasing. Chronic EMM, especially EMM associated to antidesmoplakin autoantibodies, is an inflammatory disease in which the role of B cells is not well understood. However, we report a favourable benefit of RTX treatment for months in five patients with severe disease. RTX could be a therapeutic option in severe, difficult-to-treat EMM.

Summary Background Acute exanthemas (AEs) are frequently seen; they can be caused by drugs or viruses but often the cause is unknown. Objectives To describe the clinical, virological and histological aspects of AEs and explore their cytokinic and metagenomic profiles. Methods This prospective study examined 98 patients with AE, from February to July 2014. Clinical data were recorded in a standardized chart. Virological investigation and skin biopsies were performed. In addition, blood and skin samples were analysed for cytokines and then by a shotgun metagenomic approach. We identified five groups of patients: those with maculopapular exanthemas (MPEs) that were virally induced (group 1); those with drug‐induced MPEs (group 2), those with MPEs that were both viral and drug induced (group 3), those with idiopathic MPEs (group 4) and those with pityriasis rosea (group 5). Results A virus was identified in 29 cases (human herpesvirus 6, 72%). Cytokinic analysis of the skin (n = 23 MPEs) showed higher levels of interferon‐γ and interleukin‐1 receptor‐α in viral MPEs, higher interleukin‐33 levels in idiopathic MPEs, and higher macrophage inflammatory protein 1α levels in drug‐induced MPEs. By metagenomics analysis (n = 10 MPEs), viruses identified with routine practice methods were not found in group 1 (n = 4 MPEs). However, Enterovirus A was detected in two cases, especially in a group 1 patient for whom metagenomic analysis rectified the diagnosis of the culprit agent. Conclusions Human herpesvirus 6 was the virus most frequently identified, and histology did not discriminate MPEs. In addition, the level of interleukin‐33 seen in idiopathic MPEs suggests that an environmental factor may be the trigger for these. The results bring into question the utility of routine polymerase chain reaction analysis and viral serology for determining cause in AE. What's already known about this topic? Acute exanthemas, especially maculopapular exanthemas, are a frequent reason for patients consulting emergency and dermatology departments. It is difficult to evaluate the aetiology of acute exanthema based on the clinical aspects. Few data are available on the investigations needed in routine practice, and no prospective series have been published. What does this study add? Our study provides a global and prospective description of acute exanthemas. Cytokine analysis could help to investigate the pathophysiology of idiopathic eruptions. Metagenomic analysis provides new insights about the value of routine practice virological investigations. We show for the first time the feasibility of metagenomics analysis in the skin, which results question the interest of routine PCR and viral sérologies for the exploration of such acute exanthemas.

K E Y W O R D S : allergic contact dermatitis, case report, mupirocin, polysensitization Allergic contact dermatitis caused by mupirocin is rarely reported. We report a particularly severe case with a prolonged course associated with a polysensitization background. CASE REPORTA 37-year-old woman applied a mupirocin cream (Mupiderm; Almirall Hermal, Reinbek, Germany) to a benign fibrous histiocytoma of the thigh. Because of exacerbation of the lesions, she consulted repeatedly for 6 weeks in emergency rooms, and was treated with roxithromycin tablets and multiple topical medications: clobetasol propionate cream (Clarelux; Pierre Fabre Dermatologie, Paris, France), ciclopirox olamine cream (Mycoster; Pierre Fabre Dermatologie), desonide cream (Tridesonit; Alliance Pharma, Paris, France), and an econazole cream.None of the prescriptions prevented gradual spread of the rash to the whole thigh and the appearance of nummular lesions of the trunk. A drug-related eruption or allergic contact dermatitis was finally suspected. All treatments were stopped, and the eruption resolved with the use of diflucortolon valerate cream applied for a period 3 weeks.The patient had a past history of contact allergies previously confirmed by patch tests: Biseptine lotion (Bayer Healthcare, Gaillard, France), containing chlorhexidine and benzalkonium chloride, Zovirax cream (GlaxoSmithKline, Rueil-Malmaison, France), containing acyclovir, hexamedine, methylisothiazolinone, budesonide, Myroxylon pereirae, fragrance mix I, and nickel sulfate. Roxithromycin had been previously administered without side-effects. Skin biopsy findings were consistent with contact dermatitis. New patch tests were performed for the present event: the main results, including an extensive reaction to Mupiderm (Figure 1), are shown in Table 1. Almirall Hermal declined to provide us with the different ingredients of the cream. The patient was therefore tested with Bactroban ointment (GlaxoSmtihKline) containing mupirocin but with different excipients from those of Mupiderm. To better control the reaction, we performed an open test on the arm. The test elicited extensive contact dermatitis of the entire arm, which confirmed the mupirocin allergy.We diagnosed severe allergic contact dermatitis caused by mupirocin associated with polysensitization to topical drugs. DISCUSSIONMupirocin is a topical antibiotic approved for treating cutaneous staphylococcal and streptococcal infections. It is the only compound of its pharmacological class, and is only available as topical treatment.Despite its widespread use, contact allergies are rarely reported. 1-5 We report a case that was severe and prolonged because of the association with polysensitization to a dozen allergens of various families. As in our patient, it is known that polysensitized patients may show strong reactions to patch tests. 6 Our case shows that clinical manifestations of the allergy may also be strong. Indeed, our patient developed multiple FIGURE 1 Vesicular and maculopapular eruption spreading from the pa...