[Paradoxical cutaneous reactions associated with tocilizumab therapy]. / Réactions cutanées paradoxales sous traitement par tocilizumab.

INTRODUCTION: Tocilizumab (TCZ) is a humanized antihuman interleukin (IL)-6 receptor antibody recommended for the treatment of moderate to severe active rheumatoid arthritis, adult-onset Still disease, Castleman disease and more recently, systemic juvenile idiopathic arthritis. Like anti-TNFα, rituximab and less frequently abatacept, TCZ can induce paradoxical cutaneous eruption like psoriasis with predominantly palmoplantar presentation. CASE REPORT: We report a 47-year-old woman with psoriastic arthritis who developed under anti-TNFα therapy and later under tocilizumab a paradoxical palmoplantar eruption. CONCLUSION: The specific underlying mechanisms of this side effect are unclear but relapse of these lesions seems to be observed with certain biological agents.

Neurofibromatosis 1 phenotype associated to malignant peripheral nerve sheath tumours: a case-control study.

BACKGROUND: Malignant peripheral nerve sheath tumours (MPNSTs) are the main cause of death in neurofibromatosis 1 adult patients. OBJECTIVES: To determine the clinical type of neurofibromas associated to MPNSTs. METHODS: Case-control study. Cases were neurofibromatosis 1 adults with MPNSTs and controls were patients without MPNSTs individually matched by age and sex (1 : 3). Both were recruited from our database. The following variables were studied: clinical presence of cutaneous, subcutaneous or plexiform neurofibromas and of internal neurofibromas. Internal neurofibromas were confirmed by clinical imaging. Multivariate odds ratios (aORs) were estimated with their 95% confidence interval (CI). RESULTS: From January 1995 to December 2007, 52 patients (cases) were identified with a MPNSTs, 155 controls could be recruited. In the multivariate analysis, MPNSTs were significantly associated with the presence of internal NFs (aOR: 7.5; 95% CI: 3.2-17.4), a trend for an association was observed for the presence of subcutaneous neurofibromas (aOR: 2.11; 95% CI: 0.89-5). CONCLUSIONS: This study confirms the association between the MPNSTs and the internal neurofibromas. The later are indeed associated with a high risk of malignant transformation.

[Two cases of psoas abscesses caused by group A beta-haemolytic streptococcal infection with a cutaneous portal of entry]. / Abcès du psoas à streptocoques bêta-hémolytique du groupe A à point de départ cutané : deux cas.

BACKGROUND: Psoas abscess is a rare clinical entity that occurs chiefly after intra-abdominal or retroperitoneal infection. We report two cases of psoas abscesses caused by group A beta-haemolytic streptococcal infection having a cutaneous portal of entry. CASE REPORTS: The first patient, a 50-year-old man, was feverish and had ulcerative and necrotic cutaneous lesions evocative of ecthyma that were progressing for three months and were recently associated with a painful mass in the left iliac fossa, leading to difficulties in walking. The second patient, a 35-year-old woman with a medical history of intravenous drug addiction, was admitted to intensive care for sepsis syndrome following group A beta-haemolytic streptococcal infection with a cutaneous portal of entry (swelling on left lower limb). She remained unaccountably subfebrile 10 days after the start of antibiotic therapy with amoxicillin. Abdominal CAT scans for each patient confirmed the diagnosis of left psoas abscess. For the first patient, the same group A beta-haemolytic streptococcus was isolated in drainage fluid and at the cutaneous injury site. The outcome was favourable in both cases following extensive intravenous antibiotic therapy (amoxicillin) combined with percutaneous drainage (in the first case). DISCUSSION: Psoas abscess can occur after locoregional infection and the portals of entry are usually gastro-intestinal, musculoskeletal or genitourinary, with many organisms capable of causing such secondary abscesses. Psoas abscess can also be a primary clinical event. Staphylococcus aureus is the most common causative organism. The presented cases comprised secondary psoas abscesses with a cutaneous portal of entry. Since the complete set of three evocative symptoms (prolonged fever, pain and psoitis) is frequently seen late, diagnosis must be made on the basis of prolonged infectious state or unaccountable feverish abdominal pain. Diagnosis is based on abdominal CAT scan and treatment involves the use of appropriate antibiotics as well as percutaneous or surgical drainage of the abscess. The mortality rate in this patient population remains high with survival being dependent on prompt initiation of therapy.

[Aseptic meningitis during Sweet syndrome]. / Méningite aseptique au cours d'un syndrome de Sweet.

BACKGROUND: Sweet syndrome is a neutrophilic skin disease that can involve extracutaneous signs. Here we describe a case of aseptic meningitis, a rare potential extracutaneous sign of Sweet syndrome. CASE REPORT: A 42-year-old man was hospitalized for non-pruritic maculoerythematous skin lesions of the legs and back with subsequent myalgia. A histology specimen taken from a skin lesion revealed an acute neutrophilic disease consistent with Sweet syndrome. Marked inflammation and cholestasis were observed. Systemic corticosteroid therapy was given and resulted in good clinical and laboratory response. Two weeks later, in a setting of gradual dosage reduction, the patient was hospitalized for intense headaches associated with meningeal irritation in an inflammatory context. Liver function tests were again abnormal. We concluded on a diagnosis of Sweet syndrome complicated by aseptic meningitis and hepatic sites. Investigation for underlying disease, particularly digestive or hematologic, was negative. A favorable outcome was achieved following administration of higher doses of systemic corticosteroids. DISCUSSION: Aseptic meningitis constitutes an extracutaneous localization of Sweet syndrome. A multidisciplinary approach and exclusion of infectious origin are required in order to institute systemic corticosteroid therapy.