This is the largest series of BCCs in the literature, and shows striking differences in anatomical distribution, sex and mean age according to histological type. The results suggest that the tumours of the trunk, and not only those of the superficial type, could represent a particular subtype of BCC. The analysis also suggests that the hypothesis of chronic vs. intermittent sun exposure cannot be simply extrapolated to BCC. Other causal factors, such as a genetic predisposition, could be involved in the development of carcinomas located on the trunk.

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Our data confirm the predominance of streptococcal infections and sarcoidosis among patients with EN. Tuberculosis has virtually disappeared, since the last case was observed in 1962. Various viral or bacterial diseases are rarely associated with EN, but all patients were not thoroughly investigated. A large and prospective study should be performed in order to determine the true prevalence of associated diseases in EN. In the absence of specific symptoms, exhaustive investigations are not cost-effective.

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Panton-Valentine leukocidin (PVL) is a Staphylococcus aureus (SA) exotoxin, which kills human granulocytes and monocytes in vitro. Among 43 SA strains from cutaneous infections, 12 were PVL producers, whereas among 49 blood culture strains, only 1 produced PVL. Most PVL-producing strains (11/22) came from 22 primitive cutaneous infections, especially furuncles and abscesses, while only 1 PVL-producing strain came from 21 secondary infections of dermatoses such as bullous or pruritic diseases. Intradermal injections of PVL in rabbits induced edema, erythema and necrosis; histopathological changes at the injection sites consisted mainly in leukocytoclasis and vascular necrosis. All changes were dose dependent, and previous immunization of rabbits partially neutralized PVL-induced effects. Production of PVL in vivo after injections of bacteria seems to be low, and the histopathological lesions induced in the rabbit skin do not appear to be specifically related to PVL activity. However, PVL is a good candidate as a new virulence factor in cutaneous SA infections.

The Schnitzler syndrome is characterized by a chronic urticarial eruption with a monoclonal IgM gammopathy. The other signs of the syndrome include intermittent elevated fever, joint and/or bone pain with radiologic evidence of osteosclerosis, palpable lymph nodes, enlarged liver and/or spleen, elevated erythrocyte sedimentation rate, and leukocytosis. The mean delay to diagnosis is more than 5 years, and this syndrome is of concern to internists and many medical specialists. Patients with this syndrome are often initially considered to have lymphoma or adult-onset Still disease, which are the main differential diagnoses. However, hypocomplementic urticarial vasculitis, systemic lupus erythematosus, cryoglobulinemia, acquired C1 inhibitor deficiency, hyper IgD syndrome, chronic infantile neurologic cutaneous and articular (CINCA) syndrome, and Muckle-Wells syndrome should also be excluded, because diagnosis relies on a combination of clinical and biologic signs and there is no specific marker of the disease. The disease pursues a chronic course, and no remissions have yet been reported. Disabling skin rash, fever, and musculoskeletal involvement are the most frequent complications. Severe anemia of chronic disease is another serious complication. The most harmful complication, however, is evolution to an authentic lymphoplasmacytic malignancy, which occurs in at least 15% of patients. This hematologic transformation can occur more than 20 years after the first signs of the disease, thus patients deserve long-term follow-up. Treatment is symptomatic and unsatisfactory. The skin rash is unresponsive to treatment, and nonsteroidal antiinflammatory drugs, antihistamines, dapsone, colchicine, and psoralens and ultraviolet A (PUVA) therapy give inconstant results. Fever, arthralgia, and bone pain often respond to nonsteroidal antiinflammatory drugs. In some patients, these symptoms and/or the presence of severe inflammatory anemia require steroids and/or immunosuppressive treatment, which ameliorate inflammatory symptoms but do not change the course of the skin rash.

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