Sweet syndrome (SS) has been described as a rare but distinct disorder, characterized by 4 clinical features: fever, neutrophilic leukocytosis, sudden onset of asymmetric erythematous, and often-painful skin lesions and dense dermal infiltrates of mature neutrophils without signs of vasculitis. Behçet disease (BD) demonstrates symptoms similar to those of SS, although the incidence and clinical courses of these 2 disorders are different. Peripheral neutrophilia, enhanced neutrophil activity, and dense dermal infiltration of cutaneous lesions have also been noted in both disorders. Neutrophils may play an important role in the pathogenesis of these 2 diseases, as neutrophils are increased in blood and skin lesions.¹

Objective: To investigate possible correlations between cutaneous polyarteritis nodosa (CPN) and antiphospholipid syndrome–associated antibodies.Methods: Sixteen patients were referred with CPN features. To investigate the possible role of antiphospholipid antibodies (aPL) in CPN, we measured serum lupus anticoagulant (LAC), IgG and IgM anticardiolipin (aCL) and anti–phosphatidylserine‐prothrombin complex (anti‐PS/PT) antibodies, and anti–β₂‐glycoprotein I–dependent cardiolipin (anti‐β₂GPI/CL) antibodies in the 16 CPN patients, 8 microscopic polyangiitis (MPA) patients, 33 systemic lupus erythematosus (SLE) patients, and 23 healthy controls. LAC was determined according to the Subcommittee on Lupus Anticoagulant/Phospholipid Dependent Antibody guidelines. Anti‐PS/PT, aCL, and anti‐β₂GPI/CL antibodies were measured by enzyme‐linked immunosorbent assay.Results: Anti‐PS/PT antibodies and/or LAC were detected in all CPN patients, but not in any controls. Serum IgM anti‐PS/PT antibody was found in 13 (81.3%) CPN patients. The mean ± SD serum anti‐PS/PT IgM level (19.9 ± 12.4 units/ml) in CPN patients was significantly elevated compared with SLE patients (5.7 ± 5.9 units/ml). IgG anti‐PS/PT antibody was detected in 5 (31.3%) CPN patients, but not in any controls. The IgG PS/PT antibody titers were similar in CPN patients (12.3 ± 12.0 units/ml) and SLE patients (13.8 ± 14.3 units/ml). Three (18.8%) CPN patients were positive for IgG aCL antibody and 2 (12.5%) for IgM aCL antibody. No MPA patients had aPL. CPN skin manifestations included livedo reticularis (14 [87.5%]). Direct immunofluorescence (DIF) revealed C3 within the affected vessels in 7 (77.8%) of 9 CPN patients.Conclusion: Our study demonstrated that presence of anti‐PS/PT antibodies and/or LAC could serve as markers in CPN patients. CPN could be dependently associated with the presence of anti‐PS/PT antibody. Clinicians need to recognize these titers to permit early accurate diagnosis and treatment. We believe that anti‐PS/PT antibodies will become widely recognized as a new factor when diagnosing CPN.

There is a current lack of consensus regarding methods of assessment of vitiligo. Recently, the Vitiligo Area Scoring Index (VASI) and the Vitiligo European Task Force (VETF) were proposed to offer more accurate measures of disease severity indexes and treatment evaluation criteria. It would make sense to combine the VASI with the VETF system. We proposed an original scale for treatment evaluation criteria in vitiligo based on VASI. We plan to add the digital image analysis system, health-related quality of life questionnaire, affected skin location, and skin color in the original scale.

Background Churg-Strauss syndrome (CSS), also known as allergic granulomatous angiitis, is a rare entity that is characterized by systemic vasculitis in patients with a history of asthma. Patients with CSS show a marked peripheral blood eosinophilia, but the pathogenesis remains unknown. Observations A retrospective review was performed in 9 cases of CSS in whom cutaneous findings were present as an initial manifestation. All 9 patients had purpura and petechiae as well as severe pain and paresthesias of the lower extremities. Four patients (44%) used leukotriene receptor antagonists to treat their asthma, and 3 (75%) of them developed CSS within 3 months. Five patients (56%) were positive for perinuclear antineutrophil cytoplasmic antibodies before therapy, but in all 5 the levels of perinuclear antineutrophil cytoplasmic antibody normalized. Serum IgE levels were elevated in all patients before treatment but decreased after treatment. Histologically, all patients demonstrated leukocytoclastic vasculitis and eosinophilic infiltration. Eight biopsy specimens (73%) revealed marked eosinophilia around the nerve fibers in the dermis. Palisading granulomas in association with vessel-based changes were present in 4 (36%) of 11 biopsy specimens. Conclusions These characteristic cutaneous clinical patterns that are consistent with the presence of mononeuropathy multiplexes in the lower extremities may help physicians establish an earlier diagnosis. Both eosinophils and IgE, as well as perinuclear antineutrophil cytoplasmic antibodies to some degree, likely participate in skin lesion development in CSS. Furthermore, there appears to be a correlation between treatment with leukotriene receptor antagonists and the onset of CSS in some cases.