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Mast cells and basophils interact with various cells in the urticaria lesion microenvironment, such as macrophages,.which form an essential component of innate immunity, and are involved in numerous functions including protein secretion. Objective: The aim of the present study was to characterize the macrophage phenotype in urticarial lesions of patients with chronic spontaneous urticaria (CSU) nonresponsive to antihistamines at optimized doses. And compare the phenotype with clinical and laboratory parameters such as age, gender, urticaria time, C-reactive protein (CRP), and total serum IgE, and autologous serum skin test (ASST). Methods: Twenty-eight patients with CSU refractory to antihistamines were included in the study. Epidemiological data, C-reactive protein, D-dimers, basophils in peripheral blood, and total serum IgE and ASST were assessed. The mannose receptor (CD206), CD163, CMAF, and pSTAT 1 were used to characterize the M1/M2 macrophage subpopulations. The immunolabeled cells per square millimeter were manually enumerated at a 400× magnification in 12 optical fields via light microscopy. Results: A predominance of M2 macrophages was seen in CSU patients. Statistical differences were observed between the CD206 marker and the disease course. No correlation was found between biomarkers and macrophage populations. Expression of CMAF was significantly higher in the patient sample compared to that in the control skin (patients without history of urticaria; p-value < 0.001). Conclusion: M2 macrophages were seen with significantly higher CMAF expression, which indicates macrophage activation in patients with CSU. CD206 expression was inversely correlated with disease time.

The non- or low-sedating H1 receptor antagonists represent the basic therapy for urticaria.To test an alternative approach to patients unresponsive to conventional treatment.A total of 22 patients with chronic urticaria unresponsive to conventional antihistamine treatment were enrolled for this study. They had uncontrolled urticaria even using multiple combinations of antihistamines on maximum doses and corticosteroids in short cycles (prednisone 20-40 mg, per os once a day, 3-7 days per month). Cutaneous biopsies of the urticaria lesions were taken. These findings were classified as: (I) a mixture of perivascular dermal inflammatory infiltrate composed of lymphocytes, monocytes and neutrophils and/or eosinophils; (II) inflammatory infiltrate composed chiefly of neutrophils; and (III) inflammatory infiltrate composed mainly of eosinophils. According to histology, the patients were submitted to one of the following therapeutic schemes: class A - antihistamine treatment plus dapsone; class B - colchicine or dapsone; class C - montelukast.Four patients in class A, 08 in class B and seven in class C displayed complete control of urticaria after 12 weeks of treatment; one patient in class B and two in class C did not respond to treatment. Two years after discontinuation, 16 patients are still free of urticaria.This study suggests an alternative approach for treating unresponsive chronic urticaria.

Chronic urticaria has been explored in several investigative aspects in the new millennium, either as to its pathogenesis, its stand as an autoimmune or auto-reactive disease, the correlation with HLA-linked genetic factors, especially with class II or its interrelation with the coagulation and fibrinolysis systems. New second-generation antihistamines, which act as good symptomatic drugs, emerged and were commercialized over the last decade. Old and new drugs that may interfere with the pathophysiology of the disease, such as cyclosporine and omalizumab have been developed and used as treatments. The purpose of this article is to describe the current state of knowledge on aspects of chronic urticaria such as, pathophysiology, diagnosis and the current therapeutic approach proposed in the literature.

Few studies have addressed the ultrastructure of vascular permeability in urticaria.To describe the types of endothelial cell organelles involved in vascular permeability in drug-induced acute urticaria (DIAU).Seven patients with DIAU were enrolled in the study. Biopsies of urticarial lesions and apparently normal skin were performed. The 14 collected fragmentswere processed with immunogold electron microscopy using single stains for tryptase and factor XIIIa (FXIIIa) and double immunogold labeling for both tryptase and FXIIIa.Some sections demonstrated mast cells in the degranulation process, in both anaphylactic and piecemeal degranulation. After double immunogold staining, 10 nm (FXIIIa) and 15 nm (tryptase) gold particles wereboth present, covering the granules in the mast cells, indicating that both tryptase and FXIIIa were localized within the granules of these cells. Interestingly, we found strong evidence of the presence of caveolae and vesico-vacuolar organelles (VVOs) in the endothelial cells of the biopsies. In addition to these findings, we were able to demonstrate the presence of tryptase and FXIIIa in the endothelial celIs, in urticarial lesions and in apparently normal skin.VVOs are present in the endothelial cells of post-capillary venules in DIAU. This is the first report on the expression of FXIIIa and tryptase in the cytoplasm of endothelial cells in urticaria.

Background: The cardinal signs and symptoms of adult-onset Still's disease (AOSD) include periodic fever, arthralgia and arthritis, lymphadenopathy, hepatosplenomegaly, an evanescent rash accompanied by neutrophilic granulocytosis, and a negative rheumatoid factor and antinuclear antibody test. Objective: To alert clinicians and dermatologists to internal diseases such as AOSD when assisting patients with urticarial eruptions and systemic symptoms. Methods: A case report of a 52-year-old white woman who received conventional therapy for urticaria for 3 years, with no improvement. Following this period, a diagnosis of AOSD was performed based on the presence of systemic symptoms. Results: The inflammatory activity markers decreased by the second month of methotrexate therapy; however, the cutaneous lesions failed to disappear. Thalidomide was initiated, and total improvement of the cutaneous lesions was observed after 2 weeks. Conclusion: Urticarial rash is an uncommon presentation of AOSD, and clinicians must be alert to the possibility of a misdiagnosis in these cases.

Drug-induced hypersensitivity syndrome (DIHS) usually refers to severe cutaneous drug eruption associated with systemic involvement and potentially fatal outcome. We report a 2-year-old Caucasian boy who developed DIHS due to phenytoin and phenobarbital and who showed extensive internal organ involvement. We are alerting that failure to recognize this drug eruption and discontinue the culprit drug may result in increased severity, greater extent of internal organ involvement, and fatal outcome. The recent research about the influence of human herpesvirus 6 co-infection on the pathogenesis of DIHS is also discussed by the authors in this paper.