Mast Cells in Cutaneous Allergic Vasculitis: A Case Report

Inamura, Hiroaki; Igarashi, Yasushi; Kashiwase, Yayoi; Morioka, Junichiro; Suzuki, Katsuhiro; Kurosawa, Motohiro

doi:10.2332/allergolint.55.343

Cited by 7 publications

(5 citation statements)

References 9 publications

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“…Therefore, tryptase may play an important role in the pathogenesis of the Koebner phenomenon. [9] Although not extensively studied in vasculitis, recent studies showed that immuno-enzyme-histological staining of tryptase (a marker for mast cell activation) was found in cutaneous allergic vasculitis[10] or HSP nephritis. [11]…”

Section: Discussionmentioning

confidence: 99%

Koebners phenomenon in Henoch-Schonlein purpura

Naveen

Pai

Raju

2014

Indian Dermatol Online J

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Section: Discussionmentioning

confidence: 99%

Koebners phenomenon in Henoch-Schonlein purpura

Naveen

Pai

Raju

2014

Indian Dermatol Online J

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“…In conditions such as leukocytoclastic vasculitis, activated MCs contribute to enhancing vascular permeability and facilitating the migration of leukocytes. An increased perivascular presence of MCs has been demonstrated in skin lesions characteristic of cutaneous allergic vasculitis and in urticarial vasculitis associated with systemic sclerosis 50 , 51 .…”

Section: Mast Cellsmentioning

confidence: 99%

Cutaneous vasculitis: insights into pathogenesis and histopathological features

Cassisa,

Cima

2024

Pathologica

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Summary The mechanisms underlying the onset and progression of vasculitis remain poorly understood. This condition is characterized by damage to the vascular wall, recruitment of inflammatory cells, and subsequent structural remodeling, which are hallmarks of vasculitis. The histopathological classification of vasculitis relies on the size of the affected vessel and the predominant type of inflammatory cell involved – neutrophils in acute cases, lymphocytes in chronic conditions, and histiocytes in granulomatous forms. Pathological changes progress in every context, and a single vasculitic pattern can be associated with various systemic conditions. Conversely, a single causative agent may lead to multiple distinct clinical and pathological manifestations of vasculitis. Moreover, many cases of vasculitis have no identifiable cause. A foundational understanding of the normal structure of the cutaneous vascular network is crucial. Similarly, identifying the cellular and molecular participants and their roles in forming the “dermal microvascular unit” is propedeutical. This review aims to elucidate the complex mechanisms involved in the initiation and progression of vasculitis, offering a comprehensive overview of its histopathological classification, underlying causes, and the significant role of the cutaneous vascular network and cellular dynamics. By integrating the latest insights from studies on NETosis and the implications of lymphocytic infiltration in autoimmune diseases, we seek to bridge gaps in current knowledge and highlight areas for future research. Our discussion extends to the clinical implications of vasculitis, emphasizing the importance of identifying etiological agents and understanding the diverse histopathological manifestations to improve diagnostic accuracy and treatment outcomes.

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“…The results are expressed as the mean ± SD. The ratios Chy act /Chy prot and Chy act /Try prot were calculated from each individual value * p = 0.029 when PP was compared with IP Previously, one case study [13] has examined mast cell tryptase in leukocytoclastic vasculitis. This study reported high numbers of tryptase ?…”

Section: Correlation Between Mast Cell Proteinases and Immunofluorescmentioning

confidence: 99%

“…Tryptase and chymase are the major proteins in MC TC mast cells and, therefore, they can have profound effects whenever released upon mast cell activation in vasculitis. Although mast cell tryptase and chymase have been studied in many different skin diseases [4,10], only very limited information on them is available in human cutaneous vasculitis [13]. In some older publications, mast cells have been examined in cutaneous vasculitis, but the reports deal with mast cell degranulation [23,26].…”

Section: Introductionmentioning

confidence: 99%

Mast cell tryptase and chymase in the progress of cutaneous vasculitis

Lipitsä

Harvima

2015

Arch Dermatol Res

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In animal models of vasculitis, mast cells are essential in the pathogenesis, but their involvement in human skin vasculitis is obscure. Because tryptase and chymase are potent serine proteinases in the secretory granules of mast cells, the purpose was to examine the number of mast cells expressing tryptase and chymase during the progress of cutaneous vasculitis. These numbers were correlated with the appearance of immunoreactants (C3c, fibrin, IgM, IgA and IgG) in vessel walls. For this, skin biopsies were taken from the healthy-looking skin, initial petechial lesion (IP), and palpable purpura (PP) of the leg of patients with leukocytoclastic vasculitis (n = 10). The frozen biopsies were analysed using enzyme- and immunohistochemistry and direct immunofluorescence (IF) staining. The results show that there are no marked changes in the numbers of mast cells expressing chymase or tryptase proteins. Instead, chymase enzyme activity decreased, but the score of α1-antichymotrypsin staining increased, during the progress of vasculitis. The IF positivity of fibrin correlated positively with chymase activity (p = 0.01) and the ratio of chymase activity to tryptase protein in IP (p = 0.03), as well as with mast cells showing tryptase (p = 0.03) and chymase (p = 0.01) proteins in PP. The IF positivity of C3c correlated with the ratio of chymase activity to tryptase protein in IP (p = 0.01). In conclusion, chymase is partially inactivated in vasculitis possibly due to α1-antichymotrypsin. Several positive correlations between chymase and fibrin and/or C3c in IP or PP suggest that this enzyme is involved in the deposition of immunoreactants in the vessel wall.

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Mast Cells in Cutaneous Allergic Vasculitis: A Case Report

Abstract: Mast cells may increase in the skin lesion of cutaneous allergic vasculitis.

Cited by 7 publications

References 9 publications

Koebners phenomenon in Henoch-Schonlein purpura

Koebners phenomenon in Henoch-Schonlein purpura

Cutaneous vasculitis: insights into pathogenesis and histopathological features

Mast cell tryptase and chymase in the progress of cutaneous vasculitis

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