Leukocytoclastic Vasculitis; Sequential Appearance of Immunoreactants and Cellular Changes in Serial Biopsies

Gower, Richard; Sams, W. Mitchell; Thorne, E. George; Köhler, Peter F.; Claman, Henry N.

doi:10.1111/1523-1747.ep12511631

Cited by 117 publications

(43 citation statements)

References 26 publications

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“…5 The importance of the timing when taking biopsy specimens in a dynamic process such as vasculitis has been emphasized by several investigators. 6,7 Zax et al 7 clearly demonstrated that different histologic patterns can be seen depending on the timing of biopsy in sequential biopsy specimens obtained from a single patient with leukocytoclastic vasculitis. They argued that it is the natural course of leukocytoclastic vasculitis to be initially a predominantly neutrophilic process and to evolve into a lymphocytic process.…”

Section: Discussionmentioning

confidence: 99%

Cellular and Molecular Dynamics in Exercise-Induced Urticarial Vasculitis Lesions

Kano

Orihara²,

Shiohara³

1998

Arch Dermatol

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Section: Discussionmentioning

confidence: 99%

Cellular and Molecular Dynamics in Exercise-Induced Urticarial Vasculitis Lesions

Kano

Orihara²,

Shiohara³

1998

Arch Dermatol

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“…From cxperimental studies on both the Arthus reaction animal model (14,15) and human LCV (16), the immunoglobulins are detectable for a short time after initiation of the LCV lesions; by 18-48 hours, immunoglobulin epitopes are no longer detectable. From histochemical analysis the LCV lesions in this study were most likely more than 18 hours old.…”

Section: Discussionmentioning

confidence: 99%

Localization of hepatitis C virus in cutaneous vasculitic lesions in patients with type II cryoglobulinemia

Agnello

Ábel²

1997

Arthritis & Rheumatism

142

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Objective. To investigate the role of hepatitis C virus (HCV) in the pathogenesis of the cutaneous vasculitis in patients with type I1 cryoglobulinemia.Methods. Using in situ hybridization detection of HCV, we studied 6 test patients and various control subjects. Serum HCV was quantitated, cryoglobulins were analyzed by column chromatography at 37"C, and lowdensity lipoprotein (LDL) receptors on keratinocytes were detected using LDL labeled with fluorescent dye.Results. In the cutaneous vasculitic lesions from test patients, but not control subjects, the HCV virion was found in association with IgM and IgG. HCV alone was detected in some vessel walls, and in skin and ductal epithelium and vascular endothelium in inflamed, but not normal, skin. Cryoglobulins showed HCV, monomeric IgM, and monomeric IgG, with little or no immune complexes. The extent of the lesions correlated with levels of viremia. Up-regulation of LDL receptors on keratinocytes was detected in inflamed, but not normal, skin.Conclusion. HCV was present in the cutaneous vasculitic lesions, most likely in complexes with IgM and IgG formed in situ. These findings and the correlation of the severity of the rash with the level of viremia suggest that HCV plays a major role in the pathogenesis of cutaneous vasculitis in these patients and strength- The hallmark of type TI cryoglobulinemia is palpable purpura, a cutaneous vasculitis thought to be caused by the deposition of the components of cryoglobulins, polyclonal IgG, and monoclonal rheumatoid factor (RF) in the vessel walls (1). A strong association of hepatitis C virus (HCV) infection and type I1 cryoglobulinemia has been established (2,3), and the virus is specifically concentrated in the cryoglobulins (4). These findings suggest that HCV is the etiologic agent for the disease and that the virus may be involved in the pathogenesis of the systemic vasculitis that occurs in these patients.HCV is a single-stranded RNA virus, and both the positive strand, the putative virion RNA, and the negative strand, the putative replicative RNA, have been detected in hepatocytes of infected patients by polymerase chain reaction (PCR) assays ( 5 ) and by in situ hybridization and in situ PCR (6). HCV RNA has not been reported to be localized in cutaneous vasculitic lesions, but HCV has been detected in RNA extracted from these lesions using a PCR assay (7). However, because of the exquisite sensitivity of the PCR assay, the extraction technique does not distinguish between HCV RNA in the lesion and HCV RNA that may be present in small amounts of residual serum in unaffected blood vessels.We investigated the role of HCV in the pathogenesis of the cutaneous vasculitis in type I1 cryoglobulinemia by examining biopsy specimens of the palpable purpuric lesions from patients with type I1

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“…Similar positive results were reported previously. 1,7,[28][29][30] Destruction and removal of immunoglobulins deposited in the affected dermal vessels takes place in less than 48 hours, and direct immunofluorescence studies of vasculitic lesions older than 48 hours are frequently negative. 29 The positivity of the immunofluorescence test was inversely correlated with the duration of the lesion studied by biopsy (PϽ.001).…”

Section: Commentmentioning

confidence: 99%

Prognostic Factors in Leukocytoclastic Vasculitis

Sais¹,

Vidaller²,

Jucglà³

et al. 1998

Arch Dermatol

133

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Leukocytoclastic Vasculitis; Sequential Appearance of Immunoreactants and Cellular Changes in Serial Biopsies

Cited by 117 publications

References 26 publications

Cellular and Molecular Dynamics in Exercise-Induced Urticarial Vasculitis Lesions

Cellular and Molecular Dynamics in Exercise-Induced Urticarial Vasculitis Lesions

Localization of hepatitis C virus in cutaneous vasculitic lesions in patients with type II cryoglobulinemia

Prognostic Factors in Leukocytoclastic Vasculitis

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