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PubMed1976

Studies on vasculitis. VII. C-reactive protein as a substance perpetuating chronic vasculitis. Occurrence in lesions and concentrations in sera.

Previous findings were confirmed that C-reactive protein (C-RP) occurs in some vasculitis lesions, particularly those infiltrated mainly by neutrophils (necrotizing vasculitis). The C-RP was usually in lesions also containing complement C1 or C3c, and in some, IgG was present. Using a procedure that reliably detected 200 ng C-RP/ml serum, C-RP was found in sera of many normal persons, and the amount was influenced by the occupation of the donor. Sera of thirty-one persons with vasculitis with mainly mononuclear cell-infiltrated lesions had about four-fold more C-RP (mean 28, 200 ng/ml serum) than found in normal persons, and sera of thirty-nine persons with mainly neutrophil-infiltrated lesions had eight times the normal amount (mean 56,400 ng C-RP/ml). The amount of C-RP was influenced by the severity, extent and duration of the disorder in most patients. Experimental data suggests that C-RP may contribute to the perpetuation of inflammation in chronic vasculitis.

Animals↗

PubMed2005

Streptococcus induced pustular vasculitis affecting the hands resembling pustular vasculitis of the hands--first reported case.

Pustular vasculitis of the hands is a distinctive clinical entity. It has recently been proposed by some authors to rename pustular vasculitis of the hands as 'neutrophilic dermatosis of the hands' to reflect its histological resemblance to the neutrophilic dermatoses. We report the case of a 66-year-old woman who presented with clinical appearances resembling pustular vasculitis of the hands associated with palmo-plantar pustulosis due to Streptococcus-induced 'pustular vasculitis'.

Aged↗

PubMed2006

EULAR recommendations for conducting clinical studies and/or clinical trials in systemic vasculitis: focus on anti-neutrophil cytoplasm antibody-associated vasculitis.

OBJECTIVES: To develop the European League Against Rheumatism (EULAR) recommendations for conducting clinical studies and/or clinical trials in systemic vasculitis. METHODS: An expert consensus group was formed consisting of rheumatologists, nephrologists and specialists in internal medicine representing five European countries and the USA, a clinical epidemiologist and representatives from regulatory agencies. Using an evidence-based and expert opinion-based approach in accordance with the standardised EULAR operating procedures, the group identified nine topics for a systematic literature search through a modified Delphi technique. On the basis of research questions posed by the group, recommendations were derived for conducting clinical studies and/or clinical trials in systemic vasculitis. RESULTS: Based on the results of the literature research, the expert committee concluded that sufficient evidence to formulate guidelines on conducting clinical trials was available only for anti-neutrophil cytoplasm antibody-associated vasculitides (AAV). It was therefore decided to focus the recommendations on these diseases. Recommendations for conducting clinical trials in AAV were elaborated and are presented in this summary document. It was decided to consider vasculitis-specific issues rather than general issues of trial methodology. The recommendations deal with the following areas related to clinical studies of vasculitis: definitions of disease, activity states, outcome measures, eligibility criteria, trial design including relevant end points, and biomarkers. A number of aspects of trial methodology were deemed important for future research. CONCLUSIONS: On the basis of expert opinion, recommendations for conducting clinical trials in AAV were formulated. Furthermore, the expert committee identified a strong need for well-designed research in non-AAV systemic vasculitides.

Antibodies↗

PubMedDate not supplied

Birmingham vasculitis activity score, disease extent index and complement factor C3c reflect disease activity best in hepatitis C virus-associated cryoglobulinemic vasculitis.

OBJECTIVE: Clinical measures of vasculitis activity (Birmingham vasculitis activity score = BVAS) and disease extent (Disease Extent Index = DEI), serological and immunological parameters were evaluated for the monitoring of hepatitis C virus (HCV)-associated cryoglobulinemic vasculitis (CV), treated with either cyclophosphamide or interferon-alpha 2b depending on disease severity. METHODS: Serial serum samples of 15 patients with HCV-associated CV were analyzed, and BVAS, DEI, serological and immunological parameters were recorded at diagnosis and during therapy. Eight patients were treated with interferon-alpha 2b and 7 patients with cyclophosphamide. RESULTS: A complete or partial response of the CV was seen in both treatment groups. BVAS, complement factor C3c, cryoglobulinemia, and rheumatoid factor significantly decreased in both treatment groups during 6 months (p < 0.05). DEI decrease was significant in the cyclophosphamide group (p < 0.05), and there was a trend in the interferon-alpha 2b group (p = 0.06). BVAS and DEI were significantly positively correlated, and both parameters were significantly negatively correlated with C3c levels in both treatment groups (interferon-alpha 2b/cyclophosphamide: r = -0.89, p = 0.001 versus r = -0.87, p < 0.001, respectively) whereas other parameters were not, e.g. ESR and CRP. CONCLUSIONS: Patients with different degrees of disease severity, treated with either cyclophosphamide or interferon-alpha 2b depending on their disease activity, achieved remission of their CV. BVAS, DEI and C3c were especially useful in the follow-up of HCV-associated CV. C3c correlated with BVAS and DEI during therapy and provided additional information about vasculitis activity that was not reflected by other serological or immunological parameters, e.g. ESR or CRP.

Adult↗

PubMed1998

Induction of endothelial cell adhesion molecules by serum and immunoglobulins G from a patient with vasculitis and monoclonal gammapathy: potential relevance to vasculitis.

Interactions between endothelial cell adhesion molecules and their beta2 integrin adhesive receptors on leukocytes are thought to play a role in the pathogenesis of inflammatory diseases and probably vasculitis. We describe a case in whom leukocytoclastic vasculitis was associated to a monoclonal immunoglobulin G2 kappa (IgG2K). During the vasculitic crisis, the patient's serum and the isolated IgG from this serum induced the expression of E-selectin, VCAM-1 and ICAM-1 at the HUVEC surface, but not tissue factor activity, whereas normal, control serum and patient serum at remission were without any effect. A close relationship between the vasculitis and the serum level of the monoclonal IgG was observed. We suggest that the monoclonal IgG might induce the vasculitis by increasing the expression of E-selectin, VCAM-1 and ICAM-1 which facilitate the interaction of leukocytes with vascular endothelium.

Aged↗

PubMed1975

[Symptomatic or secondary allergic vasculitis. Pathogenesis of cutaneous vasculitis].

The histopathologic alterations of the allergic cutaneous vasculitis (fibrinoid necrosis of the walls of the small blood vessels with infiltration of neuthrophils in Karyorrexis) is seen in several entities. It is possible to divide such entities in two groups: a) Primitive allergic vasculitis in which the vascular lesion is dominant and. b) Secondary allergic vasculitis in which the vascular alterations, not constant, are integrants of variable histopathologic conditions. Many classifications have deen done on clinical and pathological bases. Such classifications are not satisfactory. A classification in base of physiopathologic and immunologic mechanisms could permit adequate therapeutic planning. In this paper we consider the secondary vasculitis only. The secondary angitis are seen in: 1) Difuse colagen diseases. 3) Conditions related to infections or inflamatory processes. 3) Angitis produced by drugs. 4) Conditions produced by insects or parasites bites. 5) Heterogeneous group that include diferent tipes of not necrotizing sistemic angitis in uhich, some times, trombosant and necrotizing processes are associated.

Arteritis↗

PubMed2007

Retinal vasculitis and vitreous hemorrhage associated with mixed connective tissue disease: retinal vasculitis in MCTD.

BACKGROUND: Retinal vasculitis associated with mixed connective tissue disease (MCTD) has rarely been reported in the literature. We describe a rare case of a patient with serious retinal vasculopathy and vitreous hemorrhages associated with MCTD. CASE: A 53-year-old woman with MCTD who has had recurrent retinal vasculitis and vitreous hemorrhage in the right eye since 2000 presented with blurred vision in the right eye in April 2003. The best-corrected visual acuity was counting finger in the right eye. The patient was clinically diagnosed as having retinal and vitreous hemorrhages and retinal infarction. Prednisolone was administered orally in a daily dose of 20 mg. RESULTS: The retinal and vitreous hemorrhage improved in 7 days. The best-corrected visual acuity improved to more than 20/20 on prednisolone alone. CONCLUSION: MCTD can be associated with retinal vasculitis and vitreous hemorrhage which in our case responded well to systematic low doses of corticosteroid therapy.

Adult↗

PubMed1995

Eosinophilic vasculitis syndrome: recurrent cutaneous eosinophilic necrotizing vasculitis.

We recently identified a syndrome of recurrent cutaneous eosinophilic vasculitis in three patients. These patients had in common widespread pruritic, erythematous, purpuric papules and angioedema of face and hands associated with peripheral blood eosinophilia. Eight skin biopsies from these three patients all showed necrotizing vasculitis of the small vessels of the skin, with exclusively eosinophilic infiltration and minimal or no leukocytoclasis. The disease followed a chronic course, with recurrent, itchy, swelling skin lesions and without evidence of systemic involvement over observation periods of 3, 17, and 23 years. The skin lesions responded promptly to systemic steroid treatment, but two patients required maintenance doses for control of the disease. Immunofluorescence studies showed marked deposition of the cytotoxic eosinophil granule major basic protein in the affected vessel walls. Eosinophil-active cytokine IL-5 was detected in the serum of one patient. Expression of the vascular cell adhesion molecule-1 for eosinophil adherence was detected on the endothelium of the affected vessels. Because this disease showed distinctive clinical manifestations and characteristic histopathological features, we believe it is a distinct entity and should be distinguished from other types of vasculitis.

Adolescent↗

PubMed1976

Studies on vasculitis. VI. Antiglobulins or rheumatoid-like factors in cutaneous vasculitis lesions detected by an improved immunofluorescence procedure.

Human cutaneous vasculitis lesions tend to be chronic in contrast to ephemeral experimental Arthus responses. Human lesions were examined for fixed antiglobulin antibodies, as occur in rheumatoid joint synovia, which could bind globulins to form tissue-damaging complexes and perpetuate the inflammation. The immunofluorescence procedure was modified by pretreating sections with 5% bovine serum albumin, and by using fluorescein conjugates of F(ab)2 portions of antibodies to avoid the antigen-nonspecific binding that sometimes occurs in inflamed or necrotic tissue. Previous findings of immunoglobulins in lesions were confirmed by the more discriminating technique. IgG and IgM was present more frequently in lesions with mainly mononuclear cell changes, than in those with mainly neutrophil changes, leucocytoclastic or necrotizing vasculitis. Fab occurred in some lesions without Fc of IgG or IgM. Three lesions containing IgM or IgM and IgG, specifically bound heat-aggregated whole IgG or Fc of IgG. None bound IgM. The results indicate that the immunoglobulin in some cutaneous vasculitis lesions is locally formed or fixed antiglobulin, which will bind aggregated IgG possibly forming complexes perpetuating the lesion.

Antibodies, Anti-Idiotypic↗

PubMed1986

Urticarial vasculitis and recurrent pleural effusion: a systemic manifestation of urticarial vasculitis.

A 62-year-old woman with an 8-year history of urticaria, arthralgia and arthritis developed recurrent pleural effusion. A thorough laboratory workup during repeated attacks of concomitant urticaria and pleural effusion disclosed only hypocomplementemia and the histopathological finding of the skin biopsy revealed leukoclastic vasculitis. These findings are compatible with the entity of urticarial vasculitis. It is thus suggested that pleural effusion can form part of the systemic manifestations of urticarial vasculitis.

Complement Pathway, Classical↗

PubMed1984

The vasculitis of atrophie blanche (livedoid vasculitis) and abdominal aortic pathology.

Seven of forty-two patients with livedoid vasculitis whose cases were reviewed at the Mayo Clinic were found to have abdominal aortic disease, in the form of aortic calcification and atherosclerosis or aneurysm. None of these patients had any associated systemic mesenchymal disease (lupus erythematosus, periarteritis nodosa, rheumatoid arthritis, Sjögren's syndrome, or carcinomatous diseases). Three patients received graft replacements for aneurysm or vascular occlusive disease. Removal of the aneurysm in one case was associated with resolution of the livedoid vasculitis. Abdominal aortic changes should be considered in patients with diagnosed livedoid vasculitis.

Aged↗

PubMed1975

Livedo vasculitis (the vasculitis of atrophie blanche). Immunohistopathologic study.

Hyalinizing segmental vasculitis or livedo vasculitis (atrophie blanche) is a clinical entity with a distinctive immunohistopathologic morphology that can be distinguished from other forms of cutaneous vasculitis by histologic and direct immunofluorescent studies. Our studies showed that immunoglobulins and complement components (C-1g, C-3, and properdin) were localized in diseased vessel walls, suggesting an immune pathogenesis.

Atrophy↗

PubMed2001

"Essential" cutaneous vasculitis: what every rheumatologist should know about vasculitis of the skin.

Although the classification of small-and medium-vessel vasculitides involving the skin remains complex and imperfect, a substantial body of knowledge related to cutaneous vasculitis exists. Some components of this knowledge, though beyond the usual purview of rheumatologists, are essential to understanding the vasculitides. The correct interpretation of cutaneous findings combined with a properly performed skin biopsy yields important insights not only into underlying diagnoses, but also into the pathophysiological mechanisms of individual cases. In this review, we discuss a classification scheme for the cutaneous vasculitides, outline the work-up for evaluating patients with these disorders, and describe the essential features of the major categories of skin vasculitis.

Behcet Syndrome↗

PubMed2026

IgA Vasculitis with necrotizing arteritis: a multicenter retrospective study from the French Vasculitis Study Group and systematic review of the literature.

IgA vasculitis (IgAV) primarily affects small vessels, but rare cases with necrotizing arteritis (NA) raise questions about overlap with polyarteritis nodosa (PAN). To characterize IgAV with necrotizing arteritis (IgAV-NA) and compare its phenotype with classical IgAV and PAN. We performed a multicenter retrospective study combined with a systematic literature review (1990-2025). Patients fulfilled EULAR/PRINTO/PRES IgAV criteria, had pathological or imaging evidence of NA in small or medium arteries, and were ANCA-negative. Thirty patients were included (7 from databases, 23 from the literature). NA was confirmed by biopsy (n = 16) or vascular imaging (n = 14). Clinical features, treatments, remission, and mortality were compared with 257 adult IgAV and 196 PAN patients. Median age was 54.5 years. IgAV-NA was characterized by severe manifestations, including gastrointestinal bleeding, perforation, surgical abdomen, neuropathy, pancreatitis, and livedo. Compared with classical IgAV, IgAV-NA showed significantly higher rates of multi-organ involvement and mortality. Compared with PAN, IgAV-NA shared vascular complications but had less fever and neuropathy. Despite arterial involvement, patients did not fulfil PAN criteria. IgAV-NA represents a rare, severe IgAV phenotype with life-threatening complications rather than an IgAV-PAN overlap. Severe or atypical IgAV presentations should prompt vascular imaging and intensified immunosuppression.

Humans↗

PubMed1995

Idiopathic retinal vasculitis, aneurysms, and neuro-retinitis. Retinal Vasculitis Study.

PURPOSE: The authors describe the clinical feature of ten patients with a new syndrome characterized by the presence of retinal vasculitis, multiple macroaneurysms, neuro-retinitis, and peripheral capillary nonperfusion. METHODS: The authors evaluated ten patients identified to have clinical features compatible with the syndrome of idiopathic retinal vasculitis, aneurysms and neuroretinits (IRVAN). Clinical examination findings, sequential funds photographs (when available), fluorescein angiograms, systemic investigations, response to therapy, and visual outcomes were reviewed. RESULTS: Seven eyes of four patients sustained a marked decrease in visual acuity of 20/200 or worse. Visual loss was due to a combination of an exudative maculopathy and sequelae of retinal ischemia. Capillary nonperfusion was seen in all ten patients and was severe enough to warrant panretinal laser photocoagulation in six patients. Systemic investigations were uniformly noncontributory. Oral prednisone appears to have little beneficial effects on patients with this disorder. CONCLUSIONS: Patients with IRVAN have characteristic retinal features that readily identify this syndrome. An increased awareness of this rare syndrome may help to identify sight-threatening complications at an earlier stage. The authors caution against extensive medical investigations.

Adult↗

PubMed2002

ANCA-positive periaortic vasculitis: does it fall within the spectrum of vasculitis?

Retroperitoneal fibrosis (RPF) is a disease of unknown aetiology that has sometimes been reported in association with connective tissue disorders and systemic vasculitis. We report here two cases of antineutrophil cytoplasmic antibody (ANCA)-positive RPF showing clinical evidence of rapidly progressive glomerulonephritis. Although treatment with prednisone and cyclophosphamide led to a remission of RPF in both cases, renal function was restored in only one patient and the other progressed to chronic renal failure. The paper reviews the literature concerning ANCA-positive RPF and discusses the relationship between ANCA-positive vasculitis and RPF.

Aged↗

PubMed1992

Livedo vasculitis: vasculitis or thrombotic vasculopathy?

Elevated fibrinopeptide A levels, suggestive of a thrombogenic state, were observed in six patients with livedo vasculitis. Serological studies demonstrated normal complement levels, and circulating immune complexes were not identified by standard assays. Morphological studies showed no evidence of immune complex deposition or a neutrophilic vascular reaction. These results support classification of this disorder as a thrombogenic vasculopathy rather than as a small vessel vasculitis. Further investigations into the thrombotic abnormalities underlying this entity are warranted.

Adult↗

PubMed1995

Necrotizing vasculitis associated with hepatitis C virus infection: successful treatment of vasculitis with interferon-alpha despite persistence of mixed cryoglobulinemia.

Type II cryoglobulinemia may be associated with chronic hepatitis C virus (HCV) infection and may be characterized by vascular purpura. We report on a case of histologically proven necrotizing vasculitis associated with type II cryoglobulinemia and HCV infection. Within 14 days of interferon-alpha therapy (3 x 3 million IU/ml/week), purpuric skin lesions disappeared as well as fatigue and arthralgia; 9 months after initiation of therapy, liver enzyme values were nearly normal despite persistence of HCV RNA tested by PCR and mixed cryoglobulinemia. Rheumatoid factor activity, however, decreased markedly. To our knowledge, our patient is the first reported case with histologically proven necrotizing vasculitis with a beneficial effect of interferon-alpha. Because of the persistence of cryoglobulins, but reduction of the IgM fraction in the cryoglobulin complex under interferon-alpha treatment, it would seem worthwhile to further elucidate the pathogenic role of qualitative instead of quantitative changes of cryoglobulins and the mechanism of action of interferon-alpha.

Arthralgia↗