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At least 19 recordsLinked to original sources
PubMed1978

Small vessel vasculitis caused by hepatitis B virus immune complexes. Small vessel vasculitis and HBsAG.

In a comprehensive study of 80 patients with vasculitis, 4 had concurrent hepatitis B virus (HBV) infection. Polyarteritis nodosa was present in 2 and in the other 2, cutaneous vasculitis, presenting clinically as palpable or Henoch-Schönlein purpura. In one of these patients skin biopsies demonstrated granular deposits of IgM, C3, C4, and the hepatitis B surface antigen (HBsAg) and electron-dense deposits of aggregated 20-nm particles resembling HBsAg in postcapillary venules. Evidence for circulating HBsAg-immune complexes included increased serum Clq binding activity, decreased serum complement, and a cryoprecipitate containing both HBsAg and IgM anti-HBs. Aggregated 20-nm particles resembling intact HBsAg were also seen by negative staining electron microscopy of the serum cryoprecipitate. This patient fulfills all the criteria for a specific immune complex vasculitis caused by his immune response to a chronic HBV infection. These findings emphasize that HBV infection may be associated with small vessel vasculitis as well as polyarteritis nodosa, mixed cryoglobulinemia, and glomerulonephritis. A similar immune response to other viral infections may be expressed as palpable (Henoch-Schönlein) purpura also.

Adult↗
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↗
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↗
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↗
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↗
PubMed1979

Circulating immune complexes in cutaneous vasculitis. Detection with C1q and monoclonal rheumatoid factor.

To investigate the pathogeneic significance of immune complexes in cutaneous vasculitis, 107 patients with various forms of cutaneous vasculitis, including 59 patients with necrotizing (leukocytoclastic) vasculitis (group 1), and 48 patients with lymphocytic vasculitis, or a predominately lymphocytic perivascular infiltrate (group 2), were studied. Immunoglobulins or complement components in cutaneous blood vessels were detected by direct immunofluorescence in high frequency in both groups (91 and 88%, respectively). Using two radioassays for circulating immune complexes, Clq or monoclonal rheumatoid factor (mRF) reactive material was detected in 68% of the patients with necrotizing vasculitis but only 44% of the patients in the lymphocytic-perivascular group. The mRF radioassay was elevated in 58% of the first group of patients and 41% of the patients in group 2, although Clq binding activity was increased in 54% of the patients with necrotizing vasculitis but only in 9% of the patients with a lymphocytic vasculitis or lymphocytic perivascular infiltrate. By using both sucrose density gradient ultracentrifugation and Sepharose 6B gel filtration, the Clq and mRF reactive material detected in some patients with necrotizing vasculitis eluted in high molecular weight fractions that were also anticomplementary. In one patient with necrotizing vasculitis and hepatitis B antigenemia, these heavy molecular weight Clq and mRF reactive fractions contained a two- to three-fold increase in hepatitis B surface antigen when compared with lighter molecular weight fractions. Heavy and light molecular weight mRF reactive material could be detected in selected patients in the lymphocytic-perivascular group as well as in the necrotizing vasculitis group. These studies suggest that cutaneous vasculitis, including acute necrotizing (leukocytoclastic) vasculitis and some forms of lymphocytic vasculitis, and perhaps some diseases characterized by a lymphocytic perivascular infiltrate, may represent cutaneous expressions of immune complex disease.

Antigen-Antibody Complex↗
PubMed1976

Immunologic mechanisms in systemic vasculitis.

Thirty-four patients with systemic vasculitis were studied to determine the possible type and frequency of associated immunologic abnormalities. The patients were divided into three clinical groups--those with systemic vasculitis without respiratory tract involvement, those with systemic vasculitis with respiratory tract involvement (particularly Churg-Strauss vasculitis and Wegener's granulomatosis), and those with limited vasculitis without visceral involvement. A diminished level of serum complement was found in half the patients with systemic vasculitis without respiratory tract involvement. These patients usually had diffuse skin disease that often was associated with the presence of rheumatoid factor and cryoglobulinemia and most likely represented an immune-complex induced disease. The serum IgE often was elevated in patients who had systemic vasculitis with respiratory tract involvement, particularly those with Churg-Strauss vasculitis and Wegener's granulomatosis, and may be a clue to the pathogenesis in this group of patients.

Adult↗
PubMed1975

Cryoimmunoglobulinemia in rheumatoid arthritis. Significance in serum of patients with rheumatoid vasculitis.

Cryogloculins were examined in a standardized manner in an unselected group of 35 patients with rheumatoid arthritis (RA) and 8 patients with RA complicated by cutaneous vasuclitis and neuropathy. Optimum conditions for detection and characterization of cryoglobulins were established; the proportion of resolubilized to total precipitable protein remained constant in an individual patient under these conditions. All 8 vascultis patients and 9 of 35 other patients with RA exhibited cryoglobulins; total protein and immunoglobin content were significantly higher in the cryoglobulins of patients with vasculitis. Immunoglobulins G and M constituted two-thirds and three-quarters of the total protein in the cryoglobulins from uncomplicated rheumatoid and vasculitis patients, respectively. Serum antiglobulin titers were higher, and serum C3 levels were lower, in vasculitis patients compared to rheumatoid patients without vasclitis. Anti-gamma globulin activity was detected in all cryoglobulins from vasculitis patients. Cryoglobulin IgG and IgM were polyclonal. Density gradient analyses demonstrated the majority of the cryoglobulin activity to reside in the 19S IgM fraction. There was no evidence of a light weight (8S) IgM. A monoclonal rheumatoid factor did not detect 7S-ANTI-7S complexes in the cryoprecipitates, but acid eluates from some cryoglobulins absorbed with insoluble IgG revealed an antiglobulin of the IgG class. Serial studies performed on vasculitis patients treated with cyclophosphamide disclosed a relationship between clinical evidence of vasculitis and the presence of cryoglobulins. The antigen (IgG) and antibody (largely IgM rheumatoid factor) nature of these cryglobulins is presented as evidence that the widespread vascular complications of RA are mediated, at least in part, by circulating immune complexes.

Aged↗
PubMed1979

Management of necrotizing vasculitis with colchicine. Improvement in patients with cutaneous lesions and Behcet's syndrome.

Six patients with necrotizing vasculitis were treated with oral colchicine as part of an open study. Four patients with cutaneous vasculitis and normal levels of serum complement and one patient with vasculitis associated with Behcet's syndrome demonstrated clinical improvement while receiving colchicine. One patient with cryoglobulinemia, hypocomplementemia, and cutaneous vasculitis showed no response to colchicine therapy. In three patients, clinical improvement persisted after its withdrawal. Colchicine may be effective in controlling cutaneous necrotizing vasculitis and Behcet's syndrome through its effect on polymorphnuclear leukocyte function.

Administration, Oral↗
PubMed1975

Necrotizing vasculitis. Etiologic aspects of immunology and coagulopathy.

Thirty-one patients with cutaneous necrotizing vascultis were studied for immunological and coagulation disturbances. Serum immunoglobulin levels did not correlate with tissue deposition of the corresponding immunoglobulins in the lesions of cutaneous necrotizing vasculitis. In all instances, localization of immunoglobulins, complement, and fibrinogen, when present in the lesions of necrotizing vasculitis, was limited to the vascular wall or perivascular space. Soluble fibrinogen-fibrin complexes (cryoprofibrin) were detected in the blood of four of 17 patients with cutaneous necrotizing vasculitis. Since it represents a product of the limited action of thrombin on fibrinogen, its presence in the blood in some patients with necrotizing vasculitis suggests that intravascular coagulation may play a part in the pathogenesis of the disease. In 12 of the 31 patients studied, a cause of the vasculitis was found or presumed.

Adolescent↗
PubMed1979

Drug related vasculitis. Clinicopathologic correlations in 30 patients.

Drug related vasculitis has variously been described as necrotizing hypersensitivity or allergic angiitis or microscopic panarteritis nodosa. We reviewed tissue sections from 30 patients with validated drug hypersensitivity and vasculitis in order to precisely define this entity. No evidence of necrotizing vascular lesions or of fibrinoid associated with necrosis was found. The vascular lesions in all 30 patients involved small arteries, arterioles, capillaries, and venules. The inflammatory infiltrate consisted primarily of mononuclear cells and prominent numbers of eosinophils and was present in all three layers of the involved vessel walls. Clinically the patients developed either localized or systemic vasculitis, which could not be predicted on the basis of the associated drug. The findings of a skin rash, fever, or eosinophilia and the development of symptoms consistent with a hypersensitivity reaction while medication was being taken were all suggestive of the diagnosis of drug related vasculitis.

Adolescent↗
PubMed1978

The spectrum of vasculitis: clinical, pathologic, immunologic and therapeutic considerations.

Vasculitis is a clinicopathologic process characterized by inflammation and necrosis of blood vessels. Certain disorders have vasculitis as the predominant and most obvious manifestation, whereas others have various degrees of vasculitis in association with other primary disorders. Within the entire spectrum of vasculitis virtually any size or type of blood vessel in any organ system can be involved. Most of the vasculitides can be associated directly or indirectly with immunopathogenic mechanisms. In this regard, immune complex mediation is being increasingly recognized as the underlying mechanism in several of the vasculitides. With clinical, pathologic, and immunologic criteria, certain vasculitic disorders can be clearly recognized and categorized as distinct entities, whereas in others there is an overlap of different diseases within a broader category. In recent years, several of the more serious vasculitides, such as Wegener's granulomatosis and the systemic necrotizing vasculitides of the polyarteritis nodosa group, which formerly had extremely poor prognoses, have been shown to be extraordinarily responsive to chronic low-dose cytotoxic therapy, particularly cyclophosphamide.

Adult↗
PubMed1979

Urticarial vasculitis: report of a case and review of the literature.

A woman with cutaneous vasculitis had a severe bullous eruption that was suggestive of erythema multiforme. The patient also had a history of recurrent urticaria that continued intermittently for over a year of follow-up examination. Skin biopsy specimens of both urticarial and erythema and multiforme lesions showed leukocytoclastic vasculitis. An illness resembling systemic lupus erythematosus (SLE) is suggested by transient, low-titer, positive antinuclear antibody tests, persistent deposits of immunoglobulin and complement in normal skin, arthralgias, circulating immune complexes, and chronic hypocomplementemia. This case is similar to cases previously reported as "hypocomplementemic vasculitis," an "unusual SLE-related syndrome," and "urticaria with vasculitis."

Adult↗
PubMed1977

Leukocytoclastic vasculitis: sequential appearance of immunoreactants and cellular changes in serial biopsies.

To study the mechanisms responsible for leukocytoclastic vasculitis, we evaluated the kinetics of immunologic and cellular changes in induced vasculitis lesions. In four of five consecutive patients with active vasculitis, lesions were induced by increasing vascular permeability via injecting histamine into the skin. Biopsies were obtained for light and electron microscopy and immunofluorescence at 1, 4, 8, and 24 hr after injection. The results show that immunoglobulin, C3, and electron-dense material are deposited in vessel walls early and are followed by cellular infiltration. The characteristics of the cellular infiltrates were quite diverse at different times after histamine provocation and no distinctive patterns were seen. Nevertheless, the kinetics of the appearance of immunoreactants and cells implies that immunoglobulin and probably circulating immune complexes are present prior to the development of inflammation and supports the contention that deposition of immune complexes within vessel walls is responsible for leukocytoclastic vasculitis.

Adult↗
PubMed1979

[Circulating immune complexes and necrotizing vasculitis].

55 patients with necrotizing and with various forms of lymphocytic vasculitis were investigated for the presence of vascular deposits of immunoglobulins (Ig) and C3 by immunofluorescence testing of skin biopsies and with a 125I-Clq-binding assay for the presence of circulating immune complexes. Vascular deposits of Ig and C3 were found frequently both in patients with necrotizing and with lymphocytic vasculitis. In contrast, C1q binding activity was found almost exclusively in sera of patients with systemic necrotizing vasculitis. With one exception, all sera with C1q binding activity were from patients with vascular deposits of Ig and C3. The implications of these findings for our understanding of the development of system involvement in necrotizing vasculitis are discussed.

Antigen-Antibody Complex↗
PubMed1976

Vasculitis with hepatitis B antigenemia: long-term observation in nine patients.

The development of generalized necrotizing vasculitis in association with hepatitis B antigenemia is the first example in man of a chronic rheumatic disease presumably caused by a viral infection. This report reviews the experience in nine biopsy-proven cases of hepatitis B-associated necrotizing vasculitis followed for up to six years. The natural history of the disease is emphasized and the manifestations of patients with vasculitis who carry hepatitis B antigen are compared with those of vasculitis patients who are antigen negative.

Adult↗