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PubMed2005

Anti-endothelial cell antibodies (AECA) in patients with propylthiouracil (PTU)-induced ANCA positive vasculitis are associated with disease activity.

Increasing evidence has demonstrated that propylthiouracil (PTU) could induce ANCA positive vasculitis. However, our previous work has suggested that only one-fifth of the PTU-induced ANCA positive patients had clinical vasculitis and so the mechanism is not clear. Anti-endothelial cell antibodies (AECA) have been implicated in the pathogenesis of various vasculitides, including primary ANCA positive systemic vasculitis. The purpose of this study is to investigate the prevalence of AECA and their possible role in the pathogenesis of patients with PTU-induced ANCA positive vasculitis. Sera from 11 patients with PTU-induced ANCA positive vasculitis at both active and quiescent phases, and sera from 10 patients with PTU-induced ANCA but without clinical vasculitis, were studied. Sera from 30 healthy blood donors were collected as normal controls. Soluble proteins from 1% Triton-100 extracted in vitro cultured human umbilical vein endothelial cells were used as antigens and an immunoblotting technique was performed to determine the presence of AECA, and their specific target antigens were identified. In patients with PTU-induced ANCA positive vasculitis, 10 of the 11 patients in an active phase of disease were serum IgG-AECA positive and six protein bands of endothelial antigens could be blotted (61 kD, 69 kD, 77 kD, 85 kD, 91 kD and 97 kD). However, in the quiescent phase, seven of the 10 positive sera turned negative. None of the ANCA positive but vasculitis negative patients or normal controls were AECA positive. In conclusion, AECA could be found in sera from patients with PTU-induced ANCA positive vasculitis and were associated more closely with vasculitic disease activity.

Adolescent↗
PubMed2005

Circulating endothelial cells in relapse and limited granulomatous disease due to ANCA associated vasculitis.

OBJECTIVES: To evaluate numbers of circulating endothelial cells (CECs) in ANCA associated vasculitis and compare vasculitic relapse with limited granulomatous disease. METHODS: Sixteen patients with vasculitic relapse of ANCA associated vasculitis and 12 patients with limited granulomatous disease due to Wegener's granulomatosis (WG) were studied. Six patients with newly diagnosed vasculitic disease and six patients with vasculitis with infectious complications were also studied. Twenty two patients in remission were studied, as were 20 healthy controls. Counting of CECs was performed with anti-CD146 driven immunomagnetic isolation and staining with Ulex Europaeus lectin 1(UEA-1). RESULTS: Patients with vasculitic relapse had markedly increased numbers of circulating endothelial cells (12-800 cells/ml, median 88 cells/ml) as did patients with newly diagnosed systemic vasculitis (20-216 cells/ml, median 56 cells/ml). Patients with limited granulomatous disease due to WG had only slightly increased cell numbers (4-44 cells/ml, median 20 cells/ml), which were similar to those of patients in remission (4-36 cells/ml, median 16 cells/ml). Numbers of CECs in patients with granulomatous disease were significantly lower than in those patients with relapse or new onset vasculitis (p<0.001). Cell numbers in patients with relapse and new onset vasculitis declined with immunosuppressive treatment. Patients with infection had 4-36 cells/ml (median 10 cells/ml). A cut off value of 20 cells/ml for a positive result yielded 64% specificity and 95% sensitivity for active systemic vasculitis; the positive predictive value was 63% and the negative predictive value 95%. CONCLUSION: Markedly increased numbers of CECs discriminate active vasculitis from limited granulomatous disease and remission. These findings add further proof to the concept of CECs as a marker of ANCA associated small vessel vasculitis.

Acute Disease↗
PubMed1981

Rectal biopsy in the diagnosis of systemic vasculitis.

Vasculitis has been seen in rectal biopsies from 22 patients over a six year period. The most common finding was a necrotising vasculitis of small arteries, indistinguishable from that seen in polyarteritis nodosa (PAN). Sub-acute, chronic ("burnt out") and leucocytoclastic changes were also seen. Sixteen patients had vasculitis complicating rheumatoid arthritis (RA), 3 PAN and 3 overlap syndromes. Patients with RA and rectal vasculitis had a higher mortality, and a greater incidence of neuropathy than those with negative biopsies. An adequate biopsy is positive in 40% of patients with clinical vasculitis and RA but was only positive in one of a control series of 46 RA patients with no clinical vasculitis. Rectal biopsy in experienced hands is a safe, and repeatable procedure. It is useful as a "blind" biopsy site in the diagnosis of systemic vasculitis, especially that complicating RA. It can also be used for serial studies of the evolution of vasculitis. Serial sections of the entire biopsy may be required to reveal the vasculitis which is often focal in nature.

Adult↗
PubMed2000

Vasculitis and leukemia.

Vasculitis may accompany neoplasias and be of paraneoplastic type or associated with drugs used in patient treatment. We evaluated skin biopsies of twenty-eight cases with vasculitis accompanying leukemias reviewed and clinical outcome was evaluated. Eleven of the 28 cases had paraneoplastic vasculitis and 17 had vasculitis associated with various drugs including chemotherapy, cytokines and antibacterial agents. Paraneoplastic vasculitis was seen in 3 cases with chronic myelocytic leukemia in blastic phase, 5 patients with acute myeloblastic leukemia, and 3 with myelodysplastic syndrome. Drugs responsible for the 17 cases of vasculitis included hydroxyurea, vincristine, cytosine-arabinoside, methotrexate, all-trans retinoic acid, granulocyte-colony stimulating factor, interferon and antibiotics. Paraneoplastic vasculitis is not rare in leukemias and may be a manifestation of the blastic phase of chronic myeloid leukemia. Furthermore paraneoplastic vasculitis can be fatal in myelodysplastic syndromes and may be present clinically before the specific diagnosis is made. Drugs used in routine therapy may be the cause of the vasculitis, thus skin biopsy should be performed in all cutaneous lesions in patients with hemopoietic neoplasias.

Adolescent↗
PubMed1992

[Immunohistochemistry of nodular vasculitis. A possible role of delayed cellular hypersensitivity].

The physiopathogenesis of nodular vasculitis is still unknown: there is probably an initial Arthus' phenomenon responsible for the lesions of the deep vessels, but the frequent recurrences and the long time duration of the hypodermic nodules are still not understood. Dendritic protein S100 positive cells had previously been observed within hypodermal granulomas. The purpose of this study was to confirm these observations in a large group of nodular vasculitis, and to compare the expression of S100 protein in other vascular diseases and in pure panniculitis. Immunohistochemical staining for S100 protein was performed on paraffine-embedded samples: 45 cases of nodular vasculitis, 21 of panniculitis, 10 of superficial leucocytoclastic vasculitis, 10 of periarteritis nodosa, and 10 of erythema nodosum were analyzed by means of optic microscopy. Numerous dendritic S100 protein positive cells were found within hypodermal granulomas in most of the cases of nodular vasculitis, but these cells were absent in the 3 cases of initial deep leucocytoclastic vasculitis lesions of nodular vasculitis. The mean percentage of these cells was 4.5 p. 100 in the hypodermal inflammatory areas; they were observed mainly around vascular lesions. Hypodermal dendritic cells were absent or less numerous in all other cases, and a high number of such cells seems to be observed only in nodular vasculitis. Because of their dendritic morphology, and the high expression of S100 protein, these cells could be interdigitated cells, which are known to present antigens to T-lymphocytes. They could play an important role in generating the chronicity of nodular vasculitis, by a mechanism of delayed cell-mediated hypersensitivity, after the initial lesions caused by immune complexes.

Dendritic Cells↗
PubMed2006

[18F-FDG PET in the diagnosis of large vessel vasculitis].

INTRODUCTION: Positron emission tomography (PET) is a non-invasive diagnostic method which shows the bio-distribution of positron emitter labelled radiopharmaceuticals in the body. Due to the fact that not only timorous, but in certain conditions also some inflammatory cells may exhibit increased accumulation of 18F-FDG, 18F-FDG PET can be used in the diagnosis of both tumours and certain types of inflammations. OBJECTIVE: The objective of the study is to asses the benefits of 18F-FDG PET in the patients examined for symptoms of fever of uncertain origin whose results suggested the possibility of large vessel vasculitis. SAMPLE AND METHODS: In the years 2003 and 2004, the positron emission tomography centre at Masaryk Oncological Institute in Brno examined 35 patients in order to establish the cause of febrilia using 18F-FDG PET. The suspicion of large vessel vasculitis was based on the detection of high accumulation of radiopharmaceuticals in large vessels walls (in the aorta and the larger outgoing branches). The patients underwent a further standard imaging test to diagnose large vessel vasculitis as follows: CT angiography (CTA) in 4 patients, MR angiography (MRA) in 3 patients and duplex ultrasonography (USG) in 7 patients. A definitive diagnosis of primary autoimmunity of large vessel vasculitis was counter checked histologically or based on a therapeutic test by means of the effect of corticotherapy in immunosuppressive doses. RESULTS: Positive PET findings were recorded in 23 out of 35 patients (65.7%). 11 out of 23 PET positive patients (47.8% of PET positive persons and 31.4% of all patients with febrilia) were suspected to have active large vessel vasculitis based on PET examination. In 10 of the 11 patients, it was possible to perform additional examinations necessary to confirm the diagnosis: a histological test of arteria temporalis in one case, and a therapeutic test using corticotherapy in all 10 cases. Large vessel vasculitis was confirmed in all 10 individuals (2 men and 8 women aged 53-66, median age of 62 years). None of the CTA, MRA or USG examinations in any of the cases detected direct or clear signs ofvasculitis, but 3 CTA and 1 MRA examinations could be considered abnormal. The detection of temporal (giant cell) arteritis based on excision of arteria temporalis superficialis points to the limits of PET examination which is unable to assess veins with a diameter of less than 5 mm. On the other hand, it documents the possibility of extra-cranial damage being proved in this diagnosis with the use PET. In seven of the ten cases, a control PET scan was done during corticotherapy. It showed a drop in the accumulation of radiopharmaceuticals, and therefore a drop in the inflammatory metabolic activity on the walls of the large vessels, which was in line with the drop in the laboratory parameters of the inflammation (FW, CRP). CONCLUSION: Positron emission tomography using 18F-FDG can be used to detect active large vessel vasculitis in patients examined for symptoms of fever of uncertain origin. Apparently, PET can detect cases of large vessel vasculitis where other imaging methods have failed and can be also used to follow the development of vasculitis activity during therapy.

Adolescent↗
PubMed1994

Circulating soluble adhesion molecules in systemic vasculitis.

The plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1), E-selectin (sE-selectin), and vascular cell adhesion molecule-1 (sVCAM-1), might reflect endothelial activation and injury and would therefore be useful markers of disease activity in vasculitis. To investigate this we measured the levels of sICAM-1, sE-selectin, and sVCAM-1 by two-site ELISAs in the plasma of patients with (a) active vasculitis (n = 16), (b) vasculitis in remission (n = 15), (c) chronic renal failure (CRF) (n = 10), and (d) normal healthy controls (n = 10). Plasma sICAM-1 levels were significantly higher in patients with active vasculitis, 323 ng/ml (193-607) compared with patients with inactive vasculitis, 199 ng/ml (131-297); P = 0.0006 and healthy controls, 188 ng/ml (138-259); P = 0.0002. Plasma sE-selectin levels were also significantly higher in the patients with active vasculitis, 45 ng/ml (15-65) compared with patients with inactive vasculitis, 25 ng/ml (15-55); P = 0.027 but not when compared with healthy controls, 35 ng/ml (20-55); P = 0.16. There was no difference in plasma sVCAM-1 levels between patients with active vasculitis, OD 0.56 (0.45-0.85) and inactive disease, OD 0.58 (0.47-0.79) (P = 0.12) or with healthy controls OD 0.49 (0.42-0.68) (P = 0.48). There were no significant differences between the plasma levels of any of the soluble adhesion molecules between patients with active vasculitis and patients with chronic failure.(ABSTRACT TRUNCATED AT 250 WORDS)

C-Reactive Protein↗
PubMed1997

Mercuric chloride-induced vasculitis in the Brown Norway rat: alpha beta T cell-dependent and -independent phases: role of the mast cell.

Mercuric chloride induces a necrotizing vasculitis in the Brown Norway (BN) rat. This occurs in two phases, between 1 and 5 days (early) and between 12 and 20 days (late) after initiation of HgCl2. One outbred and four inbred rat strains were found to be susceptible to early vasculitis, but only the BN strain developed late vasculitis. In the BN strain, treatment with the mAb R73 (anti-alpha beta TCR) inhibited T cell function, completely prevented the late vasculitis, but had no effect against early vasculitis, indicating that early and late vasculitis is controlled by different genetic and cellular mechanisms. The role of the mast cell in the alpha beta T cell-independent early phase was studied. Serum concentrations of rat mast cell protease II rose following HgCl2 treatment, indicating mast cell degranulation. The reagents Doxantrazole and the mAb G63, which suppress mast cell secretory responses, also prevented the rise in rat mast cell protease II and significantly reduced the early vasculitis. The demonstration of an alpha beta T cell-dependent phase supports previous experimental data that T cells play an important role in the pathogenesis of vasculitis. The presence of an earlier alpha beta T cell-independent phase is a unique observation. The data support a role for the mast cell in the early vasculitis.

Animals↗
PubMed1997

Systemic vasculitis and epithelioma. A report of three cases with a literature review.

Coexistence of a systemic vasculitis and an epithelioma is rare. The prevalence of malignancies in patients with vasculitis has been estimated at about 5%, with about two thirds hematological malignancies and one third solid tumors, although the actual figure may be higher. We report three cases of vasculitis in patients with solid tumors. A review of the literature yielded 77 additional cases. A total of 56 cases were fully documented. The sex ratio was 1.26, and mean age was 62.5 years. The most common vasculitides were leukocytoclastic vasculitis (33%), polyarteritis nodosa (16.5%) and Henoch-Schönlein purpura. The most common sites of cancer formation were the lung (23%), the digestive system (17.5%) and the kidney (14%). The diagnosis of vasculitis antedated that of cancer in most patients. Radical cancer treatment was often followed by resolution of the vasculitis and vasculitis recurrences occurred concomitantly with tumor recurrences in some patients, suggesting that the vasculitis was a paraneoplastic syndrome. Patients with unexplained chronic vasculitis with or without a history of cancer should undergo extensive investigations for an occult neoplasm.

Aged↗
PubMed2004

Systemic Lupus Erythematosus Vasculitis: A Current Therapeutic Overview.

The development of systemic lupus erythematosus (SLE) vasculitis is of prognostic value. The earlier the vasculitis is treated, the better the prognosis for SLE. Cutaneous vasculitis is common in SLE, whereas visceral vasculitis is rare. Skin SLE vasculitis is successfully treated with antimalarials, but its discontinuation may result in an SLE flare even among patients in remission. When visceral SLE vasculitis is encountered, or when a disease state is perceived to be life-threatening, a more aggressive therapy is warranted. A combination of medications, plasmapheresis, and intravenous immunoglobulin treatment, along with high-dose steroids and cytotoxic drugs, are typically employed in the treatment of severe SLE vasculitis. Finally, patients with SLE vasculitis may benefit from a number of autoimmune disease therapies currently under investigation, such as switching cytokine responses from Th1 to Th2, and the manipulation of toll-like receptors, chemokines, and FcR receptors. Specific B-cell therapies (eg, anti-Blys, B-cell depletion) may also emerge as potential treatments for SLE vasculitis.

Journal Article↗
PubMed1998

Prognostic factors in leukocytoclastic vasculitis: a clinicopathologic study of 160 patients.

OBJECTIVE: To analyze risk factors for systemic involvement and long-term course in leukocytoclastic vasculitis. DESIGN: A clinicopathological study of 160 patients with leukocytoclastic vasculitis followed up for at least 3 years. Univariate and multivariate analysis were conducted by logistic regression methods. SETTING: The Bellvitge Hospital, a referral center in Barcelona, Spain. PATIENTS: One hundred sixty patients with cutaneous leukocytoclastic vasculitis. Patients in the categories cutaneous/systemic vasculitis and acute/chronic cutaneous vasculitis were selected for comparative analysis. MAIN OUTCOME MEASURES: Clinical, laboratory, and histopathological findings. RESULTS: Of 89 females and 71 males, aged 14 to 89 years, systemic involvement was documented in 20% of cases. Perinuclear-staining antineutrophil cytoplasmic autoantibodies were found in 21% of patients and cryoglobulins in 25.4%. Of the patients, 1.9% died of systemic vasculitis. The average duration of cutaneous lesions was 27.9 months. In 67.2%, a cause or associated condition was identified. Of the skin specimens, 59.6% showed vasculitis limited to superficial dermal vessels. Direct immunofluorescence was positive in 84.3% of cases. In the multivariate analysis, paresthesia, fever, and absence of painful lesions were found to be risk factors for systemic involvement. Cryoglobulins, arthralgia, and normal temperature were risk factors for chronic cutaneous disease. CONCLUSION: Our results identify prognostic factors in leukocytoclastic vasculitis and may provide some aid in the management of this heterogeneous group of patients.

Adolescent↗
PubMed1989

Elevated plasma levels of alpha 2-plasmin inhibitor-plasmin complex in patients with rheumatic diseases. Possible role of fibrinolytic mechanism in vasculitis.

Plasma levels of alpha 2-plasmin inhibitor (alpha 2PI) and alpha 2-plasmin inhibitor-plasmin complex (alpha 2 PIPC) were measured by sandwich enzyme-linked immunosorbent assay, using a recently developed monoclonal anti-alpha 2PI antibody, in patients with collagen diseases. Twenty patients had systemic lupus erythematosus (SLE), 4 of whom also had vasculitis, 11 patients had rheumatoid arthritis (RA), 4 of whom also had vasculitis, and 5 patients had other types of vasculitis. There was no significant difference in alpha 2PI levels between the 3 patient groups and the control groups. However, plasma levels of alpha 2PIPC in all 3 patient groups were significantly higher than those in the control group. Moreover, plasma concentrations of alpha 2PIPC in SLE patients with vasculitis were statistically significantly higher than those in SLE patients without vasculitis. These concentrations were also higher in RA patients with vasculitis than in RA patients without vasculitis, although the difference was not statistically significant. Our findings indicate that measurement of plasma alpha 2PIPC levels is useful for detecting and evaluating the severity and activity of vasculitis in patients with collagen diseases.

Adolescent↗
PubMed2003

Genetic basis of tissue specificity of vasculitis in MRL/lpr mice.

OBJECTIVE: To clarify the mode of inheritance of the tissue distribution of vasculitis in MRL/Mp-lpr/lpr (MRL/lpr) lupus-prone mice and to identify the susceptibility loci. METHODS: Vasculitis in individual MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr x C3H/lpr)F(1), and (MRL/lpr x C3H/lpr)F(2) intercross mice was analyzed by histopathologic grading of main branches of the aorta and of medium-sized arteries in the lower limbs. Genomic DNA samples from F(2) intercross mice were examined by simple sequence-length polymorphism analysis, and the polymorphic microsatellite markers highly associated with vasculitis in each tissue were determined as vasculitis susceptibility loci. RESULTS: A susceptibility locus with significant linkage to vasculitis of main branches of the aorta was mapped on chromosome 4 at D4Mit213 (map position 13.3cM) selectively in males, while vasculitis of medium-sized arteries in the lower limbs was mapped to different chromosomes: at D8Mit31 on chromosome 8 (map position 33.0) selectively in females and at D5Mit36 on chromosome 5 (map position 65.0). All of these were different from the previously defined loci governing susceptibility to vasculitis involving the kidneys. CONCLUSION: Systemic vasculitis in MRL/lpr mice is genetically controlled with cumulative effects of multiple gene loci, each of which has tissue specificity.

Animals↗
PubMed2006

Association of HLA-C3 and smoking with vasculitis in patients with rheumatoid arthritis.

OBJECTIVE: To compare HLA-C genotypes and smoking habits in patients with vasculitis or other severe extraarticular manifestations of rheumatoid arthritis (ExRA) with those in RA patients without extraarticular disease. METHODS: Patients were recruited from a large research database of patients with RA at the Mayo Clinic, from 2 Swedish cohorts of prevalent RA cases, and from a regional Swedish early RA cohort. Patients with severe ExRA (n = 159) and control patients with RA but no history of ExRA (non-ExRA controls) (n = 178) were matched for duration of RA and for clinical center. Data on smoking at RA onset, rheumatoid factor (RF) status, and antinuclear antibodies (ANAs) were extracted from the medical records. Polymerase chain reaction-based HLA-C genotyping was performed using a sequence-specific primer kit. RESULTS: The distribution of HLA-C alleles was significantly different between patients with RA-associated vasculitis and non-ExRA controls (P = 0.014). This was mainly due to a positive association of the HLA-C3 allele with vasculitis (allele frequency 0.411 in vasculitis patients versus 0.199 in non-ExRA controls; P < 0.001) and a decreased frequency of HLA-C7 (0.122 and 0.243, respectively; P = 0.018). The association between HLA-C3 and vasculitis was not due to linkage disequilibrium with HLA-DRB1. Smoking (P = 0.001), RF positivity (P < 0.0001), and presence of ANAs (P < 0.0001) were all associated with ExRA. HLA-C3 and smoking were both significant predictors of vasculitis in a multivariate model. CONCLUSION: Vasculitis in RA is associated with HLA-C3. Smoking is an independent predictor of vasculitis and other types of severe ExRA. Our results suggest that these variables are among the genetic and environmental factors that contribute significantly to the pathomechanisms of systemic RA.

Adult↗
PubMed2006

Increased serum levels of soluble fractalkine (CX3CL1) correlate with disease activity in rheumatoid vasculitis.

OBJECTIVE: To determine levels of soluble fractalkine (sFkn) in rheumatoid arthritis (RA) patients with and without rheumatoid vasculitis (RV), and to assess the relationship of sFkn levels to disease activity. METHODS: Serum was obtained from 98 RA patients (54 without vasculitis, 36 with extraarticular manifestations but without histologically proven vasculitis, and 8 with histologically proven vasculitis) and from 38 healthy individuals. Levels of sFkn were measured by enzyme-linked immunosorbent assay. Expression of Fkn and CX(3)CR1 was quantified by real-time polymerase chain reaction. Vasculitis disease activity was assessed using the Birmingham Vasculitis Activity Score and the Vasculitis Activity Index. RESULTS: Serum sFkn levels were significantly higher in patients with RA than in controls and were significantly higher in RA patients with RV than in those without vasculitic complications. Statistically significant correlations were observed between serum sFkn levels in RA patients and levels of C-reactive protein, rheumatoid factor, immune complex, and complement. In the RV group, sFkn levels also correlated with disease activity. Immunohistochemical analysis indicated that Fkn levels were associated mainly with endothelial cells in vasculitic arteries. In addition, expression of CX(3)CR1 messenger RNA was significantly greater in peripheral blood mononuclear cells from patients with active RV than in those from other RA patients or controls. Notably, serum sFkn levels were significantly diminished following successful treatment and clinical improvement. CONCLUSION: These findings suggest that Fkn and CX(3)CR1 play crucial roles in the pathogenesis of RV and that sFkn may serve as a serologic inflammatory marker of disease activity in RA patients with vasculitis.

Aged↗
PubMed1983

Rheumatoid vasculitis: diagnostic and therapeutic decisions.

Rheumatoid vasculitis is an uncommon but potentially catastrophic complication of RA. There are few extensive experiences recorded in the current literature and there is no consensus regarding the clinical features, laboratory findings, histologic pattern, prognosis, or appropriate management of this syndrome. We therefore surveyed 1,947 North American ARA members for their perceptions of rheumatoid vasculitis. Four hundred twenty-eight surveys were returned, of which 290 were suitable for analysis. The majority of respondents were within 10 years of fellowships and were evenly distributed among private practice, and part-time and full-time academic positions. The respondents saw 15-50 rheumatoid arthritis (RA) patients weekly and less than five RA vasculitis patients annually. The majority correctly diagnosed two actual and complex case histories from patients with and without autopsy-proven vasculitis. Respondents associated the following features most strongly with rheumatoid vasculitis - mononeuritis multiplex, digital gangrene, digital ischemic lesions, nailfold ischemic lesions, non-healing leg ulcers, palpable purpura, fingertip nodules, sensory neuropathy, scleromalacia perforans, high titer rheumatoid factor, positive visceral angiography, cryoglobulinemia, hypocomplementemia, circulating immune complexes, and histologic necrotizing vasculitis or vascular transmural neutrophilia. Digital lesions or sensory neuropathy alone were not viewed as portending an ominous prognosis by most respondents and would have been treated with nonsteroidal anti-inflammatory drugs, antimalarials, gold salts, or D-penicillamine. Other clinical manifestations considered as reflecting rheumatoid vasculitis (gangrene, mononeuritis multiplex, ulcers) were thought to worsen prognosis and would have been managed more often with corticosteroids, D-penicillamine, cytotoxic agents or plasmapheresis. Rheumatoid vasculitis is viewed as a heterogeneous group of syndromes with varying clinical and histopathologic features,which have different prognostic implications, and therefore should be managed differently. While these dta do not substitute for an extensive recorded series of patients, they provide useful information about community perceptions of an uncommon but difficult clinical problem. They identify the need for additional data to examine the validity of these attitudes.

Arthritis, Rheumatoid↗
PubMed2005

Difficult to diagnose manifestations of vasculitis: does an interdisciplinary approach help?

In the early stages of disease, primary systemic vasculitides often present with non-specific symptoms that make early diagnosis a challenge. The variety of clinical manifestations found in systemic vasculitis is huge, and some manifestations are frequently not clinically overt at first presentation. A logical implication of the often non-specific and sometimes subclinical presentation of vasculitis is that a systematic diagnostic work-up is necessary. This requires a multidisciplinary approach involving the expert opinion of specialists from many disciplines, such as neurology, radiology, respiratory medicine, pathology and microbiology. There are no generally accepted diagnostic criteria for primary systemic vasculitides, and the application of classification criteria as diagnostic criteria is not feasible and may even be misleading. The demonstration of vasculitis on biopsy is still the gold standard for the diagnosis of vasculitis. In cases where biopsies cannot be obtained, surrogate parameters of vasculitis (e.g. glomerular hematuria or mononeuritis multiplex), along with serology and imaging, can support a clinical diagnosis of vasculitis. This review discusses the approach to the diagnosis of central nervous system and pulmonary manifestations of primary systemic vasculitis. These two examples of difficult to diagnose manifestations of vasculitis illustrate the necessity of an interdisciplinary approach to the diagnostic work-up.

Diagnosis, Differential↗
PubMed2005

How to diagnose and treat secondary forms of vasculitis.

Vasculitis is considered to be secondary when it arises either in the context of a pre-existing connective tissue disease, as a result of direct infection with a limited range of organisms, especially viruses, or when it arises in response to exposure to a number of medications. Rheumatoid vasculitis is probably the most widely recognised form of secondary vasculitis, and in this article we review the incidence, clinical features and management of this condition. Infections may either trigger or cause some types of vasculitis. Drug therapy is a common cause of limited forms of vasculitis and may enhance our understanding of the mechanism of these diseases. The premature development of atherosclerosis in patients with existing connective tissue diseases or indeed primary vasculitis has been recognised for some time, and the underlying mechanisms are currently being studied. An appreciation of the complex and varied pathophysiology of secondary vasculitis may further our understanding of primary vasculitis.

Antibodies, Antineutrophil Cytoplasmic↗