Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoimmune diseases have been studied from the perspective of an abnormal immune response in genetically vulnerable hosts. Although the immune response is responsible for the initiation of autoimmune diseases, the effectors of the disease process likely involves cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). These polypeptides induce a wide variety of inflammatory events which contribute to the destruction of tissue and tissue remodeling in several autoimmune diseases. Blocking IL-1 with its naturally occurring receptor antagonist, the IL-1 receptor antagonist reduces the severity of disease in animal models of inflammation and autoimmune processes. Clinical studies with the IL-1 receptor antagonist will define the role for this cytokine in the pathogenesis of autoimmune diseases such as arthritis, inflammatory bowel disease, type I diabetes and vasculitis.
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PMID:Interleukin-1 and tumor necrosis factor: effector cytokines in autoimmune diseases. 132 Sep 50

Both immunological hypersensitivity and vascular abnormalities have been implicated in the pathogenesis of inflammatory bowel disease. In an attempt to link the two hypotheses, we sought evidence of local production of endothelin-1, a potent vasoconstrictor, in patients with Crohn's disease and ulcerative colitis. An immunohistochemical method was used to detect endothelin-1 in tissue samples from sixteen Crohn's disease patients, nine ulcerative colitis patients, and thirteen controls. In the controls, positively staining cells were infrequent in both lamina propria (mean 0.9% of total cells, 95% confidence interval 0.1-1.7%) and submucosa (2.3%, 0.4-4.1%). The percentage of endothelin-immunoreactive cells was significantly higher in the two disease groups than in the controls. Among the Crohn's disease patients, there were more immunoreactive cells in the submucosa than in the lamina propria (19.1%, 15.2-22.1% vs 12.3%, 8.1-16.5%; p less than 0.001), whereas the converse was true for the ulcerative colitis group (8.6%, 1.1-16.1% vs 24.4%, 14.1-34.6%; p less than 0.001). Immunoreactive macrophage aggregates around submucosal blood vessels were common in samples from Crohn's disease patients. Endothelin concentrations, measured by radioimmunoassay, in supernatants of homogenised tissue samples were significantly higher in Crohn's disease and ulcerative colitis than in controls. We suggest that local endothelin production by inflammatory cells may contribute to vasculitis in chronic inflammatory bowel disease by inducing intestinal ischaemia through vasoconstriction.
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PMID:High endothelin-1 immunoreactivity in Crohn's disease and ulcerative colitis. 134 93

Interleukin-1 (IL-1) is a 17-kDa pro-inflammatory cytokine synthesized from a variety of cell types primarily in association with disease states or during host perturbation such as immune responses. At pM or even fM concentrations, IL-1 triggers various responses in nearly all cells. It appears that there is little or no major role for IL-1 in homoeostatic mechanisms. There are two IL-1's (alpha and beta) each with its distinct sequence; there are two IL-1 receptors. Disease states such as local and systemic infection, septic shock, degenerative arthritis and autoimmune diseases such as nephritis, vasculitis and inflammatory bowel disease appear to be mediated, in part, by IL-1. Organ failure, capillary leak and death occur in animals after a combination of tumour necrosis factor (TNF) and IL-1 which is more effective in inducing these changes than either cytokine alone. IL-1 is also a potent inducer of endothelial cell adhesion molecules, IL-6, and IL-8, a neutrophil chemotactic and activating factor. Strategies for reducing the effects of IL-1 have been based on suppression of transcription, translation, or secretion; more recently, receptor blockade has been a new approach. A naturally occurring IL-1-specific receptor antagonist (IL-1ra), which shares 40% conserved amino-acid homology with IL-1 beta, binds to IL-1 surface receptors with the same affinity as IL-1 but does not possess agonist activity and acts as a competitive inhibitor of IL-1. Studies using the IL-1ra to block endogenous IL-1 in a variety of animal disease models suggest that IL-1 plays a key role in triggering the cascade of inflammatory responses. In addition, the IL-1ra reduces the spontaneous production of growth factors and proliferation of leukaemic cells. The IL-1ra may be an advantageous therapy in patients with sepsis, diabetes, inflammatory bowel, arthritis and cancer.
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PMID:Reduction of inflammation by decreasing production of interleukin-1 or by specific receptor antagonism. 139 23

The case is reported of a 50 year old man with longstanding seronegative rheumatoid arthritis who developed ulcerative colitis. The patient also had sacroiliitis and his tissue was typed as HLA-A2-B27 several years before the bowel disease began. A possible overlap between primary inflammatory bowel disease, complications to the treatment of rheumatoid arthritis with drugs, and gastrointestinal rheumatoid vasculitis is discussed.
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PMID:Ulcerative colitis complicating seronegative HLA-A2-B27 rheumatoid arthritis with sacroiliitis. 141 8

Sera from 103 patients with chronic inflammatory bowel disease (IBD) were tested prospectively for antibodies against neutrophil cytoplasmic antigens (anti-neutrophil cytoplasm antibodies, ANCA) and endothelial cell surface antigens (anti-endothelial cell antibodies, AECA) by indirect immunofluorescence (IIF) and assays based on whole fixed neutrophils, purified neutrophil enzyme substrates and human umbilical vein endothelial cells. Using IIF, ANCA were found in 26 IBD sera (25%) and in none of 51 controls. Twenty-two positive sera (85%) were from patients with ulcerative colitis (UC). The pattern of distribution of immunofluorescence was always perinuclear (P-ANCA). A majority of UC patients positive for these autoantibodies (68%) had active colitis, but none had evidence of vasculitis. Using a whole neutrophil ELISA, binding was demonstrable in 73% of UC sera compared to 27% of Crohn's (CD) sera and only 4% of controls. Unlike vasculitis sera, UC sera with P-ANCA did not bind strongly to myeloperoxidase (MPO). Forty-five per cent of IBD sera tested positive for IgG AECA in an endothelial cell ELISA, compared to seven of 51 (14%) controls. Binding correlated with both active and extensive colitis. A type of P-ANCA, in most cases distinct from MPO-specific P-ANCA observed in vasculitis, is detected in a significant proportion of patients with UC, but rarely Crohn's colitis and therefore may be of differential diagnostic value. IgG AECA are also frequent in CIBD sera but are less disease specific than ANCA.
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PMID:Autoantibodies to neutrophil cytoplasmic (ANCA) and endothelial cell surface antigens (AECA) in chronic inflammatory bowel disease. 148 88

Anti-neutrophil antibodies have been shown in sera from patients with a variety of inflammatory diseases. Those reacting with components of neutrophil cytoplasm are associated with systemic vasculitis. Both nuclear and perinuclear staining patterns on human neutrophils have been reported using sera from patients with inflammatory bowel disease. We have evaluated the reactivity against human neutrophils of sera from 100 patients with inflammatory bowel disease, 14 disease controls, and 20 normal volunteers. Altogether 27/50 (54%) sera from patients with ulcerative colitis contained antibodies that reacted with cytospun ethanol fixed neutrophils compared with 5/50 (10%) from Crohn's disease (p less than 0.001) and 0/34 control sera (p less than 0.001). All seven sera from patients with proctitis alone were negative (p less than 0.01). There was no correlation between presence or titre of anti-neutrophil antibodies and either disease activity or treatment. Positive sera gave three different staining patterns on human neutrophils. The predominant pattern was perinuclear (17/32); 12 sera gave a cytoplasmic and three a homogeneous nuclear staining pattern. None of the patients or the controls had antibodies to myeloperoxidase, elastase, or serine proteinase 3, all of which are recognised by anti-neutrophil cytoplasmic antibodies. Only 2/27 sera positive by indirect immunofluorescence reacted with an extract of neutrophil primary granules. In conclusion, anti-neutrophil antibodies occur more commonly in ulcerative colitis than in Crohn's disease or control subjects and the anti-neutrophil antibodies found in inflammatory bowel disease are different from those associated with vasculitis.
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PMID:Anti-neutrophil antibodies in inflammatory bowel disease: prevalence and diagnostic role. 161 85

We have investigated the effect of volume and concentration of exametazime on the labelling efficiency of 99Tcm-exametazime-labelled leucocytes. The first study examined the effect of varying the volume of exametazine solution whilst the concentration remained constant. A vial of Ceretec (Amersham Ltd plc) was reconstituted with sodium chloride injection BP. Aliquots of 0.25-2.0 ml were removed, added to sodium pertechnetate injection BP and incubated with 2 x 10(7)-5 x 10(7) leucocytes from 25 ml blood. The labelling efficiency decreased from 65 +/- 10% S.D. (0.25 ml) to 45 +/- 8% (2.0 ml) (n = 4). In a second study different concentrations of exametazime solution were used whilst the volume remained constant. A vial of Ceretec was reconstituted with sodium chloride injection BP. Aliquots of 25-200 micrograms were removed, made up to a fixed volume of 0.6 ml, added to pertechnetate and incubated with the plug of leucocytes as before. The labelling efficiency decreased as the concentration of ligand decreased. Thus for 200 micrograms/0.6 ml the labelling efficiency was 64 +/- 5% and for 25 micrograms/0.6 ml the labelling efficiency was 43 +/- 18% (n = 4). Clinical studies were performed using 50 ml blood from patients with a wide range of inflammatory disorders including inflammatory bowel disease, abdominal abscess and vasculitis. The concentration of ligand used was 83 micrograms/0.25 ml. The labelling efficiency was found to be 82 +/- 7% (n = 36).
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PMID:99Tcm-exametazime-labelled leucocytes: effect of volume and concentration of exametazime on labelling efficiency, and clinical protocol for high efficiency multi-dose radiolabelling. 143 98

The starting point in the evaluation of vasculitis is the clinical examination. The character and location of the primary lesions determine the type of biopsy specimens and additional tests needed to classify vasculitis. The most common causes of cutaneous vasculitis are drug reactions, infectious diseases, reactions to inflammatory diseases such as rheumatoid arthritis or inflammatory bowel disease, or association with malignant disease, especially lymphoproliferative disorders. Direct immunofluorescent techniques and leukocyte monoclonal antibody studies are useful for the diagnosis of selected cases of vasculitis. The clinical and histopathologic data help delineate an approach for further investigation of potentially associated systemic disorders or underlying causes. Although some cases of cutaneous vasculitis are not associated with systemic disorders, this possibility should never be assumed but considered only as a diagnosis of exclusion after careful examination of each patient.
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PMID:Cutaneous vasculitis: approach to diagnosis and systemic associations. 196 12

Gastrointestinal involvement occurs frequently in essential mixed cryoglobulinemia, and most often involves the liver and spleen. Intestinal involvement is much less common and is generally felt to be a late and often catastrophic manifestation of the disease due to severe vasculitis. Occasionally, the disorder mimics inflammatory bowel disease, both clinically and radiographically. We recently cared for a patient with essential mixed cryoglobulinemia who developed persistent diarrhea. Endoscopic evaluation revealed scattered petechial lesions in the duodenum and colon as well as prominent lymphoid hyperplasia in the terminal ileum. Mucosal biopsies disclosed the presence of diffuse inflammation. We suggest that this patient's diarrhea was due to intestinal vasculitis and that prominent ileal lymphoid hyperplasia may be a manifestation of essential mixed cryoglobulinemia.
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PMID:Chronic diarrhea in essential mixed cryoglobulinemia: a manifestation of visceral vasculitis? 201 55

Antineutrophil cytoplasmic antibodies (ANCAs) have recently been demonstrated to be of importance in Wegener's granulomatosis and certain other forms of vasculitis associated with glomerulonephritis. With a fixed-cell ELISA, we demonstrated that ANCAs occur in the serum of patients with inflammatory bowel disease (IBD) involving the colon. In a blinded study, sera from 21 of 25 patients with ulcerative colitis (UC) and five of 25 patients with Crohn's disease had binding in the fixed-cell ELISA. The five reactive sera from patients with Crohn's disease were associated with the presence of clear colonic involvement. The presence of ANCA in patients with UC was not influenced by disease distribution or activity. Indeed, such antibodies were present in four subjects with UC more than 5 years after colectomy. The IBD-associated ANCAs were distinct from ANCAs reported in patients with Wegener's granulomatosis since the pattern of staining on indirect immunofluorescence exhibited a nongranular perinuclear distribution (P-ANCA). The P-ANCA observed in IBD did not react with myeloperoxidase and thus was distinct from the P-ANCA observed in vasculitis with cresentric glomerulonephritis. IBD and, in particular, UC, is associated with a distinct subset of P-ANCA, which may have important diagnostic and potential pathophysiologic implications.
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PMID:A distinct subset of antineutrophil cytoplasmic antibodies is associated with inflammatory bowel disease. 220 Aug 20


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