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)

A woman, aged 26 years, who died of progressively worsening demyelinating encephalomyelitis in the course of 4 years is reported. The neuropathological findings included large subcortical softenings in the cerebral hemispheres, tiny perivenous demyelinated foci in their neighborhood and scattered in the white matter. There was an acute vasculitis with fibrinoid exudation in the affected as well as unaffected areas. Focal perivenous mononuclear cell infiltrations are conspicuous in the white matter. The laboratory and postmortem examinations suggested a collagen disease like SLE. The abnormalities included marked increase of serum gamma-globulin, especially of IgG, and elevation of CRP, RA, and ANA titer, moderate thickening of the basement membranes of the renal glomeruli, onion skin-like periarteriolar fibrosis in the spleen, fibrous pericarditis and periadventitial fibrosis of myocardial arteries. Bilateral degeneration of the spinal posterior columns and dorsal roots was also observed. A probable relationship of the modified features in this example of demyelinating encephalomyelitis with abnormal immune mechanisms in the background is discussed.
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PMID:A case of demyelinating encephalomyelitis with some resemblance to collagen disease. 7 51

Clustering of ANA and SMA was evaluated in patients with various internal diseases as a pattern of autoantibody formation. SMA was found in ANA positive patients with chronic hepatitis, undefined collagenoses and autoallergic thyroid diseases significantly more frequently, than in patients without any autoallergic disorders. The incidence of SMA in ANA positive cases with SLE and RA did not exceed their predictable by chance incidence. It was not found that clustering of autoantibodies is correlated with the E and C lymphocyte receptor abnormality as compared to the control group. The lowest count of E-RFC was found in SLE cases which differed significantly in this respect from the control group and also from chronic vasculitis cases. The clustering of autoantibodies is not correlated with hyperimmunoglobulinemia.
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PMID:Diagnostic specificity of autoantibodies. II. Clustering of autoantibodies--role in diagnosis and in comparison to E--and EAC-RFC peripheral blood profiles and immunoglobulin levels. 31 92

The term "pseudo-LE syndrome" was previously used to describe an SLE-like disease in which AMA, but not ANA, were found in serum. In an attempt to find patients with this syndrome, we tested 9 358 sera for AMA and ANA. AMA without ANA was found in six patients without liver disease. One of these patients had an SLE-like disease. Two of the others had diseases of the thyroid and one had rheumatoid arthritis--diseases in which AMA have previously been described. One patient had allergic vasculitis and one hypercholesterolaemia; these diseases are not known to be associated with the presence of AMA.
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PMID:Mitochondrial antibodies without antinuclear antibodies in non-hepatic diseases. 33 86

A 57-year-old white man presented with unilateral optic neuritis. General physical examination and neurologic consultation revealed no further findings. Laboratory investigation, however, yielded an elevated sedimentation rate, positive LE preparation, elevated ANA titer, false-positive VDRL, and red blood cell casts in the urine. A diagnosis of systemic lupus erythematosus (SLE) was made. The patient was treated with sub-Tenon and systemic corticosteroids. There was a moderate improvement in central visual acuity. The suspected pathophysiology of SLE is reviewed. The papillitis presumably reflects the generalized vasculitis of SLE and may be responsive to corticosteroids as are other signs and symptoms of this disease.
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PMID:Systemic lupus erythematosus presenting as optic neuritis. 67 40

Beginning with lesions of the capillary wall, rheumatoid arthritis is morphologically expressed by an aseptic inflammation of the synovia with following necrosis of the cartilage and the underlying bone tissue. Only little is known regarding the pathogenesis but most porbably immune mechansims are involved. There is evidence for the participation of type IV and type III-reactions i.e. sensitized lymphocytes as well as immune complexes. Equally the etiology of RA is totally unknown. Once the inflammatory process has reached some activity, in most cases it shows the character of a selfpertetuation as in other autoimmune diseases. Laboratory examinations include BSR, blood count, measurement of Fe, Cu, RF, complement, streptolysins, staphylolysins, ANA, and in doubtful cases synovial biopsy. Furthermore, effusion fluid of the joint may be examined for RF, ANA, complement, rhagocytes, crystals, protein content etc.--Among the collagen diseases sensu strictori, systemic lupus erythematosus is the most important. The underlying process may be characterized as vasculitis due to immune complexes and local activation of the complement system, the complexes containing native and/or denatured DNA, and antibodies mostly of the IgG class. Laboratory examinations include the demonstration of ANA but should concentrate on the measurement of DNA-antibodies using radioimmunological or at least a sensitive and specific immunofluorescence technique. The value of the various tests is discussed.
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PMID:[Pathophysiology and laboratory diagnosis of collagen diseases (author's transl)]. 79

A long-term study of cyclophophamide-induced suppression of auto-immune disease in NZB/NZW mice demonstrated the oncogenic potential of this alkylating agent. In seven of ten mice dying with lymphomas, retrospective examination of serial tests for heterogeneous ANA showed terminal decreases of titres or reversion of tests to negative. Suppressed titres were found in one of seven mice dying with other tumours and in four of twenty-nine mice succumbing to renal disease-vasculitis. Transplantation studies confirmed the association between growing lymphoma tissue and decreasing ANA titres. In the immunosuppressed host with connective tissue disease, the loss of certain auto-antibodies may signal development of a lymphoreticular neoplasm. Tumour-induced impairment of auto-immune responsiveness may reflect the loss of specific ANA that fulfil a protective role and inhibit neoplastic growth.
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PMID:Suppressed hetergeneous antinuclear antibody response in lymphomabearing NZB/NZW mice. 108 17

Autoimmune responses were assayed in 80 cyclophosphamide-treated and control NZB/NZW mice over a period of 1 year. Fluctuation between positive and negative immunofluorescent heterogeneous ANA tests and daily alterations of ANA titers were detected in young mice of both sexes. Although high-dose cyclophosphamide therapy (8 mg/kg/day) failed to prevent the spontaneous appearance of ANA, titered ANA values were partially suppressed in high-dose treated mice. This study permitted sequential comparisons between ANA titers and anti-DNA as useful indices of cyclophosphamide-induced suppression of autoimmune disease. ANA titers were relatively resistant to cyclophosphamide therapy. Antibodies directed specifically against DNA were suppressed mice receiving high-dose cyclophosphamide. In treated animals, decreased anti-DNA levels were associated with protection from severe glomerulonephritis and renal vasculitis. Treatment with low-dose cyclophosphamide (1 mg/kg/day) appeared paradoxically to stimulate autoantibody production and renal disease/vasculitis.
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PMID:Selective suppression of autoantibody responses in NZB/NZW mice treated with long-term cyclophosphamide. 109 22

The diagnostic potential of assays detecting anti-neutrophil cytoplasm antibodies (ANCA), anti-GBM antibodies and anti-dsDNA antibodies was evaluated by examining sera from time of admission in a consecutive series of 455 patients with biopsy verified primary or secondary glomerulonephritis (GN). ANCA were classified into c- and p-ANCA by indirect immunofluorescence (IIF) and ELISAs using alfa-granule extract, proteinase-3, myeloperoxidase (MPO), elastase and lactoferrin. C-ANCA was virtually confined to 64 patients with systemic small vessel vasculitis, 66-74% being c-ANCA positive. P-ANCA against MPO, seen in 47 patients, segregated through many diagnostic categories of primary and secondary severe GN. ANCA against lactoferrin and elastase were rare. Anti-dsDNA positive patients constituted 57% of the 44 ANA-positive patients with systemic lupus erythematosus. It is concluded that the IIF and ELISAs for anti-proteinase-3, anti-MPO, anti-dsDNA and anti-GBM have an acceptable performance and are useful in the primary diagnostic work-up of patients suspected for secondary GN as the majority of such patients will be classified by these assays.
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PMID:Anti-neutrophil cytoplasm antibodies, anti-GBM antibodies and anti-dsDNA antibodies in glomerulonephritis. 147 49

Aortic valve lesions in progressive systemic sclerosis (PSS) are very uncommon. To our knowledge, aortic regurgitation (AR) associated with PSS has not been reported previously. We would like to report the case of a 58-year-old woman who had PSS with AR due to Raynaud's symptom, fever, positive ANA, accelerated ESR, and diastolic blowing murmur along the left sternal border. After treatment with adreno-cortico steroid and an immunosuppressive agent, the patient improved serologically and symptomatically. However, she was later admitted to our hospital again due to heart failure with progressive AR. She died of refractory heart failure with severe AR and tricuspid regurgitation (TR). The former was caused by aortic cusp lesions and the latter by pulmonary hypertension. An autopsy confirmed the diagnosis of PSS, which was found to have involved the heart, lungs and pancreas. Vasculitis with infiltration and fibrotic changes were noted in these organs. Moreover, there were fibrotic thickenings and shortenings in the aortic cusps with cell infiltration. There were no indications of rheumatic disease. These results suggest that the cause of our patient's aortic valve disease may have been PSS vasculitis.
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PMID:[Report of a case with aortic regurgitation in progressive systemic sclerosis]. 151 78

Serum lipid peroxide (LPO) levels, superoxide dismutase (SOD) activity in peripheral blood erythrocytes, serum ANA, anti-dsDNA, and C3 were measured in 83 patients with systemic lupus erythematosus (SLE) and in 29 healthy controls. Compared to the controls, LPO levels were significantly increased in active SLE patients while SOD activity was markedly decreased. From the active phase to the inactive phase, a gradual decline in LPO levels and an increase in SOD activity were observed. There was a close correlation between LPO levels and disease activity or the parameters including ANA titers, anti-DNA titers, and C3 levels; a significant negative correlation was found between SOD activity and LPO levels or these parameters. Further, a marked difference in SOD activity was found in untreated active cases with and without nephritis. As the SLE patients improved, LPO levels gradually declined and SOD activity increased. The present study indicates that free radicals and resultantly formed lipid peroxide levels are higher in patients with SLE than those in normal persons, probably contributing to the production of autoantibodies, nephritis, and vasculitis of other organs, and that excessively generated free radicals may play an important role in the pathogenesis of SLE, which is possibly due to diminished SOD activity.
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PMID:The effect of lipid peroxides and superoxide dismutase on systemic lupus erythematosus: a preliminary study. 159 81


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