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)

The key to symptomatology in uremia is nitrogen retention leading to amidination and transmidination of a variety of substrates. The product of this activity is a series of guanidino acids which are methyl receptors converting S-adenosylmethionine to adenosine and homocysteine. Adenosine is a potent inhibitor of the enzyme ATPase and, in this way, contributes to the anemia, the bleeding diathesis and the CNS symptoms of uremia. Homocysteine is an inhibitor of pyridoxal phosphate-induced reactions and contributes to the angiitis and thromboembolism so unexpectedly encountered in chronic uremia.
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PMID:Alternate reasons for atherogenesis in uremia. 15 May 96

Six patients with extrinsic allergic alveolitis had weak immediate and strong late reactions of intracutaneous injection of bird serum. Biopsy of the late reaction revealed vasculitis and immunoglobulin and complement deposition in one. The antibody responsible for the immediate hypersensitivity could be transferred in serum. It was short lasting (4 hr) and resistant to heat and 2-mercaptoethanol. No evidence of an immediate reaction in the lungs could be detected following inhalation challenge as judged by examination of spirometry, flow volume loops and single breath nitrogen washout curves.
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PMID:Extrinsic allergic alveolitis from bird exposure. Studies on the immediate hypersensitivity reaction. 56 7

Criteria for the classification of polyarteritis nodosa were developed by comparing 118 patients who had this disease with 689 control patients who had other forms of vasculitis. For the traditional format classification, 10 criteria were selected: weight loss greater than or equal to 4 kg, livedo reticularis, testicular pain or tenderness, myalgias, mononeuropathy or polyneuropathy, diastolic blood pressure greater than 90 mm Hg, elevated blood urea nitrogen or serum creatinine levels, presence of hepatitis B reactants in serum, arteriographic abnormality, and presence of granulocyte or mixed leukocyte infiltrate in an arterial wall on biopsy. The presence of 3 or more of these 10 criteria was associated with a sensitivity of 82.2% and specificity of 86.6%. A classification tree was also constructed, with 6 criteria being selected. Three of these, angiographic abnormality, biopsy-proven granulocyte or mixed leukocyte infiltrate in arterial wall, and neuropathy, were criteria used in the traditional format. The other 3 criteria used in the tree format included the patient's sex, weight loss greater than 6.5 kg, and elevated serum aspartate aminotransferase or alanine aminotransferase levels above the range of normal. The classification tree yielded a sensitivity of 87.3% and a specificity of 89.3%.
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PMID:The American College of Rheumatology 1990 criteria for the classification of polyarteritis nodosa. 197 74

Effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, on blood pressure and hypertensive complications in stroke-prone spontaneously hypertensive rats (SHRSP) were investigated. Betaxolol was provided in a dose of 33 +/- 1.8 mg/kg/day, orally in drinking water, throughout the experimental period. The chronic treatment with betaxolol inhibited the development of hypertension in SHRSP and reduced values of blood urea nitrogen, creatinine, total cholesterol, free cholesterol, triglyceride, phospholipid and HDL-cholesterol in serum. Treatment with betaxolol apparently inhibited the incidence of hypertensive lesions such as cardiac fibrosis, mesenteric vasculitis, proliferative and/or necrotic vasculitis and glomeruli showing collapse or vasculitis in the kidneys. To shorten the time before the onset of hypertension and the subsequent stroke, SHRSP were kept on a SP diet containing 0.39% Na instead of the F-2 diet. When the SHRSP were kept on the SP diet, all of the control SHRSP had cerebral apoplexy and severe hypertensive lesions in the heart and kidney. When betaxolol was chronically administered to SHRSP, cerebral apoplexy and hypertensive lesions in the heart and kidney were inhibited, but the effect on blood pressure was slight. Treatment with betaxolol reduced serum creatinine levels. Our observations show that betaxolol reduces blood pressure and potently inhibits hypertensive complications in SHRSP.
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PMID:[Antihypertensive effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, in stroke-prone spontaneously hypertensive rats (SHRSP)]. 197 70

Ibuprofen-associated, acute, reversible renal failure with hyperkalemia, tubular necrosis, and proteinuria developed in a patient who had no predisposing underlying disease. A renal biopsy specimen revealed mesangial hypercellularity without glomerular crescent formation. A profound interstitial nephritis with focal inflammatory cell infiltrates of predominantly mononuclear cells and neutrophils as well as focal tubular destruction was seen. Vasculitis was not observed. Ultrastructural studies confirmed the light microscopic diagnosis of a tubulointerstitial nephritis and, in addition, indicated the presence of electron-dense mesangial and subepithelial deposits. Direct immunofluorescence examination showed diffuse mesangial IgM and C3 deposition as well as vascular C3 deposition. Renal failure rapidly resolved after discontinuation of ibuprofen therapy and initiation of steroid therapy, with return to normal levels of serum creatinine, urea nitrogen, potassium, and sodium. Proteinuria also resolved.
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PMID:Ibuprofen-associated renal dysfunction. Pathophysiologic mechanisms of acute renal failure, hyperkalemia, tubular necrosis, and proteinuria. 368 62

Experiments aimed at producing a model of Kawasaki's disease by injecting animals intraperitoneally with Pseudomonas bacilli are described. Injection of large numbers of bacilli into mice caused rapidly fatal sepsis. With appropriate numbers of organisms, some mice died within 3 days, most remained healthy, while in some an inapparent chronic disease developed. Positive blood cultures were occasionally obtained 4-17 weeks after the slow infection. An alcohol-precipitable polysaccharide, which could be measured by Roe's procedure for levan, was found in 20% of the experimentally infected mice. We suggest that this substance was partly responsible for the course of the infection. Severe vasculitis with little acute inflammatory reaction and carditis with coronary aneurysms were often obtained by injecting mice and guinea-pigs with supraliminal doses of bacilli at the same time as their immune system was impaired by treatment with either nitrogen-mustard or cyclophosphamide. We suggest that pseudomonas infection in immunologically deficient animals may mimic Kawasaki's disease and that a similar mechanism may operate in the natural form of the disease in children.
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PMID:Can pseudomonas infection in experimental animals mimic Kawasaki's disease? 654 20

Clinical sarcocystosis was studied in 37 goats after inoculation with graded doses of sporocysts of Sarcocystis capracanis. Eight uninoculated goats served as controls. Clinical response varied with the dose. Goats inoculated with 10-40 million sporocysts died between 11 and 13 days after inoculation (DAI), from interstitial pneumonia, vasculitis, and necrosis of mesenteric lymph nodes. All goats inoculated with 100,000 or 1 million sporocysts died between 19 and 23 DAI; clinical signs were anorexia, fever (40-41 C), anemia, and weight loss. Four of 4 goats inoculated with 50,000 sporocysts and 1 of 4 inoculated with 10,000 sporocysts died 24, 28, 39, 68, and 61 DAI, respectively. Goats inoculated with 1,000 sporocysts and uninoculated goats remained clinically normal. After day 18 and before day 68, packed cell volume and hemoglobin content decreased to as low as 11% and 3.6 g/dl, respectively. Alanine aminotransferase and lactic dehydrogenase activities were inconsistently increased. Blood urea nitrogen and bilirubin values were increased, reaching as high as 63 mg/dl and 10 mg/dl, respectively. Histologically, thymic atrophy, vasculitis, hepatitis, cholangitis, myocarditis, generalized myositis, and encephalomyelitis were the main microscopic findings. The cause of the anemia in goats that died after day 19 was not determined.
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PMID:Sarcocystosis in goats: clinical signs and pathologic and hematologic findings. 678 65

MRL/MpJ-Fas(lpr) (Fas(lpr)) mice develop a rapidly fatal form of systemic autoimmune disease characterized by glomerulonephritis and vasculitis similar to severe cases of systemic lupus erythematosus in humans. To evaluate the requirement for intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of tissue injury in this model, we created ICAM-1-deficient MRL/MpJ-Fas(lpr) (ICAM-1/Fas(lpr)) mice. ICAM-1 deficiency resulted in a striking improvement in the survival of Fas(lpr) mice (median +/- SEM survival of Fas(lpr) = 26 +/- 1.7 vs ICAM-1/Fas(lpr) = 47 +/- 2.4 wk, p < 0.0001) and the increased survival was associated with delayed elevations of blood urea nitrogen levels in the ICAM-1/Fas(lpr) mice. Histologic examination of the ICAM-1/Fas(lpr) mice revealed an overall reduction in glomerular disease and a significant reduction in vasculitis in the kidney, lung, skin, and salivary glands when compared with Fas(lpr). These findings indicate that ICAM-1 plays a major role in development of glomerular and vascular injury in Fas(lpr) mice.
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PMID:Intercellular adhesion molecule-1 deficiency protects MRL/MpJ-Fas(lpr) mice from early lethality. 925 74

Various chemicals found in the environment have been suspected of initiating or contributing to conditions such as asthma, dermatitis, irritability, headaches, cardiac arrhythmias, thrombophlebitis, and vasculitis. The increasing number and variety of chemicals present in the environment has led to the hypothesis that there may also be a corresponding increase in the number of people who are sensitive to these chemicals. Sensitive individuals may be continually exposed to chemical insults in their normal environment and may be experiencing a chronic reaction; however, an exposure-response relationship is difficult to establish. An Environmental Care Unit (ECU) provides an atmosphere that minimizes exposures to potential insults so patients symptoms of reaction to chemical insult may be relieved before challenge testing. Air quality required within an ECU to achieve this symptom remission is not known; therefore, this study was designed to document and compare concentrations of six criteria pollutants (sulfur dioxide, carbon monoxide, nitrogen dioxide, hydrocarbons, total suspended particular, and ozone) and formaldehyde within the ECU, the hospital outside the ECU, and the ambient atmosphere of the neighborhood around the hospital. Air movement studies indicated that the ECU was under positive pressure with respect to the rest of the hospital and had an air supply to air exhaust ratio of approximately two. Overall, no significant differences were found for any sampled pollutant at sites within the ECU or between ECU sites and the hospital proper. With an exception of ozone, significant differences among contaminant concentrations were noted between the atmosphere of the surrounding neighborhood and the hospital proper.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The determination of ambient air quality within an environmental care unit. 1028 81

We report a case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive, rapidly progressive glomerulonephritis(RPGN). A 60-year-old woman was admitted to our hospital for evaluation of RPGN. Laboratory evaluation revealed microhematuria, proteinuria(800 mg/day), anemia, renal failure(blood urea nitrogen 27 mg/dl, serum creatinine 2.2 mg/dl), cryoglobulinemia, hypocomplementemia, positive MPO-ANCA(232 EU), and hepatitis C virus infection(GOT 58 IU/l, GPT 38IU/l, HCV-RNA(PCR) 1,200 kcopy/ml, serotype 1). After admission, the patient's renal function and anemia deteriorated rapidly, then prednisolone(30 mg/day) was started. After treatment her renal function gradually improved, then a renal and liver biopsy was performed. The renal biopsy revealed six sclerosing fibrous crescentic glomeruli in twelve glomeruli. Immunofluorescent examination revealed granular deposits of IgG, C3, and fibrinogen along the glomerular basement membrane and mesangial matrix. The pathogenesis of RPGN in this case may relate to the deposition of immune complexes in the glomeruli because immunofluorescent examination was revealed to be the immune-complex type, but not pauci immune type nephritis. Liver histology revealed chronic active hepatitis with mild piecemeal necrosis and did not reveal vasculitis. Although her renal function was improved after treatment with prednisolone, she suffered from pulmonary manifestations(dry cough etc.) on the 120th hospital day. Suddenly she died because of pulmonary hemorrhage on the 180th hospital day. These findings suggest that various HCV-induced immunological abnormalities, such as positive MPO-ANCA, cryoglobulinemia and hypocomplementemia, play an important role in the pathogenesis of this RPGN, although we could not demonstrate deposition within glomeruli of immune complexes containing HCV. The effect of interferon therapy on such immunological abnormalities remains to be documented. Since interferon is known to have immunomodulatory effects, we selected corticosteroid therapy. Future studies need to focus on the optimal treatment strategy for hepatitis C virus-associated glomerulonephritis.
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PMID:[A case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive rapidly progressive glomerulonephritis]. 1089 95


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