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)

Effect of sodium copper chlorophyllin (SCC) on experimental allergic reaction was investigated. IgE antibody mediated reactions, homologous passive cutaneous anaphylaxis (PCA) in rats and the release of anaphylactic mediators (histamine and/or slow reacting substance of anaphylaxis (SRS-A] from sensitized guinea pig lung tissues or rat peritoneal mast cells classified as a Type I reaction were clearly inhibited by SCC at a similar potency as N-(3',4'-dimethoxy cinnamoyl) anthranilic acid (N-5'). The increase of vascular permeability in rat skin caused by autacoids or enzymes that participate in the Type I reaction was also inhibited by SCC. Type II or III, complement dependent, reactions including reversed cutaneous anaphylaxis (RCA) in rats and Forssman cutaneous vasculitis (FCV) in guinea pigs were inhibited by SCC. Prednisolone inhibited RCA in rats, but did not inhibit FCV in guinea pigs. Two experimental types of glomerulonephritis, nephrotoxic serum (NTS) nephritis in rats and immune complex nephritis in (NZW X NZB) F1 mice, in which Type II and III reactions might participate in the onset and the development of the disease, were slightly inhibited by SCC in terms of the biochemical changes of blood and urine parameters and histopathological scores. A moderate remission of the onset and development of these two experimental types of nephritis was recognized by the administration of prednisolone. Delayed hypersensitivity reaction as a Type IV reaction caused by sheep red blood cells (SRBC) in sensitized mouse footpad was not affected by SCC. Prednisolone clearly inhibited the SRBC induced footpad reaction in mice. IgM antibody production in mice and IgE antibody production in rats were not influenced by daily injection of SCC.
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PMID:Immunopharmacological studies of sodium copper chlorphyllin (SCC). 619 83

The studies reported here were designed to determine whether sera from various patients could prevent neutrophils from responding to the lymphokine, neutrophil migration inhibition factor from T lymphocytes (NIF-T). Neutrophils from healthy donors were treated with sera from 84 subjects and assayed for responses to NIF-T. Serum from 7 of 37 patients (19%) with rheumatoid arthritis, systemic lupus erythematosus, and various forms of vasculitis showed blocking activity. In contrast, none of 47 subjects, including healthy individuals and patients with spondylarthropathies, cancer, and active infections had a serum factor that prevented neutrophils from responding to NIF-T (P less than 0.01). Serum blocking activity occurred transiently in association with infection by Staphylococcus aureus in one patient with rheumatoid arthritis. Moreover, autologous neutrophils from this same patient showed impaired responses to NIF-T. Blocking activity could be eluted from protein A-Sepharose in three of three patients studied. In three of seven patients, blocking activity was detected in serum cryoprecipitates, with a recovery of 46 to 78% of the blocking activity and overall enrichment (purification) of 137- to 281-fold. Analysis of cryoprecipitates by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed the predominance of immunoglobulins M and G. In one patient, the serum blocking activity was not cryoprecipitable, and cryoprecipitates from a patient with essential cryoglobulinemia failed to prevent neutrophils from responding to NIF-T. Blocking activity was relatively specific for NIF-T, as there was no effect on F-met-leu-phe-induced chemotaxis of neutrophils. Serum blocking activity in patients with connective tissue disease showed some correlation (r = 0.50; P less than 0.01) with immune complexes detected by polyethylene glycol precipitation but not Clq binding. These studies suggest that the response of neutrophils to NIF-T may be blocked by serum, possibly as a result of immune complexes or autoantibodies found primarily in patients with connective tissue disease.
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PMID:Impaired response of neutrophils to a lymphokine by sera from patients with connective tissue disease. 664 68

A case of skin necrosis caused by subcutaneously administered heparin is reported. A 76-year-old woman received subcutaneous injections of porcine sodium heparin twice a day to prevent deep vein thrombosis. Nineteen days after heparin therapy began, black necrotic areas were noted on her abdomen, and heparin injections were discontinued. The patient received small amounts of heparin intravenously for three additionally days without apparent complications. Proposed mechanisms for heparin-induced skin necrosis include allergic vasculitis and localized platelet aggregation with intravascular thrombosis. Heparin therapy should be stopped if necrosis develops. Intravenous administration of heparin to sensitive patients may be followed by life-threatening reactions. Necrotic areas may heal spontaneously, but often require debridement and skin grafting. Various agents, including steroids, may be useful in preventing the development of necrotic lesions.
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PMID:Heparin-induced skin necrosis. 671 77

Atrophie blanche vasculitis is due to thromboocclusion of dermal blood vessels. A 28-year-old white man with a very severe case of this disease had a complete remission when he was treated with minidose heparin sodium injections. As little as 5,000 U of heparin every 3 days controlled his vasculitis. Further reduction of heparin dose resulted in an exacerbation of disease which was controlled with more vigorous heparin therapy. The role of minidose heparin in cutaneous disease is discussed.
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PMID:Minidose heparin therapy for vasculitis of atrophie blanche. 682 6

Two cases of cutaneous necrosis occurred that were caused by intravenous administration of porcine heparin for deep venous thrombophlebitis. The lesions grossly resembled those of warfarin sodium-induced skin necrosis. However, histologically, no fibrin thrombi were noted in capillaries and vessels, a characteristic finding in warfarin necrosis. There was no evidence of vasculitis in the lesions. Both patients subsequently received warfarin without complications.
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PMID:Cutaneous necrosis caused by systemically administered heparin. 702 74

A tissue plasminogen activator was extracted from skin lesions with allergic vasculitis and purified by successive column chromatography on Sephadex G-200, DEAE-cellulose, Hydroxyaptite-cellulose and polyacrylamide gel electrophoresis. By these procedures, 160 micrograms of enzyme with a specific activity of 843.8 international units/mg protein was obtained from 5 g of original skin. The purified material was homogeneous as ascertained by sodium dodecyl sulfate polyacrylamide gel electrophoresis and had an apparent molecular weight of 110,000 as measured by gel filtration on Sephadex G-200. Its identity with human urokinase was investigated and was found to possess the same plasminogen activator activity as that of urokinase. It had high amindolytic activity, but only slight N-alpha-acetyl-glycyl-L-lysine methyl ester esterolytic activity. This tissue plasminogen activator was confirmed to be immunologically identical to human urokinase.
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PMID:Isolation of tissue plasminogen activator from skin lesions with allergic vasculitis. 719 68

Experimental infection was produced by two of four isolates of ovine Haemophilus somnus given by intracisternal inoculation into two to three-month-old lambs. Isolate 2041 (originally obtained from a septicemic lamb in Alberta) caused lethal infection in eight of nine lambs, isolate 67p from the prepuce of a normal lamb produced less acute disease in four of nine lambs, and the other two isolates (93p and 1190) caused no detectable disease. Significant lesions were limited to the brain and spinal cord. Purulent meningitis was characteristic but vasculitis or septicemia were not detected, perhaps due to the route of inoculation. Since a difference in virulence was noted among strains, we analyzed surface proteins thought to be virulence factors of bovine H. somnus. Protein profiles of bovine and ovine H. somnus done by sodium dodecyl sulphate-polyacrylamide gel electrophoresis showed similar patterns for virulent bovine isolates and ovine septicemic isolates. Preputial isolates showed a lower molecular mass major outer membrane protein than septicemic isolates. Antigenic analysis revealed that outer membrane proteins p270, p78, p76, p40, and p39 were detected in both ovine and bovine isolates except for 1190, which was probably not a true H. somnus isolate. Thus the preputial and septicemic isolates of ovine H. somnus were similar to bovine H. somnus in pathogenicity and in surface antigens.
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PMID:Ovine Haemophilus somnus: experimental intracisternal infection and antigenic comparison with bovine Haemophilus somnus. 795 23

Recognition of sulfite sensitivity by the practicing dermatologist has become increasingly important. A wide spectrum of anaphylactoid reactions can occur after ingestion of sulfite additives in foods and medications. We report the case of a 47-year-old man with severe acute intermittent urticaria. A placebo-controlled oral challenge test with 50 mg sodium disulfite resulted in an acute urticaria attack. A biopsy taken 5 h after the appearance of the urticaria demonstrated a leukocytoclastic vasculitis with eosinophilia. Avoiding foods and drugs containing sulfites is often difficult due to its widespread use. Therefore, the patient should be equipped with a medical emergency kit.
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PMID:Disulfite-induced acute intermittent urticaria with vasculitis. 827 92

Carpal tunnel syndrome is well known to be associated with hypothyroidism, but other mononeuropathies have been rarely reported. We report a 65-year-old male who showed right deep peroneal nerve palsy caused by hypothyroidism. The patient was admitted to our hospital because of general fatigue and right drop foot. On admission, bilateral pretibial pitting edema was observed, predominant on the right side. There was no muscle contraction in the right anterior tibial muscle and extensor hallucis longus in addition to slight weakness of the proximal muscles; whereas, muscle atrophy of the anterior tibial muscle was not noted. There was no sensory disturbance. On an electrophysiological examination, there was no muscle action potentials by the stimulation of the right deep peroneal nerve. Other nerves showed normal results both in the conduction velocity and in the compound action potential. Two months after the administration of levothyroxine sodium (0.025 mg/day), the right deep peroneal nerve palsy was completely recovered, associated with disappearance of pretibial edema. It is not yet determined which of axonopathy or demyelination is dominantly responsible for neuropathy associated with hypothyroidism. These results suggested a conduction block in deep peroneal nerve associated with focal edema. It is necessary to consider hypothyroidism as well as trauma, diabetes mellitus, and vasculitis when investigating mononeuropathy of deep peroneal nerve.
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PMID:[Deep peroneal nerve palsy associated with hypothyroidism]. 839 65

A 24-year-old woman was admitted to our hospital because of pulmonary hypertension. Five years earlier, she had been given a diagnosis of systemic lupus erythematosus. The pulmonary hypertension was believed to have been caused by pulmonary vasculitis, because pulmonary angiography, nuclear perfusion scans, and axial magnetic resonance imaging of the pulmonary artery showed no evidence of pulmonary thromboembolism. Steroids, a calcium antagonist, and home oxygen therapy did not reduce the patient's pulmonary hypertension. The level of thromboxane B2, a stable metabolite of thromboxane A2, in the pulmonary artery was abnormally high (140 pg/ml). This suggested that vasoconstriction of the pulmonary artery and microthrombosis would cause continuous pulmonary hypertension. Beraprost sodium (120 micrograms/day, p.o.) was administered. This analogue of prostaglandin I2 is a potent relaxer of vascular smooth muscle, and it inhibits platelet aggregation. The pulmonary artery pressure was normal eight months after the start of therapy with beraprost sodium.
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PMID:[Systemic lupus erythematosus with pulmonary hypertension--normalization of pulmonary artery pressure by long-term administration of beraprost sodium]. 858 27


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