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 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

Defibrotide, a polydeoxyribonucleotide, has been found to modulate endothelial cell function, causing an increase in tissue plasminogen activator (t-PA) levels, a decrease in plasminogen activator inhibitor (PAI) levels, and an increase in prostaglandin I2 (PGI2) formation in humans. Defibrotide has no direct anticoagulant effect but has a synergistic action with heparin. A strong antithrombotic effect has been observed in animal models. Thus, defibrotide has a beneficial effect in cases of deep venous thrombosis (DVT), peripheral obliterative vascular disorder (POVD), stroke, vasculitis, and thromboembolism. Defibrotide also inhibits platelet function and activation. A significant decrease in platelet aggregate formation on the suture line in microarterial anastomosis in rats is one way defibrotide can inhibit platelet function and activation. In humans, a slight prolongation' of the lag period in collagen-induced aggregation has been observed. In addition, a slight decrease in the maximum amplitude of the secondary wave of ADP and adrenalin-induced aggregations was also found. Platelet adhesion is diminished, the platelet differential count on formvar membrane is altered, and platelet aggregate formation is significantly inhibited. With an increase in platelet cyclic AMP (cAMP) content and a decrease in malonyl dialdehyde (MDA) and thromboxane B2 (TXB2) formation, the levels of platelet secretion products such as PF-4 and beta-thromboglobulin (beta-TG) in plasma decreased progressively. It was also demonstrated that the 14C-glucose transport defect of the platelet membrane of atherosclerotic patients was partially corrected with defibrotide treatment.
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PMID:Effect of defibrotide on platelet function. 880 24

Severe, white sheathing of the retinal vessels and yellowish-white placoid lesions, suggesting frosted-branch angiitis, were found in both fundi of a 24-year-old woman. Fluorescein angiography showed hypofluorescence of the placoid lesions in the early phase and hyperfluorescence in the late phase. Indocyanine green angiography showed hypofluorescence during all phases. These findings imply an occlusion of the choriocapillaris. Fluorescein angiography also showed occlusion of the peripheral retinal vessels. With systemic corticosteroids and prostaglandin I2 derivative, the fundi recovered almost completely to normal 3 months later.
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PMID:A case of frosted branch angiitis with yellowish-white placoid lesions: fluorescein and indocyanine green angiography findings. 988 40