Disease relevance of 11-dehydrothromboxane B2

• The fractional conversion of exogenous thromboxane B2 (infused at a rate of 4.5, 45.3, or 226.4 fmol per kilogram of body weight per second) to urinary 11-dehydro-thromboxane B2 was assessed in four patients, in whom it averaged 5.4 +/- 0.1 percent; this value did not differ from that measured in healthy subjects [1].
• No detectable increase of urinary 11-dehydrothromboxane B2 was measured in patients with stable angina after exercise-induced myocardial ischemia [2].
• Comparisons of platelet COX-1 or -2 expression and urinary 11-dehydro-thromboxane B2 excretion suggested that aspirin was less able to block platelet activation in vivo in hypercholesterolemia [3].
• The level and dynamics of 11-dehydro-thromboxane B2 excretion were related neither to the neurological symptoms nor to the type or site of the cerebral ischemia [4].
• The change of urinary 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F1 alpha in arteriogenic impotence [5].

Psychiatry related information on 11-dehydrothromboxane B2

• This study investigated the effects of smoking cessation with and without nicotine substitution on the excretion of major urinary metabolites of thromboxane A2 and prostacyclin, 11-dehydrothromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1alpha, respectively, as well as on the excretion of leukotriene E4 in man [6].

High impact information on 11-dehydrothromboxane B2

• In all three infants, urinary concentrations of beta-thromboglobulin and 11-dehydrothromboxane B2 levels were much higher during the hyperammonaemia than those in ten control preterm infants [7].
• The urinary excretion of a major enzymatic metabolite of thromboxane A2, 11-dehydro-thromboxane B2, was measured in 57 patients with stable coronary artery disease undergoing cardiac catheterization (n = 28) or elective single-vessel percutaneous transluminal coronary angioplasty (n = 29) [8].
• The urinary excretion of the major enzymatic metabolite of thromboxane B2, 11-dehydro-thromboxane B2, was measured by a previously validated radioimmunoassay [4].
• COX activity was decreased, as were the brain concentrations of 11-dehydrothromboxane B2 and prostaglandin E2 (PGE2), metabolites of arachidonic acid (AA) produced via COX [9].
• Correlation among urinary eosinophil protein X, leukotriene E4, and 11-dehydrothromboxane B2 in patients with spontaneous asthmatic attack [10].

Chemical compound and disease context of 11-dehydrothromboxane B2

• In this study, to clarify whether eosinophil protein X (EPX) is a marker which is distinct from leukotriene E4 (LTE4), or 11-dehydrothromboxane B2 (11DTXB2), we measured the urinary excretion of EPX, LTE4, and 11DTXB2 in 14 asthmatics who were admitted to the hospital with either an acute asthmatic attack or status asthmaticus [10].
• Experimental fat embolism induces urine 2,3-dinor-6-ketoprostaglandin F1alpha and 11-dehydrothromboxane B2 excretion in pigs [11].
• For the 13 patients with arteriogenic impotence (group 3) we compared the urinary 11-dehydro-thromboxane B2 and prostaglandin F1 alpha levels before and after intracavernous injection of prostaglandin E1 by using a paired t test [5].
• The mean urinary 11-dehydro-thromboxane B2 level of 3 patients with arteriogenic impotence was significantly greater than that of the 57 control volunteers: 2.66 +/- 0.65 versus 1.74 +/- 0.56 (plus or minus standard deviation) ng./mg. creatinine (p = 0.008) [5].

Biological context of 11-dehydrothromboxane B2

• Production of urinary 11-keto-thromboxane B2 in normal and hypertensive pregnancies [12].
• Urinary levels of 11-keto-thromboxane B2 (11-keto-TXB2), were elevated at all gestational ages (12-41 weeks) compared with non-pregnant levels [12].
• On postinfusion day 8, urine protein, thromboxane B2, and 11-dehydro-thromboxane B2 excretion, glomerular epithelial crescent formation, and glomerular cell proliferation in the CGS 12970-treated dogs were significantly decreased when compared with values in the placebo-treated group [13].
• Pulmonary capillary permeability, central venous triglyceride levels, 11-dehydro-thromboxane B2 (dh-TXB2) levels, and pulmonary artery pressure were determined [14].
• At baseline aPL participants showed higher plasma levels of vWF (P = 0.006), ET-1 (P = 0.0002) and enhanced urinary excretion of 11-dehydro-thromboxane-B2 (TXB2) (P = 0.0004), F2-isoprostanes (marker of lipid peroxidation) (P = 0.02) and albumin (P = 0.04) than controls [15].

Anatomical context of 11-dehydrothromboxane B2

• Analysis of urinary 11-dehydrothromboxane B2 in patients with occluded retinal vein using GC/SIM [16].
• The urinary excretion of the major arachidonic acid metabolite of platelet origin (11-dehydro-thromboxane B2) and of the vascular endothelial cell (2,3-dinor-6-ketoprostaglandin F1 alpha) were very significantly increased (p < 0.0002) in the patients [17].
• Monitoring thromboxane in body fluids: a specific ELISA for 11-dehydrothromboxane B2 using a monoclonal antibody [18].
• Blood cell counts, plasma endothelin (ET), alpha-human atrial natriuretic peptide (ANP), platelet activating factor (PAF), 6-keto-prostaglandin F1 alpha (PGF1 alpha), and 11-dehydro-thromboxane B2 (TXB2) were evaluated before rHuEPO treatment; at 4, 8, and 12 weeks during treatment; and 5 weeks after the end of treatment [19].

Associations of 11-dehydrothromboxane B2 with other chemical compounds

• METHODS: We measured the urinary excretion of products of platelet (11-dehydro-thromboxane B2 [TXB2]) and renal (prostaglandin IF2 alpha [PGF2 alpha]) arachidonate metabolism as in vivo indexes of the constitutive PGHS-1 pathway [20].
• Moreover, the urinary excretion of 11-dehydro-thromboxane-B2 was 54% higher during treatment with gemfibrozil (P < .001), whereas the excretion of beta-thromboglobulin in urine was unaltered [21].
• Blood levels of LTB4, LTC4, LTD4, 11-dehydrothromboxane B2, eosinophil cationic protein, and histamine were measured at reaction phases of pre-BPT, IAR, and LAR [22].
• Immunoreactive thromboxane B2 (i-TXB2, mainly reflecting 2,3-dinor-TXB2) and immunoreactive 11-keto-thromboxane B2 (i-11-keto-TXB2) were measured by direct enzyme immunoassays [23].

Gene context of 11-dehydrothromboxane B2

• In addition to the biological markers of TPA-induced ODC activity in skin biopsies and urinary polyamine levels, we measured urinary 11-dehydrothromboxane B2, a specific metabolite of thromboxane A2 [24].
• Administration of aspirin caused significant suppression of 11-dehydrothromboxane B2 excretion in both the AIA and ATA groups [25].
• Antibodies were generated against 11-dehydro-thromboxane B2 conjugated to bovine thyroglobulin [26].

Analytical, diagnostic and therapeutic context of 11-dehydrothromboxane B2

• In patients undergoing coronary angioplasty treated with aspirin, 75 mg/day, urinary 11-dehydro-thromboxane B2 averaged 180 +/- 112, 223 +/- 178 and 294 +/- 260, respectively, before, during and after the procedure [8].
• Rapid, direct enzyme immunoassay of 11-keto-thromboxane B2 in urine, validated by immunoaffinity/gas chromatography-mass spectrometry [27].
• After both optimized steps in the extraction procedure were combined, immunoreactivity was found only in HPLC fractions corresponding to the retention volume of authentic 11-dehydrothromboxane B2 [28].
• A fully validated stable isotope dilution method for rapid quantification of 11-dehydrothromboxane B2 by gas chromatography/negative chemical ionization tandem mass spectrometry is reported [29].
• The plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2 were higher in the asymptomatic cerebral infarction group than in the control group [30].

References