Search Results (6)

Introduction: There is limited data in the literature on the effect of prostaglandins (PG) and thromboxanes (TX) on the development and severity of Hashimoto’s Thyroiditis (HT). This article aimed to analyze the association between blood count and the cyclooxygenase (COX) pathway in 39 women with HT. Methods: Biochemical analysis of PGE2 and TXB2 was performed using liquid chromatography (HPLC). Results: Morphological abnormalities were found in the women studied, particularly with regard to white blood cell parameters. An increase in thyroid-stimulating hormone (TSH) was associated with significantly higher levels of monocytes (p = 0.041). Correlations were also noted between the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) with TXB2 and PGE2. Furthermore, a very strong correlation was demonstrated for the first time between antibodies against tissue transglutaminase (anti-tTG) and antibodies against thyroglobulin (ATG) (r = 0.781; p = 0.007). Correlations between blood count and eicosanoids were also demonstrated. Conclusions: The results suggest the involvement of COX products in the pathogenesis of HT and hematopoiesis; therefore, this study may contribute not only to advancing knowledge, but also to developing new guidelines for diagnosing and treating autoimmune diseases. Full article

Introduction: Pulmonary hypertension due to chronic obstructive pulmonary disease (COPD) is classified as Group 3 pulmonary hypertension, with no current proven targeted therapies. It has been shown that cigarette smoke, the main risk factor for COPD, can increase thromboxane A₂ production in healthy human pulmonary artery smooth muscle cells and pulmonary artery endothelial cells, and that blocking the effect of increased thromboxane A₂ using daltroban, a thromboxane A₂ receptor antagonist, can inhibit cigarette smoke-induced pulmonary artery cell proliferation. However, it is largely unknown whether thromboxane A₂ is increased in smokers with COPD. Therefore, the aim of this study was to assess the level of thromboxane A₂ production in patients with COPD who smoke. Methods: Pulmonary artery smooth muscle cells from three smokers with COPD and three healthy donors were cultured in cell culture medium. The culture medium was collected and the thromboxane B₂ (a stable metabolite of thromboxane A₂) released in the culture medium was quantified using an ELISA kit. The data were normalised with the total protein concentration and then expressed in pg/mg protein. Demographic data were collected and baseline pulmonary function tests of patients with COPD were conducted. Results: The mean age of patients with COPD was 69 ± 7 years. All patients were smokers and had a mean smoking history of 39.66 ± 9.50 packs per year. The mean forced expiratory volume in one second, that is, FEV1%, and the ratio of forced vital capacity (FVC) to FEV1% of COPD patients were 63.33 ± 19.60% and 52.66 ± 14.64%, respectively. The results revealed that thromboxane A₂ production was significantly increased in pulmonary artery smooth muscle cells from smokers with COPD (434.56 ± 82.88 pg/mg protein) compared with the thromboxane _A2 levels in pulmonary artery smooth muscle cells from healthy donors (160 ± 59.3 pg/mg protein). Conclusions: This is the first report of increased thromboxane A₂ production in pulmonary artery smooth muscle cells from smokers with COPD. This observation strongly suggests that thromboxane A₂ can be used as a novel therapeutic target for the treatment of patients with COPD-associated pulmonary hypertension. Full article

Introduction: Aspirin resistance may be associated with various conditions. We measured serum thromboxane B₂ (TXB₂) and platelet function using the Multiplate^® Analyzer with arachidonic acid (ASPI) in patients on long term aspirin therapy to identify aspirin resistance and associated factors. Materials and Methods: Chinese patients with stable coronary heart disease had samples for serum TXB₂ and ASPI measurement taken before and 1 h after taking a morning dose of 80 mg aspirin. Results: In 266 patients with mean age 66.6 ± 10.7 years, 17% were female and 55% were current or previous smokers. TXB₂ and ASPI measurements were significantly higher before the dose than at 1 h post dose, with 46% of subjects having high ASPI values (AUC > 300 AU*min) pre dose compared with 27% at 1 h post dose. TXB₂ and ASPI measures of platelet aggregation showed weak correlations, which were only significant before the dose (r = 0.219, p = 0.001). Increased ASPI measurements were associated with white blood cell (WBC) count, haematocrit, platelet count and heart rate at 24 h post dose but only with WBC count, smoking history and heart rate at 1 h post dose. Diabetes was not associated with reduced platelet response to aspirin. The WBC count associated with aspirin resistance was over 6.55 × 10⁹/L by receiver operating characteristic analysis. Conclusions: The antiplatelet response to aspirin was reduced in a large proportion of patients. Patients with higher WBC count within the normal range appear to be at increased risk of aspirin resistance. Higher or more frequent doses of aspirin may be needed in many patients. Full article

Recently, an increase in the incidence of inflammatory bowel disease (IBD) has been observed, especially among children and adolescents. Currently, few studies focus on the differentiation of inflammation in IBD subunits, i.e., Crohn’s Disease (CD) and Ulcerative Colitis (UC). The aim of this study was to compare the concentrations of proinflammatory mediators of arachidonic acid (ARA) and linoleic acid (LA) in patients with CD (n = 34) and UC (n = 30), in order to identify differences in inflammation in both diseases and within the same entity, according to disease activity. Sixty-four adolescents with a mean age of 13.76 ± 2.69 and 14.15 ± 3.31, for CD and UC, respectively, were enrolled in the study. Biochemical analysis of ARA and LA derivatives was performed using a liquid chromatography. A trend was observed in the concentration of 15S-HETE (hydroxyeicosatetraenoic acids) in CD relative to UC. The active phase of both diseases showed a higher 15S-HETE concentration in active CD relative to active UC. Comparing patients with CD with active and inactive disease showed a trend of increased levels of thromboxane B2, leukotriene B4 and 9S-HODE (hydroxyoctadecadienoic acid) in the active versus the inactive disease. We also observed statistically significantly higher levels of 12S-HETE in inactive CD relative to active CD. In the UC group, on the other hand, statistically significantly higher levels of prostaglandin E2 and 16RS-HETE were observed in active UC relative to inactive UC. Moreover, significantly higher concentrations of LTX A4 5S, 6R were observed in inactive UC relative to the active phase. In conclusion, the present study indicated the activity of the 15-LOX pathway in CD. Further studies involving lipid mediators in patients with IBD may contribute to the development of new therapies for the treatment of IBD. The identification of differences in the course of inflammation may help to target therapy in CD and UC, and perhaps allow the introduction of an additional diagnostic marker between the two main IBD subtypes. Full article

Introduction: Polycystic ovary syndrome (PCOS) is an endocrinological disorder that affects 5–15% of women of their reproductive age and is a frequent cause of infertility. Major symptoms include hyperandrogenism, ovulatory dysfunction, and often obesity and/or insulin resistance. PCOS also represents a state of chronic low-grade inflammation that is closely interlinked with the metabolic features. “Classical” pro-inflammatory lipid mediators such as prostaglandins (PG), leukotrienes (LT), or thromboxanes (TX) are derived from arachidonic acid (AA) and are crucial for the initial response. Resolution processes are driven by four families of so-called specialized pro-resolving mediators (SPMs): resolvins, maresins, lipoxins, and protectins. The study aimed to establish lipid mediator profiles of PCOS patients compared to healthy women to identify differences in their resolutive and pro-inflammatory lipid parameters. Material and Methods: Fifteen female patients (18–45 years) were diagnosed with PCOS according to Rotterdam criteria, and five healthy women, as a comparator group, were recruited for the study. The main outcome measures were: pro-inflammatory lipid mediators (PG, LT, TX) and their precursor AA, SPMs (resolvins, maresins, protectins, lipoxins), their precursors EPA, DHA, DPA, and their active biosynthesis pathway intermediates (18-HEPE, 17-HDHA, 14-HDHA). Results: The level of pro-inflammatory parameters in serum was significantly higher in PCOS-affected women. The ratio (sum of pro-inflammatory molecules)/(sum of SPMs plus hydroxylated intermediates) reflecting the inflammatory state was significantly lower in the group of healthy women. Conclusion: There is a strong pro-inflammatory state in PCOS patients. Further research will clarify whether supplementation with SPMs or their precursors may improve this state. Full article

Bradykinin (BK) plays an important role in different physiological processes including the general preservation and modulation of vascular systems. The present study was designed in order to examine the effect of BK on isolated rat femoral artery rings and to investigate the participation of intact endothelium, cyclooxygenase products, Ca²⁺ channels, Na⁺/K⁺–ATPase, and B₂ kinin receptors in BK-induced action. Circular artery segments were placed in organ baths. The endothelium was mechanically removed from some arteries. Concentration–contraction curves for BK were obtained in the rings previously equilibrated at the basal tone. BK produced a concentration–dependent contraction, which was reduced by endothelial denudation. The BK–induced effect was almost completely inhibited by indomethacin (cyclooxygenase inhibitor) or OKY–046 (thromboxane A₂–synthase inhibitor). Nifedipine (Ca²⁺ channel blocker), ouabain (Na⁺/K⁺–ATPase inhibitor), or HOE–140 (selective B₂ kinin receptor antagonist) significantly reduced the BK–evoked effect. In conclusion, it can be proposed that BK produces concentration– and endothelium–dependent contractions of the isolated rat femoral artery, which is for the most part a consequence of B₂ kinin receptor activation. Cyclooxygenase contractile products, especially thromboxane A₂, play a significant role in this course of action. The transduction mechanism involved in the process of BK–induced femoral artery contraction include the activation of voltage–gated Ca²⁺ channels, and in a smaller extent Na⁺/K⁺–ATPase as well. Full article