1,721,236 research outputs found
Combined Oral Contraceptives Increase High-Sensitivity C-Reactive Protein but Not Haptoglobin in Female Athletes.
No full textBACKGROUND:
No studies have examined the effects of oral hormonal contraception on chronic low-grade inflammation as assessed by stratified levels of high-sensitivity C-reactive protein (hsCRP) in athletes. We explored the impact of combined oral contraceptives (OCs) on serum hsCRP, haptoglobin, triglycerides and cholesterol in white female athletes.
METHODS:
Italian sportswomen (n = 205; mean age 24 ± 5.3 years; body mass index 21 ± 2.2 kg m-2; sport activity 8.7 ± 3.65 h week-1) were analyzed according to OC use.
RESULTS:
Progressive hsCRP levels were evaluated in OC users (n = 53) compared to non-OC users (n = 152). Levels of hsCRP from 3.0 to <10.0 mg L-1 (at high risk of future cardiovascular events) were found in 26.4 % (14/53) of OC users and only in 2.6 % (4/153) of non-OC users (OR = 13.3, 95 % CI 4.14-42.6, P < 0.001). Risky hsCRP levels ≥1.0 mg L-1 were found in 62.3 % of OC users versus 13.2 % non-OC users (OR = 10.9, 95 % CI 5.26-22.5, P < 0.001). Protective hsCRP levels (<0.5 mg L-1) were found in 17.0 % of OC users and in 64.5 % of non-OC users (OR = 0.11, 95 % CI 0.05-0.25, P < 0.001). OC use increased serum triglycerides (P < 0.001), total cholesterol (P = 0.027) and HDL cholesterol (P = 0.018), whereas haptoglobin was unaffected. Hours of exercise week-1 had a mild inverse association with hsCRP (P = 0.048) in non-OC users only.
CONCLUSIONS:
OC use markedly elevated chronic low-grade inflammation in athletes, which could predispose to a higher inflammatory response to physical stress and elevate cardiovascular risk. Physical activity without OC use seemed to favor low hsCRP. Further research is needed to extend our results and to elucidate the potential effects on athletic performance of chronically elevated hsCRP. Our findings would be useful for sport physicians interpreting blood tests in athletes
Thyrotropin stimulates production of procoagulant and vasodilatative factors in human aortic endothelial cells
No full textThyroid diseases have been associated with pathophysiological changes in the vasculature that may result from altered thyroid hormone production or to direct effect of elevated thyrotropin (TSH) levels on smooth muscle cells. A direct effect of TSH on vascular endothelium has not been considered. In the present study a strain of human aortic endothelial cells has been stimulated with TSH, and vascular parameters correlated with the atherosclerotic process have been analyzed. Addition of TSH induced an increase of cyclic AMP (cAMP) concentration in human aortic endothelial cells. Furthermore it induced a decrease of endothelin (from 30 +/- 2.5 to 13 +/- 1 fmol/mL) and of tissue plasminogen activator secretion (from 2,800 +/- 200 to 1,600 +/- 150 ng/mL). On the other hand, it increased nitric oxide (from 148 +/- 8 to 211 +/- 12 muM). TSH did not affect plasminogen activator inhibitor 1. Similar results were obtained when immunoglobulin Gs (IgGs) from Graves' disease patients were used. In conclusion, our findings suggest that TSH and IgGs from Graves' disease patients could stimulate endothelial cells, increasing the secretion of procoagulant and vasodilatative factors, and that cAMP is involved in the transduction pathway. These findings are consistent with modifications of the fibrinolytic system reported in hypothyroidism and in Graves' disease. On the other hand, the increase of vascular resistance found in patients with hypothyroidism may be due to the altered thyroid hormone production and not to TSH directly, or to a different effect of TSH on peripheral vessels
A fast, nondestructive, low-cost method for the determination of hematocrit of dried blood spots using image analysis
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