6-ketoprostaglandin-f1-alpha and Sleep-Apnea--Obstructive

6-ketoprostaglandin-f1-alpha has been researched along with Sleep-Apnea--Obstructive* in 3 studies

Trials

1 trial(s) available for 6-ketoprostaglandin-f1-alpha and Sleep-Apnea--Obstructive

ArticleYear
Modulation of inflammatory and hemostatic markers in obstructive sleep apnea patients treated with mandibular advancement splints: a parallel, controlled trial.
    Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine, 2014, Mar-15, Volume: 10, Issue:3

    Obstructive sleep apnea (OSA) is associated with systemic inflammation and a hypercoagulable state. The current study aim was to investigate whether mandibular advancement splint (MAS) therapy affects inflammatory and hemostatic parameters in patients with mild-to-moderate OSA.. Twenty-two patients with mild-to-moderate OSA and 16 control subjects were studied. OSA subjects were treated with a titratable MAS for 6 months. Baseline plasma C-reactive protein, interleukin-1β, interleukin-10, interleukin-6, P-selectin, fibrinogen, D-dimer, plasminogen activator inhibitor-1 (PAI-1), thrombin-antithrombin complex, activated thrombin-activatable fibrinolysis inhibitor (TAFIa), 6-keto-PGF1α, glucose, and fibrin clot lysis time (CLT) were measured in all subjects. After 3 months of MAS therapy, measurements were repeated for the 22 patients, and after 6 months all measurements were repeated for all study subjects.. MAS treatment reduced significantly AHI at 3 months (24 vs 13.1/h) and further improved it at 6 months (13.1 vs 7.05/h). Compared with controls, OSA subjects had a significant higher baseline mean levels of fibrinogen, TAFIa, 6-keto-PGF1α, and glucose. MAS treatment significantly improved levels of IL-1β, D-dimer, TAFIa, and CLT. Despite residual apneas, MAS treatment group presented similar measured homeostatic and inflammatory levels to controls except for glucose.. Treatment with MAS in mild-to-moderate OSA subjects improves the inflammatory profile and homeostatic markers.. Niżankowska-Jędrzejczyk A; Almeida FR; Lowe AA; Kania A; Nastałek P; Mejza F; Foley JH; Niżankowska-Mogilnicka E; Undas A. Modulation of inflammatory and hemostatic markers in obstructive sleep apnea patients treated with mandibular advancement splints: a parallel, controlled trial.

    Topics: 6-Ketoprostaglandin F1 alpha; Antithrombin III; Biomarkers; Blood Glucose; C-Reactive Protein; Carboxypeptidase B2; Case-Control Studies; Fibrin Clot Lysis Time; Fibrin Fibrinogen Degradation Products; Fibrinogen; Humans; Interleukin-10; Interleukin-1beta; Interleukin-6; Male; Mandibular Advancement; Middle Aged; P-Selectin; Peptide Hydrolases; Plasminogen Activator Inhibitor 1; Polysomnography; Sleep Apnea, Obstructive

2014

Other Studies

2 other study(ies) available for 6-ketoprostaglandin-f1-alpha and Sleep-Apnea--Obstructive

ArticleYear
Systemic prostacyclin and thromboxane production in obstructive sleep apnea.
    Advances in medical sciences, 2016, Volume: 61, Issue:1

    Obstructive sleep apnea increases the risk of cardiovascular diseases. Alternations in prostacyclin and thromboxane concentrations and balance could constitute one of mechanisms linking sleep apnea and cardiovascular events. Thus we aimed to assess the concentrations of 6-keto-prostaglandin F1α (6-keto-PGF1α) (metabolite of prostacyclin) and thromboxane B2 (TXB2) (metabolite of thromboxane A2) in urine and blood of obstructive sleep apnea patients and controls (snoring subjects with otherwise normal polysomnogram).. Overnight urine and morning blood samples were taken from subjects and controls at baseline and in sleep apnea group during continuous positive airway pressure (CPAP) treatment. Samples were analyzed using mass chromatography/gas spectrometry.. We analyzed data from 26 obstructive sleep apnea subjects (mean apnea-hypopnea index 45.4±17.3) and 22 well-matched controls. At baseline sleep apnea patients, when compared to controls, have higher 6-keto-PGF1α in urine (0.89±0.15 vs 0.34±0.06, p=0.01) and blood (24.49±1.54 vs 19.70±1.77, p=0.04). TXB2 levels in urine and blood were not different across groups. CPAP treatment significantly decreased 6-keto-PGF1α in urine (0.92±0.17 vs 0.22±0.10, p=0.04), but not in blood. TXB2 levels during CPAP treatment did not change significantly.. These results suggest augmented systemic prostacyclin production in obstructive sleep apnea patients, which potentially could constitute a protective mechanism against detrimental effects of sleep apnea.

    Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Case-Control Studies; Continuous Positive Airway Pressure; Epoprostenol; Female; Humans; Male; Middle Aged; Sleep Apnea, Obstructive; Thromboxane B2; Thromboxanes

2016
[Detection of thromboxane B2, 6-keto-prostaglandin F1alpha and anticardiolipin antibody in patients with obstructive sleep apnea-hypopnea syndrome].
    Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases, 2004, Volume: 27, Issue:5

    To observe the changes of thromboxane B(2) (TXB(2)), 6-keto-prostaglandin F1alpha (6-K-PGF1alpha) and anticardiolipin antibody (ACA) in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) before and after institution of nasal continuous positive airway pressure (nCPAP).. Sixty cases of OSAHS confirmed by polysomnography (PSG) were selected as the trial group, and 20 normal donors without OSAHS were recruited as the control group. Nineteen patients with severe OSAHS were treated by nCPAP. Plasma levels of TXB(2), 6-K-PGF1alpha were detected by enzyme-linked immunosorbent assay (ELISA).. Plasma (serum) level of TXB(2) (ACA) was significantly higher in patients with moderate to severe OSAHS than that in control group (P < 0.01), and nCPAP therapy decreased its level significantly (P < 0.01). Plasma level of 6-K-PGF1alpha was significantly lower than that in the control group (P < 0.01), and nCPAP therapy increased its level significantly (P < 0.01). TXB(2) and ACA were correlated positively with AHI, and negatively with minimal oxygen saturation (P < 0.01). 6-K-PGF1alpha was correlated negatively with AHI, and positively with minimal oxygen saturation (P < 0.01).. The results indicate that patients with OSAHS are susceptible to thromboembolism disease. TXB(2), 6-K-PGF1alpha, ACA may be associated with the high prevalence of thromboembolism in patients with OSAHS. nCPAP therapy is effective in correcting TXB(2), 6-K-PGF1alpha, ACA.

    Topics: 6-Ketoprostaglandin F1 alpha; Adult; Antibodies, Anticardiolipin; Continuous Positive Airway Pressure; Female; Humans; Male; Middle Aged; Sleep Apnea, Obstructive; Thromboembolism; Thromboxane B2

2004