Respiratory Insufficiency in Postmenopausal Women

Saaresranta, Tarja; Polo-Kantola, Pa¨ivi; Irjala, Kerttu; Helenius, Hans; Polo, Olli

doi:10.1378/chest.115.6.1581

Cited by 48 publications

(4 citation statements)

References 24 publications

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“…Their common conclusion was that there was some decrease in apnea hipoapnea index (AHI) or shortening of apnea duration. In postmenopausal females with chronic respiratory failure, the ventilatory improvement was sustained for at least three weeks after cessation of the hormone [86]. As stated by the authors, the sustained ventilatory effect of short-term medroxyprogesterone acetate suggest that periodic administration might be sufficient to improve ventilation in females.…”

Section: C) Use Of Progesterone In the Treatment Of Sleepdisordered mentioning

confidence: 73%

Effects of Progesterone on Sleep: A Possible Pharmacological Treatment for Sleep-Breathing Disorders?

Andersen¹,

Bittencourt²,

Antunes

et al. 2006

CMC

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Progesterone is present in a wide spectrum of biological activity within a variety of tissues. This hormone is also known to affect reproduction, sleep quality, respiration, mood, appetite, learning, memory and sexual activity. Progesterone exerts a sleep induction or hypnotic effect and is a potent respiratory stimulant that has been associated to a decrease in the number of central and obstructive sleep apnea episodes in men. The literature also contains a substantial amount of data on the effect of apnea in women with obesity-hypoventilation during menopause. This review attempts to outline the specific role of progesterone in normal sleep and breathing as well as its possible therapeutic effects in the treatment of sleep-disordered breathing.

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Section: C) Use Of Progesterone In the Treatment Of Sleepdisordered mentioning

confidence: 73%

Effects of Progesterone on Sleep: A Possible Pharmacological Treatment for Sleep-Breathing Disorders?

Andersen¹,

Bittencourt²,

Antunes

et al. 2006

CMC

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“…In addition, s120S decreased significantly as symptoms (MRC dyspnea score) increased ( Fig 3 E). The severity of hypoxia (Pa o 2 or desaturation on movement) and oxygenation capacity of lung (Pa o 2 /Fi o 2 or Aa do 2 ) did not show any correlation with s120S ( Table 2 ); however, s120S showed positive correlation with Pa o 2 /Pa co 2 ratio representing the combined effect on gas exchange 42 ( r = 0.28 ; P = .034) ( Fig 3 F), which suggested that the impairment of aerobic metabolism might contribute to the s120S protein level. Other patient background characteristics ( Table 2 ) or subject comorbidities (such as cardiovascular disease or diabetes mellitus) and Charlson index did not show any association with serum levels of SIRT1.…”

Section: Resultsmentioning

confidence: 94%

Decreased Serum Sirtuin-1 in COPD

Yanagisawa

Papaioannou

Papaporfyriou

et al. 2017

Chest

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BackgroundThe protein deacetylase sirtuin-1 (SIRT1) is an antiaging molecule that is decreased in the lung in patients with COPD. Recently, SIRT1 was reported to be detectable in serum, but serum SIRT1 (s120S) levels have not yet been reported in patients with COPD.MethodsSerum SIRT1 protein of all samples was measured by Western blot, and the SIRT1 protein band densities were calculated and compared with clinical parameters.ResultsSeveral molecular sizes of SIRT1, including 120 kDa (actual size) and fragments (102 and 75 kDa) were quantified by Western blot. Among them, only the 120-kDa s120S was significantly decreased in patients with COPD compared with the control subjects without COPD (s120S ratio in healthy subjects = 0.90 ± 0.34 vs those with COPD = 0.68 ± 0.24; P = .014) and was positively correlated with airway obstruction (FEV1/FVC, r = 0.31; P = .020); its severity measured by FEV1 % predicted (r = 0.29; P = .029). s120S also showed a positive correlation with BMI (r = 0.36; P = .0077) and diffusing capacity of the lung per unit volume (the carbon monoxide transfer coefficient: KCO%) (r = 0.32; P = .025). It was also significantly decreased with increasing severity of lung emphysema (r = –0.40; P = .027) and with a clinical history of frequent COPD exacerbations (infrequent vs frequent, 0.76 ± 0.20 vs 0.56 ± 0.26; P = .027). SIRT1 was not detected in supernatant of A549 and primary epithelial cells in normal culture conditions.Conclusionss120S was decreased in the patients with COPD, potentially as reflected by the reduced SIRT1 within cells as a result of oxidative stress, and might be a potential biomarker for certain disease characteristics of COPD.

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“…It is possible that low progesterone levels in postmenopausal women are responsible for these changes. 19,20 Figure 4 shows representative nasal pressure profiles from each study group. Control subject 1 demonstrates the most "normal" of all control subjects, with 62% of sinusoidal flow shapes and 19% of class 4 (see Fig 5 for the flow-shape indexes).…”

Section: Discussionmentioning

confidence: 99%