Erectile dysfunction is a marker for obstructive sleep apnea

Abstract

Purpose: To investigate the prevalence of erectile dysfunction (ED) in patients with obstructive sleep apnea (OSA) with and without any other comorbidities.

Methods: The patient group was newly diagnosed as having OSA (apnea–hypopnea index [AHI] > 5/h) using a polysomnographic examination. A group of subjects with simple snoring were included into the control group. Clinically relevant comorbidities were systematically assessed in face-to-face interviews. All patients were asked to complete the 15-item International Index of Erectile Function (IIEF-15) questionnaire for the evaluation of ED. The patients with OSA and ED were evaluated according to these comorbidities.

Results: Of the 94 patients, 39 patients were excluded because of severe diseases. OSA was observed in 38 (69.1%) of the 55 patients. ED was seen in 24 (63.2%) patients with OSA, and in 8 (47.1%) patients without OSA (p > 0.05). There were no statistical differences between the groups’ ages, IIEF scores, and body mass index (BMI) scores. There were statistically significant differences between the groups’ AHI scores (p < 0.05). There was a significant correlation between the groups’ AHI scores, BMI, and age (p < 0.05). There was no statistically significant difference in patients with OSA, with and without comorbidity in terms of ED.

Conclusion: The rate of ED was higher in patients with OSA who had no other comorbidities. Therefore, ED can be a sensitive marker of OSA.

• Comorbidity
• erectile dysfunction
• obstructive sleep apnea
• prevalence

Introduction

Erectile dysfunction (ED) is defined as the consistent inability to obtain and/or maintain a penile erection sufficient to permit satisfactory sexual intercourse [1]. ED is a common problem in middle-aged to elderly men. There are many causes of ED including medications (e.g. thiazides, β-blockers, and antidepressants), neurogenic disorders, metabolic problems, aging, psychologic causes, and vascular diseases [2]. ED can be a sensitive marker of a systemic disease such as diabetes mellitus or atherosclerosis.

Obstructive sleep apnea syndrome (OSAS) is characterized by repetitive episodes of airflow limitation lasting at least 10 s [3]. The prevalence of OSA based on the current definition is rising worldwide. OSA has become a common and serious health problem and also has a negative effect on the quality of life [4].

OSA affects 4% of men aged between 30 and 60 years [5]. However, it is believed that the proportion of clinically diagnosed OSA is underestimated [6,7]. Several studies confirmed the increased prevalence of ED in patients with OSAS [8,9].

In this prospective study, we investigated the prevalence of ED in patients with OSA, with and without any other comorbidity that could lead to ED. In addition, we correlated apnea–hypopnea index (AHI) and erectile function scores.

Materials and methods

Study population

A total of 94 patients were evaluated for potential OSA. The patient group (group 1) were newly diagnosed as having OSA (>5/h) using a polysomnographic examination in Yüzüncü Yil University Dursun Odabaş Research Hospital Sleep Disorders Laboratory between November 2014 and April 2015. A group that comprised subjects with simple snoring was included as the control group (group 2).

The inclusion criteria for the study group were AHI >5 under polysomnography. Smoking, medication use, and comorbid diseases such as cardiovascular, pulmonary, or neurologic; current treatment with phosphodiesterase-5 inhibitors; proven hypogonadism; and severe lung disease were the exclusion criteria. Clinically relevant comorbidities including systemic hypertension, diabetes, hyperlipidemia, coronary heart disease, surgical prostate interventions, psychiatric/neurologic disorders, and history of chronic obstructive pulmonary disease were systematically assessed by asking the patients and/or referring to current documented medical treatment. The patients with OSA and ED were evaluated according to comorbidity.

The study was approved by the Ethics Committee of the University of Yüzüncü Yil, Van, Turkey, and was undertaken in accordance with the Helsinki Declaration of 1975, as revised in 1983.

Assessment of polysomnography

Overnight polysomnography was performed with 16-channel Embla (Medcare Inc., Reykjavik, Iceland) continuous sleep technician monitoring. The system consists of 4 channels of electroencephalogram, 2 channels of electrooculography, submental and bilateral tibialis anterior electromyograms, oronasal air flow, thoracic and abdominal movements, pulse oximeter oxygen saturation, body position detector, electrocardiogram, and a tracheal sound detector. Apnea was defined as the complete cessation of airflow lasting more than 10 s. Hypopnea was defined as a >30% reduction in airflow lasting more than 10 s accompanied by >4% desaturation and/or arousal. The average number of episodes of apnea and hypopnea per hour of sleep were measured as AHI. The OSA diagnosis was made on the basis of an AHI > 5. Sleep stages were scored following standard criteria with 30-s epochs and were reviewed and verified by a certified sleep physician.

Assessment of IIEF-15

All the 55 patients were interviewed face-to-face and asked to complete the 15-item International Index of Erectile Function (IIEF-15) questionnaire for evaluation of erectile and sexual dysfunction, which comprises 15 questions across five sexual domains [1]. It includes erectile function, intercourse satisfaction, orgasmic function, sexual desire, and overall satisfaction. ED was defined by 25 points of the EF subscore, whereby values of 17–25 indicate mild, 11–16 moderate, and 10 severe ED. Patient interviews were performed by a urologist. The urologist was unaware of the severity of the patient’s sleep problem.

Statistical analysis

Descriptive statistics for studied variables (characteristics) are presented as mean, standard deviation, minimum and maximum values. One-way ANOVA test was used to compare group means for the studied variables. In addition, Z-test was performed to compare two proportions. Pearson’s correlation analysis was used to determine linear relations among the variables. Statistical significance levels were considered as 5% and Statistical Package for the Social Sciences (SPSS Inc., Chicago, IL) version 13 statistical program was used for all statistical computations.

Results

Of the 94 patients, those who had smoked (n = 27), had severe cardiovascular (n = 3) and neurologic diseases (n = 2), current treatment with phosphodiesterase-5 inhibitors (n = 1), hypogonadism (n:1), and severe lung disease (n:5) were excluded from the study. The control group consisted of 17 patients who snored.

OSA was observed in 38 (69.1%) of the remaining 55 patients. ED was seen in 24 (63.2%) patients with OSA, and in 8 (47.1%) patients without OSA (p > 0.05) (Table 1). The number of patients with mild-, moderate-, and severe ED, was 21, 9, and 2, respectively.

Table 1. The relation between ED and OSA patients.

Group	ED+, n (%)	ED−, n (%)	Total, n (%)	p
Group 1, n (%)	24 (63.2%)	14 (36.8%)	38 (69.1%)	0.264
Group 2, n (%)	8 (47.1%)	9 (52.9%)	17 (30.9%)
Total, n (%)	32 (58.2%)	23 (41.2%)	55 (100%)

ED, erectile dysfunction; OSA, obstructive sleep apnea.

The mean age of the controls, and those with mild-, moderate-, and severe OSA was 41.7 ± 1.27 years, 39.2 ± 1.11 years, 47.27 ± 9.04 years, and 46.08 ± 1.13 years, respectively. The demographic characteristics of the subjects in the study are shown in Table 2. There were statistically significance differences between the groups’ AHI scores (p < 0.05); however, there were no statistical differences between the groups’ ages, IIEF scores, and body mass index (BMI) scores.

Table 2. Descriptive statistics and comparative results according to OSA groups.

		N	Mean	SD	Min.	Max.	p
Age	Control	17	41.7059	12.736	21.00	63.00	0.239
	Mild	15	39.2000	11.130	22.00	62.00
	Moderate	11	47.2727	9.045	32.00	64.00
	Severe	12	46.0833	11.325	27.00	61.00
	Total	55	43.0909	11.48	21.00	64.00
AHI	Control	17	2.10	1.385	0	4	0.001
	Mild	15	8.40	2.621	5	14
	Moderate	11	18.36	2.461	15	23
	Severe	12	55.08	24.467	30	101
	Total	55	18.63	23.148	0	101
IIEF	Control	17	23.9412	4.06925	14.00	29.00	0.642
	Mild	15	22.0667	6.37480	10.00	30.00
	Moderate	11	21.0909	6.62502	12.00	30.00
	Severe	12	22.2500	7.13665	8.00	30.00
	Total	55	22.4909	5.92194	8.00	30.00
BMI	Control	17	28.89	3.909	22	37	0.078
	Mild	15	26.89	3.287	19	31
	Moderate	11	29.82	5.293	24	40
	Severe	12	30.88	3.670	24	38
	Total	55	28.97	4.174	19	40

There was a significant correlation between the groups’ AHI scores, BMI, and age (p < 0.05). However, there was no correlation between the AHI scores and IIEF.

Comorbidities were seen in 16 patients: systemic hypertension (n = 3), diabetes mellitus (n = 7), hyperlipidemia (n = 2), coronary heart disease (n = 1), psychiatric/neurologic disorders (n = 1), and history of chronic obstructive pulmonary disease (n = 2). There was no statistically significant difference between patients with OSA, with and without comorbidities in terms of ED (Table 3).

Table 3. Prevalence of ED and OSA according to comorbidity.

	Comorbidity – (n:39)			Comorbidity + (n:16)
Group	OSA+	OSA−	p	OSA+	OSA−	p	p (C − versus C+)
ED+	15	7	0.546	9	1	0.233	0.225
ED−	10	7		4	2
Total	25	14		13	3

ED, erectile dysfunction; OSA, obstructive sleep apnea; C−, patients without comorbidity; C+, patients with comorbidity.

Discussion

ED as a symptom of OSA has been previously reported in the literature [10,11]. ED prevalence has been reported as 64.4% in men with OSA [12]. Although the mechanism that underlies ED in patients with OSA remains unclear, sexual problems are common among men with sleep apnea/hypopnea.

Hirshkowitz et al. verified that 91.3% patients with ED symptoms also had OSA [13]. Hirshkowitz et al. concluded that 40% of patients with OSA had ED [13]. Santos et al. reported ED prevalence in 64.4% of men with OSA and they revealed that ED determinants were age, diabetes, and past smoking habits. Hypertension and angiotensin converting enzyme inhibitors and angiotensin receptor blocker (ACEI/ARB) therapy also revealed a statistically significant association with ED [12]. Budweiser et al. reported that ED and overall sexual dysfunction were highly prevalent in patients with suspected OSA [14]. Irrespective of known risk factors, mean nocturnal SaO₂ was an additional independent correlate of these dysfunctions, which suggests that OSA-related intermittent nocturnal hypoxemia specifically contributes to their development [14].

Notably, intermittent nocturnal hypoxemia is likely to contribute to impaired penile tumescence by promoting endothelial dysfunction and altered vasoregulation, which might be mediated by a reduction of nitric oxide (NO) production, as well as elevated levels of endothelin [15,16]. Increased oxidative stress markers might result in an additive effect in the aetiopathogenesis of ED [17]. It was reported that oxidative stress markers increased in the blood of patients with OSAS to a variable degree, depending on the severity of the syndrome [18]. Also, oxidative stress was detected increased in patients with ED, whereas antioxidative parameters were found decreased [17].

As endothelial dysfunction, induced by inflammatory cytokines, chemokines, has been proposed as a possible mechanism, AHI may play a pivotal in determining the patients who are at risk of developing ED. In our study, mean AHI in control group was 2.1 while it was 18.6 in OSA group (p < 0.01). Future studies may address the relation between AHI and the degree of ED.

In contrast, the association between OSA and ED was rejected by Schiavi et al. and Gürbüz et al. [19,20]. Gürbüz et al. reported that the high incidence of ED in patients with OSA seemed to be related with concomitant comorbidities such as diabetes, atherosclerosis, and neuroendocrine disorders rather than sleep apnea [20]. Thereby, we investigated patients with OSA with and without comorbidities.

In the present study, we solely focused on erectile function. There was no statistically significant difference between ED and OSA in our study. However, the ratio of ED in the OSA group was higher when compared with the control group (63.2% in OSA group versus 47% in the control group, p > 0.05). Thus, we propose cautiousness when evaluating a patient with OSA or ED. We suggest that ED can be a sensitive marker of OSA like DM and other systemic diseases.

We excluded comorbidities unlike other studies. When comorbidities were excluded, we found that the prevalence of ED was 60% in patients with OSA. We also detected that there was no statistical significant difference between patients with and without comorbidities. This result showed that ED may be related with OSA.

Moreover, trials evaluating OSA treatment found improvements in ED, which hypothesized that there may be an association between both disorders [21–23]. The authors revealed that patients on continuous positive airway pressure (CPAP) treatment showed decreased hypoxia, improved endothelial function, decreased blood pressure, and sympathetic hyperactivity. Budweiser et al. reported that long-term CPAP treatment of OSA can improve sexual function in men with OSA [24].

Margel et al. correlated severe OSA with ED [8]. However, OSA severity was not associated with ED in another study [23]. In the present study, the severity of OSA was also evaluated using the AHI. There was no significant difference between AHI scores and ED degrees.

In our study, we observed that the ED ratio was higher in patients with OSA than in the control group. There was no statistically significant rate of ED in patients with OSA when compared with the control group. The control group consisted of patients who snored. Snoring was detected as a risk factor for sexual dysfunction [25]. We suggest there may be a relation between snoring and ED. It is our assertion that there is considerable rate of ED in patients with OSA who have no comorbidities. The major limitation of this study was the low number of patients.

Conclusions

The rate of ED was higher in patients with OSA who had no other comorbidities. Therefore, ED can be a sensitive marker of OSA.

Declaration of interest

No conflict of interest was declared by the authors.