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Original Research: Sleep Disorders |

Natural History of Primary Snoring in School-aged ChildrenNatural History of Childhood Primary Snoring: A 4-Year Follow-up Study FREE TO VIEW

Albert M. Li, MD; Yin Zhu, MM; Chun T. Au, MPhil; Dennis L. Y. Lee, MB; Crover Ho, RPSGT; Yun K. Wing, MB
Author and Funding Information

From the Department of Pediatrics (Dr Li, Ms Zhu, and Mr Au), the Department of Otorhinolaryngology - Head and Neck Surgery (Dr Lee), and the Department of Psychiatry (Mr Ho and Dr Wing), Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong.

Correspondence to: Albert M. Li, MD, Department of Pediatrics, 6th Floor, Clinical Sciences Building, Prince of Wales Hospital, Shatin, Hong Kong; e-mail: albertmli@cuhk.edu.hk


Drs Li and Zhu are the joint first authors of this manuscript.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.

Funding/Support: This study was supported by a Direct Grant for Research from the Chinese University of Hong Kong [Ref. No. 2041773].


Chest. 2013;143(3):729-735. doi:10.1378/chest.12-1224
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Background:  The objective of this study was to examine the natural history of childhood primary snoring (PS) and to identify predictive clinical symptoms and risk factors associated with PS progression to obstructive sleep apnea (OSA).

Methods:  Children aged 6 to 13 years old who received a diagnosis of PS in our previous community-based OSA prevalence study were invited to undergo repeat polysomnography (PSG) at 4-year follow-up. Subjects with an obstructive apnea hypopnea index (OAHI) ≥ 1 were classified as having OSA at follow-up.

Results:  Seventy children (60% boys) with a mean age of 14.7 ± 1.8 years were analyzed in this follow-up study. The mean duration of follow-up was 4.6 ± 0.6 years. At follow-up, 26 subjects (37.1%) progressed to OSA, of whom five (7.1%) had moderate to severe disease (OAHI ≥ 5). Twenty-two (31.4%) remained at PS, and 18 (25.7%) had complete resolution of their snoring with normal PSG. Persistent snoring had a positive predictive value of 47.7% and a negative predictive value of 86.4% for progression from PS to OSA. Multivariate logistic regression analysis showed that persistent overweight/obesity was a significant risk factor for the development of OSA at follow-up, with an OR of 7.95 (95% CI, 1.43-44.09).

Conclusions:  More than one-third of school-aged children with PS progressed to OSA over a 4-year period, although only 7.1% developed moderate to severe disease. Weight control may be an important component in the management of PS because obesity was found to be a significant risk factor for PS progression.

Figures in this Article

Snoring is a common symptom of pediatric sleep-disordered breathing (SDB), and the reported prevalence of habitual snoring ranges from 4.0% to 34.5%.14 SDB includes a spectrum of diseases with severity ranging from primary snoring (PS), to upper airways resistance syndrome, to obstructive sleep apnea (OSA).5,6 In contrast to OSA, PS, which is defined as snoring without apnea, frequent arousals, or gas exchange abnormalities,7 has been positioned at the milder end of the SDB severity continuum,8 and treatment is usually not prescribed.9

Nevertheless, whether deferment of treatment of PS is safe has recently led to more research. Kwok et al10 found that children with PS had increased casual daytime BP and reduced arterial distensibility. Our research group further demonstrated that nighttime BP was also elevated in children with PS.11 A more recent study found that PS was a risk factor for hyperactive and inattentive behavior and poor school performance in children.12 Accumulating evidence suggests PS may be associated with a variety of clinical sequelae, and, therefore, it should no longer be considered as completely benign.13

Another important issue that relates to whether PS, if left untreated, progresses to OSA, persists, or resolves over time has been poorly investigated. To our knowledge, only three research studies that examined the natural history of PS in children have been published. The three studies repeated polysomnography (PSG) in cohorts of 20, nine, and 31 children with PS over a 2-year, 3-year, and 6-month period, respectively. All three studies concluded that PS in children generally did not evolve to OSA over time.1416 These studies, however, had small sample sizes and consisted of hospital-based subjects. In this study, we aimed to determine (1) the natural history of PS in school-aged children recruited from the community over a 4-year period and (2) the clinical symptoms and risk factors predictive of PS progression to OSA.

Subjects

This was a prospective study of a cohort established between 2003 and 2005 for a childhood OSA epidemiologic study.17 Children aged 6 to 13 years old from 13 primary schools were randomly recruited. A total of 619 subjects underwent PSG, and 161 were defined as having PS (see later discussion in the “Polysomnography” section for definition). For this follow-up study, as a result of limited resources, only the first 99 consecutive subjects with PS were invited to undergo repeat assessment. Subjects were excluded from the study if they had cardiovascular, renal, or neuromuscular diseases; chromosomal abnormalities; or acute illness within 2 weeks of PSG; or if they had undergone upper airway surgery or had started on CPAP treatment during the follow-up period. Written informed consent and assent were obtained from the parents and subjects, respectively. The study was approved by the Clinical Research Ethics Committee of the Chinese University of Hong Kong (CRE_2007.363).

Sleep Symptom Questionnaire

A validated sleep symptom questionnaire18 was completed by parents of recruited subjects at baseline and follow-up, and the following information was extracted: (1) snoring frequency and other sleep-related symptoms rated on a 6-point scale (0 = never, 1 = less than 1 night per month, 2 = 1 to 2 nights per month, 3 = 1 to 2 nights per week, 4 = 3 nights or more per week, 5 = unclear), snoring and other OSA-related symptoms were defined as present if their frequency scored 2 to 4; (2) clinical features: history of allergic rhinitis and asthma; and (3) socioeconomic and environmental factors. We defined “persistent” as having a positive history at both time points.

Anthropometry Assessment

The weight, height, and Tanner stage of all subjects were assessed on the day of PSG. BMI was calculated as weight/height2 (kg/m2). Weight, height, and BMI were converted to z scores appropriate for age and sex, according to local reference.19 Overweight and obese children were defined as those having a BMI z score ≥ 1.036 and 1.645, corresponding to the 85th and 95th percentile, respectively. We defined “persistent overweight/obesity” as being overweight or obese at both baseline and follow-up. Pubertal stage was evaluated using a self-assessment questionnaire to categorize Tanner stages.20 Prepubertal was defined as Tanner stage 1, and pubertal was defined as Tanner stage 2 or greater.

Tonsil and Adenoid Size Assessment

The examination was carried out in the morning after overnight PSG by an otorhinolaryngologist. The tonsils and adenoids were evaluated for size by a 4-mm rigid rhinoscope (Storz endoscopy) and a flexible laryngoscope (P4, Olympus), respectively. The sizes of tonsils and adenoids were reported as percentages of the oropharyngeal and nasopharyngeal airways, respectively. A large tonsil or adenoid was defined as the soft tissue occupying ≥ 50% of the corresponding airway. Tonsils and adenoids were further classified as “persistently large” if they were large at both time points.

Polysomnography

All recruited children underwent initial and follow-up standard overnight PSG at a dedicated sleep laboratory with CNS 1000P polygraph (CNS, Inc). In brief, the central and occipital EEG, bilateral electrooculogram, submental electromyogram, bilateral leg electromyogram, and ECG were recorded. The positions of the subject, respiratory airflow (nasal cannula connected to pressure transducer), respiratory efforts (strain gauge), and arterial oxyhemoglobin saturation (by Ohmeda 3700 pulse oximeter) were measured. All data were scored by experienced PSG technologists. At baseline, the standard criteria described in our previous publication were used for scoring,21,22 whereas at follow-up, the new American Academy of Sleep Medicine (AASM) 2007 pediatric PSG scoring criteria were used.23 Therefore, all the baseline data of subjects with PS who participated in our follow-up study were rescored using AASM criteria. Those who were not classified as having PS by the new criteria were excluded.

The obstructive apnea hypopnea index (OAHI) was defined as the total number of obstructive apneic and hypopneic episodes per hour of sleep. The oxygen desaturation index was defined as the total number of dips in arterial oxygen saturation > 3% per hour of sleep. The oxygen saturation nadir (SpO2 nadir) was also noted. The arousal index was defined as the total number of arousals per hour of sleep.

Children who snored were given a diagnosis of PS if their OAHI was < 1 and SpO2 nadir was ≥ 90%. At follow-up, children were given a diagnosis of OSA if their OAHI was ≥ 1. Normal subjects were defined as nonsnorers with an OAHI < 1 and SpO2 nadir ≥ 90%.

Statistical Analysis

Student t tests, Mann-Whitney U tests, and χ2 tests for parametric, nonparametric, and categorical data, respectively, were used to detect difference between subjects who participated in this study and those who did not. Paired t tests, Wilcoxon signed rank tests, and McNemar tests for parametric, nonparametric, and categorical data, respectively, were used to examine intragroup differences between baseline and follow-up. Sensitivity, specificity, positive predictive value, negative predictive value, positive likelihood ratio, and negative likelihood ratio, together with their 95% CIs of OSA-related symptoms, were calculated using an online software (http://vassarstats.net/clin1.html). Binary logistic regression analyses were performed separately to investigate the factors associated with the progression of PS to OSA and the resolution of PS to normal at follow-up. All statistical analyses were performed using SPSS 16.0 (IBM), and a P value < .05 was considered statistically significant.

Of the 99 subjects invited, we failed to contact six and 18 refused to participate. One case subject who had received a tonsillectomy for recurrent tonsillitis during the follow-up period was excluded. Therefore, 74 subjects with PS participated in this follow-up study. There were no significant differences in demographic, clinical, environmental, socioeconomic, or polysomnographic characteristics between the 74 who participated and the 87 who did not (Table 1). Four participants had an OAHI ≥ 1 at baseline using AASM 2007 criteria during rescoring, so a total of 70 subjects were included in the final analysis. The mean time of reevaluation was 4.6 ± 0.6 years (range, 3.4-6.2 years) after the initial assessment.

Table Graphic Jump Location
Table 1 —Characteristics of Children With PS Who Did and Did Not Participate in the Follow-up Study

Data are presented as No. (%) unless indicated otherwise. HK = Hong Kong; IQR = interquartile range; OAHI = obstructive apnea hypopnea index; PS = primary snoring; SpO2 nadir = oxygen saturation nadir.

Subjects’ Characteristics at Baseline and Follow-up

Changes in anthropometric and PSG parameters for the whole group over the follow-up period are shown in Table 2. As expected, subjects showed a significant increase in weight and height; however, their average BMI z scores remained unchanged. The proportion of pubertal children increased from 12.9% to 100%. Only six subjects had large tonsils at baseline, of whom three had persistently large tonsils at follow-up. Three subjects had large adenoids at baseline but none at follow-up. None of the subjects had new onset of large tonsils or adenoids at follow-up. The OAHI, arousal index, and oxygen desaturation index increased, whereas the SpO2 nadir decreased significantly over the follow-up period (Fig 1, Table 2).

Figure Jump LinkFigure 1. Changes in subject measurements over the follow-up period. A, Obstructive apnea hypopnea index. B, SpO2 nadir. C, Arousal index. D, Oxygen desaturation index. SpO2 nadir = oxygen saturation nadir.Grahic Jump Location
Table Graphic Jump Location
Table 2 —Anthropometric and Polysomnographic Data of the Subjects (N = 70) at Baseline and Follow-up

Data are presented as mean (SD) unless indicated otherwise. ArI = arousal index; ODI = oxygen desaturation index; REM = rapid eye movement; SWS = slow-wave sleep; TST = total sleep time. See Table 1 legend for expansion of other abbreviations.

Twenty-six of the 70 subjects (37.1%) developed OSA at follow-up. Their median OAHI was 2.05 (range, 1.00-13.01), and five subjects (7.1%) had an OAHI ≥ 5. Among the remaining subjects without OSA at follow-up, 22 (31.4%) remained as PS and 18 (25.7%) became normal. Four subjects were unclassified at follow-up, of whom two had an OAHI < 1 but unclear snoring status and two had an OAHI < 1 but a SpO2 nadir < 90%.

Predictive Clinical Symptoms and Risk Factors for PS Progression to OSA

Among the OSA-related clinical symptoms, only persistent snoring was significantly different between those who did and did not develop OSA at follow-up (P = .007). Persistent snoring had a relatively high sensitivity (87.5%; 95% CI, 66.5%-96.7%) and negative predictive value (86.4%; 95% CI, 64.0%-96.4%) despite poor specificity (45.2%; 95% CI, 30.2%-61.2%) and positive predictive value (47.7%; 95% CI, 32.7%-63.1%) for the development of OSA. The positive likelihood ratio and negative likelihood ratio of persistent snoring were 1.60 (95% CI, 1.17-2.19) and 0.28 (95% CI, 0.09-0.84), respectively, for the development of OSA.

We analyzed the effects of several potential factors in predicting progression, persistence, or resolution of PS using logistic regression models (Table 3). In identifying the risk factors for worsening of PS, the univariate analysis showed that only the presence of persistent overweight/obesity was significantly associated with progression to OSA, with an OR of 7.33 (95% CI, 1.41-38.13). In a multivariate model adjusted for baseline age, sex, persistently large tonsils, and persistent snoring, the presence of persistent overweight/obesity remained the only significant predictor, with an OR of 7.95 (95% CI, 1.43-44.09). In contrast, no factors were found to be significantly associated with remission of PS.

Table Graphic Jump Location
Table 3 —Logistic Regression Analysis Assessing the Potential Factors Associated With the Worsening or Remission of PS

OSA = obstructive sleep apnea. See Table 1 legend for expansion of other abbreviations.

a 

Adjusted for baseline age, sex, persistently large tonsils, and persistent snoring.

b 

Adjusted for baseline age, sex, and persistently large tonsils.

In this community-based follow-up study of children with PS, we demonstrated that more than one-third of the subjects progressed to OSA over a period of 4 years. Persistent snoring had a relatively high negative predictive value for PS progression. Persistent overweight/obesity placed children with PS at an increased risk of such progression. To our knowledge, this study on the natural history of PS in children is the first to report a significant proportion of subjects with disease progression to OSA and its associated risk factors.

Studies examining the natural history of PS in both adults and children are scarce. A comparison between our study and the other three published pediatric studies is shown in Table 4. None of the previous studies found significant changes in respiratory parameters for the group as a whole, and the proportion of subjects who progressed to OSA was much lower than in our study.1416 One possible explanation for this discrepancy is our longer follow-up period, which would allow subjects greater exposure time to the risk factor(s) leading to disease progression. One such risk factor was persistent overweight/obesity, which is understandable because obesity is a well-established risk factor for OSA.17,24 Our current study provided robust evidence that obesity is a significant risk factor in causing disease progression along the SDB severity spectrum in children. Therefore, weight reduction may play an important role in preventing PS from progressing to OSA for overweight/obese children. However, in our study cohort the overall magnitude of change in BMI z score was only moderate, and we were unable to demonstrate a significant association between change in BMI z score and progression of PS. Further intervention to verify this hypothesis is needed.

Table Graphic Jump Location
Table 4 —Comparison of Our Findings and Previous Studies on Natural History of PS in Children

NA = not available; PSG = polysomnography. See Table 1 and 3 legends for expansion of other abbreviations.

a 

Change in BMI.

b 

Thirteen subjects completed sleep questionnaires.

c 

Thirty-seven subjects (31 primary snorers and six children with mild OSA) completed sleep questionnaires.

The age range in our study was older than those of the other series. At follow-up, all of the subjects had reached puberty. However, we failed to find a significant effect of puberty on PS progression. Previous studies showed that the apnea hypopnea index had no correlation with Tanner stage in healthy adolescents.25 It has also been suggested that changes in sex hormones were not a primary modulator of upper airways function during transition from childhood to adulthood.26 Thus, the role of puberty in SDB remains undefined at present. On a similar note, we failed to identify sex as a significant risk factor for PS progression in the current study.

A discrepancy also exists in the percentage of resolved PS across the four studies (Table 4), likely a result of different definitions used for PS resolution. All three published studies used only decreased questionnaire-based symptom scores to define resolution of PS. We, however, classified resolution of PS as an absence of snoring together with normal PSG findings. Adenotonsillar hypertrophy was not found to be associated with PS progression in this study. It may be because the mean age of our cohort at baseline and at follow-up were both beyond the peak age of lymphoid hypertrophy.27 However, these data were not fully analyzed in the previous studies, which included younger participants (Table 4).

In school-aged children, PS does not necessarily remain stable, especially in those who remain overweight or obese. Moreover, the presence of persistent snoring can be used as a guide for disease progression. Persistent snoring has a relatively high negative predictive value for the development of OSA, meaning that if a child with PS does not continue to snore it is less likely that he/she will develop OSA. Thus, a physician could give priority for repeat assessment to children with PS who remain overweight or obese and/or to those with persistent snoring.

This study had a few limitations. Firstly, esophageal pressure monitoring was not used; thus, cases with upper airways resistance syndrome would have been missed. Nevertheless, nasal pressure was monitored in our study, which made up to some extent for this potential source of error. Secondly, other potential factors associated with the progression or resolution of PS, such as change in craniofacial structure or fat deposition in the upper airways, were not assessed in this study.

In summary, more than one-third of children with PS progressed over a 4-year period to the development of OSA, and persistent overweight/obesity was a significant risk factor. Therefore, in the management of school-aged children with PS, greater attention should be paid to weight control. Because accumulating evidence suggests PS is also associated with important sequelae, further studies should examine the potential beneficial effects of intervention for this common pediatric problem.

Author contributions: Dr Li is the guarantor of the manuscript and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Dr Li: contributed to the project planning, recruitment of subjects, revision of the article, and approval of the final manuscript.

Ms Zhu: contributed to the data analysis, revision of the article, and approval of the final manuscript.

Mr Au: contributed to the performance and scoring of the polysomnography, revision of the article, and approval of the final manuscript.

Dr Lee: contributed to the performance and assessment of the otorhinolaryngology, revision of the article, and approval of the final manuscript.

Mr Ho: contributed to the performance and scoring of the polysomnography, revision of the article, and approval of the final manuscript.

Dr Wing: contributed to the revision of the article and approval of the final manuscript.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: Unrestricted funding was provided by the CUHK Direct Grant for Research. The design, execution, data collection and analysis of the study were carried out solely by the research team without involvement of the funding body.

Other contributions: This work was performed at the Department of Pediatrics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong. We are grateful for the cooperation and participation of all the children and their parents.

AASM

American Academy of Sleep Medicine

OAHI

obstructive apnea hypopnea index

OSA

obstructive sleep apnea

PS

primary snoring

PSG

polysomnography

SDB

sleep-disordered breathing

SpO2 nadir

oxygen saturation nadir

Castronovo V, Zucconi M, Nosetti L, et al. Prevalence of habitual snoring and sleep-disordered breathing in preschool-aged children in an Italian community. J Pediatr. 2003;142(4):377-382. [CrossRef] [PubMed]
 
Li AM, Au CT, So HK, Lau J, Ng PC, Wing YK. Prevalence and risk factors of habitual snoring in primary school children. Chest. 2010;138(3):519-527. [CrossRef] [PubMed]
 
Piteo AM, Lushington K, Roberts RM, et al. Prevalence of snoring and associated factors in infancy. Sleep Med. 2011;12(8):787-792. [CrossRef] [PubMed]
 
Sogut A, Yilmaz O, Dinc G, Yuksel H. Prevalence of habitual snoring and symptoms of sleep-disordered breathing in adolescents. Int J Pediatr Otorhinolaryngol. 2009;73(12):1769-1773. [CrossRef] [PubMed]
 
Anstead M, Phillips B. The spectrum of sleep-disordered breathing. Respir Care Clin N Am. 1999;5(3):363-377. [PubMed]
 
Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med. 2001;164(1):16-30. [PubMed]
 
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Carroll JL. Sleep-related upper-airway obstruction in children and adolescents. Child Adolesc Psychiatr Clin N Am. 1996;5(3):617-647.
 
Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. American Academy of PediatricsSection on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. American Academy of Pediatrics. Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109(4):704-712. [CrossRef] [PubMed]
 
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Li AM, Au CT, Ho C, Fok TF, Wing YK. Blood pressure is elevated in children with primary snoring. J Pediatr. 2009;155(3):362-368. [CrossRef] [PubMed]
 
Brockmann PE, Urschitz MS, Schlaud M, Poets CF. Primary snoring in school children: prevalence and neurocognitive impairments. Sleep Breath. 2012;16(1):23-29. [CrossRef] [PubMed]
 
Loughlin GM. Primary snoring in children—no longer benign. J Pediatr. 2009;155(3):306-307. [CrossRef] [PubMed]
 
Marcus CL, Hamer A, Loughlin GM. Natural history of primary snoring in children. Pediatr Pulmonol. 1998;26(1):6-11. [CrossRef] [PubMed]
 
Nieminen P, Tolonen U, Löppönen H. Snoring and obstructive sleep apnea in children: a 6-month follow-up study. Arch Otolaryngol Head Neck Surg. 2000;126(4):481-486. [PubMed]
 
Topol HI, Brooks LJ. Follow-up of primary snoring in children. J Pediatr. 2001;138(2):291-293. [CrossRef] [PubMed]
 
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Redline S, Tishler PV, Schluchter M, Aylor J, Clark K, Graham G. Risk factors for sleep-disordered breathing in children. Associations with obesity, race, and respiratory problems. Am J Respir Crit Care Med. 1999;159(5 pt 1):1527-1532. [PubMed]
 
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Figures

Figure Jump LinkFigure 1. Changes in subject measurements over the follow-up period. A, Obstructive apnea hypopnea index. B, SpO2 nadir. C, Arousal index. D, Oxygen desaturation index. SpO2 nadir = oxygen saturation nadir.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 —Characteristics of Children With PS Who Did and Did Not Participate in the Follow-up Study

Data are presented as No. (%) unless indicated otherwise. HK = Hong Kong; IQR = interquartile range; OAHI = obstructive apnea hypopnea index; PS = primary snoring; SpO2 nadir = oxygen saturation nadir.

Table Graphic Jump Location
Table 2 —Anthropometric and Polysomnographic Data of the Subjects (N = 70) at Baseline and Follow-up

Data are presented as mean (SD) unless indicated otherwise. ArI = arousal index; ODI = oxygen desaturation index; REM = rapid eye movement; SWS = slow-wave sleep; TST = total sleep time. See Table 1 legend for expansion of other abbreviations.

Table Graphic Jump Location
Table 3 —Logistic Regression Analysis Assessing the Potential Factors Associated With the Worsening or Remission of PS

OSA = obstructive sleep apnea. See Table 1 legend for expansion of other abbreviations.

a 

Adjusted for baseline age, sex, persistently large tonsils, and persistent snoring.

b 

Adjusted for baseline age, sex, and persistently large tonsils.

Table Graphic Jump Location
Table 4 —Comparison of Our Findings and Previous Studies on Natural History of PS in Children

NA = not available; PSG = polysomnography. See Table 1 and 3 legends for expansion of other abbreviations.

a 

Change in BMI.

b 

Thirteen subjects completed sleep questionnaires.

c 

Thirty-seven subjects (31 primary snorers and six children with mild OSA) completed sleep questionnaires.

References

Castronovo V, Zucconi M, Nosetti L, et al. Prevalence of habitual snoring and sleep-disordered breathing in preschool-aged children in an Italian community. J Pediatr. 2003;142(4):377-382. [CrossRef] [PubMed]
 
Li AM, Au CT, So HK, Lau J, Ng PC, Wing YK. Prevalence and risk factors of habitual snoring in primary school children. Chest. 2010;138(3):519-527. [CrossRef] [PubMed]
 
Piteo AM, Lushington K, Roberts RM, et al. Prevalence of snoring and associated factors in infancy. Sleep Med. 2011;12(8):787-792. [CrossRef] [PubMed]
 
Sogut A, Yilmaz O, Dinc G, Yuksel H. Prevalence of habitual snoring and symptoms of sleep-disordered breathing in adolescents. Int J Pediatr Otorhinolaryngol. 2009;73(12):1769-1773. [CrossRef] [PubMed]
 
Anstead M, Phillips B. The spectrum of sleep-disordered breathing. Respir Care Clin N Am. 1999;5(3):363-377. [PubMed]
 
Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med. 2001;164(1):16-30. [PubMed]
 
American Sleep Disorders AssociationAmerican Sleep Disorders Association. International Classification of Sleep Disorders, Revised: Diagnostic and Coding Manual. Rochester, MN: American Sleep Disorders Association; 1997:195-197.
 
Carroll JL. Sleep-related upper-airway obstruction in children and adolescents. Child Adolesc Psychiatr Clin N Am. 1996;5(3):617-647.
 
Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. American Academy of PediatricsSection on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. American Academy of Pediatrics. Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109(4):704-712. [CrossRef] [PubMed]
 
Kwok KL, Ng DK, Cheung YF. BP and arterial distensibility in children with primary snoring. Chest. 2003;123(5):1561-1566. [CrossRef] [PubMed]
 
Li AM, Au CT, Ho C, Fok TF, Wing YK. Blood pressure is elevated in children with primary snoring. J Pediatr. 2009;155(3):362-368. [CrossRef] [PubMed]
 
Brockmann PE, Urschitz MS, Schlaud M, Poets CF. Primary snoring in school children: prevalence and neurocognitive impairments. Sleep Breath. 2012;16(1):23-29. [CrossRef] [PubMed]
 
Loughlin GM. Primary snoring in children—no longer benign. J Pediatr. 2009;155(3):306-307. [CrossRef] [PubMed]
 
Marcus CL, Hamer A, Loughlin GM. Natural history of primary snoring in children. Pediatr Pulmonol. 1998;26(1):6-11. [CrossRef] [PubMed]
 
Nieminen P, Tolonen U, Löppönen H. Snoring and obstructive sleep apnea in children: a 6-month follow-up study. Arch Otolaryngol Head Neck Surg. 2000;126(4):481-486. [PubMed]
 
Topol HI, Brooks LJ. Follow-up of primary snoring in children. J Pediatr. 2001;138(2):291-293. [CrossRef] [PubMed]
 
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