Abstract
Background
Adenotonsillar hypertrophy (ATH) may influence iron homeostasis through low-grade inflammation and upper airway obstruction, but findings in children remain inconsistent. This study aimed to compare hematologic, iron-related, and inflammatory parameters in school-aged children with and without endoscopically confirmed ATH.
Methods
This controlled cross-sectional study included 300 children aged 6–12 years (150 with ATH and 150 controls). Hemoglobin, serum iron, ferritin, mean corpuscular volume (MCV), C-reactive protein (CRP), and hepcidin were measured. Iron deficiency and anemia were defined according to World Health Organization criteria. Continuous variables were compared using parametric or nonparametric tests as appropriate, and categorical variables were analyzed using Pearson’s chi-square test.
Results
No statistically significant between-group differences were found in hematologic, iron-related, or inflammatory parameters. Iron deficiency was identified in 30% of children with ATH and 24% of controls (p = 0.24), whereas iron-deficiency anemia was present in 10% and 8%, respectively (p = 0.55). CRP and hepcidin levels were also comparable between groups.
Conclusion
In this outpatient cohort, ATH was not associated with significant differences in routine iron indices, CRP, or hepcidin. These findings do not support routine iron evaluation solely on the basis of ATH, although targeted assessment may be considered in children with relevant clinical findings.
Keywords: Adenotonsillar hypertrophy, Iron status, Hepcidin, C-reactive protein, Children
Introduction
Adenotonsillar hypertrophy (ATH) is one of the most common causes of upper airway obstruction in childhood and is frequently accompanied by mouth breathing, restless or fragmented sleep, morning fatigue, and daytime attention difficulties consistent with sleep-disordered breathing (SDB) [1, 2]. In clinical practice, these symptoms often vary considerably between children, even when the degree of adenotonsillar enlargement appears similar. This pattern suggests that the impact of ATH may not be limited to mechanical narrowing of the nasopharyngeal airway and that broader physiologic consequences may contribute to impaired sleep quality, behavior, and daytime functioning.
Among the systemic pathways that may be affected, iron homeostasis has received increasing attention. Several clinical studies have reported a higher prevalence of iron deficiency in children with ATH or SDB, and some have described improvement in hematologic or iron-related parameters after adenotonsillectomy, suggesting that these changes may be reversible in selected patients [3–6]. However, other studies have shown only modest or statistically non-significant differences, indicating that iron-related alterations may not occur uniformly across all children with ATH [7–9]. This issue remains clinically relevant because iron plays an essential role in mitochondrial energy production, neurodevelopment, immune function, and cognitive performance; therefore, even mild disturbances, including those that remain within conventional reference ranges, may still have clinical importance in school-aged children [10–13].
One possible biological link between ATH and altered iron handling involves the combined effects of upper airway obstruction, intermittent hypoxia, and low-grade inflammation. In inflammatory states, particularly through interleukin-6 signaling, hepatic hepcidin production may increase. Hepcidin is the principal regulator of systemic iron balance; it binds to ferroportin, the major cellular iron exporter, leading to ferroportin internalization and degradation. As a result, intestinal iron absorption decreases and iron becomes sequestered within macrophages and hepatocytes [14–16]. In contrast, hepcidin expression is suppressed by iron deficiency, hypoxia, and increased erythropoietic activity [15, 16]. Through these mechanisms, inflammation may produce a pattern of functional iron restriction, in which iron stores appear relatively preserved while circulating bioavailable iron is reduced. Interpretation of iron status can therefore be challenging, because ferritin also behaves as an acute-phase reactant and may remain normal or elevated despite altered iron availability [15, 17, 18].
Despite growing interest in this topic, pediatric evidence remains incomplete. Previous studies have often included small cohorts, used heterogeneous diagnostic definitions, provided limited severity phenotyping and outcome assessment, or evaluated iron status without incorporating inflammatory markers such as C-reactive protein (CRP) and hepcidin [14, 17–20]. For conceptual and operational clarity, iron deficiency was defined in this study as a serum ferritin level < 15 ng/mL. Anemia was defined according to World Health Organization criteria as hemoglobin < 11.5 g/dL for children aged 5–11 years and < 12.0 g/dL for those aged 12 years. Iron-deficiency anemia was defined as the coexistence of anemia and ferritin < 15 ng/mL [21]. In this context, it remains uncertain whether children with endoscopically confirmed adenotonsillar hypertrophy (ATH) differ from controls in routine hematologic and iron-related indices, and whether any such differences are accompanied by changes in CRP and hepcidin.
Accordingly, in this controlled cross-sectional study, we compared hematologic, iron-related, and inflammatory parameters in school-aged children with and without endoscopically confirmed ATH. We evaluated CRP and hepcidin as exploratory markers potentially relevant to iron handling rather than as indicators of a separately defined subclinical condition. Our aim was to determine whether ATH is associated with differences in routine iron indices, the prevalence of iron deficiency and iron-deficiency anemia, and levels of CRP and hepcidin when compared with controls.
Materials and methods
This controlled cross-sectional study was conducted in the Pediatric and Otorhinolaryngology outpatient clinics between October 2025 and January 2026. School-aged children who were evaluated during routine outpatient visits were screened consecutively for eligibility. Participants were assigned to either the adenotonsillar hypertrophy (ATH) group or the control group according to clinical assessment and endoscopic findings. The study protocol was approved by the local ethics committee before enrolment (Decision No. 2025 − 105). Written informed consent was obtained from the parents or legal guardians of all participants, and all procedures were carried out in accordance with the Declaration of Helsinki.
An a priori sample size analysis was performed using G*Power (version 3.1.7). Based on a two-sided alpha of 0.05, 80% power, and a moderate effect size, the minimum required sample size was 90 participants. To increase precision, 300 children were ultimately included, with 150 in the ATH group and 150 in the control group.
Children aged 6–12 years were eligible for inclusion. Before enrolment, all participants underwent both pediatric and otorhinolaryngologic evaluation. The ATH group consisted of children with endoscopically confirmed adenotonsillar enlargement causing significant upper airway obstruction, whereas the control group consisted of children without clinical findings suggestive of persistent upper airway obstruction and without endoscopic evidence of significant adenotonsillar obstruction. Children were excluded if they had a chronic systemic disease, a known hematologic disorder, a history of blood transfusion, craniofacial malformation, asthma, allergic rhinitis or other allergic airway disease, nasal septal deviation, active viral or bacterial infection, or any other condition that could affect iron metabolism.
Adenoidal hypertrophy was assessed by flexible fiberoptic nasoendoscopy (Karl Storz, Tuttlingen, Germany) and graded according to the percentage of choanal obstruction as follows: grade 1, < 25%; grade 2, 25%–50%; grade 3, 51%–75%; and grade 4, 76%–100% [22]. Palatine tonsil size was graded by oropharyngeal examination using the Brodsky classification (grades 0–4) [23]. Children with tonsil grade 3–4 and/or adenoid grade 3–4, corresponding to at least 50% upper airway obstruction, were included in the ATH group. Children with tonsil grades 0–2 and adenoidal obstruction < 50% were included in the control group.
Venous blood samples were obtained after an overnight fast of at least 8 h. Hematologic measurements included hemoglobin, hematocrit, mean corpuscular volume (MCV), and red cell distribution width (RDW). Iron-related measurements included serum iron, ferritin, unsaturated iron-binding capacity, and total iron-binding capacity. Transferrin saturation was calculated for each participant as serum iron / total iron-binding capacity × 100. C-reactive protein (CRP) and serum hepcidin were also measured to evaluate inflammatory activity and possible inflammation-related changes in iron handling. CRP was measured using the Roche Cobas c501 analyzer (Roche Diagnostics, Mannheim, Germany), with a measurement range of 0.1–10 mg/L. CRP was analyzed as a continuous variable for between-group comparison; therefore, no prespecified diagnostic cut-off value was applied in the primary analysis. Serum hepcidin was measured using a commercial Human Hepcidin ELISA Kit (Elabscience Biotechnology Inc., Wuhan, China), with an analytical range of 2.5–50 ng/mL and intra-assay/inter-assay coefficients of variation of < 8% and < 10%, respectively. Hepcidin was also treated as an exploratory continuous biomarker rather than a dichotomized diagnostic variable.
For categorical analyses, participants were classified according to the predefined diagnostic criteria for iron deficiency, anemia, and iron-deficiency anemia described in the Introduction.
Statistical analysis
Statistical analyses were performed using SPSS software (version 26; IBM Corp., Armonk, NY, USA). Normally distributed continuous variables were summarized as mean ± standard deviation, whereas non-normally distributed variables were summarized as median (95% confidence interval). Categorical variables were expressed as number and percentage. Normality was assessed using the Shapiro–Wilk test. Between-group comparisons were performed using the independent-samples t test for normally distributed variables and the Mann–Whitney U test for non-normally distributed variables. Categorical variables, including iron deficiency and iron-deficiency anemia, were compared using Pearson’s chi-square test. Correlations between hepcidin and iron-related parameters within the ATH group were assessed using Spearman’s rank correlation analysis. A two-tailed p value < 0.05 was considered statistically significant.
Results
A total of 300 children were included in the analysis, comprising 150 children in the adenotonsillar hypertrophy (ATH) group and 150 in the control group. The two groups were comparable in terms of age and sex distribution. The main hematologic, iron-related, inflammatory, and categorical findings are presented in Table 1.
Table 1.
Hematologic, iron-related, inflammatory, and categorical findings in children with and without adenotonsillar hypertrophy (n = 300)
| Parameter | Reference range / definition | Control group (n = 150) |
ATH group (n = 150) |
p-value |
|---|---|---|---|---|
| Hemoglobin (g/dL) | 11.5–15.5 | 12.6 ± 1.2 | 12.4 ± 1.3 | 0.17 |
| Hematocrit (%) | 35.0–45.0 | 38.1 ± 2.8 | 37.9 ± 3.0 | 0.55 |
| Serum iron (µg/dL) | 50–120 | 74.8 ± 24.3 | 72.5 ± 25.1 | 0.42 |
| Ferritin (ng/mL), median (95% CI) |
Iron deficiency cut-off: < 15 ng/mL |
23.9 (22.3–25.5) | 22.4 (20.9–23.9) | 0.20 |
| MCV (fL) | 77–95 | 81.7 ± 5.5 | 80.9 ± 6.0 | 0.23 |
| RDW (%) | 11.0–14.5 | 13.2 ± 1.9 | 13.5 ± 1.9 | 0.17 |
| Unsaturated iron-binding capacity (µg/dL) | 111–343 | 319 ± 74 | 324 ± 63 | 0.53 |
| Total iron-binding capacity (µg/dL) | 250–400 | 379 ± 52 | 383 ± 54 | 0.51 |
| Transferrin saturation (%) | 15–50 | 19.7 ± 7.0 | 18.9 ± 7.1 | 0.33 |
| CRP (mg/L), median (95% CI) | < 5; analytical range: 0.1–10 |
0.93 (0.82–1.04) |
1.01 (0.86–1.16) |
0.46 |
| Hepcidin (ng/mL), median (95% CI) | Assay analytical range: 2.5–50 | 12.2 (11.3–13.1) | 11.8 (10.7–12.9) | 0.59 |
| Anemia, n (%) | WHO age-specific Hb cut-off: <11.5 g/dL for 5–11 years; <12.0 g/dL for 12 years | 15 (10.0) | 20 (13.3) | 0.37 |
| Iron deficiency, n (%) | Ferritin < 15 ng/mL | 36 (24.0) | 45 (30.0) | 0.24 |
| Iron-deficiency anemia, n (%) | Anemia plus ferritin < 15 ng/mL | 12 (8.0) | 15 (10.0) | 0.55 |
Values are presented as mean ± standard deviation (SD) for normally distributed variables, median (95% confidence interval [CI]) for non-normally distributed variables, or n (%) as appropriate. Reference ranges are provided according to commonly used pediatric laboratory intervals, diagnostic definitions applied in the present study, or assay-specific analytical ranges where applicable. Anemia was defined according to World Health Organization criteria as hemoglobin <11.5 g/dL for children aged 5–11 years and <12.0 g/dL for those aged 12 years. No universally accepted pediatric reference interval was applied for hepcidin; therefore, the assay analytical range is reported. Between-group comparisons were performed using the independent-samples t test or Mann–Whitney U test for continuous variables and Pearson’s chi-square test for categorical variables. Transferrin saturation was calculated as serum iron / total iron-binding capacity × 100. Statistical significance was defined as p < 0.05
Abbreviations: ATH adenotonsillar hypertrophy, MCV mean corpuscular volume, RDW red cell distribution width, UIBC unsaturated iron-binding capacity, TIBC total iron-binding capacity, CRP C-reactive protein, CI confidence interval.
No statistically significant between-group differences were observed in the routine hematologic, iron-related, or inflammatory parameters examined. Hemoglobin, hematocrit, serum iron, mean corpuscular volume, red cell distribution width, iron-binding capacity measures, transferrin saturation, ferritin, CRP, and hepcidin were all comparable between children with ATH and controls (all p > 0.05). The prevalence of anemia, iron deficiency, and iron-deficiency anemia was also similar between the two groups (13.3% vs. 10.0%, p = 0.37; 30.0% vs. 24.0%, p = 0.24; and 10.0% vs. 8.0%, p = 0.55, respectively).
Within the ATH group, correlations between serum hepcidin and iron-related parameters were weak and did not reach statistical significance (Table 2).
Table 2.
Correlation between serum hepcidin and iron-related parameters in the ATH group (n = 150)
| Parameter | Spearman’s ρ | p-value |
|---|---|---|
| Serum iron (µg/dL) | −0.12 | 0.14 |
| Ferritin (ng/mL) | −0.11 | 0.18 |
| Transferrin saturation (%) | −0.14 | 0.08 |
| Hemoglobin (g/dL) | −0.13 | 0.11 |
| MCV (fL) | −0.10 | 0.22 |
Correlations were assessed using Spearman’s rank correlation analysis. Correlation coefficients (ρ) and corresponding p-values are reported
Abbreviation: ATH adenotonsillar hypertrophy
Correlations were assessed using Spearman’s rank correlation analysis.
Overall, the results did not indicate a statistically significant difference between children with ATH and controls in routine hematologic indices, iron-related markers, CRP, or hepcidin.
Discussion
In this controlled cross-sectional study, we examined whether adenotonsillar hypertrophy (ATH), a common cause of upper airway obstruction in school-aged children, was associated with differences in hematologic, iron-related, and inflammatory markers when compared with a control group. Although iron plays an important role in energy metabolism, neurodevelopment, and immune function, the overall laboratory profile was similar in the two groups. Routine indices such as hemoglobin, serum iron, ferritin, mean corpuscular volume, and iron-binding parameters did not differ significantly, and the proportions of children with iron deficiency or iron-deficiency anemia were also comparable. Taken together, these findings suggest that, in this outpatient cohort, ATH alone was not associated with a distinct pattern of altered iron status.
The existing pediatric literature on this topic remains inconsistent. Some studies have reported a higher prevalence of iron deficiency in children with ATH or sleep-disordered breathing and have suggested improvement after adenotonsillectomy, raising the possibility that iron-related abnormalities may be reversible in selected clinical settings [3–6]. In contrast, other studies have found only small or statistically non-significant differences, suggesting that any disturbance in iron homeostasis may depend on factors beyond adenotonsillar size alone [7–9]. Our findings are more consistent with the latter group of studies and support the view that ATH is not uniformly accompanied by measurable iron-related impairment in all children.
A potential biological explanation for altered iron handling in children with upper airway obstruction involves the interaction between inflammation, hypoxia, and hepcidin regulation. Inflammatory signaling, particularly through interleukin-6, may increase hepatic hepcidin synthesis, whereas iron deficiency, hypoxia, and increased erythropoietic drive may suppress it.14–16 Because hepcidin reduces intestinal iron absorption and promotes iron sequestration within reticuloendothelial cells, it may contribute to a pattern of functional iron restriction even in the absence of overt iron depletion. Ferritin further complicates this interpretation because it also behaves as an acute-phase reactant [15, 17, 18]. On this basis, CRP and hepcidin were included in the present study to explore whether ATH might be associated with a low-grade inflammatory laboratory pattern affecting iron availability. However, neither marker differed significantly between groups, and correlations between hepcidin and iron-related variables within the ATH group were weak and non-significant. These findings do not support a prominent inflammation-related disturbance in iron handling in this study population.
Several factors may explain the absence of significant between-group differences. First, ATH is a clinically heterogeneous condition, and the systemic consequences of adenotonsillar enlargement may depend more on the severity and chronicity of airway obstruction than on anatomic findings alone. Second, iron status in childhood is influenced by multiple factors, including baseline iron stores, nutritional intake, growth rate, and intercurrent illness. As a result, any effect of ATH on iron metabolism may be modest and difficult to detect in an otherwise mixed outpatient population. Third, subgroup effects may have been diluted because objective sleep-based phenotyping was not available; children with more pronounced sleep-disordered breathing may differ biologically from those with anatomical enlargement alone.
The present study has several limitations that should be acknowledged. Its cross-sectional design does not allow conclusions regarding causality or temporal change. Laboratory measurements were obtained at a single time point, and no postoperative follow-up was available to assess whether iron-related indices changed after treatment of airway obstruction. Objective sleep evaluation, such as polysomnography, was not performed. Therefore, the relationship between iron-related markers and the severity of sleep-disordered breathing could not be examined directly. In addition, although children with asthma, allergic rhinitis or other allergic airway disease, nasal septal deviation, and active viral or bacterial infection were excluded at enrolment, several other potentially relevant clinical factors, including the burden of recurrent infections, dietary iron intake, snoring frequency, witnessed apnea, and feeding difficulties, were not systematically quantified. These factors may have influenced the laboratory findings and may partly explain the absence of a detectable between-group difference.
Despite these limitations, the study also has strengths. The sample size was relatively large, all children were assessed within the same clinical setting, and adenotonsillar status was defined using endoscopic and clinical grading rather than symptom history alone. In addition, the inclusion of CRP and hepcidin allowed the analysis to extend beyond routine hematologic testing and to explore a possible inflammation-related mechanism, even though no significant signal was identified.
From a clinical perspective, the present findings do not support routine measurement of iron parameters, CRP, or hepcidin solely on the basis of an ATH diagnosis in a general outpatient setting. A more selective approach appears more appropriate, particularly in children with persistent fatigue, reduced daytime functioning, growth concerns, or borderline hematologic findings. Future studies that incorporate objective sleep phenotyping, validated clinical assessment of obstruction severity, longitudinal follow-up, and more detailed evaluation of inflammatory, nutritional, and endocrine-metabolic factors may help identify whether a specific subgroup of children with ATH is more likely to show clinically meaningful alterations in iron homeostasis [19, 20, 24–26].
Conclusion
In this controlled cross-sectional study, children with adenotonsillar hypertrophy did not show significant differences from controls in routine hematologic indices, iron-related parameters, CRP, or hepcidin. These findings do not support routine iron-related evaluation solely on the basis of adenotonsillar hypertrophy in a general outpatient population. A more selective approach may be more appropriate in children with relevant clinical symptoms or borderline laboratory findings. Further studies incorporating objective sleep assessment and longitudinal follow-up are needed to clarify whether specific subgroups of children with adenotonsillar hypertrophy may show clinically meaningful alterations in iron homeostasis.
Acknowledgements
None.
Authors’ contributions
SK: Concept, design, materials, data collection, literature search, writing manuscript **.** NK: Concept, design, data collection, literature search, writing manuscript.
Funding
There is no funding/ financial support.
Data availability
The datasets used and/or analysed during the current study are not publicly available due to privacy and ethical restrictions related to patient-level clinical data but are available from the corresponding author upon reasonable request.
Declarations
Ethics approval and consent to participate
The authors assert that all procedures contributing to this work comply with the ethical standards of the relevant national and institutional guidelines on human experimentation and with the Helsinki Declaration of 1975, as revised in 2008.This study received ethical approval from the Scientific Research Ethics Committee of Kocaeli City Hospital, under decision number 2025 − 105.Written informed consent was obtained from the parents of all participants.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.Gipson K, Lu M, Kinane TB. Sleep-Disordered Breathing in Children. Pediatr Rev. 2019;40(1):3–13. 10.1542/pir.2018-0142. Erratum in: Pediatr Rev. 2019;40(5):261. doi: 10.1542/pir.405261. PMID: 30600274; PMCID: PMC6557418. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Capdevila OS, Kheirandish-Gozal L, Dayyat E et al. Pediatric obstructive sleep apnea: complications, management, and long-term outcomes. Proc Am Thorac Soc. 2008;Feb 15;5(2):274 – 82. 10.1513/pats.200708-138MG. PMID: 18250221; PMCID: PMC2645258. [DOI] [PMC free article] [PubMed]
- 3.Weng W, Tan R, Giblett N, et al. Iron deficiency found to be more prevalent in children with adenotonsillar hypertrophy. Aust J Otolaryngol. 2021;4:21. 10.21037/ajo-20-89. [Google Scholar]
- 4.Elverland HH, Aasand G, Miljeteig H, et al. Effects of tonsillectomy and adenoidectomy on hemoglobin and iron metabolism. Int J Pediatr Otorhinolaryngol. 2004;68(4):419–23. 10.1016/S0165-5876(03)00480-4. [DOI] [PubMed] [Google Scholar]
- 5.Akcan FA, Dündar Y, Bayram Akcan H, et al. Is anemia in children with sleep disordered breathing actually a consequence of chronic disease? Eur Res J. 2018;4(3):220–6. 10.18621/eurj.347720. [Google Scholar]
- 6.Reynolds Z, Hibbert N, Stevenson P, et al. The effect of iron deficiency on quality of life outcomes after surgery for obstructive sleep apnoea. J Paediatr Child Health. Oct; 2022;58(10):1816–23. 10.1111/jpc.16115 . Epub 2022 Jul 12. PMID: 35819302; PMCID: PMC9795986. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Busuttil A, Kerr AI, Logan RW. Iron deficiency in children undergoing adenoid-tonsillectomy. J Laryngol Otol. 1979;Jan;93(1):49–58. PMID: 429884. 10.1017/s0022215100086710. [DOI] [PubMed]
- 8.Çıkrıkcı S, Çelik AC, Çelikkiran İH, et al. Does adenoid hypertrophy affect hemoglobin and erythropoietin levels in children? Exp Appl Med Sci. 2024;5(1):10–9. 10.46871/eams.1433494. [Google Scholar]
- 9.Somuk BT, Yamanoğlu M, Demirtaş S. Evaluation of iron and zinc levels in recurrent tonsillitis and tonsillar hypertrophy. Am J Otolaryngol. 2016;37(2):116–9. 10.1016/j.amjoto.2015.11.005. [DOI] [PubMed] [Google Scholar]
- 10.Zimmermann MB, Hurrell RF. Nutritional iron deficiency. Lancet. 2007;Aug 11;370(9586):511 – 20. 10.1016/S0140-6736(07)61235-5. PMID: 17693180. [DOI] [PubMed]
- 11.Lozoff B, Beard J, Connor J, et al. Long-lasting neural and behavioral effects of iron deficiency in infancy. Nutr Rev. May; 2006;64(5 Pt 2):S34–43. 10.1301/nr.2006.may.s34-s43. discussion S72-91. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Halterman JS, Kaczorowski JM, Aligne CA et al. Iron deficiency and cognitive achievement among school-aged children and adolescents in the United States. Pediatrics. 2001;Jun;107(6):1381-6. PMID: 11389261 10.1542/peds.107.6.1381. [DOI] [PubMed]
- 13.Lozoff B, Smith JB, Kaciroti N, et al. Functional significance of early-life iron deficiency: outcomes at 25 years. J Pediatr. Nov; 2013;163(5):1260–6. 10.1016/j.jpeds.2013.05.015 . Epub 2013 Jul 1. PMID: 23827739; PMCID: PMC3795923. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Wang Y, Chen Y, Lin W et al. Inflammatory markers in children with obstructive sleep apnea syndrome. Front Pediatr. 2023;Apr 11;11:1134678. PMID: 37114011; PMCID: PMC10127118. 10.3389/fped.2023.1134678. [DOI] [PMC free article] [PubMed]
- 15.Ganz T. Hepcidin and iron regulation, 10 years later. Blood. 2011;Apr 28;117(17):4425-33. doi: 10.1182/blood-2011-01-258467. Epub 2011 Feb 23. PMID: 21346250; PMCID: PMC3099567. [DOI] [PMC free article] [PubMed]
- 16.Ganz T, Nemeth E. Iron homeostasis in host defence and inflammation. Nat Rev Immunol. Aug; 2015;15(8):500–10. 10.1038/nri3863 . Epub 2015 Jul 10. PMID: 26160612; PMCID: PMC4801113. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Seifen C, Pordzik J, Huppertz T et al. Serum Ferritin Levels in Severe Obstructive Sleep Apnea. Diagnostics (Basel). 2023;Mar 17;13(6):1154. PMID: 36980461; PMCID: PMC10047524 10.3390/diagnostics13061154. [DOI] [PMC free article] [PubMed]
- 18.Lee NH. Iron deficiency in children with a focus on inflammatory conditions. Clin Exp Pediatr. Jun; 2024;67(6):283–93. 10.3345/cep.2023.00521 . Epub 2024 May 21. PMID: 38772411; PMCID: PMC11150987. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Marcus CL, Brooks LJ, Draper KA, et al. American Academy of Pediatrics. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. Sep; 2012;130(3):e714–55. 10.1542/peds.2012-1672 . Epub 2012 Aug 27. PMID: 22926176. [DOI] [PubMed] [Google Scholar]
- 20.Marcus CL, Moore RH, Rosen CL, et al. Childhood Adenotonsillectomy Trial (CHAT). A randomized trial of adenotonsillectomy for childhood sleep apnea. N Engl J Med. Jun 2013;20(25):2366–76. 10.1056/NEJMoa1215881 . Epub 2013 May 21. PMID: 23692173; PMCID: PMC3756808. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.World Health Organization. Iron deficiency anaemia: assessment, prevention, and control. Geneva: WHO; 2001. [Google Scholar]
- 22.Cassano P, Gelardi M, Cassano M et al. Adenoid tissue rhinopharyngeal obstruction grading based on fiberendoscopic findings: a novel approach to therapeutic management. Int J Pediatr Otorhinolaryngol. 2003;67(12):1303-9. PMID: 14643473 10.1016/j.ijporl.2003.07.018. [DOI] [PubMed]
- 23.Brodsky L, Moore L, Stanievich JF. A comparison of tonsillar size and oropharyngeal dimensions in children with obstructive adenotonsillar hypertrophy. Int J Pediatr Otorhinolaryngol. 1987;Aug;13(2):149 – 56. 10.1016/0165-5876(87)90091-7. PMID: 3667094. [DOI] [PubMed]
- 24.Lin SY, Su YX, Wu YC, et al. Management of paediatric obstructive sleep apnoea: A systematic review and network meta-analysis. Int J Paediatr Dent. Mar; 2020;30(2):156–70. 10.1111/ipd.12593 . Epub 2019 Nov 22. PMID: 31680340. [DOI] [PubMed] [Google Scholar]
- 25.Keskin N, Keskin S. Association between adenotonsillar hypertrophy and leptin, ghrelin and IGF-1 levels in children. Auris Nasus Larynx. 2021;48:248–54. [DOI] [PubMed] [Google Scholar]
- 26.Bitar MA, Rahi A, Khalifeh M, et al. A suggested clinical score to predict the severity of adenoid obstruction in children. Eur Arch Otorhinolaryngol. Oct; 2006;263(10):924–8. 10.1007/s00405-006-0086-y . Epub 2006 Jun 24. PMID: 16799801. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets used and/or analysed during the current study are not publicly available due to privacy and ethical restrictions related to patient-level clinical data but are available from the corresponding author upon reasonable request.