Adenoid hypertrophy (AH) commonly leads to upper airway obstruction, obstructive sleep apnea and hypoxia in children [1] . Obstructive sleep apnea causes hypoxia, pulmonary hypertension and right ventricle (RV) dysfunction [2] . Obstructive sleep apnea exists in 1% - 3% of children and can occur at any age [3] . The adenoids, like all lymphoid tissue, enlarge when infected. Although lymphoid tissue does act to fight infection, sometimes bacteria and viruses can lodge within it and survive. Chronic infection, either viral or bacterial, can keep the pad of adenoids enlarged for years, even into adulthood. Some viruses, such as the Epstein-Barr Virus, can cause dramatic enlargement of lymphoid tissue. Primary or reactivation infections with Epstein Barr Virus, and certain other bacteria and viruses, can even cause enlargement of the adenoidal pad in an adult whose adenoids had previously become atrophied. Enlarged adenoids can become nearly the size of a ping pong ball and completely block airflow through the nasal passages. Even if enlarged adenoids are not substantial enough to physically block the back of the nose, they can obstruct airflow enough so that breathing through the nose requires an uncomfortable amount of work, and inhalation occurs instead through an open mouth. Adenoids can also obstruct the nasal airway enough to affect the voice without actually stopping nasal airflow altogether [4] .

Platelet size is correlated with platelet activation and large platelets have more hemostatic activation [5] . So mean platelet volume (MPV) may be used as a marker of platelet activation and may also be associated with atherosclerosis as a simple assessment tool [6] . MPV levels increase in some conditions such as hypertension, hypercholesterolemia, diabetes mellitus, acute myocardial infarction and acute ischemic stroke [7] . Varol et al. [8] suggested that MPV levels were higher in adult patients with severe obstructive sleep apnea than healthy patients. Sagit et al. [9] showed that patients with septal deviation had increased MPV levels. Onder et al. [10] revealed no significant relation between MPV levels and obstructive adenoid hypertrophy.

There are conflicting studies on MPV levels in patients with obstructive conditions. So we aimed to investigate the MPV levels in AH patients and the relationship between MPV levels and adenoid size in children.

The current study consisted of 95 patients presented to the pediatrics outpatient clinic of Bozok University Medical faculty with AH (45 male, 50 female; mean age: 6.47 years).

Children with nasal septal deviation, sinonasal infection, hematological disease, chronic diseases, and history of previous adenoidectomy were excluded from the study

Routine preoperative blood samples were drawn from the antecubital vein by careful vein puncture. Blood samples were collected in EDTA, and laboratory data were screened via a computerized database in the hospital. The reference values for MPV ranged between 5.0 and 15.0 f L.

Lateral cephalometric graphs were obtained from all patients to measure adenoid/nasopharynx (A/N) ratio. A/N ratio has been shown to have a good correlation with endoscopic examination findings [11] . A/N ratio was calculated as defined by Fujioka et al. [12] before. The distance between the outermost point of convexity of adenoid shadow and basiocciput was divided to the distance between sphenobasiocciput and posterior end of the hard palate.

The statistical analyses were carried out by Statistical Package for Social Sciences (SPSS) 18. Before performing the Student t test, the data was checked for normality of distribution by Kolmogorov-Smirnov test. Variables were expressed as mean ± SD. Comparisons of variables were performed using unpaired Student t test and Chi-square test. Bivariate associations of the variables were assessed using Pearson’s correlation coefficients and p value < 0.05 was considered indicate statistical significance.

The AH group consisted of 95 patients (50 females and 45 males) with a mean age of 6.47 years, and the control group had 99 patients (57 females and 42 males) with a mean age of 5.77 years. There were no significant differences between the study and control groups in terms of age and sex. All characteristics of the AH and control groups, including MPV, hemoglobin, WBC, MCV and MPV are listed in Table 1.

The mean MPV levels were 9.39 f L in patients with AH and 9.64 f L in the control group and there was no statistical differences (p = 0.156). The mean ANS level was 0.78 ± 0.065 in patients with AH.

There were no correlation between ANS and other parameters by Pearson correlation analysis.

Student’s t test, ^&Chi-square test, p level is significant at the <0.05 level. WBC: white blood cell, Hb: hemoglobin, MCV: mean corpuscular volume, MPV: mean platelet volume.

AH causes upper airway obstruction and leads to increased pulmonary hypertension and corpulmonale [13] and also upper airway resistance syndrome by increased upper airway resistance as a result of labored breathing [14] . It is shown that adenotonsillectomy decreases pulmonary arterial hypertension to normal values in children [15] . When sufficient airflow is not meet nasal way, mouth breathing begins and this causes turbulent airflow. The intraluminal air pressure cannot reach the appropriate level to keep the nasopharyngeal and orophayngeal structures open in the supine position; moreover, the bulk of the tongue is displaced backwards by the influence of gravity, obstructing the airway. Therefore, this chain of events results in alveolar hypoventilation, hypoxia, and hypercarbia during sleep [14] [16] .

If the children who had AH or tonsillar hypertrophy left untreated, they can experience abnormal orofacial anatomy, poor appetite, growth retardation, aggressive behavior, anxiety, impaired attention, depression, and somatization disorders over the long term [17] [18] .

Chronic alveolar hypoxia causes hypoxemic pulmonary vasoconstriction that leads to hypertension and RV heart failure [19] [20] . MPV level is showed to be higher in patients with pulmonary hypertension [21] . MPV shows platelet activity and large platelets are more active and have more prothrombotic potential [9] .

In current study we didn’t found any differences between AH and healthy controls in terms of MPV level and we didn’t detect any relationship between MPV values and adenoid size. One possible reason for this is that the study group included pediatric patients; chronic hypoxia exposure time is shorter in the pediatric population than in adult patients. MPV values in children may not be related to upper airway obstruction. Önder et al. [10] revealed that there was no significant relation between MPV levels and obstructive adenoid hypertrophy consisted with our results. Cevik et al. [22] found that MPV values were significantly lower in patients with nasal polyps than controls. Yılmaz et al. [23] been showed that adenotonsillary hypertrophy causes higher pulmonary artery pressure values and adenotonsillectomy is an effective therapeutic measure in such patients. Varol et al. [24] revealed that six months of CPAP therapy caused significant reductions in median MPV values in adult patients with severe OSA. Sagit et al. [9] found that septoplasty has a curative effect for hypercoagulopathy with reducing MPV values. Kucur et al. [25] found that MPV values were found to be higher in children with AH than controls and there was a significant reduction in MPV levels after adenoidectomy. They demonstrated that MPV levels may indicate the risk of cardiopulmonary diseases. Steiropoulos et al. [26] also reported that patients with chronic obstructive pulmonary disease had high MPV values. In contrast, Çevik et al. [27] suggested that MPV values in children with AH were significantly lower than those in control subjects. It has been suggested that chronic hypoxia causes catecholamine-dependent platelet activation and that this leads to changes in platelet shape with an increase in platelet swelling, leading to an increase in MPV and PDW [28] [29] . Tuncel et al. [30] found that there is no significant difference in MPV values between asthmatic children and control groups.

MPV values are in normal limits in children with AH and are not correlated with adenoid size.

Esra Akyüz Özkan, (2016) MPV Values in Children with Adenoid Hy-pertrophy and Correlation with Adenoid Size. Open Access Library Journal,03,1-5. doi: 10.4236/oalib.1102315