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Table of Contents
ORIGINAL ARTICLE
Year : 2019  |  Volume : 68  |  Issue : 3  |  Page : 310-316

Vitamin D level and mean platelet volume in patients with obstructive sleep apnea syndrome


1 Department of Chest, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Medical Biochemistry, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Department of Chest Department, Chest Hospital, Shebin El-Kom, Egypt

Date of Submission06-Jan-2019
Date of Acceptance31-Mar-2019
Date of Web Publication4-Sep-2019

Correspondence Address:
Hebatallah A Sharaf El-Din
Master of chest Diseases and Tuberculoses (MSC), Faculty of Medicine Menoufia University, Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejcdt.ejcdt_4_19

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  Abstract 


Objectives To assess the serum level of vitamin D and mean platelet volume (MPV) in patients with obstructive sleep apnea syndrome (OSAS) and whether their levels correlate with OSAS severity or not.
Background OSAS is a clinical disorder characterized by recurrent episodes of upper airway collapse during sleep. Studies show a link between low levels of vitamin D ‘25(OH) D’ and obstructive sleep apnea. Some studies showed that patients who have OSAS also have raised platelet aggregation and activation. MPV is considered an indicator of activation of platelet and its size. Limited studies have informed a relationship between MPV and sleep apnea.
Patients and methods A total of 65 patients with OSAS and 24 age-matched controls with completed Epworth sleepiness scale were included. OSAS diagnosis was based on polysomnography. Vitamin D was measured by ELISA, and MPV was measured by Sysmex xn-10 machine.
Results A prospective case–control study was done on 65 OSAS cases and 24 age-matched and sex-matched controls. Vitamin D level was significantly lower among OSAS cases than controls, with lowest 25(OH) D in severe OSAS cases, whereas MPV showed nonsignificant difference between them, and the higher MPV was among severe cases. There was a significant negative correlation between vitamin D level and neck circumference (NC), apnea–hypopnea index (AHI), and desaturation index. There was a significant positive correlation between MPV level and each of NC and AHI. NC was an independent predictor for both vitamin D and MPV levels. NC, AHI, and vitamin D level are the independent risk factors for obstructive sleep apnea, with odds ratios of 2.09 and 1.6, respectively.
Conclusion Patients with OSAS have decreased vitamin D level. Patients with severe OSAS have lower vitamin D level and higher MPV than other groups. Obesity may be the cause that explains this relation regarding high NC.

Keywords: apnea–hypopnea index, mean platelet volume and neck circumference, obstructive sleep apnea, vitamin D


How to cite this article:
Azab NY, El-Wahsh RA, El-Helbawy RH, El-Ghobashy YA, Sharaf El-Din HA. Vitamin D level and mean platelet volume in patients with obstructive sleep apnea syndrome. Egypt J Chest Dis Tuberc 2019;68:310-6

How to cite this URL:
Azab NY, El-Wahsh RA, El-Helbawy RH, El-Ghobashy YA, Sharaf El-Din HA. Vitamin D level and mean platelet volume in patients with obstructive sleep apnea syndrome. Egypt J Chest Dis Tuberc [serial online] 2019 [cited 2022 Jun 27];68:310-6. Available from: http://www.ejcdt.eg.net/text.asp?2019/68/3/310/266035




  Introduction Top


Obstructive sleep apnea syndrome (OSAS) is a disease in which there is narrowing of the upper airway, which interferes with ventilation during sleep, causing recurrent attacks of apnea and hypopnea [1]. Airflow cessation partially or totally leads to arousals, fragmentation of sleep, and desaturation of oxyhemoglobin. It is considered a systemic inflammatory disease [2].

The receptors for vitamin D are widely distributed and mainly responsible for regulation of calcium and phosphate flux across bone, gut, and kidney [3].

Vitamin D regulates gene expressions that might affect various tissues and metabolic pathways; it controls the appearance of the RelB gene, which plays an essential role in the advancement of inflammation. The RelB gene and inflammation have been related to sleep apnea [4].

Insufficiency of vitamin D could furthermore deteriorate sleep apnea. Actually, it affects the advancement of chronic rhinitis and tonsil hypertrophy. Correspondingly, vitamin D deficiency negatively encourages function and structure of the airway. Chronic low vitamin D level results in a noninflammatory skeletal myopathy, and thus decreasing the power of contraction. These elements could later aggravate sleep-related airway obstruction and then deteriorate OSAS [5].

Decreased vitamin D levels are common in OSAS, because this sleep disorder causes daytime sleepiness and fragmentation of sleep, which may raise the possibility of the deficiency of vitamin D [6].

Platelets are cytoplasmic fragments without nuclei. Platelets are important markers for pathophysiology of many diseases. Platelets are involved in more activities and also in some intercellular interactions, which make their role important in inflammation [7].

Activation of platelets plays a role in some ‘cardiovascular diseases,’ so elevated mean platelet volume (MPV) may be a marker for cardiovascular crises. Patients who have OSAS are known to have a high cardiovascular risk. So, the MPV is a sign of platelet activation in patients with OSAS [8].

MPV reflects the activity of platelets. The real mechanism of activated platelet in patients with OSAS is unknown. Hypoxia plays a main role in OSAS pathophysiology; it can also stimulate prothrombotic and proinflammatory flow, which in turn activates the platelets [9].


  Patients and methods Top


The current prospective study was conducted on 89 patients who were divided into two groups: group 1 consisted of 65 patients attending the chest and ENT clinics of Menoufia University Hospitals and who were diagnosed to have obstructive sleep apnea in Sleep Laboratory Unit of Chest Department of Menoufia University, and group 2 consisted of 24 healthy volunteers who served as a control group.

This study was done in the Sleep Laboratory Unit in Chest Department and Medical Biochemistry Department, Menoufia University, during the period from December 2016 to December 2017.

Exclusion criteria

OSAS cases with comorbid conditions, including cardiopulmonary disease, metabolic and endocrinal disorders, and renal or hepatic diseases were excluded. Participants who now use supplementations of vitamin D or prescriptions that may affect the metabolism of vitamin D were also excluded.

Health Research Ethics Board of Menoufia University permitted the study. Informed consent was taken from all participants, and each patient underwent the following:
  1. Medical full history taking, including sleep habits.
  2. Physical examination (general and local), including anthropometric measurements:
    1. Neck circumference (NC): using a nonstretchable plastic tape, with the individuals stand-up, NC was measured in the middle of the neck, between mid-cervical spine and mid-anterior neck. In men with a laryngeal prominence (Adam’s apple), NC was measured just below the prominence [10].
    2. BMI was calculated by dividing weight (kg) with square of height (m2) [10].
  3. Chest radiography (posteroanterior and lateral views).
  4. Routine laboratory investigations.
  5. Vitamin D was measured by Human Vitamin D ELISA Kit. The blood sample was collected and then coagulated at room temperature for 10–20 min. Then, it was centrifuged at the speed of 2000–3000 rpm for 20 min to gather supernatant in Medical Biochemistry Department, Menoufia University. The serum was isolated soon and then stored at −20°C for long term. Serum concentration of 25(OH) D is the best indicator of vitamin D status in humans. Level of 25(OH) D less than 10 ng/ml is considered as severe deficiency, more than or equal to 10 to less than 20 ng/ml as moderate deficiency, more than or equal to 20 to less than 30 ng/ml as mild deficiency, and more than or equal to 30 ng/ml as optimal [11].
  6. MPV was measured by Sysmex laser machine (Automated CBC analyzers), which measures the degree to which the cells scatter light in a forward direction (low-angle light scatter). The machine computes the average size of platelets in blood and typed in blood tests as part of the complete blood count. In general, a reference range of 7–12 fl is used [12].
  7. Epworth sleepiness scale is a self-reported questionnaire involving eight questions to assess the propensity for daytime sleepiness or dozing [13].
  8. Overnight polysomnography was performed using Embla S4000 Medicare, Ireland. The PSG consisted of Somnologica studio software (Embla s 4000 PSG, Ireland), electroencephalography sensor with its cables, electrooculography electrodes, electromyography electrodes for the chin and anterior tibialis muscle, nasal cannula and nasal thermistor, thoracic and abdominal belts, pulse oximetry sensor, electrocardiography electrodes with its cables, snoring microphone, and body position sensor. All studies were analyzed using the criteria of Rechtschaffen and Kales [14].


Data obtained from this study were as follows:
  • The apnea–hypopnea index (AHI) is the sum of apnea–hypopnea events per hour. If AHI is less than 5, one is not considered to have OSAS. In contrast, an AHI of more than or equal to 5 and less than 15, is classified as mild, more than or equal to 15 and less than 30 is moderate, and more than or equal to 30 is severe OSAS [15].
  • Desaturation index (DI) was measured as the number of desaturation episodes per hour, which are decrease in saturation by approximately 4% from the baseline saturation in the previous 120 s, and lasting more than 10 s [15].
  • Total sleep time.
  • Snoring time.
  • Percent time sleeping in supine position.



  Results Top


This work was done on 65 patients and 24 controls matched in age and sex.

Male patients represented 55.4% among cases, and among controls, males represented 62.5%, with a nonsignificant difference between both groups. The patients demonstrated significantly higher BMI, NC, Epworth sleepiness scale, AHI, oxygen DI, and snoring time during sleep. However, total sleep time and percentage of sleep in supine position were of lower level in patients than in controls ([Table 1]).
Table 1 Statistical comparison between patient group and control group regarding personal data, clinical data, polysomnographic parameters, and Epworth sleepiness scale questionnaire

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A significant lower level of vitamin D was found among patients than controls, with nonsignificant difference between them regarding MPV level ([Table 2]).
Table 2 Statistical comparison between patient group and control group regarding vitamin D level and mean platelet volume

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Both vitamin D level and MPV differed significantly with the degree of severity of obstructive sleep apnea. The proportion of participants with vitamin D deficiency and high MPV was found in severe OSAS than mild and moderate OSAS ([Table 3]).
Table 3 Statistical comparison between different grades of severity of obstructive sleep apnea syndrome regarding vitamin D and mean platelet volume

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There is a significant adverse relation between vitamin D level among patients and each of NC, Epworth sleepiness scale, AHI, oxygen DI, snoring time, and MPV level (r=−0.39, −0.26, −0.37, −0.32, −0.22, and −0.21, respectively), and a positive correlation was found among MPV level and each of NC and AHI (r=0.26 and 0.24, respectively). MPV demonstrated a significant negative correlation with vitamin D level (r=−0.21) ([Table 4]).
Table 4 Correlation between vitamin D, mean platelet volume, and other measured parameters in patients with obstructive sleep apnea syndrome

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NC was the independent predictor for both vitamin D and MPV levels, with standard β=−0.27, P=0.03, and standard β=−0.28, P=0.03, respectively ([Table 5]).
Table 5 Multivariate linear regression analysis for independent risk factors affecting vitamin D level and mean platelet volume level in patients with obstructive sleep apnea syndrome

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NC, AHI, and vitamin D level were the independent risk factors for OSAS, with an odds ratio of 2.09, 1.6, and 0.11, respectively ([Table 6]).
Table 6 Binary logistic regression analysis for independent risk factors for obstructive sleep apnea syndrome

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  Discussion Top


The present study revealed that levels of vitamin D were decreased significantly in patients (37.6±28.7 ng/ml) than in controls (76±65.1 ng/ml) ([Table 2]). Vitamin D level in patients with severe OSAS was lower than its level in moderate OSAS, and both were much lower than in patients with mild OSAS ([Table 3]).

According to the studies by Kerley et al. [6] and Erden et al. [16], vitamin D levels were decreased in both OSAS groups (moderate and severe) than in control. Furthermore, Toujani et al. [17] and Archontogeorgis et al. [18] found that vitamin D levels were decreased in patients with OSAS compared with controls. Goswami et al. [19] found that the severe OSAS had lower vitamin levels. Barceló et al. [20] also revealed that vitamin D levels were decreased in patients with severe OSAS than mild and moderate OSAS.

Vitamin D receptors are located in skeletal muscles and are connected to muscle cell proliferation and differentiation into mature type II muscle fibers. Vitamin D deficiency is linked to proximal myopathy [21]. High levels of parathyroid hormone and hypophosphatemia lead to decrease in vitamin levels, causing weakness of the muscle [22]. This muscle weakness in vitamin D deficiency affects pharyngeal patency and causes apnea while sleeping [23].

On the contrary, OSAS might predispose to deficiency of vitamin D. Because of obesity or sleepiness all over the day, which leads to decreased exposure to sunlight, it causes decrease in the formation of vitamin D [24].

Age, obesity, and inflammation may be the most important risk factors that cause vitamin D deficiency in patients with OSAS [17].

On the contrary, Mete et al. [24] and Bozkurt et al. [25] reported a nonsignificant difference in vitamin D levels between patients and controls. However, the lowest level of vitamin D was found in the severe group. Salepci et al. [26] also found no difference in vitamin D levels between patients with OSAS and controls.

In the current study, no relation was found between BMI and vitamin D level, although an inverse relation was demonstrated between vitamin D and NC in OSAS patients ([Table 4]).

These findings are in agreement with those of the studies by Mete et al. [24] and Toujani et al. [17], who reported a nonsignificant difference between vitamin D levels among different BMI classes, and Salepci et al. [26], who could not find a relation between levels of vitamin D and BMI.

However, Kerley et al. [6] reported a significant negative correlation between vitamin D, BMI, and total percentage body fat but found no relation between vitamin D and NC, and also Erden et al. [16] and Bozkurt et al. [25] reported negative correlation between BMI and vitamin D level.

Goswami et al. [19] found that lower vitamin D concentrations and higher variations of OSAS were associated with increased BMI and larger NC.

Bad diet habits lead to obesity, and these diets usually contain low amount of vitamin D. In addition, the need for sleep during daytime and restricted physical activity is frequent among obese participants limiting their exposure to sunlight, which could decrease vitamin D levels [17]. Vitamin D deficiency predispose to obesity by increasing parathyroid hormone which in turn increases the entry of calcium to adipocytes, and causes deposition of fat and prevent its destruction [6]. Furthermore, inflammatory cytokines found in obesity affect the formation of vitamin D negatively and enhance its clearance [27].

In this study; there is a significant negative relation between vitamin D and some sleep parameters (Epworth sleepiness scale, AHI, oxygen DI, and snoring time) ([Table 4]). Regression analysis for significant correlated factors revealed that NC was an independent predictor for vitamin D deficiency in patients with OSAS ([Table 5]).

This finding was in accordance to Mete et al. [24], who stated that the vitamin D levels were lower in the severe OSAS group compared with the other groups, and Bertisch et al. [28], who reported that patients with low vitamin D had a high AHI. Archontogeorgis et al. [18] found vitamin D levels were negatively related with oxygen DI and AHI. Kerley et al. [6] also reported that there is an inverse relationship between vitamin D and AHI, and it is an independent factor. On the contrary, Goswami et al. [19] reported that the AHI is not an independent factor.

Low vitamin D affects the inflammatory pathways; this leads to or deteriorates OSAS, as they sharing the same disorders and comorbidities [3]. Hypoxia also stimulates inflammatory pathways [21]. So, hypoxia could be the cause of vitamin D deficiency (VDD) in patients with OSAS [29]. The chronic inflammation in OSAS diminishes the stocks of vitamin D. A study explained this theory, showing increased vitamin D levels in patients with OSAS on CPAP for 7 days [30].

Contrary to this and other published studies, Salepci et al. [26], Erden et al. [16], and Toujani et al. [17] reported no difference in vitamin D levels in relation to OSAS severity grade (AHI or DI).

There is a significant negative relation between vitamin D and MPV in the current research ([Table 4]), which is comparable to Cure et al. [30]. This may be owing to that low level of vitamin D enhances the discharge of some cytokines such as IL-6 and TNF-α, which cause high MPV [30].

Regarding MPV, there was a nonsignificant difference in MPV between patients with OSAS (9.25±0.99 fl) and controls (9.1±1.0 fl) ([Table 2]).

In accordance with the current results, Sarioglu et al. [31] and Sökücü et al. [9] found no significant difference in MPV among patients with OSAS and controls. Topçuoğlu et al. [32] studied severe OSAS and nonsevere OSAS. The difference in MPV between both groups was not significant. Karakaş et al. [33] found nonsignificant changes between patients (mild and moderate) and controls, but there was a significant change comparable to the severe group.

Akyüz et al. [34] also could not find change in MPV of patients and controls. They reported that patients with OSAS who have no substantial cardiovascular risk factors do not have high MPV.

On the contrary, Nena et al. [35] and Varol et al. [8] showed high MPV in patients with severe OSAS. They did not exclude patients who had cardiovascular diseases and smokers, so there was high MPV. Akyol et al. [36] reported that the highest MPV was in severe group compared with mild and moderate groups.Hypoxia affects the pathophysiology of OSAS; it stimulates proinflammatory and prothrombotic pathways, which enhance platelets’ size and activity [8]. Possible mechanisms are indirect effect of increased sympathetic activation causing catecholamine discharge that activates platelets, chronic recurrent hypoxia which has direct effect on platelets’ activity, and chronic inflammation [9]. Chronic inflammation in OSAS causes releasing of proinflammatory cytokines and IL-6. IL-6 and IL-3 affect megakaryocyte activity and lead to the creation of more active and greater platelets. So, elevated IL-6 levels in patients with OSAS lead to high MPV by enhancing the megakaryocyte ploidy [8].

MPV was higher in severe group than in moderate, and both were higher than in mild OSAS ([Table 3]). This adds to the previous hypothesis that MPV increases owing to inflammation and not just because of obesity.

Positive relation existed among MPV and each of NC and AHI, with no relation between MPV and BMI or other sleep parameters ([Table 5]). Regression analysis for significant correlated factors revealed that NC was the only factor that explained high MPV levels in patients with obstructive sleep apnea ([Table 5]).

In agreement with this study, Nena et al. [35], Sökücü et al. [9], and Akyol et al. [36] reported that the highest MPV was found in severe OSAS group. They found that in severe OSAS, MPV is high and related to AHI. Varol et al. [8] reported a significant difference, with high MPV of patients in severe group compared with the controls, and there is a relation between MPV, AHI, and DI.

Unlike most studies, Topçuoğlu et al. [32] and Sarioglu et al. [31] reported that when all comorbidities and cardiovascular risk factors were excluded, the MPV was not significantly related to AHI and other parameters of polysomnography.

The more the severity, the more the risk of having cardiovascular diseases and systemic inflammation, which results in high MPV [9].

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]



 

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