• Sonuç bulunamadı

Effects of Smoking Cessation Therapies on the Mean Platelet VolumeIclal Hocanli

N/A
N/A
Protected

Academic year: 2021

Share "Effects of Smoking Cessation Therapies on the Mean Platelet VolumeIclal Hocanli"

Copied!
5
0
0

Yükleniyor.... (view fulltext now)

Tam metin

(1)

1 Department of Chest Disease, Medical Faculty, Dicle University, Diyarbakir, Turkey

2 Department of Public Health, Medical Faculty, Dicle University, Diyarbakir, Turkey Correspondence: Abdurrahman Abakay,

Department of Chest Disease, School of Medicine, Dicle University, Diyarbakir, Turkey Email: arahmanabakay@hotmail.com Received: 05.05.2016, Accepted: 16.05.2016

RESEARCH ARTICLE / ARAŞTIRMA

Effects of Smoking Cessation Therapies on the Mean Platelet Volume

Iclal Hocanli1, Abdurrahman Abakay1, Abdullah Cetin Tanrikulu1, Hadice Selimoglu Sen1, Yilmaz Palanci2, Ozlem Abakay1

ABSTRACT

Objective: The aim of the current study was to investigate the effects of smoking on mean platelet volume (MPV) in different age groups.

Methods: This study included a total of 150 patients (105 men and 45 women). Demographic data and other laboratory data were recorded for each patient. Patients were divided into two groups based on their smoking cessation status as follows: Those who quit smoking (n = 72) and those who continued to smoke (n = 78).

Results: At the end of the study, 50.4% (n = 53) of the 105 male patients and 42.2% (n = 19) of the 45 female patients quitted smoking. Of those who quit, 73.6% (n = 53) were male and 26.4% (n = 19) were female. The mean age of the patients who did not quit smoking was 34.9 ± 10.1 years, and 35.8 ± 10.1 years in quitter group. Mean annual cigarette consumption was 18 packs/year in not-quitted group, and 17 packs/year in stop smoking group. The pre- and post- treatment MPV values were 7.2 ± 1.0 fl and 7.3 ± 1.2 fl in non-quitting group (p>0.05), while 7.5 ± 1.0 fl and 7.2 ± 1.0 fl in quitted group (p<0.05).

Conclusion: Significant decreases were observed in MPV of smoking quitters following cigarette cessation treatment.

Arch Med Invest 2016; 1 (1): 1-5

Key words: Mean platelet volume, smoking cessation, treatment

Sigara Bırakma Tedavilerinin Ortalama Trombosit Hacmi Üzerindeki Etkileri

ÖZET

Amaç: Bu çalışmanın amacı farklı yaş gruplarında sigara içiminin Ortalama trombosit hacmi (MPV) üzerindeki etkisini araştırmaktır.

Yöntemler: Bu çalışmaya 105 erkek ve 45 kadın toplam 150 hasta dahil edildi. Her bir hasta için demografik veriler ve diğer laboratuvar bulguları kaydedildi. Hastalar sigarayı bırakma durumuna göre sigara içmeyi bırakanlar (n = 72) ve içmeye devam edenler (n = 78) olmak üzere iki gruba ayrıldı.

Bulgular: Bu çalışmanın sonucunda 105 erkek hastanın %50,4’ü ve 45 kadın hastanın %42,2’ü sigarayı bıraktı. Sigarayı bırakanların %73,6’ü (n=53) erkek, %26,4’ü (n=19) kadındı. Sigarayı bırakmayan grubun yaş ortalaması 34,9 ± 10,1 yıl iken, sigarayı bırakan grubun yaş ortalaması 35,8 ± 10,1 yıl idi. Sigarayı bırakmayan grubun ortalama sigara tüketimi 18 paket / yıl iken sigarayı bırakan grubun ortalama sigara tüketimi 17 paket/yıl olarak tespit edildi. Tedavi öncesi ve sonrası MPV değerleri sigarayı bırakmayan grupta 7,2 ± 1,0 fl ve 7,3 ± 1,2 fl (p>0.05); sigarayı bırakan grupta ise 7,5 ± 1,0 fl ve 7,2 ± 1,0 fl olarak saptandı (p<0.05).

Sonuç: Sigara bırakma tedavisi sonrası sigarayı bırakan hastalarda MPV değerlerinde anlamlı düşme gözlendi.

Anahtar kelimeler: Ortalama trombosit hacmi, sigara bırakma, tedavi

INTRODUCTION

Currently, tobacco dependence is the largest prevent- able cause of death in the world [1] and smoking is a risk factor for six of the eight most common causes

of death in the world. Cigarette smoke contains more than 4,000 pharmacologically active, antigenic, cyto- toxic, mutagenic, and carcinogenic components [2]. In addition, smoking is associated with up to 50 chronic diseases that do not directly result in death [3]. Smok-

(2)

ing was found to be responsible for 80% of all chronic lung diseases, and for one-third of all deaths due to heart disease and cancer [3].

Mean platelet volume (MPV) is an indicator of platelet activation that has hemostatic importance.

MPV has been reported to increase during acute myocardial infarction, acute cerebral ischemia, and in transient ischemic attacks [4]. It has been reported that MPV is elevated in healthy elderly smokers, but the relationship between smoking habit and MPV in young healthy individuals is not known [5].

In this study, we aimed to investigate hematologi- cal parameters, such as MPV, in individuals who quit smoking after smoking cessation treatment.

METHODS

The study included patients who had applied to The Chest Diseases and Smoking Cessation Clinic at the Dicle University Research Hospital between January 2011 and January 2012. We accessed the files of 450 patients who were admitted to the Smoking Cessation Clinic and were able to reach 300 patients. Among those 300 patients, 150 regularly came for their post- treatment follow-ups; these 150 patients were includ- ed in the study. Local ethical committee approval was obtained from the Dicle University Medical Faculty Ethics Committee for Non-interventional Studies.

The patients (105 men, 45 women) were asked to fill out the study form. The demographic data, smok- ing duration (packs/years), body mass index (BMI), treatment regimen, drugs used in the pharmacological treatment and their side effects, comorbidity status, Fagerström test for nicotine dependence (FTND) score, the presence of another smoker in the same home, and laboratory data before and after treatment were re- corded for each patient. Patients were divided into two groups: those who quit smoking after the treatment (n

= 72) and those that did not quit smoking (n=78). The Fagerström Nicotine Dependence Test consists of six questions, and each question is scored differently. Af- ter evaluating the test results, the patients were divided into five groups based on the total number of points as follows: very low (0-2 points), low (3-4 points), mod- erate (5 points), high (6-7 points), and very high (8-10 points) nicotine dependence.

Blood samples were taken from the brachial vein into a hemogram tube and were analyzed with a CELLDYN 3700 Hematology Analyzer (USA) at the Central Laboratory of the Dicle University Faculty of

Medicine. The white blood cells (WBC), hemoglobin (Hb), hematocrit (Hct), MPV, and platelet (Plt) values were evaluated.

Statistical Analysis

The SPSS 15.0 software package for Windows was used for statistical analysis. The quantitative variables were presented as means ± standard deviations, and categorical variables were presented as numbers and percentages (%). The data was analyzed whether it was normally distributed or not. Conforms to the nor- mal distribution of data were measured. A one-way analysis of variance was used to compare the means of normally distributed groups that had more than two choices. The variance homogeneity test was used for multiple comparisons. The Tukey test was used for variables that had P> 0.05, while variables that had P <0.05 were tested by Tamhane’s T2 test. The chi- square test was used to compare qualitative variables between the groups. P <0.05 was considered statisti- cally significant.

RESULTS

Among the 150 patients enrolled in the study, 105 (70%) were men and 45 (30%) were women. Forty- eight percent of the patients (n = 72) were in the smok- ing cessation group, while 52% (n = 78) were in the group that did not quit smoking. Among the individu- als that quit smoking, 73.6 % (n = 53) were male and 26.4 % (n = 19) were female. In the group that did not quit smoking, 66.6 % (n = 52) were male and 33.4% (n

= 26) were female. Fifty-three of the 105 (50.4%) male patients and 19 of the 45 (42.2%) female patients quit smoking. There was no statistically significant differ- ence between men and women in terms of smoking cessation (p = 0.35). The mean age of the 29 male pa- tients who quit smoking was 52.5 ± 10.7 years, while that of the 38 male patients who did not quit smoking was 48.5 ± 12.3 years. The mean age of the 13 women who quit smoking was 46.5 ± 10.7 years, while that of the 26 women who did not quit smoking was 45.6

± 9.0 years, and there was no significant difference in terms of mean age between the groups (p = 0.12). In addition, there was no significant difference in BMI between the groups (p = 0.32).

The group that did not quit smoking smoked 18 packs/year while the group that quit smoking smoked 17 packs/year (p = 0.27). Nine of the patients (11.5%) who did not quit smoking and three patients (4.1%) who quit smoking were diagnosed with asthma or

(3)

COPD. Comorbidities were present in 31 of the pa- tients who did not quit smoking and in 21 of the pa- tients who quit smoking. There was no significant difference in terms of frequency of comorbidities between the groups (Table 1) (p = 0.075). WBC de- creased from 8.1 to 7.6 after treatment in the group that did not quit smoking, while the WBC of the group that quit smoking decreased from 7.9 to 7.8 following

the treatment. This difference was not statistically sig- nificant (p = 0.15). In addition, the hemoglobin (Hb), hematocrit (Htc), and platelet (PLT) values were not significantly different between the groups (p = 0.85 for Hb, p = 0.002 for Htc, p = 0.070 for PLT). The mean MPV value in the group that quit smoking decreased from 7.5 to 7.2 after the treatment, which was statisti- cally significant (Table 2) (p = 0.014).

Table 1. Frequency of co morbidities between the patient groups

Comorbidities Patients who did not quit smoking (n=78) n (%) Patients who quit smoking (n=72) n (%) p

Asthma or COPD 9 (11.5) 3 (4.1)

0.075

Psychiatric Diseases 6 (7.6) 4 (5.5)

DM 5 (6.4) 3 (4.1)

Others 11 (14.1) 11 (15.2)

Total 31 (39.6) 21 (28.9)

COPD: Chronic obstructive pulmonary disease, DM: Diabetes mellitus, Others: Goiter, cerebrovascular accident, Behcet’s dis- ease, etc.

Table 2. Comparison of MPV values between the patient groups

Parameter Patients who did not quit smoking (n=78) Patients who quit smoking (n=72) p Pre-treatment Post-treatment Pre-treatment Post-treatment

MPV (fL) 7.2±1.0 7.3±1.2 7.51±1.0 7.2±1.0 0.014

MPV: Mean platelet volume

DISCUSSION

Many studies have been conducted in our country and others regarding the health problems caused by tobacco exposure. Published work describes that the prevalence of pulmonary and systemic diseases has significantly changed the success of smoking cessa- tion among smokers [6] However, in our study, we did not observe a significant difference in terms of smok- ing cessation in patients that had pulmonary and sys- temic diseases and those that didn’t.

There are many published studies evaluating the factors thought to be effective in smoking cessation, including age, sex, socio-economic status, occupation, education level, housing conditions, existing pulmo- nary and cardiovascular system diseases, the number of cigarettes smoked per day, and nicotine depen- dence [6-10]. Age, gender, socioeconomic status, and nicotine dependence are well-defined determinants in smoking cessation [6,10]. In addition, some studies have identified gender as a determinant that affects the success of treatment [10]

Smoking has acute and chronic effects on the he- matological system. Although the causes and mecha- nisms are not clear, acute cigarette smoking leads to elevated leukocytes, eosinophils, and platelets in the peripheral blood. These blood values have been shown to return to normal 5 years after smoking ces- sation [11]. The mechanism of smoking-associated leukocytosis is not clear [11]. In our study, WBC and PLT counts were not elevated in either group. A 1x103 unit decline in the number of leukocytes has been sug- gested to lead to a 14% decrease in the risk of death due to coronary artery disease and a 6.2% decrease in all-cause mortality [12]. It has been shown that smok- ing, diabetes mellitus, and hypertension increase the platelet volume [13-14].

Diabetes, pre-diabetes, smoking, hypertension, hypercholesterolemia, obesity, coronary heart disease, metabolic syndrome, statins, anti-hypertensives, and atrial fibrillation can significantly affect MPV values [15]. In accordance with previous studies [16,17]. We also found that smoking increased platelet reactivity and MPV values.

(4)

In our study, MPV was not significantly different between the group that stopped smoking and the group that did not stop. Martin et al. [18] measured MPV in 1,716 patients with myocardial infarction. They re- assessed the MPV values two years later and found that patients who had ischemic attacks and died as a result of those attacks had significantly higher MPV values. The conclusions from the study by Martin et al. were that MPV is an independent risk factor for recurrent myocardial infarction and that vascular risk factors, such as blood pressure, plasma cholesterol levels, leukocyte count, fibrinogen levels, and smok- ing, were not significantly related to recurrent myo- cardial infarction.

Cigarette smoking increases MPV levels in elder- ly patients with risk factors for atherosclerosis. Kario et al. conducted a study with 142 adults with and with- out atherosclerotic risk factors who were smokers and non-smokers to investigate the effects of smoking on MPV in arterial diseases. While the MPV was high in smokers with atherosclerosis, it was significantly higher in smokers that did not have atherosclerosis.

They also determined that MPV decreased significant- ly 1-3 months after smoking cessation [2]. Gasparyan et al. [19,20] reported that patients with high-grade in- flammatory diseases had low MPV values. In contrast, Önder et al. [20] reported a decrease in platelet count and elevated MPV levels in patients with COPD. Gas- paryan et al. [19] reported that smoking and exposure to nicotine have more effects on platelet function than do age, gender and other risk factors. Previous studies have shown that chronic cigarette smoking can cause platelet activation [21-24]. MPV is a potential maker for platelet reactivation [25,26]. Large platelets con- tain more granules than do smaller platelets, aggregate faster with collagen, have high thromboxane A2 lev- els, and have more glycoprotein Ib and IIb / IIIa recep- tors [27-29]. While some studies report that smoking does not affect MPV (105,106), Kario et al. reported that MPV values are elevated in smokers [2].

In our study, MPV values were significantly de- creased in smokers who quit smoking after treatment.

Platelets play an important role in the pathophysiol- ogy of atherosclerotic diseases. It has been reported that changes in platelet volumes might have predic- tive and diagnostic significance in thrombotic and prothrombotic events [30]. Some studies have report- ed co-occurrence of decreased platelet count and in- creased MPV [26,27]. There is a negative correlation between MPV and the total number of platelets, which

has been suggested to lead to the production of large reticulocytes as compensation for the consumption of small platelets [28]. Platelet activation can cause ath- erothrombotic complications. Platelet activation in hy- pertension includes renin activation, endothelial dys- function, increased catecholamines, and the presence of comorbid conditions [31]. Those comorbid condi- tions include DM, smoking, stress, and hypercholes- terolemia. Giles and Inglis reported that MPV values are higher in gestational hypertensive patients when compared to normal pregnant women [32]. Similar to other studies in the literature, our study also verifies that smoking has adverse effects on blood parameters, such as MPV. Unlike other studies in the literature, our results indicate that cessation of smoking is associated with a significant decrease in MPV levels.

Declaration of Conflicting Interests: The authors declare that they have no conflict of interest.

Financial Disclosure: No financial support was received.

REFERENCES

1. Greisenegger S, Endler G, Hsieh K, et al. Is Elevated mean platelet volume associated with a worse outcome in pa- tients with acute ischemic cerebrovascular events? Stroke 2004;35:1688-1691.

2. Kario K, Matsuo T, Nakao K. Cigarette smoking increases the mean trombosit volume in elderly patients with risk fac- tors for atherosclerosis. Clin Lab Haematol 1992;14:281- 287.

3. Behr J, Nowak D. Tobacco smoke and respiratory disease.

Đn D’Amato G, Holgate ST; eds. The Impact of Air Pollu- tion on Respiratory Health. First Ed. Sheffield: ERS Jour- nals Ltd. Eur Respir Mon 2002;21:161-179.

4. Global Adult Tobacco Survey Turkey Report; 2010. Avail- able from: http://www.who.int/tobacco/surveillance/en_tfi_

gats_turkey_2009.pdf

5. Bath PM, Missouris CG, Buckenham T, MacGregor GA. In- creased platelet volume and platelet mass in patients with atherosclerotic renal artery stenosis. Clin Sci 1994;87:253- 257.

6. Monse E, Campell J, Tonnesen P, Gustavsson G.

Socıodemographıc predıctors of success in smoking inter- vention. Tobacco Control 2001;10;165-169.

7. Dale LC, Glover ED, Sachs DPL, Schoeder DR, Bupropion for smoking cessation : Predictors of succesful outcome.

Chest 2001;119:1357-1364.

8. Osler M, Prescott E. Psyholosocial, behavioral and health determinants of succesful smoking cessation: a longitudinal study of Danish adults. Tobacco Control 1998;7:262-267.

9. Gorecka D, Bednarek M, Nowinski A, Puscinska E. Diagno- sis of airflow limitation combined with smoking cessation

(5)

advice increases stop-smoking rate. Chest. 2003;123:1916- 1923.

10. Kenford SL, Fiore MC, Jorenby DE, Smith SS. Predicting smoking cessation:Who will quit with and without the nico- tine patch. JAMA 1994:271;589-594.

11. Bain BJ, Rothwell M, Feher MD, et al. Acute changes in haematological parameters on cessation of smoking. J R Soc Med 1992;85:80-82.

12. Grimm RH, Neaton JD and Ludwig W. Prognostic impor- tance of the white blood cell count for coronary, cancer, and all-cause mortality. J Am Med Assoc. 1985:254;1932–

1937.

13. Pathansali R, Smith NM, Bath PM. Prothrombotic mega- karyocyte and platelet changes in hypertension are reversed following treatment: a pilot study. Platelets 2001;12:144- 149.

14. Tschope D, Langer E, Schauscil S, et al. Increased platelet volume-sign of impaired thrombopoiesis in diabetes mel- litus. Klinische Wochenschrift 1989;67:253-259.

15. Vizioli L, Muscari S, Muscari A. The relationship of mean platelet volume with the risk and prognosis of cardiovascu- lar diseases. Int J Clin Pract 2009;63:1509–1515.

16. Hawkins RI. Smoking, platelets and thrombosis. Nature 1972;236:450–452.

17. Giles C. The platelet count and mean platelet volume. Br J Haematol 1981;48:31–37.

18. Martin JF, Bath PM, Burr ML. Influence of platelet size on outcome after myocardial infarction. Lancet 1991;338:1409-1411.

19. Gasparyan AY, Ayvazyan L, Mikhailidis DP, Kitas GD.

Mean platelet volume: A link between thrombosis and in- flammation? Current Pharmaceutical Design 2011;17:47- 58.

20. Onder I, Topcu S, Dökmetas HS, Türkay C, Seyfikli Z.

Platelet aggregation size and volume in chronic obstructive pulmonary disease. Materia Medica Polona 1997;29:11–13.

21. Takajo Y, Ikeda H, Haramaki N, et al. Augmented oxida- tive stress of platelets in chronic smokers. Mechanisms of impaired platelet-derived nitric oxide bioactivity and augmented platelet aggregability. J Am Coll Cardiol.

2001;38:1320-1327.

22. Lupia E, Bosco O, Goffi A. Thrombopoietin contributes to enhanced platelet activation in cigarette smokers. Athero- sclerosis. 2010;210:314-319.

23. Rangemark C, Benthin G, Granstrom EF, et al. Tobacco use and urinary excretion of thromboxane A2 and prosta- cyclin metabolites in women stratified by age. Circulation.

1992;86:1495-500.

24. Hung J, Lam JY, Lacoste L, Letchacovski G. Cigarette smoking acutely increases platelet thrombus formation in patients with coronary artery disease taking aspirin. Circu- lation. 1995;92:2432-2436.

25. Park Y, Schoene N, Haris W. Mean platelet volume as an in- dicator of platelet activation: methodological issues. Plate- lets. 2002;13:301-306.

26. Boos CJ, Lip GY. Assessment of mean platelet volume in coronary artery disease-what does it mean? Thromb Res 2007;120:11-13.

27. Martin JF, Trowbridge EA, Salmon GL, Plumb J. The bio- logical significance of platelet volume: its relationship to bleeding time, platelet thromboxane B2 production and megakaryocyte nuclear DNA concentration. Thromb Res 1983;32:443-460.

28. Jakubowski JA, Thompson CB, Vaillancourt R, et al. Ara- chidonic acid metabolism by platelets of differing size. Br J Haematol 1983;53:503-511.

29. Giles H, Smith REA, Martin JF. Platelet glycoprotein IIb–

IIIa and size are increased in acute myocardial infarction.

Eur J Clin Invest 1994;24:69-72.

30. Trowbridge EA, Martin JF. The platelet volume distribu- tion: a signature of the prethrombotic state in coronary heart disease. Thromb Haemost 1987;58:714-717.

31. Punda A, Polic S, Rumboldt Z, et al. Effects of atenolol and propranolol on platelet aggregation in moderate essen- tial hypertension: randomized crossover trial, Croat Med J 2005;46:219–224.

32. Giles C, Inglis TC. Thrombocytopenia and macrothrombo- cytosis in gestational hypertension. Br J Obstet Gynaecol 1981;88:1115-1119.

Referanslar

Benzer Belgeler

No significant difference was found between the patient group with acromegaly and the healthy control group in terms of peripheral systolic blood pressure, peripheral main arterial

Increased mean platelet volume in patients with familial Mediterranean fever may not be a marker of atherosclerosis risk.. Ailevi Akdeniz Ateşli olgularda ortalama trombosit

Although there are no statistically difference between three groups in terms of diabetes mellitus, hypertension and smoking, they did not mention about the body mass

Conclusion: Patients with idiopathic or ischemic CMP have higher MPV values indicating tendency to platelet aggregation regardless of the etiology, when compared to controls and

In conclusion, significantly higher MPV in patients with HcV infection may be responsible for the viral effect that causes platelet dysfunction, supporting the association between

In harmony with literature, it was identifi ed in our study that both platelet number and MPV level had been signifi cantly higher in the group where colorectal malignancy

The main reason why political values meet the requirements of the development of our society, the vital needs of the state independence of Uzbekistan, the interests of our people

The patients were divided into two groups as SAI positive group includ- ing patients with ascitic culture positive and/or ascites polymorphonuclear leukocyte count (PMNL) &gt;250 mm 3