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Калашник Д.М. Дисфункція тромбоцитарної ланки у курців, хворих на хронічне обструктивне захворювання легенів
02.08.2014, 17:05

Резюме
Калашник Д.М. Дисфункція тромбоцитарної ланки у курців, хворих на хронічне обструктивне захворювання легенів.
У роботі розглянуті морфологічні та функціональні характеристики тромбоцитів у пацієнтів з хронічне обструктивне захворювання легенів (ХОЗЛ), які курять. Встановлено, що рівень тромбоцитів у пацієнтів з ХОЗЛ III - IV ст. достовірно вищий ніж у здорових осіб (p<0,001). АДФ -індукована агрегація тромбоцитів у курців, хворих на ХОЗЛ збільшується пропорційно стадії захворювання.
Ключові слова: агрегація тромбоцитів, куріння, хронічне обструктивне захворювання легенів.

Резюме
Калашник Д.Н. Дисфункция тромбоцитарного звена у курящих пациентов с хроническим обструктивным заболеванием легких.
В работе рассмотрены морфологические и функциональные характеристики тромбоцитов у пациентов с хроническим обструктивным заболеванием легких ХОЗЛ, которые курят. Установлено, что уровень тромбоцитов у пациентов с ХОЗЛ III-IV ст. достовірно выше чем у здорових (p<0,001). АДФ-индуцированная агрегація тромбоцитов у курильщиков, больных на ХОЗЛ увеличивается пропорционально стадии заболевания.
Ключевые слова: агрегация тромбоцитов, курение, хроническое обструктивное заболевание легких.

Summary
Kalashnyk D.N. Platelet dysfunction in smoking patients with chronic obstructive pulmonary disease.
The aim of this study was to investigate morphological and functional characteristics of circulating thrombocytes in current smokers with chronic obstructive pulmonary disease (COPD). Established that platelets from patients with COPD III-IV st. higher than in healthy (p<0,001). ADP-induced platelet aggregation in smokers patients with COPD is increased in proportion to the stage of the disease.
Key words: aggregation of platelets, smoking, chronic obstructive pulmonary disease.

Рецензент: д.мед.н., проф. Л.М. Іванова

УДК 616.24-007.272-036.12-092:616.155.2:613.84

ДУ «Національний інститут терапії ім. Л.Т.Малої НАМН України» (Харків)

ГУ «Национальный институт терапии им. Л.Т. Малой НАМНУ»

GI «L. T. Mala National Therapy Institute of the NAMS of Ukraine»

darunika@rambler.ru

Introduction.

COPD is considered to be a global health care problem, which is often complicated by acute atherothrombotic events [3]. Important role in these processes is played by platelets.

Thus, with that in mind, the purpose of the given research was to study the level of aggregation and morphological characteristics of platelets in smokers, patients with COPD.

Materials and Methods: 36 COPD patients were examined: 21 men and 15 women, average age was (62,7±11,8). Anamnesis of the disease was (6,5±3,9) years. In most patients, the primary factor in the development of COPD was smoking. Thus, 19 patients (90.4 %) men and 14 (93.3 %) women are smokers. The overall experience of smoking - (24±11,3) pack/years.

All patients were divided into 3 groups: the first group (gr. 1) constituted 12 patients with COPD II st.; the second group (gr. 2) included 11 patients with COPD III st.;  the third (gr. 3) consisted of 10 patients with COPD IV st. Control - 15 almost healthy individuals aged 40-50, who do not smoke. The study excluded patients with concomitant cardiovascular disorders, and other conditions that require the appointment of antiplatelet therapy.

The diagnosis of COPD was established according to national and international standards (GOLD, 2012). The study was conducted against the background of basic therapy of metered dose inhalers. All patients had spirometry performed (spirograph Spirokom, Ukraine) routinely.

State of the hemostatic platelet level was determined by hematological parameters (platelet amount, plateletcrit) and platelet aggregation activity. Analysis of blood samples was performed in the hematology analyzer. The following reference values were used​​: PLT (platelet amount) - 150-450 m/mm3, MPV (mean platelet volume) - 6,0-13,0 fl, PDW (platelet distribution by volume) - 6.0-10,0 %; PCT (plateletcrit) - 0,15-0,40 %. Platelet aggregation analysis was performed using platelet aggregation analyzer "Extreme".

Statistical analysis was carried out using standard analysis package program Statistika for Windows Microsoft.

Results and Discussion: It was established that all examined patients’ tolerance to physical exertion was significantly lower than in healthy people (345±40) m vs. (853±27) m (p<0.05). Patients of the first group had significantly higher exercise tolerance - (365 ± 47) m compared to patients of the 2nd group - (274 ± 35) m and the 3rd group - (234 ± 53), (p < 0,05).

According to mMRC scale patients got (2±0,3) points, according to Borg scale - (3,8±1,0) points.

Average FEV1 in patients smokers - (47,3±3,7)%, among healthy individuals - (91,3±2,5)% (p <0,05).

It was revealed that in the 2nd and 3rd group patients platelet level was significantly higher than the control group (197±1,43), (p<0,05). For example, in the 1st group of patients platelet level was (199±1,37) (p>0,05), in the 2nd group - (240 ± 2,37), in the 3rd group – (354±1,79) m/mm3 (p<0,001). In 30% of patients of the 2nd and 3rd groups the increase of the MPV level wasfound and only 10% of patients with COPD I st. Negative correlation dependence between the platelet level, plateletcrit and distance meters when performing tests with the 6-minute walk (r = - 0,37; p < 0.05), and (r = - 0,35; p < 0.05) was established accordingly.

An inverse correlation relationship between the platelet level and FEV1 (r = -0,19, p=0,008) was found. Activation of platelet aggregation and growth occurs in diseases of the respiratory tract in humans and in laboratory animal models [5]. We found out that the increase in platelet aggregation occurs in patients with COPD I st. (1st gr.) - (57,14±2,68) vs. (46,51±1,32)%, (p<0.05). In patients with COPD II-III st. CIAT, induced by ADP, increased significantly in comparison with the control group, was respectively (70,37±2,76) vs. (46,51±1,32)% in the 2nd gr., (p<0,001); (91,38±1,3) vs. (46,51±1,32)% in the 3rd gr. (p<0.001).

As a pat of the study, a direct correlation dependence between CIAT and smoking (p/years) - (r=0,76, p=0,017). Thus, we confirmed the fact that with the progression of COPD occurs lesion of capillary bed, which promotes the injection in blood of procoagulants and proaggregants devastating platelets. Perhaps platelet dysfunction in smokers plays a role in the formation of bullous emphysema in severe and very severe COPD stage [2].

Conclusions: The level of platelets in patients with COPD III-IV st. is significantly higher than the level of platelets in healthy people (p<0,001). ADP - induced platelet aggregation in smokers increases in proportion to the stage of COPD.

The study of the role of antithrombotic therapy is considered to be promising, the potential benefits from which in these patients requires further study.

Література

  1. Бурдули Н.М. Нарушения агрегации тромбоцитов у больных с хронической обструктивной болезнью легких и роль лазеротерапии в их коррекции / Н.М. Бурдули, И.З. Аксенова // Клин. мед. - 2004. - № 82 (8). - С. 34–37.
  2. Привалова Е.В. Тромбоцитарная дисфункция у длительно курящих пациентов с ХОЗЛ / Е.В. Привалова, Т.В. Вавилова, Н.А. Кузубова // Пульмонология. - 2010. - № 10. - С. 40-45.
  3. Biljak V.R. Platelet count, mean platelet volume and smoking status in stable chronic obstructive pulmonary disease / V.R. Biljak, D. Pancirov, I. Cepelak [et al.] // Platelets. - 2011. - Vol. 22, № 6. - P. 466-470.
  4. Cella G. Plasma markers of endothelial dysfunction in chronic obstructive pulmonary disease / G. Cella, A. Sbarai, G. Mazzaro [et al.] // Clin. Appl. Thromb. Hemost. - 2001. - Vol. 7, № 3. - P. 205-208.
  5. Dunkel B. Platelet activation in ponies with airway inflammation / B. Dunkel, K.J. Rickards, C.P. Page, F.M. Cunningham // Equine Vet J. - 2007. - Vol. 39, № 6. - P. 557-561.
  6. Increased platelet and erythrocyte arginase activity in chronic obstructive pulmonary disease associated with tobacco or wood smoke exposure / A. Guzmán-Grenfell, N. Nieto-Velázquez, Y. Torres-Ramos [et al.] // J. Investig. Med. - 2011. - Vol. 59, № 3. - P. 587-592.
  7. MacCallum P.K. Markers of hemostasis and systemic inflammation in heart disease and atherosclerosis in smokers / P.K. MacCallum // Proc. Аm. Thorac. Soc. - 2005. - Vol. 2. - P. 34–43.
  8. Fimognari F.L. Mechanisms of atherothrombosis in chronic obstructive pulmonary disease / F.L. Fimognari, S. Scarlata, M.E. Conte, R.A. Incalzi // Int. J. Chron. Obstruct. Pulmon. Dis. - 2008. - Vol. 3, № 1. - P. 89-96.
  9. Yang Q. Dysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: basic considerations for future drug development / Q. Yang, M.J. Underwood, M.K. Hsin [et al.] // Curr. Drug. Metab. - 2008. - Vol. 9, № 7. - P. 661-667.
Категорія: 5 (119) | Додав: siderman | Теги: smoking, aggregation of platelets, chronic obstructive pulmonary disea
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