ABSTRACT
Antecedentes y objetivos: El tabaco provoca una reacción leucocitaria influida por factores como la edad, índice de masa corporal (IMC), presencia de enfermedad pulmonar obstructiva crónica (EPOC) y otras comorbilidades. Estudiamos la responsabilidad del tabaquismo en la respuesta leucocitaria, su relación con algunas comorbilidades y con la proteína C reactiva (PCR) como reactante de fase aguda. Población y método: Tres poblaciones con una edad media de 66,8 ± 8,4 años. Las dos primeras sin comorbilidades; una sin haber fumado nunca (n= 48), la otra fumadora (n= 51) y la tercera (n=63) con EPOC estable. Mediante la bioimpedancia eléctrica determinamos el IMC. La PCR se obtuvo por test de alta sensibilidad. Las comorbilidades se valoraron con el índice de Charlson y el índice de Charlson corregido. Resultados: Hubo un significativo aumento de los leucocitos en la población sana fumadora (7,9 ± 1,7 x103/mm3) respecto a la población sana no fumadora (6.4 ± 1,4 x103/mm3; p< 0,001). No hubo diferencia significativa entre el grupo EPOC, 7,4 ± 2,1 x103/mm3 y la población sana fumadora. La leucocitosis fue independiente de la carga tabáquica, edad, IMC, estadios GOLD y comorbilidades. La PCR se incrementa en la población fumadora y con presencia/diagnóstico de EPOC aunque sin relación estadística con la cifra de leucocitos. Conclusiones: El tabaquismo condiciona una repuesta leucocitaria que perdura en similar intensidad en la población con EPOC y una elevación independiente de la PCR. La enfermedad inflamatoria subclínica está ya presente en el fumador sano y se perpetúa con similar intensidad en la población con EPOC (AU)
Antecedents and objectives: tobacco produces a leukocyte reaction influenced by factors like age, body mass index (BMI), chronic obstructive pulmonary disease (COPD) and other comorbidities. We study the impact of tobacco use in the leukocyte reaction, its relationship with some comorbidities and with the C-reactive protein as a acute phase reactant. Population and method: three populations with a mean age of 66.8± 8.4 years. The first two populations without any comorbidities; one having never smoked (n=48), the other one smoking (n=51) and the third one (n=63) with a stable COPD. The BMI was determined through electrical bioimpedance. The C-reactive protein was determined by high-sensitivity CRP test. The comorbidities were assessed with the Charlson index and the corrected Charlson index. Results: the healthy smoking population presented a significant increase of leukocytes (7.9 ± 1.7 x103/mm3) in comparison with the healthy non-smoking population (6.4 ± 1.4 x103/mm3; p< 0,001). There was no significant difference between the COPD population (7.4 ± 2.1 x 103/mm3) and the healthy smoking population. Leukocytosis was independent of the tobacco load, age, BMI, GOLD stages and comorbidities. The CRP is augmented in the smoking population and with COPD present or diagnosed, although without any statistic relationship with leukocyte number. Conclusions: tobacco use determines a leukocyte response that lasts with similar intensity in the COPD population and with an independent increase of CRP. The subclinical inflammatory disease is already present in the healthy smoker and is perpetuated with similar intensity in the COPD population (AU)
Subject(s)
Humans , Pulmonary Disease, Chronic Obstructive/epidemiology , Smoking/adverse effects , Leukocytes , Leukocytes , C-Reactive Protein , Body Mass IndexABSTRACT
INTRODUCTION: The CRP is known to be an acute phase reactant, but with new high sensitivity assay methods it appears that CRP is also a marker of chronic inflammation. This study was to investigate whether smoking acts as a systemic disease and to see if there is a relation between CRP values and smoking. MATERIAL AND METHODS: 762 persons were studied, with a mean age of 41.74+/-10.03 years. 200 were smokers, 344 were non-smokers and 218 were ex-smokers. The following details were noted in the smoking history: cigarette brand, number of cigarettes/day, number of years smoking and milligrams of nicotine and tar. In the case of ex-smokers, the number of years since giving up smoking was noted. The CRP was determined using the high sensitive Tina-Quant assay. Windows SPSS version 11.0 software was used. RESULTS: The CRP values showed statistically significant differences between the smoking and non-smoking groups. A statistically significant increase in CRP was observed in relation to number of cigarettes/day (p=0.001), mg of nicotine (p=0.017), mg of tar (p=0.020) and number of years of smoking (p=0.0001). However, when analysing the relation between CRP and the number of years since giving up smoking, there was a negative curve of 0.02 in the equation, but this was not of statistical significance. CONCLUSIONS: CRP levels rise when there is an increase in number of cigarettes/day, mg of nicotine and tar and years smoking.
Subject(s)
C-Reactive Protein/analysis , Inflammation/blood , Nicotiana/chemistry , Nicotine/analysis , Smoking/physiopathology , Tars/analysis , Adult , Chronic Disease , Humans , Inflammation/etiology , Middle Aged , Smoking/adverse effectsABSTRACT
Introducción: La PCR se conoce como reactante de fase aguda, pero con los nuevos métodos de análisis ultrasensibles, aparece el concepto de PCR como marcador de inflamación crónica. En este estudio vamos a investigar si el tabaquismo se comporta como una enfermedad sistémica, ver si existe relación entre los valores de la PCR y el tabaquismo. Material y métodos: Se estudian 762 personas de edad media 41,74 (d.s.10,03) años. 200 eran fumadoras, 344 no fumadoras y 218 exfumadoras. En la historia de tabaquismo se recoge: marca de tabaco, número de cigarrillos/ día, duración en años del hábito y milígramos de nicotina y alquitrán. En los exfumadores el número de años de abandono tabáquico. La PCR se determina mediante ensayo Tina Quant ultrasensible. Se aplica el programa informático SPSS windows versión 11.0 Resultados: Aparecen valores de PCR con diferencias estadísticamente significativas entre los grupos de fumadores y de no fumadores. Se observa un aumento estadísticamente significativo de la PCR en relación con el número de cigarrillos/ día (p = 0,001), con los mg de nicotina (p = 0,017), con los mg de alquitrán (p = 0,020) y con los años de duración del hábito tabáquico (p = 0,001). Sin embargo, al estudiar la relación entre PCR y años de abandono tabáquico se observa una pendiente negativa de la ecuación de 0,02, pero no es estadísticamente significativa. Conclusiones: Los niveles de PCR aumentan al incrementarse el consumo de cigarrillos/día, los mg de nicotina, de alquitrán y la duración del hábito
Introduction: The CRP is known to be an acute phase reactant, but with new high sensitivity assay methods it appears that CRP is also a marker of chronic inflammation. This study was to investigate whether smoking acts as a systemic disease and to see if there is a relation between CRP values and smoking. Material and methods: 762 persons were studied, with a mean age of 41.74 ± 10.03 years. 200 were smokers, 344 were non-smokers and 218 were ex-smokers. The following details were noted in the smoking history: cigarette brand, number of cigarettes/day, number of years smoking and milligrams of nicotine and tar. In the case of ex-smokers, the number of years since giving up smoking was noted. The CRP was determined using the high sensitive Tina Quant assay. Windows SPSS version 11.0 software was used. Results: The CRP values showed statistically significant differences between the smoking and non-smoking groups. A statistically significant increase in CRP was observed in relation to number of cigarettes/day (p = 0.001), mg of nicotine (p = 0.017), mg of tar (p=0.020) and number of years of smoking (p = 0.0001). However, when analysing the relation between CRP and the number of years since giving up smoking, there was a negative curve of 0.02 in the equation, but this was not of statistical significance. Conclusions: CRP levels rise when there is an increase in number of cigarettes/day, mg of nicotine and tar and years smoking
