Email this article Activity of systemic inflammatory reaction in patients with chronic obstructive pulmonary disease in regard to small intestinal absorption function
- Authors: Beloborodova EI, Akimova LA, Burkovskaya VA, Asanova AV, Semenenko EV, Beloborodova EI, Akimova LA, Burkovskaya VA, Asanova AV, Semenenko EV
- Issue: Vol 81, No 3 (2009)
- Pages: 19-22
- Section: Editorial
- URL: https://journals.rcsi.science/0040-3660/article/view/30276
- ID: 30276
Cite item
Full Text
Abstract
Aim. To study the effect of systemic inflammatory reaction in patients with chronic obstructive pulmonary disease (COPD) in association with absorption of the small intestine.
Material and methods. Small intestinal absorption was studied in 93 COPD patients (22, 36 and 35 patients at stage I, II and III, respectively) in a clinically stable stage of the disease and in 35 healthy controls. The absorption was investigated biochemically and with application of radionuclide methods, blood concentration of TNFalpha was measured with enzyme immunoassay.
Results. The small intestine of patients with moderate and severe COPD showed subnormal absorption of fats, protein, carbohydrates. With the disease progression, this disorder aggravated. The same trend was seen in relation to TNFalpha concentration. A strong direct correlation was found between a high concentration of TNFalpha and a low absorption of 131I-albumin and fatty acids, this high concentration correlated negatively with low absorption of d-xilose.
Conclusion. Relationships between inflammation severity and small intestinal absorption of fats, protein, carbohydrates in patients with moderate and severe COPD means loss of essential nutrients, primarily protein and fats. This is important in understanding of pathobiological processes of development of extrapulmonary (intestinal) manifestations in COPD patients.
Material and methods. Small intestinal absorption was studied in 93 COPD patients (22, 36 and 35 patients at stage I, II and III, respectively) in a clinically stable stage of the disease and in 35 healthy controls. The absorption was investigated biochemically and with application of radionuclide methods, blood concentration of TNFalpha was measured with enzyme immunoassay.
Results. The small intestine of patients with moderate and severe COPD showed subnormal absorption of fats, protein, carbohydrates. With the disease progression, this disorder aggravated. The same trend was seen in relation to TNFalpha concentration. A strong direct correlation was found between a high concentration of TNFalpha and a low absorption of 131I-albumin and fatty acids, this high concentration correlated negatively with low absorption of d-xilose.
Conclusion. Relationships between inflammation severity and small intestinal absorption of fats, protein, carbohydrates in patients with moderate and severe COPD means loss of essential nutrients, primarily protein and fats. This is important in understanding of pathobiological processes of development of extrapulmonary (intestinal) manifestations in COPD patients.
About the authors
E I Beloborodova
L A Akimova
V A Burkovskaya
A V Asanova
E V Semenenko
E I Beloborodova
L A Akimova
V A Burkovskaya
A V Asanova
E V Semenenko
References
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO workshop report. Last updated 2006. www.goldcopd.org/.
- Rahman I., Morrison D., Donaldson K., MacNee W. Systemic oxidative stress in asthma, COPD, and smokers. Am. J. Respir. Crit. Care Med. 1996; 154: 1055-1060.
- MacNee W. Oxidative stress and lung inflammation in airways disease. Eur. J. Pharmacol. 2001; 429: 195-207.
- Burnett D., Hill S. L., Chamba A., Stockley R. A. Neutrophils from subjects with chronic obstructive lung disease show enhanced chemotaxis and extracellular proteolysis. Lancet l987; 2: 1043-1046.
- Jeffery P. K. Structural and inflammatory changes in COPD: a comparison with asthma. Thorax 1998, 53: 129-136.
- Saetta M., Baraldo S., Corbino L. et al. CD8+ve cells in the lungs of smokers with chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 1999; 160: 711-717.
- Di Francia M., Barbier D., Mege J. L., Orehek J. Tumor necrosis factor - alpha levels and weight loss in chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 1994; 150: 1453-1455.
- Agusti A. G. Systemic effects of chronic obstructive pulmonary disease. Proc. Am. Thorac. Soc. 2005; 2: 367-370.
- Dahl M., Vestbo J., Lange P. et al. C-reactive protein as a predictor of prognosis in chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2007; l75: 250-255.
- Pinto-Plata V. M., Mullerova H., Toso J. F. et al. C-reactive protein in patients with COPD, control smokers and nonsmokers. Thorax 1998; 61: 23-28.
- Agusti A. G. N., Noguera A., Sauleda J. et al. Systemic effects of chronic obstructive pulmonary disease. Eur. Respir. J. 2003; 21: 347-360.
- Gan W. Q., Man S. F., Senthilselvan A., Sin D. D. The association between chronic obstructive pulmonary disease and systemic inflammation a systematic review and a meta-analysis. Thorax 2004; 59: 574-580.
- Berkes J., Viswanathan V. K., Savkovic S. D., Hecht G. Intestinal epithelial responses to enteric pathogens: effects on tight junction barrier, ion transport, and inflammation. Gut 2003; 52: 439-451.
- Perdue M. H. Mucosal Immunity and inflammation. III. The mucosal antigen barrier: cross talk with mucosal cytokines. Am. J. Physiol. Gastrointest. Liver Physio;. 1999; 277: 1-5.
- McKay D. M., Baird A. W. Cytokine regulation of epithelial permeability and ion transport. Gut 1999; 44: 283-289.
- Elliott S. J., O'Connell C. B., Koutsouris A. et al. A gene from the locus of enterocyte effacement that is required for enteropathogenic E. coli to increase tight-junction permeability encodes a chaperone for EspF. Infect. and Immun. 2002; 70: 2271-2277.
- Fasano A. Toxins and the gut: role in human disease. Gut 2002; 50: 9-14.
- Fleckenstein J. M., Kopecko D. J. Breaching the mucosal barier by stealth: an emerging pathogenic mechanism for enteroadherent bacterial pathogens. J. Clin. Invest. 2001; 107: 27-30.
- Van De Kamer J. H., Bokkel Hunink H., Weyer H. A rapid method for the determination of fat in feces. J. Biol. Chem. 1949; 177: 347-355.
- Беленькая Т. Ю. Распознавание нарушения абсорбции липидов в кишечнике методом Камера. Казан. мед. журн. 1970; 5: 37-38.
- Ишмухаметов Л. И. Радиоизотопная диагностика заболеваний органов пищеварения. М.: Медицина; 1979.
- Беленькая Т. Ю. Проба с d-ксилозой в оценке функции кишечника. Учен. записки. Петрозавод. ун-та. Мед. науки. 1970; 17(5): 78-81.
- Roe J. H., Rice E. W. A photometric method for the determination of free pentoses animal fissues. J. Biol. Chem. 1948; 173 (2): 507-512.
- Зубова С. Г., Окулов В. Б. Молекулярные механизмы действия фактора некроза опухолей-a и трансформирующего фактора роста в процессе ответа макрофага на активацию. Пульмонология 2001; 1: 18-22.
- Agusti A. G. N., Sauleda J., Miralles C. et al. Skeletal muscle apoptosis and weight loss in COPD. Am. J. Respir. Crit. Care Med. 2002; 166: 485-489.
- Petrache I., Otterbein L. E., Alam J. et al. Heme oxygenase - I inhibis TNF-a -induced apoptosis in cultured fibroblasts. Am. J. Physiol. Lung Cell. Mol. Physiol. 2000; 278: 312-319.
- Adams V., Jiang H., Yu J. et al. Apoptosis in skeletal myocytes of patients with chronic heart failure is associated with exercise intolerance. J. Am. Coll. Cardiol. 1999; 33: 959-965.
- Vescovo G., Volterrani M., Zennaro R. et al. Apoptosis in the skeletal muscle of patients with heart failure: investigation of clinical and biochemical changes. Heart 2000; 84: 431-437.
- Gosker H. R., Wouters E. F. M., Van der Vusse G. L., Schols A. M. W. J. Skeletal muscle dysfunction in COPD and chronic heart failure: underlying mechanisms and therapy perspectives. Am. J. Clin. Nutr. 2000; 71: 1033-1047.
- Fourman L. P. R. Absorption of xylose in steatorrhea. Clin. Sci. 1948; 4: 289-294.
- Физиология всасывания / Уголев А. М., Амиров Н. Ш., Файтельберг Р. О. и др. Л.: Наука; 1977.
Supplementary files
