The aim was to highlight the leading links of pathogenesis of chronic obstructive pulmonary disease (COPD) using published data and the results of own research. Material and methods. The publications of the last 5 years have been picked up for review from Pubmed library. Own research has been based on retrospective analysis of medical records from 470 patients with COPD (246 men and 224 women, median age 62 years). Results. According to literature data chronic persistent inflammation, manifesting by activation of multiple cells with excessive production of number of biologically active substances, is a leading link of COPD pathogenesis. Second important link of COPD pathogenesis is energydependent hypoxia with signalling pathway change and super expression of hypoxia-inducible factor. An important role plays chronic disease anaemia, occurring due to effect of pro-inflammatory cytokines and hypoxia-inducible factor which, in turn, preserves inflammation and hypoxia. According to own data a decrease of blood oxygenation and decline in lung function also testify to existing relationship between inflammation and hypoxia. Active inflammation correlated with decreased bronchial patency. Anaemic syndrome in COPD patients was associated with higher levels of neutrophils, ESR, C-reactive protein, total fibrinogen, seromucoids and integral haematological indices, as well as low blood oxygenation and decrease of velocity parameters of lung function. Conclusion. Inflammation, hypoxia and anaemia are three connected links of pathogenesis of COPD, which create vicious circle and possibly determine disease progression. Key words: chronic obstructive pulmonary disease, pathogenesis, inflammation, hypoxia, hypoxia-inducible factor, anaemia.
Patients with chronic obstructive pulmonary disease (COPD) in combination with anemia of chronic disease (ACD), are of particular interest to both scientific and practical health care. The purpose of the work - to study the activity of systemic inflammation.Material and methods. The results of the examination of 475 patients with exacerbation of COPD were analyzed, which were divided into two groups: group I - 155 people (61,3% men and 38,7% women) with ACD; group II - 320 patients (46,9% of men and 53,1% of women) without the anemic syndrome. Determination of the activity of the inflammatory process was performed by hemocytogram, serum markers of inflammation and integrated hematological indices. The results of the study. It was found that COPD in combination with ACD was accompanied by activation of the inflammatory process (erythrocyte sedimentation rate, segmented neutrophils content) and suppression of lymphocyte-monocyte inflammation, significantly higher integral hematological indices (leukocyte shift index; ratio of leukocytes, non-segmented neutrophils and all neutrophils to the erythrocyte sedimentation rate; the ratio of neutrophils to lymphocytes and the integrated index of inflammation), which increased with the deepening of the anemic syndrome, increasing patients age and was more pronounced in women. Activation of inflammation was associated with deterioration of bronchial patency according velocity parameters (Tiffno index, mean and peak volumetric velocities, maximal volumetric velocities by 25% and 75% of the forced ungs vital capacity). Anemic syndrome was also associated with higher levels of C-reactive protein (p>0,05), general fibrinogen (p<0,05) and seromucoids (p>0,05), the content of which varied in parallel with the leukocyte shift index. Conclusion. Anemic syndrome, as a manifestation of persistent systemic inflammation, worsens the course of a chronic obstructive pulmonary disease through affecting the respiratory function and the inflammatory process activation.
Aim. Comparative efficacy analysis of autologous hematopoietic stem cells (HSC) prior to auto-HSCT in patients with lymphoproliferative disorders (LPDs) and multiple sclerosis (MS). Materials & Methods. The trial included 237 patients: 103 LPD and 134 MS patients. In 225 patients HSC mobilization involved only colony-stimulating factors (CSFs), in 12 patients chemotherapy (cyclophosphamide, etoposide) was combined with CSFs. On the intended date of cytapheresis all the patients were tested for CD34+ marker expression. Сytapheresis followed in the patients with CD34+ count more than 0.01 x 10<sup>6</sup>/mL. Results. In 23 (22 %) LPD patients CD34+ count was too low for auto-HSCT (‘collection failure group'). Within this group 19 patients received CSF mobilization, and 4 patients received chemotherapy + CSF. Plerixafor was administered in 5 patients, in 4 of them a repeated mobilization also failed to collect enough cells. In 80 LPD patients the number of mobilized and collected CD34+ cells was sufficient for auto-HSCT (‘collection success group'). Within this group 77 patients received auto-HSCT, 74 patients were treated with CSF mobilization, 6 patients received chemotherapy + CSF, and in 11 patients plerixafor was administered. Median total number of CD34+ cells in the ‘collection success group' was 2.7 x 10<sup>6</sup>/kg. All 134 MS patients had enough CD34+ cells for auto-HSCT. All of them received CSF mobilization. Median total number of CD34+ cells in the MS group was 2.34 x 10<sup>6</sup>/kg. Potential risk factors for HSC mobilization failure in LPDs were evaluated. They included age, gender, prior radiotherapy, number of antitumor treatment lines prior to auto-HSCT, clinical response prior to auto-HSCT (complete/partial remission or stabilization), and HSC mobilization regimen. These factors with the exception of gender were not associated with mobilization failure parameters. The worst mobilization outcomes were reported in male patients. Conclusion. In 22 % of LPD patients the planned high-dose chemotherapy and auto-HSCT failed due to insufficient counts of autologous CD34+ cells in apheresis product. Male gender can be considered to be a prognostic factor of mobilization failure in LPDs.
A retrospective analysis of 470 patients with chronic obstructive pulmonary disease and anemia was conducted in order to determine hematological indices. 17 markers of inflammation activity, endogenous intoxication, adaptation, nonspecific and immune reactivity were calculated during this analysis. It was established that the course of chronic obstructive pulmonary disease with anemia was accompanied by a more pronounced inflammation syndrome with a significant increase in stab and segmented neutrophilic granulocytes, an acceleration of the erythrocyte sedimentation rate, and significantly higher integral hematological inflammation indixes (leukocyte shift index, indexes of correlation: -leukocytes to erythrocyte sedimentation rate, -neutrophils to erythrocyte sedimentation rate, -nonsegonuclear neutrophils to erythrocyte sedimentation rate, neutrophils to lymphocytes; inflammation activity index, integrated inflammation index), large endogenous intoxication (neutrophil reactive response index, leukocyte intoxication index), change in adaptation, nonspecific reactivity (decrease in adaptation index, immune reactivity and allergization, and increase in the ratio indices: lymphocytes to monocytes, - lymphocytes to eosinophils) with activation of the phagocytic link of nonspecific protection over cell-humoral. The determination of integral hematological indices is an important, informative and accessible method for assessing the general condition of a patient with chronic obstructive pulmonary disease and anemia.
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