STOP LEUKEMIA

When conducting this study, CLL patients were divided into two subgroups. When leukocytosis is more than 50 × 10 9 / L , the risk of development of leukostasis in the vessels of the lungs increases significantly, and when leukocytosis is more than 200 × 10 9 / L, leukostasis almost always develops . The first subgroup included 10 patients with benign course of CLL (from group I), leukocytosis in peripheral blood of which did not exceed 50 × 10 9 / l. The second subgroup consisted of 15 patients from groups II and III, with the level of leukocytes in peripheral blood from 100 to 850 × 10 9 / l.

The indicator of the microcirculation parameter (PM), which characterizes the state of tissue perfusion, was significantly decreased as the CLL progressed and leukocytosis increased in peripheral blood (Table 10). In patients of the first subgroup, the PM index, despite its decline in some patients, was generally not significantly different from the PM index in healthy individuals. Patients of the second subgroup were diagnosed with a significant decrease in PM . A reliable inverse correlation was established between the level of leukocytosis and a decrease in PM (r = –0.75, P <0.01), between the duration of CLL disease and a decrease in PM (r = –0.6, P <0.05).

The values ​​of the mean square deviation of PM (σ), reflecting the preservation of the mechanisms of blood flow regulation in the microcirculatory bed, did not differ in patients of both subgroups from the control group . The coefficient of variation (Kv), which characterizes the dependence of tissue perfusion on the modulation of blood flow, increased during the tumor progression and in the second subgroup significantly exceeded the control .

When analyzing the rhythmic components of blood flow oscillations, no significant differences in the e-range of patients with CLL have all x subgroups (P> 0.05) . Fluctuations in the e-range on the dopplerograms are due to the metabolic activity of the vascular endothelium, namely the production of nitric oxide. Since no endothelial fluctuations were diagnosed in CLL patients, it was concluded that there were no significant impairments to the metabolic activity of the vascular endothelium of the microcirculatory bed, in this disease.

The amplitudes of oscillations in the N-range (due to sympathetic effects on smooth muscle cells of arterioles and arterio-venular anastomoses) and in the M-range (characterizing the state of the muscle tone of the pre-capillaries regulating blood flow to the nutritive channel) did not have significant differences with control .

The amplitudes of oscillations in the D-range in patients of the first subgroup did not have significant differences compared with the control indicators; in the second subgroup, there was a decrease in the amplitudes of oscillations in the D-range (P <0.05). The decrease in the amplitudes of the respiratory waves is due to insufficient blood flow into the venules, which may be due to the presence of leucostasis in CLL patients in the later stages of the tumor progression.

The amplitudes of oscillations in the C-band decreased during the tumor progression, in the first subgroup they did not have significant differences compared with the control, in the second subgroup the cardiac wave indices decreased (P <0.01). A decrease in cardiac wave values ​​indicates a decrease in arterial blood flow into the microvasculature, which may be due to the presence of vascular accumulations of lymphocytes, in some cases completely blocking the gaps of small vessels.

Significant inverse correlations were found between the level of leukocytosis in peripheral blood and a decrease in the fluctuations in the D and C ranges (respectively, r = –0.64, P <0.01 and r = –0.68, P <0.01), between duration of illness and a decrease

It can be concluded that in patients with CLL, in the process of tumor progression, the parameters characterizing the passive factors of LDF grams (causing fluctuations in blood flow outside the microcirculation system) —the amplitudes of fluctuations in the heart and respiratory ranges (pulse wave from the arteries and suction action ” respiratory pump “from the veins). These oscillations propagate with the bloodstream into the probed area, since the microvasculature, which is an integral part of the circulatory system, is topographically located between the arteries and the veins. Thus, in patients with CLL in the late stages of tumor progression, the flow of arterial blood into the microvasculature and its outflow to the venules due to the presence of leukostasis decrease.Indicators of active factors controlling microcirculation (directly affecting the microcirculation system — amplitudes of vibration in the EH and M bands), modulating blood flow from the vessel wall and realized through its muscular component, change to a much lesser extent. One of the reasons for this can be the fact that active mechanisms create transverse oscillations of the blood flow as a result of alternation of contraction and relaxation of vascular muscles (alternating episodes of vasoconstriction and vasodilatation); passive factors organize longitudinal blood flow oscillations, expressed in periodic changes in the blood volume in the vessel; in the arterioles, the nature of the volume change is determined by the pulse wave, in the venules the workermodulating blood flow from the vascular wall and implemented through its muscular component, change to a much lesser extent. One of the reasons for this can be the fact that active mechanisms create transverse oscillations of the blood flow as a result of alternation of contraction and relaxation of vascular muscles (alternating episodes of vasoconstriction and vasodilatation); passive factors organize longitudinal blood flow oscillations, expressed in periodic changes in the blood volume in the vessel; in the arterioles, the nature of the volume change is determined by the pulse wave, in the venules the workermodulating blood flow from the vascular wall and implemented through its muscular component, change to a much lesser extent. One of the reasons for this can be the fact that active mechanisms create transverse oscillations of the blood flow as a result of alternation of contraction and relaxation of vascular muscles (alternating episodes of vasoconstriction and vasodilatation); passive factors organize longitudinal blood flow oscillations, expressed in periodic changes in the blood volume in the vessel; in the arterioles, the nature of the volume change is determined by the pulse wave, in the venules the workerthat active mechanisms create transverse blood flow oscillations as a result of alternation of contraction and relaxation of vascular muscles (successive episodes of vasoconstriction and vasodilatation); passive factors organize longitudinal blood flow oscillations, expressed in periodic changes in the blood volume in the vessel; in the arterioles, the nature of the volume change is determined by the pulse wave, in the venules the workerthat active mechanisms create transverse blood flow oscillations as a result of alternation of contraction and relaxation of vascular muscles (successive episodes of vasoconstriction and vasodilatation); passive factors organize longitudinal blood flow oscillations, expressed in periodic changes in the blood volume in the vessel; in the arterioles, the nature of the volume change is determined by the pulse wave, in the venules the worker rhythm of the respiratory pump . Lecostasis in small vessels of the lungs and bronchi present in a significant number of CLL patients to a greater extent impede longitudinal fluctuations in blood flow.

All patients who underwent diffuse endobronchitis during PBS underwent therapeutic measures: active aspiration of the bronchial contents, selective / partial lavage with dioxidine solution, local administration of antibiotics, etc. Two to three weeks after the start of treatment, endobronchial LDF was re-performed in these patients. Changes in the microcirculatory blood flow in the mucous membrane of the proximal bronchi in CLL patients, after normalization of the bronchoscopic picture, were preserved, which is explained by the morphological changes in the microvasculature vessels in CLL patients.

Disruption of microhemocirculation leads to the development of tissue hypoxia, metabolic disturbances in the mucous membrane cells of the bronchi and, along with marked secondary immunodeficiency, contribute to the occurrence of the inflammatory process in the bronchi. Violation of microhemocirculation supports the inflammatory reaction in the bronchi, contributes to its recurrent course, the development of disturbances in gas exchange and the ineffectiveness of antibacterial therapy. In 60% of patients with a progressive course of CLL (40% of the total number of patients with CLL), with PBS, an inflammatory process in the bronchi has been diagnosed with no pronounced clinical manifestations. However, the presence of a chronic focus of infection may contribute to the development of pneumonia in patients with a progressive course of CLL. Considering the above, patients with a progressive course of CLL,in the absence of contraindications, diagnostic bronchoscopy is recommended, and in the presence of an inflammatory process in the bronchi, the appointment of therapeutic measures.

The presence of the inflammatory process in the bronchi, along with their leukemic infiltration, contributes to an increase in bronchial resistance in patients with CLL group III.

Violation of microhemocirculation indices is registered earlier than the clinical manifestations of the bronchopulmonary system lesions appear. Thus, the study of endobronchial microcirculation can help predict the occurrence of inflammatory diseases of the bronchopulmonary system in patients with CLL.

The effect of cytostatic therapy on microcirculation in patients with CLL was studied. Currently, in patients with a progressive course of CLL, in the absence of severe concomitant pathology and autoimmune complications, the treatment of choice are protocols containing fludarabine (monotherapy with fludarabine or its combination with cyclophosphamide, rituximab, mitoxantrone). The use of these protocols allows in most cases to achieve complete or partial remission of the disease. One of the criteria for complete remission is a reduction in the number of lymphocytes <4.0 × 10 9 / l, partial remission , a reduction by 50% in the number of lymphocytes of peripheral blood . In patients with groups II and III treated according to these protocols, after the normalization of the number of leukocytes, endobronchial LDF was repeated. All of them showed a significant improvement in the PM indicators, but in no case did the PM indicators completely normalize. An improvement (but not normalization) of the oscillation amplitudes in the respiratory and cardiac ranges was noted .

The persistence of endobronchial microhemocirculation disorders in patients with CLL, after achieving complete remission, is explained by the etiology of factors affecting the microcirculation indices. In addition to leukocytosis and anemia, abnormalities of platelet and plasma hemostasis, the state of the endothelium of the vessels, regulation of tissue vascular tone, pH and pO 2 , hormonal function and many other factors affect the reduction of microhemocirculation parameters .

Chlorambucil therapy, at present, is regarded only as a palliative treatment and is used in cases of a calm course of B-CLL in elderly patients with an adverse somatic status. In case of chlorambucil therapy, complete remission of CLL was not achieved in any case, leukocytosis was preserved. In patients treated with this drug, there was no significant improvement in microhemocirculation indices.

Advantage of modern CLL chemotherapy protocols (FC, FCR, FCM, etc.) when using which appeared the possibility of achieving complete remission, besides a significant reduction in the tumor mass, is an improvement in microcirculation in the vessels of the bronchopulmonary system. The restoration of microhemocirculatory blood flow contributes to the improvement of tissue trophism and, accordingly, to a decrease in the incidence of AML in CLL patients in remission.

Note: P 1 – significance of differences compared with control; P 2 – the significance of the difference between the indices of LDF, before and after achieving remission.

Thus, the study of endobronchial microhemocirculation can help predict the occurrence of inflammatory diseases of the bronchopulmonary system in patients with CLL. The informativity of the endobronchial LDF method is highly informative in diagnosing vascular and intravascular disorders of the microcirculatory bed of the bronchial mucosa, in identifying early signs of microhemocirculation disorders. The use of this method allows the assessment of the dynamics of microcirculatory disorders in the mucosa of the proximal bronchi during the treatment of CLL.

In the study of general and zonal ventilation of the lungs using the rheography method in patients of group I, no significant changes were found, compared with the control. In group II, there was a decrease in the eographical index of the respiratory volume (DOR) and the eographical indicator of the minute ventilation volume (MVD) of the middle and lower zones of both light, and an increase in the DOF and MVR of the upper zones. The total value of the MPR from all zones of the lungs was reduced by 25.9% (P <0.05) as compared with the control. The greatest changes in regional ventilation were found in patients of group III, they showed a significant decrease in dose rates and MOP in each zone of the lungs, a decrease in the total indicator of MOV from all zones of the lung, compared with controls , by 43.8% (P <0.001) . In patients with groups II and III, there was a redistribution of ventilation from the lower and middle zones to the upper zones of both lung, as can be seen from the increase in the MOVr ratio of the upper zones / MOVr of the lower zones of the lungs .

Indicators of eographically minute minute pulsatory blood flow (MCR) from each of 6 light zones in group I did not significantly differ from those of control. In patients of group II, there was a decrease in perfusion in the middle and lower zones of both lungs and its increase in the upper zones (since areas with increased ventilation are supplied with blood), the overall intensity of MPKr from all zones of the lungs is reduced by 17.4% (P <0.05). In group III, a significant decrease in perfusion was noted in the middle and lower zones of both lungs, in the upper zones, the perfusion indices did not significantly differ from the control, the total intensity of MPCr from all lung zones was reduced by 34.3% (P <0.001). In patients with groups II and III, there was a redistribution of pulmonary blood flow from the lower and middle zones to the upper zones of both lungs. . Redistribution of blood flow to the upper zones was achieved by increasing vascular resistance in the lower and middle zones of both lungs, as evidenced by a decrease in the average blood filling rate (SSC) and lengthening the a-Q interval in these zones . An important rheographic sign indicating the state of venous resistance in the pulmonary circulation is the diastolic-systolic coefficient (DSC), the highest coefficient values ​​were recorded in patients of groups II and III in the middle and lower zones of the lungs.

The development and progression of hypoxemia is associated with an increase in pressure in the pulmonary artery (LA) system. In Group I, the SrDLA indicator (14.7 ± 0.7 mm. Hg. Art.) Did not have significant differences compared with the control group (14.99 ± 0.61 mm Hg. Art.). Patients II (18.2 ± 1.08 mm. Hg. Art.) And III (22.16 ± 1.6 mm. Hg. Art.) Groups showed a significant increase in SrDLA compared with control (P <0 , 05 and Р <0.001, respectively).

EHOKG and IDKG were performed on 54 CLL patients aged from 40 to 70 years, without concomitant COPD (13 out of I, 26 out of II and 15 out of III groups). Patients with heart defects, atrial fibrillation, high blood pressure and other diseases accompanied by primary lesions of the left heart areas were excluded from the study, since this pathology has a significant impact on intracardiac hemodynamics [149, 170, 254]. In 34 patients (63%) SrD-LA indices in conditions of rest did not exceed 20 mm. Hg Art. Of these, 28 people (52%) had SrDLA values ​​within 9–16 mm. Hg Art., in 6 patients (11%) – 17 – 20 mm. Hg Art. Pulmonary hypertension (PH) was detected in 20 (37%) people. Indicators SrDL were within 21 – 32 mm. Hg St, on average – 22.5 ± 0.7 mm. Hg Art. These are patients from groups II and III, of whom 3 had progressive, 9 had tumor and 8 had splenic CLL. The highest rates of SrDLA were found in patients with splenic and neoplastic forms of CLL in the later stages of tumor progression, with a significant increase in the liver and spleen. Progressive hemoblastosis was noted in all patients with high rates of SrDLA, 6 patients were diagnosed with terminal stage of the disease.

In the study of the functional ability of the right from the heart of the business in patients of group I, a decrease in the ratio E / A TC was observed . In group II, a further decrease in the E / A TC ratio was diagnosed . In group III, a significant increase in KDR, KDO and RV CSR was diagnosed. In patients with group III, the cardiac index (SI) of the pancreas was increased, which is associated with an increase in heart rate in the later stages of hemoblastosis, due to anemia and intoxication. A decrease in the maximum blood flow velocity in the early diastole (E TC ), an increase in the maximum blood flow velocity in the late filling phase of the pancreas (A TC ) and a decrease in the E / A ratio were detected. Increase A TC in the process of tumor progression in CLL can be explained by an increase in heart rate in these patients. E TC depends on the difference in pressure gradient in the cavities of the right heart and is not related to the heart rate, therefore, this indicator does not change in groups I and II. A decrease in E TC was diagnosed only in patients of group III, where dilatation of the pancreatic cavity takes place. Thus, early signs of diastolic dysfunction of the pancreas were detected in patients with CLL I group; in the II and III groups, disturbance of the diastolic function of the pancreas progressed. A significant decrease in the fraction of the prostate ejection was diagnosed only in patients of group III. The index of TMPS PZHDincreased in patients in groups II and III .

In group I patients with CLL, there was an increase in TMZS LC , in groups II and III, it continues to increase. In patients with groups II and III, the thickness of the interventricular septum increases. An increase in the A MC and reduction ratio E / A is diagnosed at the early stages of tumor progression (I group), which is evidenced by the presence of left ventricular diastolic dysfunction. In the process of tumor development, disorders of LV diastolic function are progressing: A MKincreases, reaching maximum values ​​in group III, and, accordingly, the ratio E / A MK significantly decreases . Due to an increase in heart rate, an increase in the LV LV and LV LV . Only in group III there was a significant increase in KDR, KSR, KDO, KS O and a decrease in LV EF .

The revealed changes can be explained by tumor intoxication, cardiotoxic effects of cytostatics, rheological disorders in the coronary vessels in patients with high leukocytosis, anemia, and in some cases lymphoid infiltration of the myocardium. Dilatation of the cavities of both ventricles, an increase in their size and corresponding volumes, a decrease in the ejection fraction were diagnosed only in CLL patients in stage C (with the presence of anemic syndrome). Patients with CLL are people, in the overwhelming majority of cases, elderly, many of them had coronary heart disease, which also contributed to the violation of the LV myocardium and the development of circulatory failure.

Ultrasonic examination of the diaphragm in patients of group I showed no significant changes compared to controls. The thickness of the diaphragm (TD) did not differ from that in the control group. The position, shape, echogenicity of the diaphragm also did not change. Excursion of the diaphragm with calm (EDS) and forced (EDF) breathing did not differ from control. In patients with group II, the thickness of the diaphragm did not change. But the echo structure of the diaphragm became non-uniform, flattening of its dome was noted. The excursion of the diaphragm during calm and forced breathing decreased significantly. In group III, the largest morphological changes in the diaphragm were revealed. The dome was not clear. Its echostructure became non-uniform. Significantly decreased excursion of the diaphragm with calm and forced breathing.Violation of the excursion of the diaphragm and its morphological reorganization, in case of CLL, contributes to severe hepato- and splenomegaly, which occur in the majority of patients of groups II and III. Compression of the diaphragmatic muscle with enlarged liver and spleen significantly reduces its mobility and is one of the causes of the onset of severe and prolonged bronchopulmonary pathology in CLL. Another cause of dysfunction of the diaphragm in CLL is its specific leukemic lesion.Another cause of dysfunction of the diaphragm in CLL is its specific leukemic lesion.Another cause of dysfunction of the diaphragm in CLL is its specific leukemic lesion.

A correlation analysis was performed between indicators of pulmonary and intracardiac hemodynamics, the functional state of the diaphragm, respiratory function and blood gas composition in CLL patients at different stages of tumor progression. Patients of groups II and III showed a significant correlation between a decrease in the excursion of the diaphragm with a quiet and forced breathing and a decrease in the MOR of the lower and middle zones of the lungs. In the second group, the correlation coefficient between the decrease in the EDF and the decrease in the MOR of the lower zones was 0.87 (P <0.001); between a decrease in EDF and a decrease in the MOB of the middle zones of 0.68 (P <0.01). The correlation coefficient between the decrease in the EDS and the decrease in the MOR of the lower zones was 0.72 (P <0.01); between a decrease in the EDS and a decrease in the MOB of the middle zones of 0.64 (P <0.05). In group III, a clear correlation was also diagnosed between a decrease in EDF and a decrease in the MOBR of the lower (0.66; P <0.05) and medium (0.65; P <0.05) zones of the lungs. The correlation coefficient between the decrease in the value of the EDS and the decrease in the MOR of the lower zones was 0.64 (P <0.05), the middle zones 0.62 (P <0.05). No significant correlation was found between the EDF, EDS and MOBP indices of the upper zones of the lungs in patients with CLL. Correlation analysis confirms the assumption of the important role of a violation of the excursion of the diaphragm in CLL patients in reducing the ventilation capacity of the lower and middle zones of the lungs and the redistribution of ventilation in the upper zones.

A reliable average inverse correlation was established between a decrease in the excursion of the diaphragm during forced and quiet breathing and an increase in AHDLA in patients II (r = –0.59; P <0.05 and -0.51; P <0.05) and III (r = – 0.66; P <0.01 and – 0.61; P <0.05) groups. A strong positive correlation was found between a decrease in the MOVP of the sum and a decrease in the pO 2 of blood in patients of the II (0.86; P <0.001) and III (0.9; P <0.001) groups. The inverse correlation relationship between the decrease in blood pO 2 and the increase in SrDLA in patients of the II (r = –0.65; P <0.01) and III (r = –0.9; P <0.001) groups was diagnosed. Smaller correlation coefficient and reliability in group II is explained by insignificant changes in pO 2 indices in these patients. and SrDLA. It can be concluded that a violation of the functional capacity of the diaphragm leads to impaired ventilation of the middle and lower zones of the lungs, as a result of which hypoxemia and PH develop.

A significant increase in the liver and spleen, which occurs in many patients with a progressive course of CLL and in the terminal stage of the disease, contributes to a high standing of the diaphragm case and disruption of its excursion. The diaphragm is the main respiratory muscle, which, under physiological conditions, provides 2/3 of the vital capacity of the lungs, and 70–80% of inspiration with forced respiration [208]. So, according to J.L. Shika and V.I. Sobolev, as a result of the movement of the diaphragm, the lower and 40-50% of the ventilation volume of the upper lobes of the lungs is fully ventilated. Violation of the excursion of the diaphragm, the main respiratory muscle, is an important factor in the violation of respiratory function in the late stages of tumor progression in patients with CLL. Compression of the lower parts of the lungs with enlarged liver and spleen is an important factorreducing respiratory volume lower zones and redistribution of ventilation in the upper zones of the lungs. It can be argued that mechanical compression of the diaphragm with enlarged liver and spleen and its specific leukemic lesion contribute to impaired contractility of the diaphragm, which is one of the reasons for the development of hypoxemia and PH in patients with CLL II group without an associated broncho-obstructive process. This group included a greater number of patients with the splenic CLL.

Other causes of hypoxemia and PH in patients with CLL in stage B are a decrease in microhemocirculation and a severe, prolonged course of infections of the bronchopulmonary system, accompanied by impaired ventilation and hemodynamics of the pulmonary circulation.

In the later stages of tumor progression of CLL, the lymph nodes in the chest cavity acquire a dense texture, lymphoid infiltration appears in the lungs and pleura (with the development of specific lymphoproliferative pleurisy), a compression syndrome develops, leading to impaired bronchial patency and pulmonary ventilation, as a result of the pulmonary pulsations of the pulmonary pulmonary regimen. – gain a heavy and long current. These changes contribute to a decrease in pO2 and an increase in pressure in the aircraft system. This explains the higher value of SrDLA in patients of group III. As CLL progresses, myocardial dystrophy develops in such patients, which contributes to impaired hemodynamics of the ICC and an increase in pressure in the PA.

Thus, four mechanisms of LH development in patients with CLL who do not have a concomitant bronchial obstruction process can be distinguished: 1) thoracodiaphragmatic due to decreased excursion of the diaphragm, when it is compressed with enlarged liver and spleen and leukemic lesion ; 2) bronchopulmonary – severe and prolonged course of infectious and specific leukemic processes; 3) vascular due to impaired blood rheology in the vessels of the ICC; 4) myocardial degeneration.

For the first time, a comprehensive examination of the bronchopulmonary system (spirography, traditional X-ray, regional lung rheography) was performed in 1997 (at that time stage B according to the Binet classification was at that time). On radiographs and tomograms, an increase in mediastinal lymph nodes was determined. No other pathology was identified.

In 2006, the patient was diagnosed with stage J. according to J. Binet’s classification: hemoglobin – 75g / l, erythrocytes – 2.6 × 10 12 / l, platelets – 70 × 10 9 / l, leukocytes – 280 × 10 9 / l, lymphocytes – 98%, segmented – 2%; marked lymphadenopathy – lymph nodes of all groups up to 3-4 cm in diameter, with a densely elastic consistency; splenomegaly was the leading clinical syndrome — the spleen occupied the entire left half of the abdominal cavity; the liver was significantly enlarged .

As a result of a comprehensive examination of the bronchopulmonary system of patient A. in 2006, the following changes were diagnosed. With CT of the lungs – a significant increase in lymph nodes in the chest cavity, the high position of the dome of the diaphragm. During spirography, there were no impairments in the ventilation function of the lungs. During peak flow measurements, the PSV indicators were as follows: in the morning hours – 96% D, in the evening hours – 101% D. During pneumotachography, an increase in bronchial inhalation resistance was observed (3.3 cm.vod.st / l / s) and on exhalation (3.6 cm.v.st./l / s). When fibrobronchoscopy was diagnosed with bilateral diffuse endobronchitis, IV Art. LDF data: PM – 23.09 PE, σ – 10.89 PE, Kv – 47.16%, Ae – 6.2 PE, An – 3.93 PE, Am – 3.18 PE, Ad – 2.7 PE, Ac – 1.6 PE.

During the 13-year study period, a fatal outcome was found in 95 CLL patients. The mortality of patients with CLL was analyzed and morphological changes in the lungs, bronchi, and pleura in these patients were studied according to autopsy data. The terminal stage of CLL is more often manifested by the transformation into a large cell lymphosarcoma, the development of cachexia. Prolymphocytic crisis was observed in only two patients. Blast crisis CLL in our study is not registered. The immediate causes of death of patients with CLL are given.

Histological examination of autopsy material showed lymphoid infiltration of the lungs and bronchi in 43 patients (45%). However, only 5 patients had massive leukemic infiltration, which was radiologically detected in the form of focal or infiltrative shadows, and then the diagnosis was made after long-term follow-up of the disease and exclusion of other local processes in the lungs. In the same patients, lymphoid infiltration was diagnosed macroscopically at autopsy. Histological examination of the lungs in these situations revealed a total monomorphic leukemic infiltration along the interalveolar septa, filling the lumen of the alveoli and vessels with lymphocytes . In all other cases, lymphoid infiltration was detected only with microscopic Optical research . Lymphoid infiltration in the lungs was predominantly interstitial. Often, in the stage of malignant transformation, there was a total infiltration of the interstitial lung tissue. Lei goat infiltration was very pronounced along the bronchi, small vessels and in the interalveolar septa, often it was of a confluent nature. Hemorrhages were observed in the interstitial and respiratory tissue with a perivascular edema. Foci of leukemic infiltration in respiratory structures were less frequently observed.

Histological examination in the lungs showed an expansion and congestion of blood vessels, the lumens of many vessels were filled with lymphocytes (leukostasis) . Leukostasis was especially frequently detected in small-caliber vessels. The accumulations of lymphocytes in these situations completely blocked the gaps of small vessels, causing a significant disruption of microcirculation . In some patients, infiltration of the walls of the pulmonary vessels with tumor cells and multiple perivascular arteries of lymphoid cells were noted.

Peribronchial, perivascular, interstitial sclerosis was revealed in many patients. Multiple atelectasis of the lung tissue alternated with areas of emphysematous dilatation of the alveoli, as well as edema and sclerosis of the interalveolar septa . In patients with CLL, it is possible to express an assumption about the compensatory nature of the localized pulmonary emphysema. In some areas, in the presence of diffuse lymphoid infiltration of the pulmonary tissue and an increase in bronchopulmonary lymph nodes, alveoli are excluded from ventilation due to atelectasis. A decrease in the area and ventilation capacity of other alveoli due to edema, sclerosis of the interalveolar septa, lymphoid infiltration of the interalveolar septa, desquamation of the alveolar epithelium is noted. In the remaining parts of the lung, the expansion of the alveoli occurs compensatory. These changes are more pronounced in CLL patients in the later stages of the tumor progression. Speaking of emphysema in patients with CLL, it is also necessary to take into account the elderly age of most patients,in this case, senile emphysema may occur.

Morphometric studies were conducted in patients who died in the presence of CLL. When performing a morphometric study of the bronchi and alveoli, a comparative analysis was carried out with similar indicators of 30 absolutely healthy people, equal in age and sex, who died from injuries incompatible with life and who did not have a history of hemoblastosis and bronchopulmonary pathology (control group).