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.

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).

A morphological study of segmental bronchi in patients with CLL showed a decrease in the number of neutrophils, eosinophils, plasma and mast cells in the submucosal layer. In patients who died due to the progression of CLL, an increase in the number of lymphocytes at all levels of the bronchial tree was observed. In most patients, the height of the mucosal epithelium and the thickness of the mucous membrane of the segmental bronchi were significantly reduced. In many patients, thinning of the basement membrane is noted, and growth of connective tissue in the submucosal layer. Atrophic changes of the mucous membrane should be explained by a violation of endobronchial microhemocirculation, which largely depends on the extent of leucostasis .

The walls of many vessels of the bronchopulmonary apparatus in patients with CLL, compared with the control group, looked somewhat thickened due to edema and lymphoid infiltration. Dilation of the vessels of the lungs and bronchi, some of which was filled with lymphocytes, was noted. The ratio of vascular diameter to thickness in patients with CLL was 12.9 ± 0.05, in the control group it was slightly lower – 11.8 ± 0.04. The degree of vascular plethora was changed, in CLL patients (67 ± 2.7%) it was higher than in the control group (55.3 ± 3.7%; P <0.05).

The thickness of the interalveolar septa in many of the dead was increased due to their edema (55 ± 5.2 compared to 40 ± 0.08 μm in the control; P <0.01). Due to the large number of emphysematous transformed tissue in patients with CLL, an increase in the area of ​​the alveoli is observed (172 ± 28 μm 2 ), but due to the large variability of this indicator, this increase, compared with the control, was not significant (132 ± 10 μm 2 ; P> 0.05).

Specific lymphoproliferative pleurisy was diagnosed in 21 patients. 19 found to be fatal. In cytological examination of exudate, lymphocytes were found in a large number of these patients. Histological examination revealed diffuse or focal lymphoid pleural infiltration .

The study of the diaphragm in 45 patients with a significant increase in the liver and spleen revealed the predominance of myocytes of medium size (cross-sectional area – 501 ± 14.2 μm 2 ), but there was an increase in the newly formed large myocytes (1969 ± 31 μm 2 ) and small (286, 8 ± 17 microns 2 ) sizes. Necrobiotic changes in myocytes were diagnosed . In these patients, a significant growth of stroma was observed around the vessels and the intermuscular space. Revealed large areas lipomat Oz . Such dystrophic changes are caused by dysfunction of the diaphragm, due to its compression with enlarged liver and spleen. A histological examination showed lymphoid and filtration of the diaphragm and lymphocytic stasis in the vessels, which also contributes to the violation of the contractile ability of the diaphragm and dystrophic changes in muscle fibers. In 30 patients there was no significant increase in the liver and spleen. The sizes of myocytes of the diaphragm in such patients did not have significant differences with those of practically healthy individuals, without concomitant bronchopulmonary diseases and hemoblastosis, who died from injuries (96% were also average myocytes) . However, many patients without severe hepato – and splenomegaly showed lymphoid infiltration of the diaphragm and accumulation of lymphocytes in the lumen of the vessels. Lymphoid infiltration of the diaphragm has never reached a size where it could be determined macroscopically, in all cases these were histological findings.

An enlarged lymph nodes in the chest cavity was detected in 73 (76.8%) deaths from CLL (according to the data of an intravital radiological study of 228 patients with CLL, an increase in the lymph nodes in the chest cavity was diagnosed in 66.7% of patients). At the same time, an increase in mediastinal lymph nodes was observed in 65 patients, aortic arches in 30 people, paratracheal in 10, paraesophageal in 8, bifurcation in 12, bronchopulmonary in 65 cases.

In 14 patients, the enlarged bronchopulmonary lymph nodes appeared in the form of large packages, dense, rocky consistency, were brazed into conglomerates and caused compression, infiltration, and lung tissue and bronchi. Histological analysis of these lymph nodes revealed signs of transformation into large-cell lymphosarcoma (Richter syndrome). In all these patients, death occurred when pneumonia was added. For patients who died without obvious signs of sarcoma transformation, compression syndrome in the chest cavity is not typical. The lymph nodes of the mediastinum, even with a significant increase, remained soft consistency and did not squeeze the surrounding tissue.

Leukostasis in vessels with CLL is not clinically determined, as a rule [237]. But as mentioned earlier, their presence explains the impaired microhemocirculation , which contributes to the development of morphological changes in the bronchi and lungs, a severe and prolonged course of inflammatory processes of the bronchopulmonary system. In order to identify statistically significant indicators that could indicate the presence of leukostasis in the pulmonary vessels, a discriminant analysis was carried out for which the statistical package STATISTIKA 6.0 was used. The study included patients who did not have a concomitant pulmonary disease. All this sick a full instrumental examination of the bronchopulmonary system was performed in vivo, and after autopsy, morphological changes in the lungs and bronchi were studied. The results of discriminative analysis are as follows:

Statistically significant signs (P <0.05): 1) Leukocytosis in peripheral blood is more than 100 × 10 9 / l (p = 0.0001); 2) Reduction of PM during endobronchial LDF less than 50 PE (p = 0.001); 3) Reduction of Ac when performing endobronchial LDF less than 2.5 PE (p = 0.0015); 4) Reducing Hell when conducting endobronchial LDF less than 2.5 PE (p = 0.0025); 5) prolonged and recurrent infections of the bronchopulmonary system (bronchitis, pneumonia) (p = 0.032); 6) B – symptoms, p = 0.035.

The combination of the above indicators with a high degree of probability may indicate the presence of leucostasis in the vessels of the microcirculatory bed of the bronchopulmonary system in patients with CLL. As it was established by previous studies, the risk of developing leukostasis occurs with an increase in leukocytosis more than 50 × 10 9 / l, with leukocytosis more than 200 × 10 9 / l, they almost always develop . The decrease in the microhemocirculation parameter, the amplitudes of oscillations in the cardiac and respiratory ranges in CLL is largely due to the presence of leucostasis in the vessels of the microvasculature. “B” symptoms (fever, night sweat and weight loss) in CLL appear in the later stages of tumor progression, when the tumor process gets out of control of cytostatics and progressive leukocytosis is observed in the blood. In these patients, a prolonged and recurrent AML is observed.

Statistically insignificant signs: 1) A decrease in hemoglobin of less than 100 g / l (p = 0.2); 2) Increase in bronchopulmonary lymph nodes according to CT data (p = 0.28); 3) Reduction of the total MPKr index during lung rheography of less than 50 ohms / min (p = 0.9).

In CLL, a decrease in the hemoglobin level can be caused not only by bone marrow infiltration with tumor cells with crowding out all the hemopoiesis sprouts, but also autoimmune conflict. An enlarged lymph node, including bronchopulmonary, is not always accompanied by high leukocytosis in the peripheral blood. In the rheographic method of studying pulmonary blood flow, pulsatory vibrations of large vessels are detected. Therefore, these indicators for the diagnosis of leukostasis in the vessels of the lungs and bronchi are not reliable.

Classifying functions: Group1 = -1.21-0.57 * X1-1.62 * X2 + 0.87 * X3 + 1.77 * X4 + 0.74 * X5 + 1.07 * X6 + 0.63 * X7 + 1.05 * X8 + 1.46 * X9. Group 2 = -86.8 + 46.5 * X1 + 41.1 * X2 + 32.2 * X3 + 25.5 * X4 + 39.2 * X5- 9.7 * X6 + 4.7 * X7-2 , 8 * X8 + 1.9 * X9.

The obtained classification functions can be used to assign a patient to group 1 or group 2. For this indicator values ​​obtained from the newly admitted patient, are entered into the classification functions for groups 1 and 2. The classification functions are calculated, and the patient relates to the group for which the calculation gave a greater value.

As an example, here is an extract from the case history No 12368. Patient S., born in 1940. Diagnosis: Chronic lymphocytic leukemia, splenic form, stage C according to the classification of Binet. The diagnosis was made in 2002, death was ascertained in 2006.

Clinical research data from 2005. Peripheral lymph nodes of all groups up to 2 – 3 cm in diameter, soft-elastic consistency. The spleen is significantly enlarged, occupies the entire left half of the abdomen. The lower edge of the liver is palpable 14 cm below the right costal arch. Blood count: hemoglobin – 106 g / l, erythrocytes – 3.3 × 10 12 / l, platelets – 50 × 10 9 / l, leukocytes 150 × 10 9 / l, lymphocytes – 80%, segmented core – 12% , eosinophils – 3%, monocytes – 5%.Immunophenotyping of peripheral blood lymphocytes – CD5 +, CD19 +, CD20 +, CD22 +, CD23 +. Radiographic examination of the chest: mediastinal lymph nodes are not enlarged, the high position of the diaphragm dome. These endobronchial LDF: PM – 23.8 PE, σ – 11.7PE, Kv – 45.1%, Ae – 6.1 PE, An – 3.5 PE, Am – 3 PE, Hell – 2.4PE, Ac – 1.65 PE. When conducting a regional rheography, MOVr (soum) -70 ohm / min, MPKr (soum) – 65 ohm / min.

During the discriminant analysis, the following data was available: leukocytosis> 100 × 10 9 / l (1), PM <50 PE (1), Reduction of Ac <2.5 PE (1), Reduction of Ad <2.5 PE (1 ), relapsing and protracted AML (1), B-symptoms (1), MPKr <50 ohms / min (0), Decrease in hemoglobin <100 g / l (0), increase in bronchopulmonary lymph nodes at CT (0 ).

The following classification functions were calculated: Group 1 = -1.21-0.57 * 1-1.62 * 1 + 0.87 * 1 + 1.77 * 1 + 0.74 * 1 + 1.07 * 1 +0, 63 * 0 + 1.05 * 0 + 1.46 * 0 = 2.19. Group 2 = -86.8 + 46.5 * 1 + 41.1 * 1 + 32.2 * 1 + 25.5 * 1 + 39.2 * 1-9.7 * 1 + 4.7 * 0- 2.8 * 0 + 1.9 * 0 = 88.0.

As can be seen from the calculation results, the value of the classifying function for group 2, equal to 88.0, is greater than the value of the function for group 1. Consequently, the patient was assigned to group 2, the combination of the listed symptoms most likely indicated the presence of leucostasis in the vessels of the lungs and bronchi.

In patients with stage III, multiple destruction of the ribs characteristic of MM, pathological ribs of the ribs occurred. In 7 patients, tumors emanating from the re- cers, compressing the corresponding zones of the lung tissue and creating the effect of a lung tumor, were noted . Subsequently, after autopsy, histological examination of tumors emanating from the ribs showed characteristic myelocytocellular growths.

The presence of inflammatory infiltrates was diagnosed in 33 patients (in 44 cases, taking into account repeated pneumonia). In most cases, pneumonia was detected in patients with MM in the later stages of tumor progression with chest deformity and renal failure.

Fluid in the pleural cavities was detected in 47 patients (38.2%). Subsequently, during the pleural puncture or at autopsy, the etiology of pleural effusion was established. In 8 cases there was a specific pleurisy, due to myeloma pleural infiltration; in 11 cases, infectious pleurisy as a complication of pneumonia; 28 people were diagnosed with transudate (pleural manifestation of renal failure).

In 52 patients with MM (42.3%), complicated by myeloma nephropathy and renal failure, nephrogenic pulmonary edema of degrees I, II and III was detected according to the classification of V.M. Perelman et al. (1964). The main diagnostic sign of nephrogenic pulmonary edema is a cloud-like darkening in the central regions on the chest radiograph in a direct projection . Its shape resembled a butterfly due to the free peripheral zone 2-4 cm wide. The darkening consisted of unsharply delineated rounded foci, the size of which depended on the number of alveoli filled with transudate. With accumulation in the interstitial spaces and pleural crevices of the edematous fluid, there were visible bands of darkening radiating away from the central part of the butterfly (26 patients — 50% of the total number of patients with nephrogenic edema). However, in 26 patients (50%), the blackout was unilateral, segmental, located mainly in the lower sections, combined with hydrothorax.

Only in one patient, radiological examination was able to detect calcification in the lungs . Calcium deposits are of very small size, and in the overwhelming majority of cases it is not possible to detect them during X-ray examination.

In two patients, a mediastinal tumor was diagnosed radiologically, which later at autopsy turned out to be an extramedullary foci of blood formation in the mediastinal tissue.

Great opportunities for the diagnosis of bronchopulmonary manifestations of multiple myeloma appear when using computed tomography (CT). CT scan of the thoracic cavity organs was performed in patients with MM in cases where traditional X-ray examination did not allow to establish an accurate diagnosis, as well as in contradictions between the clinical picture and the clinical picture. Hos major task of RT – clarify the nature and localization of the pathological process Skog, its extent and prevalence with osed- of bodies . In MM CT, considerable assistance was provided in the diagnosis of tumors emanating from the ribs that squeezed the lungs and, in traditional X-ray examinations, created the effect of a “lung tumor”. 7 such patients are registered. In a traditional X-ray examination, radiologists expressed the opinion that these patients have peripheral lung cancer. Knowing the peculiarities of the osteodestructive MM process, CT scan of the chest cavity was performed. QD has a higher resolution in contrast than conventional techniques, and makes it possible to clearly identify organic structures . During the CT in these patients were able to establish that “tumor” is destroyed tissue edges, it comes out of it and causes compression of adjacent areas and second portion of the lung tissue. Pe ripheral lung cancer was excluded.

As an example, here is a brief extract from the case history No 45019. Patient M., born 1953 It was observed in the hematology department of the Amur regional clinical hospital from 1998 to 2003. with a diagnosis of multiple myeloma, diffuse-focal form, synthesizing PIg G, stage IIIA. In 2003, the development of chronic renal failure was established. From 1998 to 2003 radiographs of the chest were determined characteristic of MM destruction of the ribs. In 2003, during a survey of the lungs on the right, in the area of ​​the 6th rib, a “formation” was detected, which was initially regarded by the radiologist as peripheral lung cancer. . When performing CT, it was found that the tumor comes from the 6th rib on the right. These data were subsequently confirmed by autopsy results. In the middle third of the 6th rib on the right, a 10 × 8 cm formation was found, which gave a shadow on the radiograph. Histological examination revealed a characteristic pattern of myeloma tumor.

CT scan has provided significant assistance in the diagnosis of pleural myelomatous lesions. According to the histological examination after autopsy, specific myeloma pleural infiltration was observed in 8 patients. In 6 of them, myelomatous lesion was suspected during CT. The pleura in these patients was thickened. In two cases revealed focal, in six cases diffuse infiltration.

As an example, here is a brief extract from the history of the disease No 392. Diagnosis Multiple myeloma, which synthesizes PiGG, was exposed in 2002. At the initial course, he received treatment according to the protocol M 2 -VBMCP, reached the plateau phase, which lasted until 2007. Supportive therapy was conducted under this protocol. In January 2007, the disease recurred: a marked pain syndrome reappeared in the chest cell and spine, multiple bone destruction on radiographs of the skull, ribs, pelvic bones, and spinal column. Treatment according to the PAD protocol. The clinical effect is not marked. Since June 2007, tumor screening of the left pleura is determined on CT scan of the chest cavity, which significantly increased in size by October 2007. During the histological study of the puncture biopsy material of the “tumor” of the pleura, plasma cells were found. Currently, the patient is undergoing radiation therapy to the area of ​​pleural lesion.

When performing CT with a large degree of confidence It is intended to diagnose interstitial changes in the lungs in patients with MM: deformity of the pulmonary vascular pattern, pulmonary fibrosis, pulmonary emphysema. In patients with MM, even in the absence of a concomitant broncho-obstructive process, a large percentage of emphysematous transformed lung tissue is determined. As the tumor progresses, the percentage of emphysema increases. This was established using the method of emphysema detection when performing CT using the Hitachi W-800 computed tomography program using the Level Detect program. tomographic slice [157]. According to CT data in patients with IA and IIA disease stages (I group), the percentage of emphysematous tissue per unit. area averaged 25.14 ± 0,22; in patients with stage IIIA (group II) – 41.7 ± 0.28%; in stage IIIB of the disease (group III) – 42.21 ± 0.22%.

Computed tomography is a verification method of radiological examination of the organs of the thoracic cavity in patients with MM complicated by CRF. The sensitivity of CT in the detection of pulmonary changes in patients with chronic renal failure increases significantly. When performing CT, it is possible to diagnose not only structural, but also functional changes in the lungs in patients with MM with the presence of renal failure. Computed tomography provides significant assistance in the diagnosis of pneumonia in patients with MM, developed on the background of agranulocytosis after cytostatic treatment. Due to the deficiency of neutrophils in these patients, it is very rarely possible to identify a clear inflammatory focus in a standard X-ray study. With CT, most of these patients still managed to determine the presence of infiltration.

Myeloma, proceeding from the pleura.

Summarizing the above, we can conclude the following:

1. The main radiological manifestations of pulmonary complications of multiple myeloma are: interstitial type of changes (increased pulmonary pattern, emphysema, pneumosclerosis), presence of destruction and ribs tumors, inflammatory infiltrates, nephrogenic pulmonary edema, fluid in the pleural cavities.

2. Computed tomography is the most effective method for detecting local pathological processes in the lungs with MM. CT is the leading method of X-ray diagnostics of pneumonia adhering against the background of agranulocytosis.

3. When using the method of quantitative evaluation of radiological data at CT in patients with MM, as the tumor progression revealed an increase in the percentage of emphysematous tissue.