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As MM progressed, there was a deterioration in the indices of cellular and humoral immunity .

The respiratory function was studied by spirography in 70 patients with MM without concomitant COPD. In half of the patients (35 people), no violations of VFL were detected. These are patients from group I and group II, with a disease duration of 1-2 years, in whom no changes were detected during x-ray examination of the lungs. In 35 patients, moderate violations of VFL were diagnosed: in 10 patients in restrictive mode, and in 25 in mixed types. These are patients of group II, who had a diagnosis of MM more than two years ago, and patients from group III. In all, during the X-ray examination of the lungs, changes in the interstitial type were observed (increased vascular pattern, pneumosclerosis and emphysema). According to spirography, 19 patients with myeloma G, 10 with myeloma A,1 with non-secretive myeloma and 5 people with Bens-Jones myeloma, of whom 15 patients had ESRD. Most of these patients were diagnosed with a small reduction in lung volumes. Reduction of VC was diagnosed in all 35 patients (68.4 ± 2.0% D; P <0.001). In 25 patients, a moderate decrease in FEV was observed. 1 (72.9 ± 2.1; P <0.001).

Reduction of VC indicates a loss of elasticity in the lungs and the development of a restrictive respiratory failure (DN). Increased plasma viscosity, the presence of intravascular protein stasis, and increased protein infiltration into the alveoli lead to the lysis of the elastic framework of the lungs. Dystrophy of the elastic framework and the development of emphysema contributes to impaired blood circulation in the lungs in these patients. The filling of part of the alveoli with paraprotein with MM leads to the shutdown of these alveoli from ventilation and the development of emphysema, which in this case is also of compensatory nature. [57]. This reasoning is also supported by a large number of patients with myeloma A, who have impaired VFL, as myeloma A has a more pronounced hyperviscose syndrome . Specific lymphoid and plasma cell lung infiltration may contribute to the development of restrictive type DN. In chronic kidney disease, an important reason for the development of a restrictive type of DN is the presence of uremic changes in the lungs – uremic pulmonary edema, uremic pneumonitis and calcification. A decrease in the FEV 1 value combined with a decrease in the VC indicates the development of a mixed type of DN. When conducting radiological (including ERTG and CT) and bronchoscopic examinations, no patient had an intrabronchial myeloma growth. Therefore, the decrease in FEV 1 can be attributed to edema, specific lymphoid and plasma cell infiltration, sclerotic changes of the bronchial mucosa, with the addition of CRF to uremic lesions, nephrogenic edema and uremic bronchitis. The above changes are more pronounced in the later stages of MM tumor progression. Therefore, it was not revealed in patients with IA, IIA, or the IIA stage of myeloma with a short tumor duration of any violations of VFL recorded by the method of spirography.

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The parameters of peak flow measurements of patients with normal spirogram indices did not differ from those in the control group and were within 95% of the proper values ​​in the morning and 100% in the evening, the daily fluctuations averaged up to 5% of the initial value. The PSV data of patients who had a moderate decrease in FEV 1 during spirography were lower than in the control group, averaging 65% D in the morning and 75% D in the evening. Daily changes in HRP throughout the study did not change and were within 10%.

In group I patients, the value of bronchial resistance (R aw ) on inspiration (2.78 ± 0.1 cm water / l / s) and on expiration (3.06 ± 0.08 cm water / l / s) did not significantly differ from similar indicators in the control group (2.8 ± 0.1 and 3.0 ± 0.06 cm. water.st / l / s, respectively; P> 0.05). In group II, the value of bronchial inspiratory resistance (3.1 ± 0.2 cm. Water / l / s) did not change (P> 0.05), R aw during exhalation was increased (3.9 ± 0.2 see water.st / l / s; P <0.001). In patients with group III, a significant increase in bronchial resistance was noted: R aw on inspiration – 4.2 ± 0.15 cm water / l / s and R aw on expiration – 4.5 ± 0.26 cm. water / l / s (P <0.001). In patients of group II, plasma-cell and lymphoid infiltration of the bronchi, edema and sclerosis of the bronchial mucosa are already taking place. The leading cause of a pronounced increase in bronchial resistance in patients with group III is nephro genic edema of the lungs and bronchial mucosa, as a manifestation of renal failure.

Diagnostic fibrobronchoscopy was performed on 60 patients with MM who did not abuse smoking and did not have concomitant COPD (20 patients of group I, 20 patients of group II, and 20 patients of group III). All patients of group I had a bronchoscopic picture of a normal tracheobronchial tree. No hypersensitivity of the bronchi was observed.

In 10 patients of group II, bilateral diffuse atrophic endobronchitis was diagnosed. The bronchial mucosa in these patients was atrophied, pale, thinned. In the lumen of the bronchi mucous secret was absent or was very scarce. A bronchoscopic picture of a normal tracheobronchial tree was diagnosed in 10 patients. In all patients, contact bleeding of the bronchial mucosa was noted.

Bilateral diffuse atrophic endobronchitis was diagnosed in 12 patients of group III. The bronchial mucosa was atrophied, pale, thinned. In 8 patients of this group, there was a picture of a normal tracheobronchial tree. As in patients of group II, in all patients of group III, contact bleeding of the bronchial mucosa was observed, due to impaired hemostasis in the later stages of tumor progression in patients with MM . Thus, when conducting fibrobronchoscopy in 50% of patients with MM IIIA and in 60% of patients with renal insufficiency, bilateral diffuse atrophic endobronchitis occurs (40% of the total number of patients with MM).

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Endobronchial biopsy was performed on 10 patients of group I, 10 patients of group II and 5 patients of group III. The biopsy specimen was the same as in patients with CLL. Patients of group I were diagnosed with moderate proliferation or dystrophy of the bronchial epithelium. In patients with groups II and III, histological examination of biopsy specimens determined edema, atrophy of the bronchial mucosa, and in some cases focal squamous metaplasia of the epithelium was observed. In some patients of groups II and III, lymphocytic and plasma cell infiltration of varying severity was detected under the basement membrane. In patients of group I, there was a slight dilatation of capillaries, plethora of arterioles, capillaries and venules. Protein stasis in the vessels of the microcirculatory bed of the bronchi in patients with MM in stages IA and IIA would not be detected lo In patients with group II, dilatation and plethora of arterioles, capillaries, and venules were observed with varying degrees of severity. The number of arterio-venous anastomoses was increased. In some vessels of the microvasculature, accumulation of protein masses was noted. In patients with group III, dilatation of arterioles, capillaries, and venules was also diagnosed with varying degrees of severity. In patients with MM, complicated by CRF, in the vessels of the microvasculature, the accumulation of protein masses was more pronounced than in patients of group II. This can be explained by increased lung function in conditions of azotemic uremia .

In order to study microhemocirculation in the proximal parts of the bronchial tree, 30 patients with MM underwent endobronchal LDF (10 patients from group I, 10 from II and 10 from group III). The results were compared with the data of 20 people from the control group, who were conducted PBS and LDF. In patients with MM in the course of tumor progression, disturbances of microcirculatory blood circulation in the bronchial mucosa were recorded in terms of the nature and severity of the microcirculatory circulation.

The indicator of the microcirculation parameter (PM), which characterizes the state of tissue perfusion, was significantly reduced as MM progressed. In multiple myeloma, impaired microhemocirculation in the lungs and bronchi is primarily due to the syndrome of increased blood viscosity and anemia. In order to minimize the effect of anemia on the PM indicators, in patients with MM groups II and III, the anemic syndrome was stopped before the study. The hemoglobin level during LDF was not lower than 100 g / l, the content of erythrocytes was not lower than 3 × 10 9 / l. Thus, they tried to establish a decrease in the speed of red blood cells in the microvessels, which, in MM, is primarily due to the syndrome of increased blood viscosity. A significant inverse correlation was established between an increase in the serum paraprotein level and a decrease in PM (r = –0.8, P <0.01), between the duration of the disease MM and a decrease in PM (r = –0.64, P <0.05). ), between an increase in the level of creatinine in the blood and a decrease in the PM (r = –0.5, P <0.05).

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The values ​​of the mean square deviation of PM (σ), reflecting the preservation of the mechanisms of blood flow regulation in the microcirculatory bed, in patients of groups I and II did not have significant differences compared with the control (P> 0.05), and decreased in group III ( P <0.001) . The coefficient of variation (Kv), which characterizes the dependence of tissue perfusion on blood flow modulation, increased during tumor progression and in all groups significantly exceeded control (P <0.001) .

When analyzing the rhythmic components of blood flow oscillations, a decrease in e-range fluctuations was observed in patients of groups II and III. In group I patients, the amplitude of oscillations in the E-band did not differ from the control indices (Table 30). A decrease in the amplitude of oscillations in the E-band indicates endothelial dysfunction and a decrease in the production of nitric oxide in MM patients in the later stages of the tumor progression. The decrease in endothelial oscillations correlated with the stage of the disease (r = –0.72, P <0.01), the level of paraprotein (r = –0.56, P <0.05) and blood creatinine (r = –0.56 P <0.05). Since in patients with another lymphoproliferative disease – CLL, there are no changes in endothelial oscillations, it can be assumed that, in MM, important factors for the development of endothelial dysfunction are paraproteinmia,dysproteinemia and uremic intoxication. Endothelial dysfunction of the microvasculature vessels contributes to a severe and prolonged course of inflammatory processes of the bronchopulmonary system in patients with MM and an increase in pressure in the pulmonary artery system.

In patients with MM, no significant changes in the oscillations in the H-, M-, D- bands were detected. The amplitudes of oscillations in the C-band in patients with MM decreased in the course of tumor progression; in group I, they did not have significant differences compared to control; in groups II and III, the indices of cardiac waves decreased significantly (P <0.05 and P <0.001, respectively). A decrease in cardiac wave values ​​indicates a decrease in arterial blood flow into the microvasculature due to the development of a syndrome of increased blood viscosity. According to the data of endobronchial biopsy, in patients of the third group, protein stasis is more pronounced than in patients of the second group; therefore, in the presence of renal insufficiency, the smallest indicators of vibration amplitudes in the C-band were recorded.Significant inverse correlations were found between the level of serum paraprotein of the blood and a decrease in fluctuations in the C-range (r = –0.7, P <0.01), between the duration of MM disease and a decrease in the fluctuations in the C-range r = – 0.58, P <0.05), between the level of blood creatinine and the decrease in fluctuations in the C-band (r = –0.5, P <0.05).

It is obvious that similar violations of microhemocirculation occur in the lungs. Thus, in a significant number of patients with MM II and III groups, during radiological methods of examination, there is an increase and deformation of the pulmonary pattern, which is caused by stagnation of blood in small vessels with the development of pneumosclerosis, since due to the increased viscosity of the plasma, blood flow slows down pulmonary capillary system.

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Disruption of microhemocirculation contributes to the violation of tissue trophism, the development of tissue hypoxia, metabolic disorders in the cells of the bronchial mucosa. The consequence of this are atrophic changes in the bronchial mucosa. In 40% of MM patients, bilateral diffuse atrophic endoscopy develops. At the same time, in patients with MM, in contrast to patients with CLL, outside the attachment of AML, in no case was a latent inflammatory process occurring in the bronchial mucosa, despite the fact that CLL also shows markedly abnormal microhemomas in the process of tumor progression. – circulation. This can be explained by a more pronounced decrease in cellular and humoral immunity in patients with CLL compared with patients with MM . In patients with CLL, due to the deep mismatch of all parts of the cellular and humoral immunity, against the background of a violation of the trophism of the bronchial tissues, the inflammatory process quickly develops and then acquires a chronic course.

Disruption of microhemocirculation in the vessels of the lungs and bronchi, along with pronounced secondary immunodeficiency, lymphoid and plasma cell infiltration of the lung tissue, paraproteoinosis of the lungs, contribute to the occurrence of severe and prolonged pneumonia in patients with MM. So in patients with MM I group, where no microcirculation disorders were detected, pneumonia was not registered. In group II, pneumonia was diagnosed in 10 patients (18% of the total number of patients in this group), in group III in 23 patients (42%).

The effect of cytostatic therapy on microhemocirculation indices in patients with MM was studied. In cases where, after carrying out cytostatic treatment, it was possible to reach the phase of a stable “plateau”, a decrease in blood paraprotein was noted, endobronchial LDF was repeated for MM patients. In all, an increase in the PM indices was noted, but in no case did the PM indices completely normalize. An improvement in the amplitudes of oscillations in the endothelial and cardiac ranges was noted. (Table 31).

The persistence of endobronchial microhemocirculation disorders in patients with MM, after reaching the “stable plateau” phase, is explained by the multifactorial nature of the microcirculatory disorders. In addition to the syndrome of increased blood viscosity and anemia, impaired platelet and plasma hemostasis, vascular endothelium, regulation of tissue vascular tone, pH and pO 2 , hormonal background and many other factors affect the microcirculation . In the majority of patients with MM, the plateau phase maintains a minimum PIg production.

As in CLL patients with MM, a high degree of effectiveness of the endobronchial LDF method was noted for identifying vascular and intravascular disorders of the microvasculature of the mucous bronchi in the early stages of the pathological process. The role of LDF in the diagnosis of endothelial dysfunction of microvasculature vessels is very important . The use of this method allows to assess the dynamics of microcirculatory disorders in the mucous membrane of the proximal bronchi during the treatment of myeloma.

According to the data of zonal rheography of the lung in patients of the I group, there were no violations of the general and regional ventilation of the lungs, the vertical gradient of ventilation characteristic of healthy people remained unchanged . The ratio of MOVR of the upper zones / MOVR of the lower zones did not have significant differences compared with the control . No significant impairment of the pulsatory blood flow in this group was also detected. The regional VPO indicators and the total VPO indicator of both lungs did not differ from the control indicators.

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

In patients with MM of group II, during reopulmonography, there is a decrease in general and regional ventilation of the lungs . A significant decrease in ventilation in the middle and lower zones of both lungs, a decrease in the total MOBP from all zones of the lungs by 29.4% (P <0.05) and redistribution of ventilation from the lower and middle to the upper zones of both lungs were diagnosed . A decrease in the rheographic index of systolic blood filling (SCR) and the index of minute pulsatory blood flow (MPCr) in the right lung was diagnosed. The mccr of the right lung is reduced, compared with the control, with a reliability of <0.05. In the left lung, a significant decrease in blood flow occurred only in the middle zone. The cumulative index of MCR had no significant difference with the control (P> 0.05) . A significant increase in vascular resistance was noted in the lower and middle (to a lesser extent) zones of both lungs, which can be judged by the decrease in HSC and in the length of the Q-interval . But there was no significant redistribution of pulmonary blood flow in patients of group II. Estimating the state of the venous outflow in the small circle of blood circulation due to DSC change, an increase in this index was found in the middle and lower zones, with the greatest values ​​of the coefficient in the basal regions of the lungs. Significantly reduced VPO upper and lower zones and the left lung as a whole (P <0.001). Despite the fact that in the right lung the integral indicator of HPE did not have significant differences with the control, the total index of HPE of both lungs was reduced .

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In patients with MM of group III, pr and carrying out zonal lung reography , there is a decrease in general and regional ventilation of the lungs. A significant decrease in ventilation in all zones of both lungs and a decrease in the total MOBP from all zones of the lungs by 48.8% (P <0.001) were diagnosed. There is a redistribution of ventilation from the lower and middle to the upper zones of both lungs . A decrease in the pulsatory blood flow in both lungs was diagnosed. The cumulative MPCr index is reduced compared with the control by 46.5% (P <0.001) . In group III, due to uremic damage of the heart and blood vessels, the precapillary vascular resistance reaches maximum values. In patients with renal failure, a significant increase was diagnosed. DSC in the middle and lower zones of both lungs. In group III, the VPO in the right lung had no significant differences compared with the control (p> 0.05). On the left, the overall indicator of HPE was reduced (p <0.05), due to a decrease in the VPO of the lower zone (p <0.001). The HPE of both lungs in group III patients did not have significant differences with the control group (1.1 ± 0.053; p> 0.05).

In patients of group I, the pO2 indicator did not significantly differ from that in the control group. The decrease in pO2 in patients of groups II and III is explained by the progression of regional ventilation disorders as the tumor process develops in patients with MM. The leading role in the disturbance of blood gas composition in MM is associated with a decrease in ventilation and lung perfusion, but the progression of the anemic syndrome as the tumor process develops also plays an important role .

In group I, the SrDLA index (14.67 ± 0.5 mm Hg) did not have significant differences compared with the control group (14.99 ± 0.61 mm Hg; P> 0.05). Patients II (18.7 ± 1.0 mm Hg; P <0.05) and III (22.8 ± 0.5 mm Hg; P <0.001) of the groups showed a significant increase in SrDLA compared to control.

Echocardiography and ICGD were performed on 50 patients with MM aged 33 to 70 years without concomitant COPD (12 patients from I, 27 of II, and 11 of Group III). Patients with diseases accompanied by a primary lesion of the left heart were excluded from the study. Pulmonary hypertension was diagnosed in 26 patients (52%). The SrDLA index in these patients was within 21–39 mm Hg, and averaged 23 ± 0.9 mm Hg. All patients with PH belonged to groups II and III (17 and 9 people, respectively). In patients with renal insufficiency, the highest rates of SrDLA were noted. In 24 patients (48%), the average SrDLA in rest did not exceed 20 mm. Hg Art. Of these, in 17 people it was within 9–16 mm. Hg Art. and in 7 – 17 – 20 mm. Hg Art.

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Patients with MM, in whom, according to echocardiographic studies, an increase in SrDLA is diagnosed, these are patients with a pronounced destructive process in the bones, including the ribs, sternum, and thoracic spine. Some of them had significant chest deformity. Violation of the chest excursion (due to the osteodestructive process) is an important reason contributing to the development of hypoxemia and an increase in pressure in the aircraft system. In addition to hypoxemia, endothelial dysfunction and, in the presence of CRF, acidosis contribute to the development of PH in patients with MM without broncho-obstructive syndrome (the pH value of blood in patients of group III was on average 7.24 ± 0.03).

Indicators SrDLA in patients with MM, without broncho-obstructive process.

TMPS PZHD increases in patients of group II and reaches maximum values ​​in group III. The CRV of the pancreas reaches significant differences, compared with the control, only in group III. A study of the functional capacity of the right heart in patients of group I was diagnosed with a significant decrease in the ratio of E / A TK compared with the control, i.e. already in the early stages of the tumor diastolic dysfunction of the pancreas is formed. Patients of group II were diagnosed with a decrease in E TK and an increase in A TK , reducing the ratio of E / A. In group III, more significant impairments of pulmonary hemodynamics were revealed. Marked hypertrophy and dilatation of all cavities of the heart. Reduced ejection fraction of the pancreas. KDO and CSR RV were increased. Increased cardiac index of the pancreas, which is associated with an increase in heart rate in the terminal stage of hemoblastosis due to uremic intoxication and anemia. Revealed a reliable decrease in E TK , an increase in A TK and a decrease in the E / A ratio. Thus, in patients with MM in the presence of CRF, the greatest changes in the systolic and diastolic functions of the pancreas were observed .

TMZS LVZh increased already in patients of group I. In the process of tumor progression, it continues to increase, reaching maximum values ​​in group III. The thickness of the interventricular septum is increased in patients with groups II and III. In group I patients, the E / A MK ratio decreased ; LV diastolic dysfunction has occurred. In the process of tumor progression, the ratio of E / A MK continued to decline. Severe dilatation of the LV was diagnosed only in the presence of CRF (group III). In patients of group III, a significant increase in LV size and their corresponding volumes was observed compared with the control group . In the process of tumor howling progression (II and III group) increased MO LV SI LV after effect of increasing heart rate. LV EF was reduced only in patients with MM in the presence of renal failure .

The revealed changes can be explained by impaired blood rheology due to paraproteinemia, cardiotoxic effects of cytostatics, tumor intoxication, anemia, lymphoid and plasma cell infiltration of the myocardium. But dilatation of the cavities of both ventricles, an increase in their size and corresponding volumes, a decrease in the ejection fraction are diagnosed only in patients with MM with chronic renal failure. Many patients with MM are elderly people, they have coronary heart disease diagnosed , which also contributed to the violation of the LV myocardium trophism and the development of circulatory failure.

Thus, it can be concluded that the development of pulmonary hypertension in MM is promoted by: 1) hypoxemia due to impaired excursion of the chest and diaphragm, severe inflammatory and specific paraproteinemic and uremic processes in the lungs, and impaired blood rheology Ic in the vessels of the ICC, 2) endothelial dysfunction, 3) myocardial degeneration, 4) in the presence of renal failure – acidosis.

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An ultrasound examination of the diaphragm in patients of group I showed no significant changes compared to controls. The thickness of the diaphragm did not change. The position, shape, echogenicity of the diaphragm also did not differ from the control. Excursion of the diaphragm with calm and forced breathing did not differ from control. In patients of group II, the thickness of the diaphragm did not change, but its echo structure became heterogeneous. Marked flattening of the dome of the diaphragm. Significantly decreased excursion of the diaphragm. In group III, the largest morphological changes in the diaphragm were revealed. Its dome was not clear, the echo structure became non-uniform. The mobility of the diaphragm significantly decreased. EDS and EDF were significantly reduced. Decrease in the expansion of the diaphragm and its morphological restructuring, with MM,specific myelomatous damage to the diaphragm (plasma cell and lymphoid infiltration, the presence of protein stasis in vessels with impaired microcirculation, etc.), impaired chest movements in patients with severe osteodestructive process, in the presence of renal failure – uremic defeat afragmal muscle .

In patients of group II, a significant correlation dependence was found between a decrease in EDF and a decrease in the MOB of the lower (r = 0.89; P <0.001) and middle zones of the lungs (r = 0.56; P <0.05), between decrease EDS and a decrease in the MVR of the lower (r = 0.62 P <0.05) and middle zones (r = 0.56; P <0.05) of the lungs. In group III patients, a clear correlation was found between a decrease in EDF and a decrease in the MOBP of the lower lung zones (r = 0.56; P <0.05), between a decrease in the EDS and a decrease in the MOP of the lower lung zones (r = 0.52; P < 0.05). At the same time, no reliable correlation was found between the EDF, EDS and MOVr indices of the upper and middle zones. lungs. Smaller correlation indicators (compared to group II) between the decrease in the excursion of the diaphragm and the ventilation capacity of the lower zones of the lungs, the lack of reliable links between the excursion rates of the diaphragm and the ventilation of the middle zones is explained by the fact that in violation of the ventilation of the lungs, specific bronchopulmonary manifestations of CRF — nephrogenic edema, pneumonitis, calcification, fluid accumulation in the pleural cavities — play.

A significant inverse correlation was established between the decrease in EDF and EDS and the increase in SrDLA in patients II (r = –0.69; P <0.01 and –0.61; P <0.05) and III (r = –0.52 ; P <0.05 and – 0.5; P <0.05) groups. A positive correlation was found between a decrease in the MOVR of the sums and a decrease in the pO 2 of blood in patients of the II (r = 0.89; P <0.001) and III (r = 0.82; P <0.001) groups. A reverse correlation was diagnosed between a decrease in blood pO 2 and an increase in SrDLA in patients of the II (r = –0.96; P <0.001) and III (r = –0.79; P <0.001) groups.

Thus, in patients with MM, impaired functional ability of the diaphragm leads to impaired ventilation of the middle and lower zones of the lungs, resulting in hypoxemia and pulmonary hypertension. However, in patients with MM complicated by CRF, this relationship is less pronounced, since the uremic damage of the bronchopulmonary system plays an important role in impaired respiratory function, and the pH of the blood and endothelial dysfunction of the vessels contribute to the development of PH.

As an example, here is an extract from the outpatient card No 4569. Patient S., born in 1947. Diagnosis: Multiple myeloma, diffuse focal form, secreting P IgG, stage IIIA was exposed in November 1997. In the myelogram, 19% of plasma cells, in the immunogram, IgG is 65 g / l, on radiographs of the skull, pelvic bones and edges multiple destruction. Mild anemia has occurred. During the initial hospitalization in the hospital, treatment was carried out according to the MR protocol. The plateau phase has been reached. She subsequently received maintenance therapy according to the MR protocol for 5 years. In 2002, a relapse of the disease was established. After conducting two courses of therapy under the protocol M 2 – VBMCP reached the second phase of the “plateau”, which lasted until 2006. In 2006 a relapse of the disease developed, which was accompanied by the destruction of flat bones, a pronounced pain syndrome and a pathological fracture of the left shoulder. Attempts to strengthen cytostatic therapy led to the development of serious complications: agranulocytosis, complicated by pneumonia; toxic hepatitis; thrombocytopenia and severe hemorrhagic syndrome. In July 2006 therapy started on the Velc + dexa protocol. A stable plateau phase has been reached.

Additional survey methods (July 2006). Roentgenograms of the bones of the skull, pelvis, and ribs – multiple destruction. In myelogram 40% of plasma cells. Immunogram: IgG – 75 g / l, IgA – 0.84 g / l, IgM – 0.58 g / l. Blood count: hemoglobin – 95 g / l, erythrocytes – 3.6 × 10 12 / l, platelets – 120 × 10 9 / l, leukocytes – 3.9 × 10 9 / l, segmented nucleus – 46%, lymphocytes – 45%, eosinophils – 3%, monocytes – 6%, ESR – 65 mm / h. Biochemical analysis of blood: total protein – 95 g / l, creatinine – 90 μm / l, urea – 6 μm / l, Ca – 2.6 mmol / l. Clinical analysis of urine – proteinuria 1000 mg / l. Spirography: VC – 64% D, FEV 1 – 70% D. During peak flowmetry, the PSV indicators were as follows: in the morning hours – 69% D, in the evening hours – 74% D. Daily fluctuations PSV was 5%. During pneumotachography, an increase in bronchial inhalation resistance was observed (3.2 cm water / l / s) and exhalation (3.5 cm water / l / s). When conducting PBS, a bilateral diffuse atrophic endobronitis was diagnosed. The results of endobronchial LDF before treatment with Velcade and Dexamethasone: PM – 35.63 PE; σ – 5.8 PE; Kv – 16.28%; Ae – 1.98 PE; An – 1.93 PE, Am – 3.04 PE; Hell – 2,850 PE; Ac – 1,460 PE. The data of endobronchial LDF in the stable plateau phase: PM — 65.1 PE; σ – 8.1 PE; Kv – 17.9%; Ae – 2.3 PE; An – 2.8 PE, Am – 3.2 PE; Hell – 3.6 PE; Ac – 2,9PE. Zone rheography of the lungs (July 2006). Dore of the right lung: upper zone – 0.5, middle zone – 0.38, lower zone – 0.8 ohm;The depth of the left lung is the upper zone — 0.46, the middle zone — 0.44, the lower zone — 0.44 ohms. Dob sum = 3.02 ohms. MEP of the right lung: upper zone – 8.3, middle zone – 6, lower zone – 11.2 ohm / min; MEP of the left lung: upper zone – 7, middle zone – 8, lower zone – 6.6 ohm / min. MOVr Sum – 47.1 ohm / min. The ratio of the MOV of the upper zones / MOV of the lower zones = 0.86. SCR of the right lung: in the upper zone – 0.09, in the middle zone – 0.05, in the lower zone – 0.1 ohm; The CR of the left lung – in the upper zone – 0.1, in the middle zone – 0.06, in the lower zone – 0.1 ohm. Scr sum = 0.5 ohm MPCr of the right lung: in the upper zone – 7.5, in the middle zone 3.5, in the lower zone 9.7; MPCr of the left lung: in the upper zone – 8.6, in the middle zone 4.5, in the lower zone 9.7 ohms / min. MPKr Sum = 43.5 ohm / min. Ventilation-perfusion ratio: right lung: upper zone 1.1, middle zone 1.7, lower zone 1.15; left lung: upper zone 0.8, middle zone – 1.77, lower zone 0.7. VPO of both lungs 1.1. IKC ultrasound data (July 2006): SrDLA – 23 mm. Hg Art., KDO PZh – 126 ml, KSO PZh – 67 ml, UI PZh – 49 ml / m 2 , SI PZH – 2.6 l / min / m 2 , EF PZH – 41%, E TC – 0.36 m / s, A TC 0.53 m / s, E / A – 0.7. Diagnosed the expansion of all cavities of the heart. Ultrasonic examination of the diaphragm: TD – 6 mm, EDS – 12 mm, EDf – 28 mm.

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Based on the analysis of the data of spirography, peak flow measurements, pneumotachography and ultrasound methods for examining hemodynamics of the ICC, we can conclude:

1. In patients with MM in the late stages of tumor progression, there is a moderate impairment of ventilation function of the lung in restrictive and mixed types. This is due to a decrease in the elastic capacity of the lungs due to plasma hyperviscosity, lung paraproteinosis, impaired blood circulation in the lungs, specific lymphoid and plasma cell infiltration of the lungs and bronchi, in renal insufficiency by the presence of specific uremic lesions — nephrogenic pulmonary edema, uremic pneumonitis, calcification.

2. As MM progresses, bronchial resistance rises, reaching maximum values ​​in patients with renal insufficiency.

3. In the process of tumor progression in MM, there is a decrease in the parameters of endobronchial microhemocirculation. The leading causes of impaired microhemocirculation in patients with MM are syndrome of increased blood viscosity and renal insufficiency.

4. In patients with MM at the late stages of tumor progression, dysfunction of the vascular endothelium of the microvasculature was diagnosed.

5. Violation of microhemocirculation in patients with MM caused by atrophic changes of the bronchial mucosa. In 40% of these patients, fibrobronchoscopy was diagnosed with bilateral diffuse atrophic bronchitis.

6. After reaching the phase of a stable plateau, the main indicators of the endobronchial LDF are improved, but not fully normalized due to the multifactor nature of the microcirculatory disorders.

7. In the process of development of MM, disorders of general and regional ventilation of the lungs and pulmonary blood flow are progressing, which is characterized by a decrease in ventilation and perfusion indices each zone separately and in general for both lungs. There is a redistribution of ventilation and blood flow from the lower and middle zones to the upper zones of both lungs. These changes are due to the progression of specific myelomatous lesions of the bronchopulmonary system and the diaphragm.

8. In patients with MM with a pronounced osteo-destructive process of the chest, a significant decrease in the excursion of the diaphragm was observed with calm and forced respiration.

9. In patients with MM in the process of tumor progression, the development of pulmonary hypertension is noted. The development of pulmonary hypotension in MM is promoted by: a) hypoxemia due to impaired excursion of the chest and diaphragm, the presence of specific myelomatosis and uremic processes in the lungs, impaired microcirculation and rheology of blood in the ICC vessels, b) endothelial dysfunction, c) myocardial dystrophy, d) acidosis in the presence of renal failure.

10. With the progression of the tumor process there is a violation of the hemodynamics of the ICC. In patients with renal insufficiency, a significant impairment of the systolic and diastolic functions of the right and left ventricles was revealed.

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The lethal outcome was ascertained in 65 patients with MM. In the overwhelming majority of cases, death occurred due to the progression of the underlying disease — the presence of myeloma nephropathy, complicated by chronic renal failure (52 patients — 80%); hemorrhagic syndrome due to deep thrombocytopenia; anemic syndrome. Pneumonia and its complications were diagnosed in 28 patients (43% of all died), in all cases it was the direct cause of death. In 28 of 52 patients with MM (53.8%) who died with symptoms of myelomous nephropathy and chronic renal failure, inflammatory infiltrates were found in the lungs (in this situation, pneumonia was also the direct cause of death ).

A morphological study of the lungs, bronchi, and pleura of 65 patients who died from MM was performed . The following changes were diagnosed . In 26 people (40%), lymphoid and plasma cell infiltration took place in the form of cords or nodes in the inter-alveolar septa, along the vascular adventitia, in the bronchial mucosa and in the peri- bronchial spaces . The interalveolar septa were thickened due to their infiltration with plasma cells and / or lymphocytes.

Paraproteinosis of the lungs was diagnosed in 38 patients (58%). The protein masses filling the pulmonary alveoli created a pattern of protein pulmonary edema, impregnated thickened, hyalized interalveolar septa and filled small vessels (Fig. 36 – 37). Plasma cells and lymphocytes were often able to be detected along the periphery of protein masses . Manifestations of amyloidosis in this study were detected only in 9 patients (13.8% of all deaths). The masses of amyloid were stained red when using congo-mouth staining. In these patients, there was a deposition of protein masses in the alveolar spaces, perivascular, peribronchial, and also in the walls of blood vessels .

Plasma and lymphoid infiltration of the pleura occurred in 8 (12.3%) patients with MM and was accompanied by the development of exudative pleurisy, which is an extremely unfavorable preventive factor .

In 51 patients (78%), histological examination diagnosed pneumosclerosis. In 16 people (24.6%), foci of calcification were found in bronchial cartilage and interstitium. The occurrence of calcium deposits causes an inflammatory reaction with the next development of fibrosis . Many patients had one hundred uneven blood supply of pulmonary vessels, small perivascular hemorrhages. Foci of atelectasis alternated with areas of emphysematous expansion of the alveoli. In this case, we can speak of the compensatory nature of the localized emphysema. Since, due to the deposition of paraprotein and the development of atelectasis, some alveoli are excluded from ventilation, the ventilation capabilities of other alveoli are reduced as a result of edema, fibrosis, lymphoid and plasma infiltration of the interalveolar septa, the compensatory expansion of the preserved alveoli occurs.