Immunological studies

Immunological studies were carried out in 40 patients with COPD associated with CLL during the period of exacerbation of the disease and at 14-15 days after the start of treatment. A comparative analysis of the immunological parameters of the main and control groups was carried out. In patients with CLL, there is a significant decrease in the phagocytic activity of neutrophils, a decrease in the content of serum immunoglobulins of classes A, M and G, and immunosuppression in T-lymphocyte content. These changes are explained by the B-cell tumor nature of the disease – B-CLL. For the same reason, for 14–15 days, after the start of treatment, there were no changes in the indices of cellular and humoral immunity . Immunodeficiency dictates the need for immunomodulating therapy in the treatment of COPD in patients with CLL.

The exacerbations of COPD in patients with a progressive course of CLL often coincided with courses of polychemotherapy (CP, COP, CHOP, ATS, FC, FCR, FCM), which contributes to the progression of immunodeficiency. In patients with CLL with association with COPD treated with chlorambucil and cyclophosphamide exacerbations of the broncho obstruction was not observed.

During exacerbation of COPD in patients with progressive CLL, the clinical symptoms of which disease determine the severity of the condition at the moment were assessed. In most cases, these were symptoms of COPD. In such situations, first of all, therapy was directed to the treatment of the broncho-obstructive process and only upon achieving remission, COPD was prescribed cytostatic therapy. The appointment of aggressive chemotherapy in the period of exacerbation of COPD, in all cases led to an even greater burden of bronchopulmonary disease, and even to the development of pneumonia in patients with CLL.

The course of COPD on the background of CLL is characterized by a significant inhibition of immunity, a more severe course and a slow dynamics of clinical syndromes. All modern methods of treatment of COPD have been used to treat these patients . The dynamics of clinical manifestations of COPD in patients with CLL in the stage of exacerbation of the obstructive process in the lungs was compared with the dynamics of these indicators in patients with COPD without CLL (3rd control group) . Due to the characteristics of CLL, which is characterized by leukocytosis and absolute lymphocytosis in blood tests, indicators of the number of leukocytes and neutrophils were not taken into account when assessing the severity and dynamics of clinical manifestations of COPD during the exacerbation.

Of the 228 patients with CLL, 40 patients were diagnosed with chronic pulmonary heart (CID) according to clinical, radiographic, electrocardiographic, and echocardiographic studies. In all 40 people, the cause of the development of HPS was a prolonged course of chronic obstructive pulmonary disease (COPD). There were no diseases with a primary lesion of the pulmonary vessels and with thoracodiaphragmatic disorders in this group. In all patients, the duration of diagnosis of COPD ranged from 5 to 20 years. In all 40 patients, according to clinical and radiological data, pulmonary emphysema occurred, in 25 patients according to x-ray data, diffuse pneumosclerosis.

Clinical manifestations of HPS were detected in 40 patients . Compensated pulmonary heart was diagnosed in 28 and decompensated in 12 people. In patients with compensated HLS, the symptom complex of chronic respiratory failure prevailed. Dyspnea, fatigue during exercise, cyanosis in these patients for a long time were only manifestations of respiratory failure. An important role in the timely diagnosis of HPS in these patients was played by given target physical, laboratory and instrumental examinations. Physical examination revealed the following symptoms: an enhanced diffuse cardiac impulse in the pericardial region; tachycardia; accent II tone over the pulmonary artery her; amplified I tone over the tricuspid valve compared to the apex of the heart; amplified II tone above the xiphoid process, at the point of attachment of the IV – V ribs to the sternum to the right compared to the base of the heart; epigastric pulsation; the displacement of the right border of the relative dullness of the heart; a push of the right ventricle in the IV – V intercostal space, on the left at the edge of the sternum; presystolic or protodiastolic gallop in the zone of auscultation of the tricuspid valve or right ventricle.

Clinical manifestations of decompensated pulmonary heart were an enlarged liver (it must be borne in mind that an enlarged liver in this situation may be a clinical manifestation of CLL, therefore, when diagnosing decompensated HPS in these patients, hepatomegaly did not have an important diagnostic value), edema of the lower extremities, ascites , swelling of the cervical veins, pulsation of the liver, positive symptom of Plesch, systolic murmur at the base of the sternum, nocturia, oliguria, complications from the central nervous system and Stems Thus , the formation of decompensated pulmonary heart was characterized by adherence of right ventricular heart failure to respiratory failure.

Radiographic signs of CID in patients with CLL were bulging of the cone of the pulmonary artery and expansion of the right heart, which were detected in 32 patients.

All patients had more than two “direct” signs of pulmonary heart on an ECG: 1) Rv 1 ≥ 7 mm; 2) R / Sv 1 ≥1 mm; 3) Rv 1 + Sv 5 ≥ 10.5 mm; 4) the time of internal deviation in the lead V 1 ≥ 0.03-0.05 s; 5) QR complex in lead V 1 ; 6) incomplete blockade of the right bundle of His bundle with Rv 1 ≥ 10 mm; 7) complete blockade of the right bundle of His bundle with Rv 1 ≥ 15 mm; 8) right ventricular loading in V 1 – V 2 management (inversion of T wave).

During echocardiography and ICDH, pulmonary hypertension was diagnosed in 40 patients with COPD complicated by CPH (during ECG and ICDD, there was an increase in pressure in the LA system, hypertrophy and / or dilation of the right ventricle were detected), and 20 patients with CLL were not diagnosed. who had a history of COPD and were not abused by smoking (37% of the total number of CLL patients without COPD). In 10 patients with CLL with concomitant COPD (diagnosed according to clinical and instrumental data), pulmonary hypertension was not detected (10%).

Patients with CLL associated with COPD, and without a broncho-obstructive process, who, according to echocardiography and IDGC, were diagnosed with LH, are divided into four subgroups: subgroup A – 10 patients with CLL with COPD without LH signs; subgroup B – 28 patients with compensated HPS; subgroup C – 12 patients with decompensated HPS; subgroup D – 20 patients with CLL without COPD, but with the presence of LH signs. For comparison, an ultrasound study of the heart was carried out in patients with COPD and HPS without concomitant lymphoproliferative disease (additional control subgroups): 10 people with COPD without PH ( control subgroup A KONT ), 25 people with COPD and signs of HLS in the stage compensation (control subgroup B KONT ), 25 people with COPD and signs of HPS in the decompensation stage (control subgroup C KONT ). Patients of the control subgroups by age and sex matched the patients with CLL.

TMPS of the pancreas in patients of subgroup A differed from the same indicator in the control (P <0.01). In the stage of compensated pulmonary heart, the thickness of the myocardium of the right ventricle reached maximum values ​​(compared to control, subgroups A and C – P <0.001). In case of decompensation of the CHPS, the TMPS PZH exceeded the control indicator with a reliability of <0.001, but was significantly less than in the compensation stage (P <0.001). In subgroup D, the myocardial thickness of the pancreas was significantly different from the control indices (P <0.001) and subgroup B (P <0.001). TMPS prostate patients subgroup A Comte , it was smaller than in patients of the subgroup A (P <0.01). Increase TMPS PZH in patients with COPD occurring on the background of CLL and not complicated by pulmonary hypertension, it can be explained by tumor intoxication, cardiotoxic effects of cytostatics, anemia, lymphoid myocardial infiltration. The TMPS indicators of the pancreas of subgroups B and B KONT , C and C KONT did not have significant differences .

There was an increase in the indices of the CRV of the pancreas in patients with CLL in combination with COPD and HLS in subgroups B and C (P <0.001). In patients with compensated and decompensated CPH, an increase in the RER RV is associated primarily with prolonged pulmonary hypertension, due to the presence of a pathologic process in the lungs. No significant differences in the CRD of the main pancreas and the corresponding control subgroups were found.

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