No 35 (2014)

Background: Autoantibodies to myocardial antigenic epitopes and corresponding autoreactive T cell clones play an important role in myocardial damage and in pathogenesis of infectious immune myocarditis. T lymphocytes subpopulations/regulatory T cells balance as well as T cell-derived cytokines are crucial in the mechanisms of immune regulation in myocarditis. Aim: To assess quantitative parameters and functional characteristics of basic peripheral blood lymphocytes subpopulations in patients with infectious immune myocarditis and post-myocarditis cardiosclerosis. Material and methods: 35 patients with infectious immune myocarditis and 39 patients with post-myocarditis cardiosclerosis were included. Among infectious immune myocarditis patients, 17 patients had advanced congestive heart failure (CHF) (NYHA III), and 18 patients had mild, moderate or no heart failure (NYHA 0-II). Among cardiosclerosis patients, 18 patients had no CHF, and 21 had only mild symptoms of heart failure (NYHA I). 10 healthy volunteers were enrolled in the control group. Populations and subpopulations of peripheral blood lymphocytes and markers of lymphocytes activation were studied using quadricolor laser flow cytometry (FACSCalibur) and suitable monoclonal antibodies (Becton Dickinson, USA). Results: Inflammatory myocardial diseases are characterized by alterations of innate and adaptive immunity. In our study, patients with infectious immune myocarditis and post-myocarditis cardiosclerosis had significantly reduced numbers of natural killer T cells irrespective of CHF symptoms and disease duration. T cell immunity disturbances were characterized by decreased numbers of CD3+CD4+ cells depending from the disease duration and symptoms severity. Patients with infectious immune myocarditis also had increased numbers of B cells. Immune activation was demonstrated both in infectious immune myocarditis and (less prominent) in post-myocarditis cardiosclerosis. Increased expression of early activation marker CD25 was found during the first 2 weeks from the disease onset in patients with infectious immune myocarditis. In 1 month and during the second month of the disease, increased numbers of T cells and non-T lymphocytes were demonstrated along with late activation manifested by the expression of HLA-DR antigen. Different severity of CHF symptoms was associated with different patterns of activation markers. Increased expression of apoptosis marker CD95 was found in both infectious immune myocarditis and post-myocarditis cardiosclerosis; maximal CD95 values were demonstrated in myocarditis patients in 1 month after the disease onset. Conclusion: Disturbances of anti-infection immunity and self-limitation mechanisms of immune reactions play an important role in the development and progression of inflammatory myocardial diseases.

Background: Sarcoidosis is an inflammatory granulomatous disease of unknown origin. Lungs and thoracic lymph nodes are most frequently affected. To assess inflammatory process activity, disease activity criteria are to be identified. In clinical practice, bronchoalveolar lavage (BAL) fluid lymphocytes count and blood neopterin levels are commonly used for the monitoring of inflammatory activity in sarcoidosis, though, reliability of the methods may be inadequate. Aim: To assess reliability of BAL fluid lymphocytes count and blood neopterin levels as inflammatory markers in pulmonary sarcoidosis. Materials and methods: BAL fluid lymphocytes counts and blood neopterin levels were measured in 111 patients with pulmonary sarcoidosis. 39 patients had stage I sarcoidosis on chest radiographs, 57 patients had stage II, 15 patients had stage III sarcoidosis. In 28 patients, BAL fluid was sampled from different segments of the lung to compare lymphocytes counts. The results were paralleled with pulmonary function tests, radiographic stage and lung parenchyma changes in computed tomography. Results: Lymphocytes counts in BAL fluid correlated with blood neopterin levels (r=0.26, p=0.027), forced vital capacity value (r=-0.24, p=0.04), and did not correlate with sarcoidosis radiographic stage. In 43% of patients, relative lymphocyte counts in BAL fluid samples from different parts of the lung varied significantly (from 5 to 23%). Normal neopterin levels were detected in 40% of patients with active inflammation. Conclusion: Non-uniform pattern of pulmonary inflammation results in variable lymphocytes counts in BAL fluid samples from different parts of the lung. BAL fluid lymphocytes counts and blood neopterin levels should not be used for reliable monitoring of inflammation in sarcoidosis.

Background: Despite the number of publications related to the expression of surface antigens of periphery blood lymphocytes in chronic obstructive pulmonary disease (COPD), algorithm for interpreting of the results and implicating pathogene-tic treatments still needs to be developed. Aim: To assess the role of cytotoxic lymphocytes in the maintaining of inflammation in COPD. Materials and methods: To examine immune status in 37 patients with COPD exacerbation or remission and 24 healthy donors (control group), blood cytotoxic T-lymphocytes and NK-cells contents were measured using indirect immunofluorescence method. Absolute and relative numbers of lymphocytes expressing CD3, CD4, CD8, CD16, CD20, CD23, CD25, CD54, CD71, CD72, HLA-DR, CD95 antigens, membrane immunoglobulins  M (mIgM) and G (mIgG) were estimated. Results: In COPD, significantly increased numbers of blood cytotoxic lymphocytes were demonstrated independently from the disease stage (p < 0.001). During COPD exacerbation, significant elevations of CD4, CD8, CD20, CD72, NК-cells numbers, serum mIgM and mIgG were demonstrated. During remission, CD20 and CD72 content returned to normal, though, increased numbers of other cytotoxic cells persisted promoting inflammation and progressive damage of pulmonary and bronchial tissues. Conclusion: Observed changes may be due to excessive stimulation of T-cell component of immune system in COPD patients both in exacerbation and remission. Relative reduction of total T-lymphocyte numbers indicates non-specific (non-infectious) inflammation type. High cytotoxic potential of immune system results in pulmonary damage and promotes development of pneumosclerosis and emphysema.

This is a case presentation of hypothyroidism with symptomatic hypothyroid myopathy and 10-fold creatine kinase increase.