
Changes in the microcirculatory bed in patients with post-mastectomy syndrome
Author(s) -
О. В. Фионик,
Varvara Krasnikova,
D. A. Pokatilo,
М. Л. Поспелова
Publication year - 2022
Publication title -
voprosy rekonstruktivnoj i plastičeskoj hirurgii
Language(s) - English
Resource type - Journals
ISSN - 1814-1471
DOI - 10.52581/1814-1471/78-79/05
Subject(s) - medicine , mastectomy , lymphedema , breast cancer , fibrosis , metastasis , radical mastectomy , radiation therapy , laser doppler velocimetry , endothelial dysfunction , surgery , blood flow , cardiology , cancer , pathology
The purpose of the study: to determine the features of the state of the microcirculatory bed in women with post-mastectomy syndrome as a cause of fibrosis. Material and methods . The study involved 76 women, of whom two groups were formed. The first group consisted of 46 patients aged 25 to 49 years (mean age – (43.8 ± 3.8) years old) with post-mastectomy syndrome (PMES), the average period after radicle treatment of breast cancer was (4.3 ± 2.1) years. All patients underwent mastectomy, radiation and chemotherapy for the treatment of breast cancer, followed by a comprehensive examination to exclude metastasis and continued tumor growth, as well as to exclude hemodynamically significant violations of venous and arterial blood flow of the upper extremities. The second group was formed of 30 healthy female volunteers aged 25 to 43 years, whose average age was (33.75 ± 10.70) years old. Clinical and instrumental methods of examination were used: anthropometric method, lymphoscintigraphy of the upper extremities, laser Doppler flowmetry, determination of the expression level of intercellular adhesion molecules sICAM-1, sPECAM-1. The results . Gross violations of the function of the microcirculatory bed were revealed: endothelial dysfunction, spasm of precapillary sphincters, decrease in the intensity of blood flow in the metabolic capillaries, the predominance of passive mechanisms of blood flow regulation. These changes lead to tissue hypoxia, which may be the trigger for the development of fibrosis and lymphedema. Endothelial dysfunction, which is confirmed by increased expression of specific biomarkers, may be the basis of these disorders. A complex, long-term change in the work of microvessels leads to a breakdown of compensatory mechanisms. Conclusion. The study of the pathogenetic mechanisms of the development of post-mastectomy syndrome will allow forming preventive strategies in patients after treatment of breast cancer, improving the quality of life of these patients. Further search for promising predictors of the development of fibrosis, the study of changes in the microcirculatory bed will provide additional information about the pathogenesis of PMES, to identify changes in the soft tissues of the upper extremities at an early stage of post-mastectomy syndrome, may be important for the development of more effective methods of treatment of PMES.