According to O.A. Rukavitsin and GI Sidorovich (2006) at the time of diagnosis of MM, most often there is damage to the respiratory organs and urinary tract infections, usually they are caused by S. Pneumoniae and H. Influenzae, as a result of staphylococci and gram-negative flora begin to predominate; High-dose chemotherapy, accompanied by prolonged neutropenia, and steroid treatment promote the development of a fungal infection . At different periods of MM, the risk of developing bacterial infections is not the same: in the initial phase of the disease, it is 4 times higher than in remission; and in the first two months of chemotherapy 2 times higher than during the rest of the time . Patients with MM, as well as all patients with chronic lymphoproliferative tumors, are subject to repeated respiratory infections, especially pneumonia, which are one of the main causes of mortality in this pathology . The incidence of pneumonia in patients with MM is associated with a decrease in the function of humoral and cellular immunity . In addition, susceptibility of MM patients to infections is due to activation of endogenous infection, expansion of the entrance gate for microorganisms due to damage to the skin, mucous membranes, prolonged catheterization and central veins . Especially such complications are observed during high-dose chemotherapy or after bone marrow transplantation, when the body is weakened due to both the tumor disease and the use of aggressive chemotherapy programs . In patients with chronic renal failure (CRF), the likelihood of the addition of infectious complications increases. At the same time, any infection in MM patients can lead to the development of acute renal failure .
An important factor predisposing to the lung localization of infectious processes in MM is the pathoanatomical basis of the lesion of the lungs in this disease, designated O.V. Voyno-Yasenetskaya as “pulmonary-alveoli bright paraproteinosis” . O.V. Voyno-Yasenetskaya concluded that plasma hyper-viscosity, proteinaceous intravascular stasis with an increase in the permeability of the basement membranes and increased filtration of the protein into the alveoli underlie the aerohematic barrier and lead to lysis of the elastic framework of the lung. The release of paraprotein into the septal spaces causes proliferation of septal cells and a pronounced macrophage reaction, as well as impaired lymphatic drainage, with a consequent increase in hydrostatic pressure in the capillaries. There is a deposition of three types of substances in the tissues: amyloid, amyloid-like and crystalline. The basis of pulmonary alveolar paraproteinosis in MM is the deposition of amyloid-like substance, filling of part of the alveoli with amyloid-like bodies , “hyalinosis” of membranes. Per Primary is the lesion of blood vessels (primarily capillaries) and interalveolar septa. Circulatory impairment at the level of the aerohematic barrier leads to dystrophy of the lung skeleton and emphysema, which later becomes compensatory in nature due to the shutdown of the part of the alveoli filled with the proteinaceous polysaccharide substance. The most significant changes were observed in myeloma A. Amyloid-like deposits were found in the walls of the pulmonary vessels, in capillaries, alveolar septa, septal spaces, alveolar epithelium, alveolar lumens, from vessels, walls of arterioles .