Pericarditis Xanthomatous

Xanthomata pericarditis (lat. pericarditis xanthomatosus) is a diffuse degenerative-proliferative form of rheumatic pericarditis. It differs from classic rheumatic P in the frequent formation of massive papillary growths - “xanthoma”. The etiology is often unknown.

Pericarditis xanthomatose Infectious inflammatory process of the outer layer of the pericardium. It is characterized by loose deposition of lipids in the connective tissue and the appearance of oxalate crystals (xanthoma) in the stroma.

Etiology The etiology and pathogenesis are similar to those of exudative pericarditis. It is also possible for the disease to develop against the background of a septic condition and systemic connective tissue diseases. Pathological anatomy Microscopic examination reveals damage to pansclerotic structures with a layered organization in the area of ​​inflammation. As a result of metabolic disorders and paralysis of connective tissue synthesis, an increase in the volume of fatty cytoplasm is determined, as well as the accumulation of neutral fats. Further, there is a violation of the histoarchitectonics of the connective tissue with deformation, disintegration of fibers, invagination of the fibrous frame without the formation of cellular reactions of acute inflammation. In addition, high pericardial permeability and fibrin accumulation in the spaces are noted. At the same time, fibroplasia and polymorphic cellular infiltration of neutrophils with an admixture of lymphocytes and plasma cells are detected in the stroma zone. Decomposition of chromatin and nuclear debris is noted in the bruises. With a long course, isolated signs of atheromatous dissection appear. Such lesions are characterized by the formation of Aschoff cells with rounded nuclei and basophilia. Around areas affected by atheroma, a zone of accumulation of mononuclear cells is often found. Most often, the serous membranes, parietal and visceral, trachea of ​​the bronchial tree, fibromuscular flaps of the ischial region, mediastinum, mediastinal muscles and lungs are involved in the pathological process. A characteristic feature is that myocardial damage develops last. Meanwhile, signs of myocardial inflammation are usually present both in the etiology and in the pathomorphological study of the structure of the pericardium. The progression of erosive inflammation leads to the formation of an aseptic form and reactive fibrosis. The appearance of irreversible changes differs in nature depending on the impact of etiological factors. Viral infection stimulates lacunar, bacterial infection - obstructive pericarditis. All infectious lesions are accompanied by fever and mediastinitis (inflammation of the pericardial sac). Involvement of the serosa and myocardium is characterized by multinucleated alveolar granulocytes that cover the endocardium. The mucous sinuses of all membranes contain degenerative elements of interstitial origin that are not expressed by agglutination of immune complexes of erythrocytes. The myocardium, hyperplastic around the cavity of the heart sac, is gradually replaced by myocardial cells. The presence of a sinus is accompanied by an accumulation of neutrophils and macrophages with pronounced hypertrophy, which determines the