Pancreatic diseases and thrombotic, thromboembolic complications

Abstract

In this paper, the authors analyze the etiologic, pathogenetic, and clinical variants of thrombotic and thromboembolic complications in chronic pancreatitis and pancreatic cancer. The authors concentrate on the pathogenetic mechanisms that contribute to the development of chronic pancreatitis, hereditary pancreatitis, and pancreatic cancer. These mechanisms include participation in systemic chronic inflammation, activation of plasma cells that accelerate proliferation, progression, migration, and invasion of epithelial cancer cells, metastasis of tumor cells, and a worsening of the response to radiation and chemotherapy. The discussion focuses on the role of extracellular matrix rigidity and the transformation of plasma cells. We consider the pathogenesis of hereditary pancreatitis in detail and highlight the genetic features of its development. We emphasize the importance of paraneoplastic symptoms, which combine to form a syndrome that often manifests as thrombotic and thromboembolic complications (migrating thrombophlebitis, thrombosis, and thromboembolism of different branches of the pulmonary arteries). The significance of thrombocytosis and the synthesis of fibrinopeptide A (a biomarker for tumors) is now under scrutiny. The level of fibrinopeptide A may be directly related to the size of the tumor. We indicate the peculiar course of deep vein thrombosis, which occurs in the muscles of the calves, impacts the proximal veins of the legs, and remains undetected. We discuss the symptoms of thrombosis in the veins of the ileofemoral segment and elucidate the mechanism behind pain syndrome. Increased venous pressure in the pelvic veins, a decrease in venous wall tone due to hormonal changes, the development of stasis, and tumor masses’ compression are the causes. Thrombosis in the ileofemoral segment and deep veins of the lower extremities (both distal and proximal) is the cause of pulmonary embolism (usually with a negative prognosis).