Features of the onset of chronic pancreatitis associated with systemic connective tissue diseases (rheumatic diseases)

In the article, the authors outlined some etiological and pathogenetic links in the onset of pancreatitis, morphological features, and variants of symptoms of the pancreas associated with rheumatic diseases. It is emphasized that, more often than not, acute or chronic pancreatitis occurs in connection with vasculitis. We presented the mechanisms of development in periarteritis nodosa, systemic lupus erythematosus, and rheumatoid arthritis. Necrotizing arteritis of pancreatic vessels occurs with a frequency of 60% in periarteritis nodosa, ranging from 6.2–7.4 to 53% in systemic lupus erythematosus, 50% in rheumatoid arthritis, and 17% in scleroderma. Changes in intrapancreatic arteries of small and medium caliber occur in 71% of cases. We presented the mechanisms of development, symptoms, types, diagnostic search, and differential diagnosis of autoimmune pancreatitis. A feature of the course is the presence of both acute and chronic pancreatitis, indicating the possibility of pancreatic infarction due to thrombosis as part of the antiphospholipid syndrome. We analyzed the unique characteristics of pancreatic injury in scleroderma, which include damage to the structure and function of multiple organs and digestive systems. Changes in the vascular bed, problems with cellular immunity caused by CD4+ T lymphocytes and Th2 helper cells, and excessive fibrosis are all to blame. They cause fibrosis by releasing profibrotic cytokines and also have a direct effect on fibroblasts. In this case, dysfunctions and disturbances in the motility of the digestive canal occur; sphincter Oddi dysfunction is of great importance. This leads to the formation of pain syndrome or exocrine pancreatic insufficiency. The authors revealed in detail the features of morphological changes in the pancreas in periarteritis nodosa. The changes are associated with either destructive-productive or productive panvasculitis of the medium and small arteries. Lymphocytes, macrophages, and plasmacytes primarily determine focal infiltration in the gland’s stroma. We observed a clinical picture of classic pancreatitis. Symptoms of pancreatic attack appear with high activity of the underlying disease, while in the inactive phase, functional failure of the pancreas occurs. Attention is focused on the significance of vasculitis of large vessels in giant cell arteritis.