What causes chronic pancreatitis?

Chronic pancreatitis in children, as in adults, is of a polyethological nature and serves as the main form of pancreatic pathology. In children, duodenal diseases (41.8%), bile ducts (41.3%), and less frequent intestinal pathology, pancreatic abnormalities, and abdominal trauma are considered to be the leading etiological cause. Concomitant factors: bacterial and viral infections (hepatitis, enterovirus, cytomegalovirus, herpetic, mycoplasmal infections, infectious mononucleosis, epidemic parotitis, salmonellae, sepsis, etc.) and helminthiases (opisthorchiasis strongyloidiasis, giardiasis, etc.). Systemic diseases of connective tissue, respiratory diseases, endocrine organs (hyperlipidemia, often I and V type, hyperparathyroidism, hypercalcemia, hypothyroidism), chronic renal failure and other conditions can contribute to the development of pancreatitis. The toxic effect of some drugs on acinar tissue, leading to the development of drug pancreatitis (glucocorticosteroids, sulfonamides, cytostatics, furosemide, metronidazole, NSAIDs, etc.) is proved. Irreversible changes in the pancreas can occur due to the use of alcohol-containing beverages and other toxic substances.

Genetic and congenital factors can also cause pronounced morphological changes in the pancreas in hereditary pancreatitis, cystic fibrosis, Schwamman-Diamond syndrome, isolated pancreatic enzyme deficiency.

The frequency of hereditary pancreatitis among other etiologic forms is 3 to 5%, inheritance occurs in an autosomal dominant type. The development of the disease is due to the gene mutation of pancreatic enzymes (trypsinogen and trypsin). The mutation of the cationic trypsinogen R117H gene leads to a loss of control over the activation of proteolytic enzymes in the pancreas. As a rule, the clinical symptomatology of hereditary pancreatitis is formed in 3-5 years, the disease is characterized by the severity of pain and dyspeptic syndrome. With age, the frequency of relapse increases, and severe pancreatic insufficiency develops. In ultrasound examination, calcifying pancreatitis is diagnosed.

In the etiology of chronic pancreatitis, the role of allergic diseases, food sensitization, the use of food products containing xenobiotics and various additives that adversely affect the pancreas is great. If the cause of pancreatitis development can not be clarified, idiopathic pancreatitis is diagnosed. Some researchers identify an autoimmune variant of pancreatitis, including primary.

In most children, chronic pancreatitis develops again (86%), as a primary disease is much less common - in 14% of patients.

Pathogenesis of chronic pancreatitis

To understand the mechanism of development of the pathological process in the pancreas, all factors should be divided into 2 groups. The first is the factors that cause difficulty in the outflow of pancreatic juice and lead to ductal hypertension. The second is the factors contributing to the direct primary lesion of the acinar cells of the gland. Isolation of the leading etiologic moment is necessary for the reasonable appointment of medical measures.

The main link of the mechanism of development of most forms of chronic pancreatitis is the activation of pancreatic enzymes in the ducts and parenchyma of the gland. In a cascade of pathological reactions, a special place belongs to proteolytic enzymes (trypsin, chemotripsin, etc.) and less often - lipolytic enzymes (phospholipase A). The autolysis process leads to edema, destruction of acinar cells, infiltration. With recurrence - to sclerosis and fibrosis of the gland with the development of secretory deficiency. Thanks to powerful inhibitory systems, the pathological process in the gland can be limited to interstitial edema without the development of necrosis, which is often noted in childhood. Often, chronic pancreatitis in children - the outcome of previously transferred acute pancreatitis.

Transition to chronic forms can be subclinical, which subsequently leads to complications (cyst, changes in the duct system, etc.).

Mediators of inflammation play an important role in the genesis of chronic pancreatitis. Anti-inflammatory cytokines include interleukins 1, 6, 8. Tumor necrosis factor, platelet aggregation factor. In this case, the production of cytokines does not depend on the cause of pancreatitis. Activation of cytokine reactions has a damaging effect on pancreatic acinocytes.

The pathological process in the pancreas can begin as a result of a deficiency of gastrointestinal hormones and biologically active substances. A decrease in the number of hormone-producing cells synthesizing secretin, cholecystokinin, pancreosimine, serotonin in duodenal diseases with motor disorders and the development of atrophic processes in the mucosa has been proven. Violation of the metabolism and deposition of intestinal hormones leads to dystrophic changes in the gland, difficulty in the outflow of pancreatic secretion, disruption of the motility of the duodenum, lowering the pressure in it and dysfunction of the sphincter apparatus. Under these conditions, the atrophy of acinar cells occurs and their replacement by connective tissue.