Arterial hypertension and chronic pancreatitis: calcium dependent pathology and its complications

Abstract

The course and progression of arterial hypertension (AH) and chronic pancreatitis (CP) occurs against a background of increased consumption or insufficient intake of calcium ions into the body. Most often, the development of AH is associatedwith a genetic defect at the level of the angiotensin-converting enzyme with a violation of the permeability of the cell membrane, and, consequently, the loss of potassium against the background of accumulation of sodium and calcium inside the cell. The result of excess calcium in the cell is an increase in the vessels tone and their increased sensitivity to catecholamines. At the same time, with CP, the mechanisms of bone resorption are associated with a violation of calcium absorption as a result of the formation of maldigestion syndromes and malabsorption. The arising systemic spasm of the vascular canal with AH promotes the progression of CP and the violation of the synthesis of enzymes in the organ, which is calcium dependent. Thus, despite the different mechanisms of calcium absorption intake/impairment, the combination of these nosological forms can be considered as a predictor of the osteopenic syndrome. Purpose. Improvement of early diagnosis of metabolic bone disorders and predicting osteopenic changes in patients with combined course of AH and CP.