The effects of prolactin on ADP-induced platelet aggregation in patients with stable angina of effort and gastroesophageal reflux disease

Abstract

The combination of stable angina of effort (SEA) and gastroesophageal reflux disease (GERD) is frequently observed in the clinic of internal diseases. Thrombocytic link of homeostasis is one of the main factors in the development and progression of atherosclerosis. The long-term increase of circulation prolactin levels can result in the development of pathological changes caused by hyperprolactinemia.Objective — to investigate the effect of prolactin levels on the ADP-induced platelet aggregation in patients with SEA and GERD.Materials and methods. The study included 148 persons: 30 patients with isolated SEA (1st group), 30 patients with isolated GERD (2nd group), and 88 patients with combination of SEA and GERD (3rd group). A separate group consisted of 20 practically healthy persons (PHPs). The serum levels of prolactin and the degree, rate, and time of ADP-induced platelet aggregation were investigated in all patients, included in the study.Results and discussion. The degree, rate, time of ADP­induced platelet aggregation, as well as prolactin levels, were significantly higher in patients with SEA and comorbidity of GERD than the similar results of the PHPs group, patients with isolated SEA and isolated GERD. A high direct correlation relationship was established between the degree of ADP-induced aggregation of blood platelets in patients with SEA with comorbid GERD and serum prolactin levels (r = 0.710; r = 0.696). Conclusions. It has been established that in patients with SEA with comorbid GERD, the prolactin levels were higher than in groups with isolated SEA, isolated SEA and PHPs group and increaseв proportionally to the degree and rate of ADP-induced platelet aggregation.