Abstract
Summary. The article presents the results of the study of metabolic endogenous intoxication indexes (MEI) reflecting intoxication by organic compounds influencing the change of physiological pH balance and their correlation with the presence and severity of chronic pain syndrome and quality of life criteria. The dynamics of these indexes and improvement of QOL on the background of the suggested scheme of small volume infusion detoxification therapy (SWIDT) by hyperosmolar balanced crystalloid (HSC) containing components with reserve alkalinity in the section of 30-day period were researched. The aim of the study – to evaluate the therapeutic effect of SWIT on the severity of pH abnormalities as well as the effect of SWIT on the severity of chronic pain syndrome and related aspects of quality of life in patients with CP in comorbidity with T2DM. Materials and Methods. 115 patients divided into 5 groups were examined: Group 1 – 20 patients without complaints on the gastrointestinal tract, Group 2 – 30 patients with CP, Group 3 – 20 CP patients with concomitant T2DM received protocol treatment (PT), Group 4 and 5 – CP patients with concomitant T2DM, including 21 patients received PT with a course of SWIT for 3 days, and 24 patients – SWIT course for 5 days. The concentration of lactate and pyruvate in blood plasma was determined, the lactate/pyruvate ratio was calculated, the concentration of bicarbonates in blood plasma was determined, pain was determined by the QLQ-C30 and PAN28 questionnaires, pain syndrome severity was determined by the visual analogue scale (VAS). Statistical processing of the obtained data was performed using Microsoft Excel 2016 and Statistica 13.0. Results. A positive therapeutic effect on the dynamics of the level of mEI markers and COPD disorders in patients with CP with concomitant T2DM has been proved, which indicates the positive effect of the SWIT scheme in the program of complex treatment. A clear dependence of the rate of normalization of these parameters on the duration of the SWIT course was revealed. Conclusions. 1 Statistically significant increase of objective markers of COS impairment due to MEI (lactate, lactate/pyruvate ratio) in CP patients with concomitant T2DM in comparison with the same in isolated CP was revealed (p<0.05). Strong correlations between markers of mEI and pH disturbance towards metabolic acidosis mediated by lactate/pyruvate ratio and bicarbonate content were found. A higher level of efficiency of SWIT-5 application in complex therapy in comparison with MOIT-3 program has been established. It is proved that normalization of the specified indexes directly correlates with duration of the MOIT course.
Highlights
The causes of persistent metabolic acidosis in CP are: chronic inflammation of pancreatic tissue with the development of edema and impaired microcirculation and perfusion and, as a consequence, hypoxia [1]; oxidative stress of CP tissue with the predominance of acidic metabolites production; intestinal microflora activity with dysbacteriosis, reduced capacity of blood buffer systems [2]
Strong correlations between markers of mEI and pH disturbance towards metabolic acidosis mediated by lactate/pyruvate ratio and bicarbonate content were found
The main studied parameters in the groups changed as follows: lactate level decreased in the protocol treatment group by 9.52 %, in SWIT 3 group
Summary
The causes of persistent metabolic acidosis in CP are: chronic inflammation of pancreatic tissue with the development of edema and impaired microcirculation and perfusion and, as a consequence, hypoxia [1]; oxidative stress of CP tissue with the predominance of acidic metabolites production; intestinal microflora activity with dysbacteriosis, reduced capacity of blood buffer systems [2]. An important pathogenetic factor of pH abnormality in patients with CP is concomitant diabetes mellitus [3]. Patients with both types of diabetes have high level of lactate in plasma on an empty stomach [4]. The mechanisms underlying diabetes-associated hyperlactatemia include significant changes in intracellular glucose metabolism in insulin-sensitive tissues (decreased glycogen synthesis, impaired glucose oxidation metabolism and increased nonoxi dative glycolysis rate) [5]. Patients with insulin resistance/diabetes have increased glycolysis activity, which leads to the formation of NAD, pyruvate, and a decrease in NAD+ levels. There is a conversion of pyruvate to lactate by LDH by generating NAD+ from NAD in a redox reaction exacerbated by insulin resistance, as hyperinsulinemia causes increased glycolysis [6]
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