脂肪变性期稳定型心绞痛和非酒精性脂肪肝患者的高氨血症

E. J. Zykina, Zh. G. Simonova
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The results of laboratory examination (clinical and biochemical blood tests, lipidograms, insulin levels (calculated by HOMA-IR), glycosylated hemoglobin (HbAlc)) were evaluated; non-invasive markers for the diagnosis of liver injury. Hyperammonemia was evaluated by quantitative rapid ammonia analysis using a Pocket Chem TM BA PA-4140 analyzer. All patients underwent ultrasound of the liver using Philips Epiq 5 (USA). Results. In all patients with stable angina (group I and II), the diagnosis of non-alcoholic fatty liver disease, steatosis stage, was confirmed. The lipid profile of patients in Groups I and II showed more significant hypertriglyceridemia compared to those in the control group, with no statistical difference in Groups I and II. The mean ammonium level in patients with NAFLD in combination with stable CHD (group I, II) was above the threshold and was 87 (57-127.5) and 79 (57-97) μmol/L, respectively, and did not differ significantly (p > 0.05). 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摘要

的目标。评估伴有稳定型心绞痛的非酒精性脂肪肝患者脂肪变性期高氨血症的严重程度。研究材料和方法。在临床试验中,将稳定型心绞痛患者分为三组。第一组(n = 43)由肝脂肪变性合并肥胖和稳定型冠心病的NAFLD患者组成。II组(n = 41):体重正常、冠心病稳定的肝脂肪变性期NAFLD患者。III组(对照组)(n = 42) -无NAFLD的稳定型心绞痛患者,体重正常。评估实验室检查结果(临床和生化血液检查、血脂、胰岛素水平(通过HOMA-IR计算)、糖化血红蛋白(HbAlc));诊断肝损伤的无创标志物。采用Pocket Chem TM BA PA-4140分析仪定量快速氨分析法评估高氨血症。所有患者均使用飞利浦Epiq 5(美国)进行肝脏超声检查。结果。所有稳定型心绞痛患者(I组和II组)均确诊为非酒精性脂肪性肝病,即脂肪变性期。与对照组相比,I组和II组患者的脂质谱显示出更明显的高甘油三酯血症,但I组和II组之间无统计学差异。NAFLD合并稳定型冠心病患者(I、II组)的平均铵离子水平均高于阈值,分别为87 (57-127.5)μmol/L和79 (57-97)μmol/L,差异无统计学意义(p >0.05)。III组患者(无肝脏疾病)血氨均值在目标范围内。根据相关分析结果,建立了铵与肝酶的关系,计算了脂肪变性指数和基本代谢指标。结论。非酒精性脂肪性肝病合并稳定型心绞痛的脂肪变性期患者比不伴有肝损伤的稳定型冠心病患者有更严重的高氨血症。
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Hyperammonemia in patients with stable angina pectoris and nonalcoholic fatty liver disease at the steatosis stage
The aim. To assess the severity of hyperammoniemia in patients with non-alcoholic fatty liver disease at the steatosis stage in conditions of comorbidity with stable angina. Research materials and methods. During the clinical trial, three groups of patients with stable angina were formed. Group I (n = 43) consisted of patients with NAFLD at the stage of hepatic steatosis in combination with obesity and a stable form of CHD. Group II (n = 41) - patients with NAFLD at the stage of hepatic steatosis against the background of normal body weight and stable CHD. Group III (control) (n = 42) - patients with stable angina without NAFLD, with normal body weight. The results of laboratory examination (clinical and biochemical blood tests, lipidograms, insulin levels (calculated by HOMA-IR), glycosylated hemoglobin (HbAlc)) were evaluated; non-invasive markers for the diagnosis of liver injury. Hyperammonemia was evaluated by quantitative rapid ammonia analysis using a Pocket Chem TM BA PA-4140 analyzer. All patients underwent ultrasound of the liver using Philips Epiq 5 (USA). Results. In all patients with stable angina (group I and II), the diagnosis of non-alcoholic fatty liver disease, steatosis stage, was confirmed. The lipid profile of patients in Groups I and II showed more significant hypertriglyceridemia compared to those in the control group, with no statistical difference in Groups I and II. The mean ammonium level in patients with NAFLD in combination with stable CHD (group I, II) was above the threshold and was 87 (57-127.5) and 79 (57-97) μmol/L, respectively, and did not differ significantly (p > 0.05). In patients of group III (without liver disease), the mean values of ammonia in the blood were in the target range. According to the results of correlation analysis, we established the relationship of ammonium with liver enzymes, calculated steatosis indices and basic metabolic indicators. Conclusion. Patients with non-alcoholic fatty liver disease in the steatosis stage with a combination of stable angina have more severe hyperammonemia compared to patients with stable CHD without concomitant liver injury.
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