【Abstract】 Objective: To observe the effect of coenzyme Q10 in the treatment of acute carbon monoxide poisoning (ACOP) patients. Methods: 90 cases of ACOP patients were selected as research subjects, and were divided into 45 cases each in the observation group and the control group by randomized numerical table method. The control group was treated with conventional therapy, and the observation group was treated with coenzyme Q10 on the basis of the control group, and the cognitive ability scores, serological indexes [C-reactive protein (hs-CRP), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH), and troponin (cTnI)] levels and the incidence rate of adverse reactions were compared before and after treatment. (C-reactive protein (hs-CRP), creatine kinase isomerase (CK-MB), lactate dehydrogenase (LDH), and troponin (cTnI)] levels and the incidence of adverse events were compared between the two groups.
Results: after treatment, the Montreal cognitive assessment scale score of the observation group was significantly higher than that of the control group, and the difference was statistically significant (P<0.05); after treatment, the levels of hs-CRP, CK- MB, LDH, and cTnI of the observation group were significantly lower than those of the control group, and the difference was statistically significant (P<0.05); when comparing the incidence of adverse reactions of the two groups, the difference was not statistically significant (P>0.05). (There was no statistically significant difference in the incidence of adverse reactions between the two groups (P>0.05). Conclusion: The use of coenzyme Q10 in the treatment of ACOP patients on the basis of conventional treatment can improve the cognitive function score and reduce the level of serological indexes, and its effect is better than that of conventional treatment alone.
Acute carbon monoxide poisoning (ACOP) is caused by excessive inhalation of carbon monoxide (CO), which can combine with hemoglobin in human blood to form carboxyhemoglobin, resulting in hypoxia of vital tissues and organs, causing respiratory distress, headache, and twitching of limbs, etc. [1-2], and its morbidity and mortality rate are among the highest of poisoning diseases [3]. After timely treatment of ACOP, some patients with ACOP still have a "false healing period" of 2~30 d, and suffer from slow reaction, confused memory, urinary incontinence, etc. [4]. This paper observes the effect of coenzyme Q10 in the treatment of ACOP patients.
1 Information and methodology
1.1 General information
Ninety patients with ACOP admitted to our hospital from May 2018 to May 2019 were selected for the study. Inclusion criteria: patients who met the diagnostic criteria for CO poisoning [5]; patients who were treated in our hospital and had not received any other treatment prior to admission; patients with onset of illness within 3 h; and patients with first-time CO poisoning.
Exclusion criteria: patients with malignant tumors; pregnant or breastfeeding patients; patients with a history of allergy to the drugs selected for this study; patients with hematological or infectious diseases. The patients and their families understood the content of the study and voluntarily signed the informed consent form, and the study was approved by the Ethics Committee of the hospital. The patients were divided into 45 cases each in the observation group and the control group by using the randomized numerical table method.
Observation group: 25 males, 20 females; age 20-70 years old, mean (38.68±8.76) years old; time from poisoning to hospitalization 0.5-3 h, mean (1.02±0.16) h; 14 cases of mild, 23 cases of moderate, 8 cases of severe. In the control group, there were 30 males and 15 females, aged 21-71 years old, average (39.25±8.83) years old; the time from poisoning to hospitalization was 0.5-3 h, average (1.03±0.12) h; there were 16 cases of mild, 22 cases of moderate, and 7 cases of severe poisoning. There was no statistically significant difference between the two groups in terms of gender, age and other general information (P>0.05), and the two groups were comparable.
1.2 methodologies
The control group was treated with hyperbaric oxygen, correcting water, electrolyte and acid-base balance disorders, improving cerebrovascular circulation and other conventional treatments, of which the hyperbaric oxygen treatment time was 60~90 min/times, 1 time/d, the pressure was adjusted to be 0.15~0.20 Mpa, and the pressure was increased, stabilized and reduced for 20 min, 50 min and 20 min respectively, and at the same time, the patients were given 20% mannitol intravenously, and the specific amount of the drug was selected according to the degree of poisoning of the patients. The specific dosage should be selected according to the degree of intoxication of the patient, and the dosage can be appropriately reduced after the symptoms are relieved, but the hyperbaric oxygen therapy and the monitoring of vital signs should still be maintained.
In the observation group, Coenzyme Q10 capsule (Guangdong South China Pharmaceutical Group Co., Ltd., H19993662, 10 mg) was combined with the treatment in the control group, and one capsule was swallowed with water three times a day in the morning, noon and night. The poisoned patients were examined by cranial magnetic resonance within 48 hours after admission to the hospital, and the examination was repeated 20 days later. If delayed encephalopathy occurred during the treatment period, magnetic resonance examination was performed immediately, and the examination was repeated after 1 month of treatment. Before and after treatment, both groups collected 5 mL of venous blood from the patients and centrifuged the serum, and chose Beckman AU5800 automatic biochemical immunoassay analyzer from the United States to measure the level of C-reactive protein (hs-CRP) by scattering turbidimetry, the level of creatine kinase isoenzyme (CK-MB) by enzyme immunofluorescence, the level of lactate dehydrogenase (LDH) by rate method, and the level of troponin (ccTiP) by chemiluminescence. The enzyme-linked immunofluorescence method was used to determine the level of creatine kinase isoenzyme (CK-MB), the rate method was used to determine the level of lactate dehydrogenase (LDH), and the chemiluminescence method was used to determine the level of troponin (cTnI).
1.3 Observation indicators
(1) To compare the cognitive ability of the two groups before and 1 month after treatment, the Montreal Cognitive Assessment Scale (MoCA) was used as the basis of judgment [6], and the patients were scored in 8 cognitive domains and 11 items, such as attention and concentration, memory, language, executive function, visual structural skills, abstract thinking, computation, and orientation, etc., with a total score of 30 points, and the higher scores indicated that the higher cognitive ability of the patients.
(2) Compare the levels of serologic indexes, including hs-CRP, CK-MB, LDH and cTnI, before and after treatment.(3) Compare the incidence rates of adverse reactions during treatment between the two groups.
1.4 Statistical methods
SPSS 21.0 statistical software was used to process the data. Measurement data were expressed as (x- ± s), comparison was made by t-test, and count data were made by χ2-test, and P<0.05 was regarded as statistically significant difference.
2 Results
2.1 Comparison of cognitive ability between the two groups before and after treatment
Before treatment, there was no statistically significant difference between the MoCA scores of the two groups (P>0.05); after treatment, the MoCA scores of the two groups were significantly higher than those before treatment, and the observation group was higher than the control group, and the difference was statistically significant (P<0.05). See Table 1.
2.2 Comparison of serologic index levels between the two groups before and after treatment
Before treatment, there was no statistically significant difference in the levels of hs-CRP, CK-MB, LDH and cTnI between the two groups (P>0.05); after treatment, the levels of hs-CRP, CK-MB, LDH and cTnI were significantly lower than those before treatment, and the observation group was lower than that of the control group, and the difference was statistically significant (P<0.05). The difference was statistically significant (P<0.05).
2.3 Comparison of the incidence of adverse reactions between the two groups
Comparing the incidence of adverse reactions between the two groups, the difference was not statistically significant (P>0.05). See Table 3.
3 Discussion
ACOP is one of the common life poisoning and occupational poisoning, patients will have unconsciousness, headache, dizziness, flushing, etc. The treatment effect is better for patients with shorter time of poisoning, and it is not easy to leave after-effects, while patients with longer time of poisoning have more serious hypoxia of tissues and organs due to the accumulation of large amount of CO in the body, and they are easy to leave complications [7-8].
The levels of hs-CRP, CK-MB, LDH and cTnI can reflect the myocardial function of patients [9-10], and in patients with CO poisoning, the combination of myoglobin and CO to form carbon-oxygenated myoglobin leads to tissue hypoxia, which injures cardiomyocytes and leads to cardiac function damage [11]. Since the affinity of hemoglobin for CO is higher than that of oxygen, hyperbaric oxygen therapy can expel CO from the blood as soon as possible, so that the body can obtain enough oxygen again and stabilize the vital signs, and meanwhile, improving the cerebral vascular circulation can prevent the occurrence of cerebral infarction and reduce the occurrence of delayed encephalopathy.
The results of this study showed that the MoCA score of the observation group was significantly higher than that of the control group, and the levels of hs-CRP, CK-MB, LDH and cTnI were lower than those of the control group. The reason for this may be that conventional treatment mainly improves the symptoms of CO poisoning, but does not pay enough attention to the treatment of cognitive function and myocardial injury.
Coenzyme Q10 is a fat-soluble quinone, and its clinical effects are mainly antioxidant and neuroprotective. Coenzyme Q10 can effectively scavenge free radicals, inhibit over-oxygenation and transfer electrons in the mitochondrial respiratory chain, which can reduce oxidative damage to human epithelial cells and cognitive impairment, and inhibit iron-induced apoptosis of dopamine neurons, thereby inhibiting damage to brain cortical cells.
In addition, because of the obvious antioxidant effect of coenzyme Q10 and its membrane stabilizing effect, coenzyme Q10 can promote the oxidative phosphorylation of cardiomyocytes by repairing mitochondrial membrane phospholipids to protect the damaged myocardium and improve myocardial function. The results of this study also showed that there was no statistically significant difference in the incidence of adverse effects between the two groups. This suggests that the combination of coenzyme Q10 therapy does not increase the safety risk. Due to the small sample size of this study, the results need to be confirmed with a larger sample size.
In conclusion, the use of coenzyme Q10 in the treatment of ACOP patients can improve cognitive function scores and reduce serologic markers, which is better than the effect of conventional treatment alone.
bibliography
[1] Yang Hui . Nursing care of patients with acute carbon monoxide poisoning treated with hyperbaric oxygen [J]. Contemporary Nurses,2017 ,24( 4 ):24-25.
[2] Qin Shiyue, Zhang Yuancong, Chen Jingqing, et al. Prehospital emergency care for acute carbon monoxide poisoning
57 cases analyzed [J]. Huaxia medicine, 2017 , 30 ( 5 ): 113-114.
[3] ZHENG Quanle, FU Na, ZHOU Shunyi, et al. Progress of diagnosis and treatment of delayed encephalopathy in acute carbon monoxide poisoning [J]. Chinese Electronic Journal of Neurotrauma Surgery, 2017 , 3(1): 48-50.
[4] LI Ying, LIU Jianing. Analysis of factors related to the occurrence of acute lung injury after acute carbon monoxide poisoning [J]. Anhui medicine, 2018 , 22 ( 8 ): 1472-1474.
[5] Huang Shaoqing, Zhou Yushu, Liu Renshu . Modern diagnosis and treatment of acute poisoning [M]. Beijing: People's Army Medical Press, 2002: 188-191.
[6] WANG Wei, WANG Luning . Application of the "Montreal Cognitive Assessment Scale" in screening patients with mild cognitive impairment [J]. Chinese Journal of Internal Medicine, 2007, 46(5 ): 414- 416.
[7] Ge Huan, Gao Chunjin, Zhao Liming, et al. Clinical treatment guidelines for carbon monoxide poisoning (II)[J]. Chinese Journal of Nautical Medicine and Hyperbaric Medicine, 2012 , 19(5):315-317.
[8] LI Sheng, CHEN Qianmiao, CHI Xuefeng, et al. Study on predictors of delayed encephalopathy after acute carbon monoxide poisoning [J]. Zhejiang Medicine, 2019, 41(11 ): 1150- 1153.
[9] Liu Junge . Clinical observation of acute carbon monoxide poisoning combined with sexual pulmonary edema [J]. Clinical Medicine Literature Electronic Journal, 2017, 4 ( 68 ): 13304.
[10] JING Jianjun, ZHANG Zhengui, YU Zuofa. Predictive value of inflammatory factors on severity and prognosis of patients with acute carbon monoxide poisoning [J]. Chinese and Foreign Medical Research, 2019, 17(15 ): 1-3.
[11] ZHANG Baoping, QI Lubo, HAN Yanqiu. Study related to brain tissue and cardiomyocyte damage in patients with acute carbon monoxide poisoning [J]. Journal of Cardiovascular and Cerebrovascular Diseases of Chinese and Western Medicine, 2018 , 16 ( 16 ): 2425-2426.
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