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The Role of Helicobacter Pylori Eradication on the Glycemic Control of Type 2 Diabetes Mellitus Patients: A Prospective Study

Weaam Mohammed Ali ¹, Mohammad Alyamany Kobeisy Hussein², Soumaia Ahmed Kassem³

1Assistant lecturer of internal medicine Internal Medicine Department, Faculty of Medicine, Aswan University, Aswan 81528 ,Egypt

2Professor of Internal Medicine, Internal Medicine Department, Faculty of Medicine, Assuit University, Assuit 71515, Egypt

3Lecturer of Internal Medicine, Internal Medicine Department , Faculty of Medicine, Aswan University, Aswan, 81528 Egypt

Corresponding Author: Weaam Mohammed Ali Email: [email protected]

Abstract:

Aim: To determine the eradication effect of H.pylori infection in improving the HbA1c level in patients with type 2 diabetes

Background: The potential role of H. Pylori infection on the development and progression of type 2 diabetes mellitus (T2DM) has gained momentum over the recent years, which was supported by the observations of previous epidemiological studies. Thus, we conducted the present study in order to determine the association between H. Pylori infection and the glycemic status of T2DM, as well as the impact of H. Pylori eradication on the glycemic status of T2DM.

Methodology: it was conducted in the department of internal Medicine at Aswan university hospital, and included 200 patients: group I;100 cases divided into two equal sub-groups (A and B) controlled and uncontrolled type 2DM patients Respectively and group II; 100 non diabetic patients as control, The both groups were subjected to eradication of H.P infection according to the international guidelines then HbA1c was formed before and after 3 months for the uncontrolled group to determine

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the eradication effect of h. pylori infection in improving the HbA1c level in patients with type 2 diabetes.

Results: We observed that H. Pylori frequency detected by stool antigen among diabetic patients was 77.0% compared to 55.0% among non-diabetic patients with a statistically significant difference (p=0.001). Higher frequency of H. pylori antigen was present among uncontrolled diabetic (82.0%) compared to 72.0% among controlled diabetics without a statistically significant difference (p=0.235;). HbA1c had a mean of 9.84± 1.6 before treatment and a mean of 7.39±1.02 after treatment. A statistically significant difference has occurred in HA1c among cases with uncontrolled diabetes after eradication of helicobacter pylori. (p=0.001).

Conclusion: In conclusion, our results highlighted the high prevalence of H. Pylori infection among T2DM patients. We found that the eradication of H. Pylori infection led to significant improvements in the glycemic control among uncontrolled patients. These results add to the evidence on the

potential of H. Pylori treatment in diabetes control and should be confirmed in larger studies.

Keywords: Helicobacter Pylori; Eradication; Glycemic Control; Type 2 Diabetes Mellitus

Introduction

The past two decades have witnessed a dramatic rise in diabetes epidemic, which appears to continuously rising over the world [1, 2]. In the most recent epidemiological figures, it was noted that the expected number of the T2DM patients will rise to approximately 642 million by 2040 [3].

The same figures were projected for the Middle East, region, with expected rise in the prevalence of T2DM to reach nearly 14% by 2045 [4]. T2DM is prevalent in Egypt, which is listed among the ten top countries concerning the prevalence of diabetes. Previous reports showed that nearly nine million people are living with T2DM in Egypt, accounting for almost 17% of the whole diabetes population

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in the Middle East [5]. Thus, T2DM represents a substantial burden and attributed for a considerable amount for healthcare resources utilization and expenditures in Egypt. Besides, it poses a significant increased morbidity and mortality burden. The Egyptian dietary pattern is characterized by the consumption of food with a high glycemic load [6], which further increases the risk of hazardous outcomes in diabetic patients in Egypt.

Helicobacter pylori (H. pylori) is a highly prevalent pathogens in different parts of the world and the leading etiological agent for chronic gastritis; the cumulative body of evidence demonstrates that H. pylori infection affects nearly 45% of the global population, with wide geographical disparity and highest incidence reported in the developing and low-income countries[7, 8]. Previous reports have implicated various risk factors in increased susceptibility to H. pylori infection such as poor socio-economic status, overcrowded households, low education, and poor sanitary condition[9].

While the debate regarding the exact route of H. pylori has not been fully elucidated yet, previous experiments showed that the infection is mainly transmitted through feco-oral and oral–oral routes, and -to lesser extent- through sexual transmission[10, 11]. Once reaching the gastric mucosa, H.

pylori exerted different pathological changes for chronic infection and inflammation, these changes include mainly alteration in gastric acidity, bacterial adhesions, release of toxins, and chemokines;

which, in return, lead to subsequent inflammation, immune reactions, and tissue damage[12].

Clinically, H. pylori is asymptomatic in the vast majority of the patients; nonetheless, patients with chronic infection are at excessive risks of various gastrointestinal complications including dyspepsia, peptic ulcer, and chronic gastritis[7]. Besides, chronic H. pylori infection is a well-established risk factor for gastric carcinoma, gastric lymphoma, and esophageal carcinoma[13, 14]. Patients with chronic H. pylori infection are also prone to extra-intestinal complications such as anemia and thrombocytopenia[7].

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The potential role of H. Pylori infection on the development and progression of T2DM has gained momentum over the recent years, which was supported by the observations of previous epidemiological studies [15]. Previous reports showed that T2DM with concomitant H. Pylori infection exhibit significant upregulation in the inflammatory cytokines and other inflammatory markers, leading to progressive insulin resistance and uncontrolled glycemic status, even with medication adherence [16]. Nonetheless, the current body of evidence is equivocal, with other reports noted no significant association between H. Pylori infection and the progression of T2DM [17]. Thus, we conducted the present study in order to determine the association between H. Pylori infection and the glycemic status of T2DM, as well as the impact of H. Pylori eradication on the glycemic status of T2DM.

Materials & Methods

The manuscript was prepared in line with the recommendations of STROBE statement[18].

Study Design and Patients:

The present study was a case-control study carried out in the Department of Internal Medicine at Aswan university Hospital and included 200 patients. The patients were divided into two groups.

The group I included 100 cases divided into two equal sub-groups (A and B) controlled and uncontrolled T2DM patients, respectively; and group II included 100 nondiabetic patients.

Inclusion and exclusion criteria:

Patients > 35 years of age were included if they matched the criteria of T2DM diagnosis, had disease duration for more than five years, had poor glycemic control defined as HbA1C ≥7, had a history of dyspepsia, bloating or epigastric discomfort for more than one month.

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Data Collection and Methodology:

The following data were collected from eligible patients: demographic characteristics, T2DM- related history, Complete blood count (CBC) findings, renal and hepatic function tests, H Pylori antigen in stool, fasting (FBG) and post-prandial blood glucose (PPBG), and HbA1c level. The HbA1c was measured by affinity chromatographic methods. While the stool H. Pylori antigen test was assessed by enzyme immunoassay (EIA) test, using a commercially available polyclonal antibody (HPSA).

Patients with positive H. pylori infection were subjected to 20 mg esomeprazole, amoxicillin 1 gram, and clarithromycin 500 mg for 14 days (all twice daily). Then, all patients were followed for three months in order to assess the change in HbA1c level.

Statistical analysis:

We used the Statistical Package for Social Sciences (SPSS, version 24, for PC; IBM, Armonk, NY) for data analysis. Data were expressed as either frequencies (%) or means ± standard deviations.

The, the comparisons between the two study groups were conducted using the Chi-Square test or the independent sample t test. A p value of less than 0.05 was considered significant.

Results

Baseline Characteristics:

A similar age was present between both group IA and IB, the mean age in group IA was 45±8 years and group IB was 45±9 years. Group II had a mean age of 51±10 years old. A statistically significant difference was present between group IA and control (p=0.004). There was no statistically significant difference was present regarding gender distribution between the study groups. Regarding the anthropometric measures, a statistically significant difference was present

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between both cases and control regarding the body mass index (BMI) (p=0.001) for the difference between both IA, IB and group II (Table 1).

Oral hypoglycemic medication use was 78%, Insulin 12%, and both 10.0% among group IA, compared to group IB, oral hypoglycemic use frequency was 90%, Insulin 2% and both 8%. There was no statistically significant difference between group IA and group IB regarding anti-diabetics, but the difference was significant regarding other medications (p=0.029). Anti-hypertensives were the most common among all groups (Figure 1).

Hypertension was the most frequent co-morbidity among group IA, IB, and II (38.0%, 32.0%

and 25.0%, respectively). The second most common was obesity for group IA (28.0%), dyslipidemia for group IB and II (10.0%, 16.0%, respectively). The difference between groups was statistically significant (p<0.001). Regarding complications, most of patients in group IA (98.0%) had no complications and only one patient (2.0%) had diabetic nephropathy, while (84.0%) of group IB had complications and 7 patient (14.0%) had diabetic nephropathy and only one patient (2.0%) had diabetic nephropathy, peripheral neuropathy & amputation. There was statistically significant difference between groups (p<0.001). No statistically significant difference was present regarding the history of diabetes in years p=0.077. The mean for group IA was 8 ± 3 and 9 ± 5 for group IB (Table 2).

Hypertension was the most frequent co-morbidity among group IA, IB, and II (38.0%, 32.0%

and 25.0%, respectively). The second most common was obesity for group IA (28.0%), dyslipidemia for group IB and II (10.0%, 16.0%, respectively). The difference between groups was statistically significant (p<0.001). Regarding complications, most of patients in group IA (98.0%) had no complications and only one patient (2.0%) had diabetic nephropathy, while (84.0%) of group IB had complications and 7 patient (14.0%) had diabetic nephropathy and only one patient (2.0%) had

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diabetic nephropathy, peripheral neuropathy & amputation. There was statistically significant difference between groups (p<0.001). No statistically significant difference was present regarding the history of diabetes in years p=0.077. The mean for group IA was 8 ± 3 and 9 ± 5 for group IB (Table 3).

Helicobacter pylori prevalence:

We observed that H. Pylori frequency detected by stool antigen among diabetic patients was 77.0% compared to 55.0% among non-diabetic patients with a statistically significant difference (p=0.001; Figure 2). Higher frequency of H. pylori antigen was present among uncontrolled diabetic (82.0%) compared to 72.0% among controlled diabetics without a statistically significant difference (p=0.235; Figure 3).

Effect of H pylori eradication on diabetes control:

HbA1c had a mean of 9.84± 1.6 before treatment and a mean of 7.39±1.02 after treatment. A statistically significant difference has occurred in HbA1c among cases with uncontrolled diabetes after eradication of helicobacter pylori. (p=0.001; Table 4).

Discussion

The potential role of H. Pylori infection on the development and progression of T2DM has gained momentum over the recent years, which was supported by the observations of previous epidemiological studies [15]. Previous reports showed that T2DM with concomitant H. Pylori infection exhibit significant upregulation in the inflammatory cytokines and other inflammatory markers, leading to progressive insulin resistance and uncontrolled glycemic status, even with medication adherence [16]. Nonetheless, the current body of evidence is equivocal, with other reports noted no significant association between H. Pylori infection and the progression of T2DM [17]. Thus,

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we conducted the present study in order to determine the association between H. Pylori infection and the glycemic status of T2DM, as well as the impact of H. Pylori eradication on the glycemic status of T2DM. The current study was done in the department of internal Medicine at Aswan university hospital and included 200 patients divided into two groups. The group I included 100 cases divided into two equal sub-groups (A and B) controlled and uncontrolled T2DM patients, respectively; and group II included 100 nondiabetic patients. All participants were complaining of dyspepsia more than one month.

Our results showed that the H. Pylori infection frequency detected by stool antigen among diabetic patients was 77%, compared to 55% among non-diabetic patients with a statistically significant difference. The higher prevalence of H Pylori in diabetic patient and its higher level in uncontrolled diabetic in this study make diabetes as a suspected risk factor for H. pylori.

Theoretically, it is believed that diabetics are more susceptible to colonize H. pylori due to elevated blood glucose level and, subsequently, gastric mucosal change and increased glucose concentration in it. Another reason for the higher H. pylori infection is the higher rate of hospital admission in these patients [19]. These reasons raise the hypothesize that people with diabetes are more prone to H.

pylori infection, with associated increase in the risk of macovascular complications [20]. Besides, the fact that H. pylori infection usually occurs before the onset of diabetes raises the possibility that the H. Pylori is implicated in the development of T2DM [21]; nonetheless, the pathogenesis behind such association is not clear yet, with reported hypothesizes linking the H. Pylori-mediated inflammatory process in the development of T2DM [22].

In line with our findings, a previous report noted that 77% of diabetic patients had H. pylori infection, compared to only 60% of the normal control [23]. Likewise, Vafaeimanesh et al. [24],

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showed that H. Pylori infection was markedly more prevalent among individuals with diabetes (65.9% versus 50.5% in normal control). Our results are in consistent with the recent studies [16, 25, 26], and was confirmed in a study by Candelli et al. [27], which has the advantage of being a long- term follow-up study. Other reports from Pakistan [28], Qatar , and Italy [29] revealed significantly high risk H. pylori infection among T2DM subjects than in control. On the contrary, the results of Alzahrani et al. [17] study revealed that the prevalence of H. pylori infection was slightly higher in diabetics than in nondiabetics, with no significant difference. The same results were noted in other studies [30]. Thus, the current body of evidence is equivocal, which may be related to the method of detection of H. Pylori, different diabetes characteristics, or other demographic characteristics [31].

Concerning the impact of H. Pylori eradication on the glycemic control, we reported a statistically significant improvement in HbA1c among cases with uncontrolled diabetes after eradication of H. Pylori. This finding empower that H. pylori can be considered as risk factor for diabetes. There was significant improvement in the fasting, postprandial plasma glucose and HbA1c levels after three months following eradication of H. pylori in the T2DM patients.as mentioned by Dey L et al. [23], whereas in the patients with T2DM without H. pylori infection the change in the glycemic parameters from the baseline till the end of the study were negligible. Cheng et al. [25]

illustrated that the HbA1c level decreased following H. pylori eradication. Such results highlight the add-on beneficial role of treating H. Pylori on glycemic control. Similar findings were reported by Zojaji et al. [32], and Kato et al [33]. However, the current body of evidence is equivocal, with other reports show no changes in the HbA1c after eradication [34].

The current study has some limitations. First, we enrolled a small number of patients, which limits the external validity of our findings. Second, the follow-up period was short and should be

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extended in future studies. Third, the observational nature of the study is inherently subjected to some forms of bias as selection bias and potential confounders. In addition, we did the stool antigen test (H.

pylori), but the 13C-urea breath test and/or endoscopy were not done because of the limited access to these tests. Further randomized controlled trials are needed to adjust their findings to the confounding factors, mentioned above.

In conclusion, our results highlighted the high prevalence of H. Pylori infection among T2DM patients, with uncontrolled glycemic status. Such results indicate that H. Pylori may be considered as a risk factors for uncontrolled glycemic status. We found that the eradication of H. Pylori infection led to significant improvements in the glycemic control among uncontrolled patients. These results add to the evidence on the potential of H. Pylori treatment in diabetes control and should be confirmed in larger, longer follow-up studies.

Conclusion

Prevalence of H. Pylori infection detected by stool antigen was (77.0%) among diabetic patients compared to (55.0%) among non-diabetic patients with a statistically significant difference, Higher frequency of H. pylori antigen was present among uncontrolled diabetic (82.0%) compared to

(72.0%) among controlled diabetics without a statistically significant difference, After eradication of helicobacter pylori, a statistically significant difference has occurred in hemoglobin A1c among cases with uncontrolled diabetes, Diabetes mellitus can be considered as risk factor for H. pylori infection

Abbreviations: H. Pylori: Helicobacter Pylori, T2DM: Type 2 Diabetes Mellitus, Acknowledgement: None to declare

References

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Table 1: Demographic Characteristics of the Included Patients

Variables Group IA (n=50) Group IB (n=50) Group II (n=100)

P

Age Mean ±SD 45 ± 8 45 ± 9 51 ± 10

0.006*

Range 35 - 65 33 - 65 35 - 65

BMI Mean ±SD 25 ± 3 25 ± 3 21 ± 2 <0.001

Range 18 - 31 19 - 36 17 - 27

Gender Male 25 50.0% 24 48.0% 42 42.0% 0.59

Female 25 50.0% 26 52.0% 58 58.0%

Table 2: DM-related History

Variables Group IA

(n=50)

Group IB (n=50)

Group II (n=100)

p

Co- morbidities

Dyslipidemia 1 2.0% 5 10.0% 16 16.0%

<0.001*

Obesity 14 28.0% 4 8.0% 0 0.0%

Hypertension 19 38.0% 16 32.0% 25 25.0%

Hypothyroidism 1 2.0% 0 0.0% 0 0.0%

Chronic kidney diseases 4 8.0% 0 0.0% 0 0.0%

Ischemic heart diseases 2 4.0% 0 0.0% 0 0.0%

Gastritis 0 0.0% 0 0.0% 15 15.0%

No 9 18.0% 25 50.0% 44 44.0%

Complications None 49 98.0% 42 84.0% 100 100.0%

<0.001*

Diabetic Nephropathy

1 2.0% 7 14.0% 0 0.0%

Diabetic Nephropathy, peripheral neuropathy &

amputation 0 0.0% 1 2.0% 0 0.0%

DM Duration Mean ±SD 8 ± 3 9 ± 0.077

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Range 3 - 16 2 -

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Table 3: Baseline Glycemic Parameters

Variables Group IA (n=50) Group IB (n=50) Group II (n=100) P-value Fasting glucose Mean ±SD 97.1 ± 11.8 131.5 ± 22.4 80.7 ± 6.4 <0.001

Range 78 - 118 92 - 184 71 - 100

2HPP Mean ±SD 177.5 ± 22.9 292.9 ± 60.2 129.6 ± 10.3 <0.001

Range 140 - 230 170 - 419 110 - 148

HbA1c Mean ±SD 6.4 ± 0.6 9.7 ± 1.1 5 ± 0.2 <0.001

Range 5.5 - 7.5 7.8 - 12.1 4 - 5.5

Table 4: HbHA1c before and after H. pylori eradication for the uncontrolled diabetic patients with positive H pylori

(n=41) Before After P

HA1c

<0.001*

Mean± S.D 9.84 ± 1.06 7.39 ± 1.02 Range 7.80 - 12.1

0

5.70 - 9.50

Figure’s Legends

0 20 40 60 80 100

Group IA Group IB

78

90

12

10 2 8

%

Anti-diabetic drugs

Oral hypoglycemic Insulin Both

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Figure 1 shows the Anti-diabetic drugs between study groups.

Figure 2 shows the H. pylori Antigen between the study groups.

Figure 3 shows the H. pylori Antigen between the study groups.

77.0%

55.0%

23.0%

45.0%

0.0%

10.0%

20.0%

30.0%

40.0%

50.0%

60.0%

70.0%

80.0%

90.0%

Group I Group II

H. pylori Antigen

Positive Negative

72.0%

82.0%

28.0%

18.0%

0.0%

10.0%

20.0%

30.0%

40.0%

50.0%

60.0%

70.0%

80.0%

90.0%

Group IA Group IB

H. pylori Antigen

Positive Negative