Correlation of Vitamin B12 deficiency with H. pylori infection and other Biochemical parameters in Iraqi patients

 

Namir I. A. Haddad*, Nadia A. Abdulrahman

Department of Chemistry, College of Science, University of Baghdad, Jaddiriya, Baghdad, Iraq.

*Corresponding Author E-mail: namir.haddad@gmail.com

 

ABSTRACT:

Helicobacter pylori are implicated in the pathogenesis of several human gastric diseases and lead to significant morbidity and mortality worldwide. This study aimed to estimate serum levels of vitamin B12 in Iraqi individuals infected with H. pylori and comparing them with healthy individuals. This case–control study was performed between January and June 2019 on eighty-four participants (41 female and 43 male) distributed evenly into patients and control groups. Serum vitamin B12 was measured and complete blood count was performed. The results revealed that patients group had decreased levels of hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration, red blood cell, white blood cells and platelet compared to healthy individuals. Moreover vitamin B12 level of patients (females and males) was significantly lower than that of control group (396.2±101.3 vs. 706±269pg/ml) for females and (253±100 vs. 629±151 pg/ml) for males. Vitamin B12 might be used as a valuable indicator for anemic patients having gastritis since it is strongly correlated to Hb, HCT, MCV, MCH, MCHC and PLT level in infected patients.

 

KEYWORDS: Vitamin B12, H. pylori, ulcer, hematological parameters.

 

 


INTRODUCTION:

The bacterium that grows in close association with the lining of the stomach is called Helicobacter pylori. It is associated with several human gastric diseases and lead to significant morbidity and mortality worldwide1. These bacteria are involved in the pathogenesis of gastric cancers such as gastric adenocarcinoma and mucosa associated lymphoid tissue lymphoma as well as superficial gastritis and peptic ulcer disease2.

 

Nearly, fifty percent of the world’s populations are infected with H. pylori and this infection remains asymptomatic in majority of infected population3. Stomach infections with Helicobacter pylori mostly occur in childhood. If repeated, it might result in chronic gastritis predominantly leading to peptic ulcer disease, later on in life. Ulcer is a sore or hole in the lining of the stomach or duodenum (the first part of the small intestine)4.

 

These bacteria enfeeble the preservative mucous that covering the stomach and duodenum, which permits the passing of acid to the sensitive lining below it. Each of the bacteria and the acid irritate the lining and cause a sore, or ulcer. H. pylori secrete enzymes that neutralize the acid in stomach, so they are able to survive in stomach. The Bacterial acid tolerance and motility play critical role in gastric colonization5.

 

Infection with these bacteria will cause significant increases in the inflammation factors production such as C-reactive proteins (CRP) and interleukins (IL) in the gastric epithelial cells.  As well as, it has a central role in the elevation of oxidative stress and causing stomach inflammation, peptic ulcers, and gastric malignancy in the infected individuals6.

 

Since inflammation is a defensive multistep process for the immune system, the frequent exposure to the infection of H. pylori will result in inflammation process failure and inability to combat progress of infectious agents. This will cause numerous diseases such as heart disease and cancer, and as result, this continuous over stress causes weakening of the body7,8.

In spite of the association of H. pylori to peptic ulcers and malignancies, which cause bleeding that result in iron deficiency anemia (IDA), the majority of individuals infected with H. pylori do not have ulcers or malignancies. Infected individuals usually have chronic gastritis that is not associated with gastro-intestinal bleeding. H. pylori9. The infection of H. pylori is strongly related with chronic gastritis of the antrum of the stomach, which causes impairment in gastric acid and pepsin secretion, and is thus linked to malabsorption of food-vitamin B12. Hence, the decreasing in vitamin B12 intake and its lack may be due to this infection10.

 

This study aimed to estimate serum Vitamin B12 concentrations in Iraqi subjects infected with Helicobacter pylori and comparing them with healthy individuals.

 

MATERIAL AND METHODS:

This case–control study was performed on eighty-four participants (43 male and 41 female) between January and June 2019. The excluded patients were who had renal failure, liver failure, pregnant and any underlying medical condition, which may cause vitamin B12 deficiency.

 

H. pylori infection was diagnosed by endoscopy examination as well as by rapid test. About 4 milliliter of blood was withdrawn from every individual and distributed equally into two portions; 2 milliliter in a tube having K3-EDTA to carry out the complete blood count (CBC) using Mindray hematology analyzer. The second portion (2 mL) was dispensed in a gel tube and centrifuged for 15 minute. The obtained serum was used to determine vitamin B12 concentrations using Monobind (USA) ELISA kit.

 

Data analysis:

The obtained results were analyzed statistically by using SPSS soft-ware (version 22). The means were compared using Independent sample test, and the correlations between the vitamin B12 and other variables were detected using the Pearson’s correlation analysis, with a P value of <0.05 indicating the statistically significant difference for both tests.


 

Table 1. Clinical and biochemical characteristics of the study.

parameter

FP

FC

P

MP

MC

P

Age (year)

30.75±7.38

32.48±12.21

0.614

31.08±9.2

25.29±6.4

0.03

Vitamin B12 (pg/ml)

396.2±101.3

706±269

<0.001

253±100

629±151

<0.001

Hb (g/dl)

11.6±1.93

12.9±1.96

0.558

14.9±1.22

15.6±1.27

0.464

HCT (%)

38.15±4.96

40.31±3.18

0.899

46.8±3.02

48.38±3.68

0.648

MCV (fL)

83.45±9.5

87.34±6.8

0.135

88.44±5

91.90±10.2

0.514

MCH ( pg)

25.47±3.9

27.16±2.1

0.084

26.05±2.2

28.28±4.4

0.376

MCHC (g/dl)

30.47±1.62

31.18±0.9

0.081

30.81±1.1

31.45±0.6

0.245

RBC (1012/L)

4.33±0.56

4.40±0.37

0.357

5.13±0.3

5.21±0.6

0.601

WBC (109/ L)

6.46±1.04

6.85±2.17

0.505

7.16±1.3

7.30±1.5

0.757

PLT (109/ L)

225±65

238±54

0.393

220±59

230±45

0.527

Results were expressed as mean ± SD, Independent sample test was used for the purpose of comparison between the groups and P < 0.05 was considered statistically significant. Abbreviations: FP: Female patients, FC: Female control, MP: Male patients, MC: Male control, Hb: Hemoglobin, HCT: Hematocrit, MCV: Mean Corpuscular Volume, MCH: Mean Corpuscular Hemoglobin, MCHC: Mean Corpuscular Hemoglobin Concentration, RBC: red blood cell, WBC: White Blood Cells, PLT: platelet.

 


Table 2. The correlations of vitamin B12 with other parameters among female patients.

Parameter

Serum Vitamin B12

r

P

Age (year)

-0.222

0.412

Hb (g/dl)

0.662**

0.005

HCT (%)

0.639**

0.008

MCV (fL)

0.842**

<0.001

MCH( pg)

0.796**

<0.001

MCHC (g/dl)

0.576*

0.02

RBC (1012/ L)

0.051

0.850

WBC (109/ L)

0.370

0.158

PLT (109/ L)

0.698**

0.003

r, Pearson coefficient. *Statistically significant at P < 0.05. ** Highly significant at P < 0.01. Abbreviations: Hb: Hemoglobin, HCT: Hematocrit, MCV: Mean Corpuscular Volume, MCH: Mean Corpuscular Hemoglobin, MCHC: Mean Corpuscular Hemoglobin Concentration, RBC: red blood cell, WBC: White Blood Cells, PLT: platelet.

 

 

Table 3. The correlations of vitamin B12 with other parameters among male patients.

Parameter

Serum Vitamin B12

r

P

Age (year)

0.172

0.402

Hb (mg/dl)

0.494*

0.010

HCT (%)

0.395*

0.046

MCV (fL)

0.300*

0.036

MCH ( pg)

0.921**

<0.001

MCHC (g/dl)

0.980**

<0.001

RBC (1012/ L)

0.022

0.916

WBC (109/ L)

-0.164

0.422

PLT (109/ L)

0.435*

0.026

r, Pearson coefficient. *Statistically significant at P < 0.05. ** highly significant at P < 0.01. Abbreviations: Hb: Hemoglobin, HCT: Hematocrit, MCV: Mean Corpuscular Volume, MCH: Mean Corpuscular Hemoglobin, MCHC: Mean Corpuscular Hemoglobin Concentration, RBC: red blood cell, WBC: White Blood Cells, PLT: platelet.

 

RESULTS:

The present study included eighty-four participants divided equally into two groups, patients and control group. The patients group included 16 female and 26 male, while the control group included 17 female and 25 male. The means serum vitamin B12 of both gender in patients group were significantly lower than control group, as illustrated in Table 1. Moreover, there were slightly decreasing in hematological parameters of patients compared to control.

 

Based on the results in Table 2, serum vitamin B12 level in female patients showed a high significant positive correlation with Hb, HCT, MCV, MCH, MCHC and PLT levels. However, serum vitamin B12 level in male patients showed a positive correlation with Hb, HCT, MCV and PLT, and highly significant positive correlation with MCH and MCHC as it reveled in    Table 3.

 

DISCUSSION:

According to the obtained results from this study, we found a strong decreasing in vitamin B12 concentrations in individuals having H. pylori infection. Many researchers found that vitamin B12 levels were improved after healing from H. pylori infection11,12,13.

 

Ravi et al., revealed that the absorption of vitamin B12 is influenced by the influence of H. pylori on gastric mucosa. Therefore, persons with B12 deficiency must be underwent for diagnostic analysis of H. pylori infection and suitable treatment must be initiated14.

 

Helicobacter pylori have been characterized as an etiologic agent in the deficiency of vitamin B12. The frequency of vitamin B12 deficiency and its clinical consequences is predicted to be elevated in a population with a high incidence of H. pylori infection. These bacteria can cause B12 malabsorption by hypochlorhydria related to atrophic gastritis. Hypochlorhydria might cause a failure in the isolating of B12 from food binders and its consequent removal to salivary R-binder in the stomach15.

 

The present study illustrated that males have lower concentrations of vitamin B12 compared to females which agreed with that of Devrajani at al., who found that the deficiency of vitamin B12 was higher in males than in females16. However, Gümürdülü et al. found that the females have lower levels of vitamin B12 than males17.

 

The complete blood count is so essential in diagnosis of several diseases18. The hematological parameters; Hb, HCT, MCV, MCH, MCHC and PLT of males and females patients in this study showed a slight decreasing compared to healthy individuals. Kibru D et al., and Mwafy et al., had reported similar findings19,20. The pathogenic mechanism of reduced hematological parameters may be explained by blood losing that attributable to the chronic erosive of gastritis and reduced absorption of iron to chronic gastritis21.

 

Our results revealed that decreased vitamin B12 concentrations in both male and female patients correlated with hematological parameters; Hb, HCT, MCV, MCH, MCHC and PLT. This result partially agreed with that of Mwafy et al. who observed that vitamin B12 correlates with Hb, HCT, and RBC20. In 2000, Annibale et al. reported a reasonable mechanism that might explain IDA development in H. pylori-infected individuals. It may be a result of the gastritis pattern and associated with the effects on gastric physiology acting on the ordinary process of iron absorption; raises the pH of gastric causes reducing in iron solubility. H. pylori binding proteins lead to iron protein complex in the bacterium with decreasing in the secretion of vitamin C in gastric juices and reduces vitamin B12 and folate bioavailability22.

 

CONCLUSION:

Patients with H. pylori infection have reduced levels of vitamin B12 and hematological parameters. Vitamin B12 may possibly use as valuable indicator for anemic patients with gastritis since it is strongly correlated to Hb, HCT, MCV, MCH, MCHC and PLT level in infected patients.

 

CONFLICT OF INTEREST:

The authors declare no conflict of interest.

 

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Received on 05.01.2020           Modified on 08.03.2020

Accepted on 25.04.2020         © RJPT All right reserved

Research J. Pharm. and Tech. 2020; 13(11):5451-5454.

DOI: 10.5958/0974-360X.2020.00951.8