Peptic Ulcer Disease (PUD) is a consequence of the imbalance of acid secretion and mucosal defences which resist acid digestion thereby indicating a serious medical problem. Ulcers can manifest in the stomach or duodenum, in the oesophagus or the jejunum and can develop at the margin of a gastroenterostomy or in Zollinger-Ellison syndrome. While the mortality rates are low, peptic ulcer disease is highly prevalent, causing painful suffering and is expensive to treat [1] . Much research has pointed out that H. pylori and the deficiency of vitamin B12 are connected and they demonstrate a strong causative correlation. Even in case of those without gastritis or other gastrointestinal issues, scientists have found the H. pylori bacteria in over 50% of patients suffering from pernicious anaemia, primarily because of untreated deficiency of vitamin B12 [2] . While the drug such as lansoprazole and omeprazole is useful for PUD, its use does not come without the increased risk of having other complications. Among these are clinically relevant drug-drug interactions; an increased aspiration pneumonia risk among certain patients; and complications related to Vitamin B12 deficiency (e.g. hyperhomocysteinemia, macrocytic anaemia, and/or neuropathies) [3] .

One hundred subjects, 65 (65%) were males, while 35 (35%) were females. Table 1 shows the overall mean age ± SD of individuals, and the mean age ± SD of male and female individuals.

Table 2 shows 31 (36.0%) H. pylori infected patients had normal vitamin B12 level and 55 (64%) was Vitamin B12 deficiency in 86 (86%) H. pylori infected patients with a significant difference (P value < 0.05).

Helicobacter pylori have been determined as an etiologic factor in vitamin B 12 deficiency [4] . In populations with a high prevalence of H. pylori infection, the

P value < 0.05.

frequency of vitamin B12 deficiency and its clinical consequences can be expected to be high. In this study, the high frequency (64%) of vitamin B12 deficiency was found in patients with Helicobacter pylori infection leads to immediate development of persistent gastritis, colonization of the stomach by H. pylori is almost always accompanied by clinical and histological signs of chronic gastritis associated with both local and systemic immune response. The resolution of gastritis, mucosal immune response to H. pylori and normal appearance of gastric epithelium is demonstrated following eradication of the infection with antibiotic therapy [4] . A study by Carmel et al., who investigated the association between H. pylori infection and megaloblastic anemia, by examining patients with food-cobalamin malabsorption and the investigators found that patients with low levels of serum cobalamin had a higher seroprevalence of H. pylori infection [5] . Infection with H. pylori causes a series of changes in gastric function prior to the final stage of gastric atrophy. The initial infection causes transient hypochlorhydria and usually few or no clinical symptoms [6] . In some persons, the infection causes gastric inflammation with elevated serum gastrin and pepsinogen and reduced somatostatin concentrations [7] . The elevated gastrin and reduced somatostatin then cause elevated acid secretion from gastric parietal cells [6] , but over time (usually many years) some but not all infected persons develop peptic ulcer disease, gastric cancer, and eventually atrophic gastritis with low gastric acid secretion, and possibly inadequate production of intrinsic factor.

Helicobacter pylori have been determined as an etiologic factor in vitamin B12 deficiency. Therefore, vitamin B12 deficiency is more pronounced in Helicobacter pylori infected patient.

Kadhim, G., Shikh, M., Omar, H. and Ismail, A. (2018) Vitamin B12 Deficiency in Helicobacter pylori Infected Patients. Open Access Library Journal, 5: e4172. https://doi.org/10.4236/oalib.1104172