The aim is to study the association of H. pylori infection with T2DM and its relation with glycated hemoglobin (HbA1c) levels

Dyspepsia is a worldwide problem that affects 40% of adults. Approximately 10% of all patients presenting for endoscopy for gastrointestinal symptoms have dyspepsia [1] Helicobacter pylori is a gram-negative spiral flagellate bacillus, which normally is a resident of gastric epithelium, It can cause inflammatory cell infiltration in gastric mucosa that produces cytokines, which are not only responsible for local effects but can damage remote tissues causing extradigestive diseases like ischemic heart disease, autoimmune thyroid disease, iron deficiency anemia, idiopathic thrombocytopenic purpura, and neurologic diseases [1].

In addition to this, it is also thought to play a direct or indirect role in the pathogenesis of metabolic syndrome, non-alcoholic fatty liver disease, and type 2 diabetes [2].

Diabetes mellitus (DM) is a major public health problem, with increasing prevalence globally. The major burden (90-95%) is caused by type 2 diabetes mellitus (T2DM), which typically develops in adulthood and is characterized by variable levels of insulin resistance, impaired insulin secretion, and increased glucose production [3].

The association between DM and H. pylori infection remains controversial, although many studies have been done, which concluded that a definiterelationship exists between the two. It is hypothesized that H. pylori infection promotes atherosclerosis by altering lipid metabolism, and this leads to the metabolic syndrome, insulin resistance, and finally, to type 2 diabetes [2].

There are several lines of evidence to implicate increased susceptibility to H. pylori infection in diabetic patients. First, a diabetes-induced impairment of cellular and humoral immunity may enhance an individual's sensitivity to H. pylori infection. Second, diabetes-induced reduction of gastrointestinal motility and acid secretion may promote pathogen colonization and infection rate in the gut. Third, altered glucose metabolism may produce chemical changes in the gastric mucosa that promote H. pylori colonization [4] pylori is a gram-negative, spiral-shaped pathogenic bacterium that specifically colonizes the gastric epithelium causing chronic gastritis, peptic ulcer disease, and/or gastric malignancy [5].

H. pylori is mainly acquired in childhood by the fecaloral, oral-oral, or gastro-oral route and has been recognized as a worldwide public health problem, which is more prevalent in developing countries [6].

H. pylori infection induces an acute polymorphonuclear 7 infiltration in the gastric mucosa, which is gradually replaced by an immunologically mediated, chronic, predominantly mononuclear cellular infiltration. The mononuclear infiltration is characterized by the local production and systemic diffusion of proinflammatory cytokines that can affect remote tissues and organic [7] As a result, an increased prevalence of extradigestive diseases has been reported in those with evidence of H. pylori infection in recent years, including ischemic heart disease, autoimmune thyroid diseases, sideropenic anemia, idiopathic

thrombocytopenic purpura, neurologic diseases, and hepatobiliary diseases[8]. T2DM is an emerging pandemic, responsible for an estimated 3.8 million adult deaths worldwide [9].

The pathogenesis of T2DM is complex, with risk factors associated with lifestyle (e.g. diet, obesity, and physical activity), genetic background, and socioeconomic factors [10].

In T2DM, the pancreas can no longer produce enough insulin to overcome the cellular loss of sensitivity, resulting in the accumulation of sugar in the bloodstream [11]. Identification of treatable causes of this disease will aid in the development of strategies to delay or prevent its onset or slow its progression. Recent evidence implicates the pathological involvement of inflammation in T2DM, which is an important process induced by H. pylori infection [12]. [13], who reported that the prevalence of H. pylori infection was higher in diabetics (24%) than in controls of similar age, sex, and socioeconomical status after 3 years of follow-up, and the reinfection rate was higher in diabetic patients. [14], who reported that there was no difference in H. pylori prevalence between patient with DM and non-DM controls. [15], who reported that H. pylori infection was positively associated with HbA1c levels through a large-scale cross-sectional analysis, which indicated a role of H. pylori in impaired glucose tolerance in adults.

Inclusion Criteria:

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Exclusion Criteria:

- 1) Patients with T1DM. (2) Patients with age less than 35 years. (3) Patients with history of NSAIDs or alcohol intake. (4) Patients already on steroid or immunosuppressive. (5) Patients on proton pump inhibitors. (6) Patients with history of H. pylori-eradication therapy in the previous 6 months.

(7) Patients with diagnosed malignancy in previous medical records. (8) Patients with history of hematemesis. (9) Patients with severe weight loss

cross-sectional study