Helicobacter pylori infection among patients with type II diabetes mellitus

Abstract

T2DM formerly known as non-insulin-dependent diabetes mellitus or adult-onset diabetes is a metabolic disorder that is characterized by high levels of blood glucose resulting from insulin resistance and relative insulin deficiency. It is an emerging pandemic and is rapidly becoming a serious threat to public health.1 H. pylori is a gram-negative, spiral shaped pathogenic bacterium that specifically colonizes on the gastric epithelium, it is one of the most common human bacterial pathogens and infection causes a wide array of gastric disorders, including simple gastritis, peptic ulcers and gastric malignancies. Gastrointestinal inflammation caused by H. pylori can influence the absorption of glucose and lipids, which are also abnormal in DM patients.2,3 It is a common infection in diabetic patients who have inadequate metabolic control, individuals are colonized by H. pylori infection in the gastric antrum, probably because of chemotactic factors such as tumor necrotic factor (TNF), interleukins-IL-1, IL-2, and IL-8, which are present in gastric epithelium.4,5 Beside DM the H. pylori is also a well be established cause of dyspepsia, the incidence of H. pylori is increased in DM may be due to delay gastric emptying and antraldy smotility, which are important causes of dyspepsia in diabetes, the role of H. pylori infection in diabetic dyspepsia is mainly related to blood glucose concentration, reduce of acid secretion and secrete higher of pro-inflammatory cytokines.5,6 Recent evidence has shown that qat chewing does indeed delay gastric emptying of a semisolid meal, probably as a result of the sympathomimetic action of cathinone in qat. Inflammation and activated innate immunity have been implicated in pathogenesis of diabetes through insulin resistance, for example, elevated levels of inflammatory cytokines may lead to phosphorylation of serine residues on the insulin receptor substrate, which prevents its interaction with insulin receptors, inhibiting insulin action or altered glucose metabolism may produce chemical changes in the gastric mucosa that promote H. pylori colonization So, individuals with diabetes are more frequently exposed to pathogens than their healthy counterparts.7–10 This study was conducted to reveal the prevalence of H. pylori among T2DM and non-DM patients with the association between Qat chewing and potential risk factors.