Helicobacter pylori and Hematologic Diseases

Abstract

Helicobacter pylori infection is the most common infection of the human species, with developing countries displaying a marked disadvantage in contrast to developing countries. While H. pylori infection is asymptomatic in most infected individuals, it is intimately related to malignant diseases of the stomach, such as gastric cancer and gastric MALT lymphoma, as well as benign diseases, for example chronic gastritis and duodenal and gastric peptic ulcers. Since the discovery that gastric mucosa could be colonized by bacteria, evidence of greater than 50 extragastric manifestations has been reported, linking H. pylori infection and the development of diseases associated with cardiology, dermatology, endocrinology, obstetrics and gynecology, hematology, pneumology, neurology, odontology, ophthalmology, otorhinolaryngology, and pediatrics. This chapter presents the extragastric manifestations of H. pylori infection expressed through hematologic diseases; particularly those included in the international consensus, and discusses guidelines for the management of H. pylori infection, such as iron deficiency, vitamin B 12 (cobalamin) deficiency, and immune thrombocytopenia. Other manifestations reviewed include immune neutropenia, antiphospholipid syndrome, and plasma cell dyscrasias, such us monoclonal gammopathy of undetermined significance, multiple myeloma, and Henoch-Schönlein purpura.

Anemia and its association with Helicobacter pylori infection among adult dyspeptic patients attending Wachemo University Nigist Eleni Mohammad Memorial Referral Hospital, Southwest Ethiopia: A cross-sectional study

“…H . pylori infection is associated with anemia by impairing iron absorption as a result of chronic gastritis which causes gastric hypochlorhydria, leading to impair reduction of the dietary iron from the ferric to ferrous form [ 13 , 14 ]. Because most dietary iron is in the ferric form, and an acidic intragastric pH and ascorbic acid are needed to reduce it to the ferrous form for absorption [ 15 ].…”

Anemia and its association with Helicobacter pylori infection among adult dyspeptic patients attending Wachemo University Nigist Eleni Mohammad memorial Referral Hospital, Southwest Ethiopia

“…Considering the morphological classification of anemia, normocytic-normochromic anemia (63.5%) was the predominant type of anemia among H.pylori infected study participants followed by microcytic hypochromic anemia (34.6%) in this study. This might be due to the reason that blood loss secondary to chronic erosive gastritis, decreased iron absorption secondary to chronic gastritis and hypochlorhydria, and also rises in hepcidin level after H. pylori infection which might contribute in anemia [11,14].…”

“…The possible mechanism that might explain the association between anemia and H. pylori infection may include; consumption of iron by the organism itself [41], gastrointestinal blood loss due to H. pylori-induced gastrointestinal lesions [14], and gastritis increased levels of neutrophil-derived lactoferrin, and since H. pylori has a lactoferrin-binding protein receptor, the infection may result in increased iron losses related to bacterial turnover. Since these bacteria have a high turnover rate, a large amount of iron may be lost in stools in the form of dead bacteria [11,42].…”

“…H. pylori infection is associated with anemia by impairing iron absorption as a result of chronic gastritis which causes gastric hypochlorhydria, leading to impair reduction of the dietary iron from the ferric to ferrous form [13,14]. Because most dietary iron is in the ferric form, and an acidic intragastric pH and ascorbic acid are needed to reduce it to the ferrous form for absorption [15].…”

“…pylori uptakes iron for their growth by competing with their host [4], and increased hepcidin production secondary to H. pylori infection decreases the release of iron from macrophages and entrecote [17]. Because hepcidin, act as an acute-phase reactant in response to the inflammation produced in the gastric mucosa, resulting in anemia of inflammation or chronic disease [14]. Other possible mechanism includes iron loss via hemorrhagic gastritis and active bleeding peptic ulcers [18].…”