Helicobacter pylori-Related Extraintestinal Manifestations—Myth or Reality

Abstract

It is well documented that Helicobacter pylori (H. pylori) can cause both gastrointestinal and extraintestinal manifestations. The latter one represents a major burden in terms of diagnosis and treatment. H. pylori-associated systemic subclinical inflammation is mostly responsible for the development of extraintestinal manifestations, and its early eradication might result in preventing all adverse events related to their occurrence. Thus, it was suggested that H. pylori might be associated with iron deficiency anemia, thrombocytopenia (immune thrombocytopenic purpura), Schonlein Henoch purpura, failure to thrive, vitamin B12 deficiency, diabetes mellitus, body mass index, cardiovascular diseases, as well as certain neurological conditions. Nevertheless, studies showed both pros and cons in terms of the role of H. pylori in the development of previously mentioned clinical entity underlining the crucial need for further studies on these topics. Although most of these extraintestinal manifestations occur during adulthood, we must not forget that H. pylori infection is acquired mainly during childhood, and thus its early diagnosis and eradication might represent the cornerstone in the prevention of H. pylori-induced inflammatory status and consequently of all related extraintestinal conditions.

An Overview of Clinical Manifestations of Dermatological Disorders in Intensive Care Units: What Should Intensivists Be Aware of?

“…It is an autoimmune disease in which the body’s immune system incorrectly recognizes skin proteins as foreign and thus produces antibodies to attack the foreign protein [ 15 , 16 ]. Trigger factors include medications [ 17 ] such as antibiotics, calcium channel blockers, ACE inhibitors, NSAIDs, salicylates, and interleukins, vaccines such as influenza [ 18 , 19 ], swine flu [ 20 ], tetanus toxoid [ 21 ], and COVID-19 vaccines [ 22 , 23 , 24 ], viral infections such as herpes simplex [ 25 ], hepatitis B and C [ 26 , 27 , 28 ], bacterial infections such as Helicobacter pylori [ 29 ], parasitic infections such as Toxoplasma gondii [ 30 , 31 ], and following organ transplantation [ 32 , 33 ]. Physical factors such as trauma, surgical interventions, thermal or electric burns, ultraviolet exposure, radiotherapy, and photodynamic therapy can also cause PV [ 34 ].…”

Helicobacter pylorivirulence factors: subversion of host immune system and development of various clinical outcomes

“…Although H. pylori numerous virulence factors are responsible for the induction of local damage in gastric mucosa, the host's innate and adaptive immunity including the pattern recognition receptors (PRRs), pro-inflammatory cytokines, chemokines, chemotactic factors, monocytes, macrophages, neutrophils, natural killer cells (NK cells), dendritic cells (DCs), B cells, and T cells facilitate the development of subclinical systemic inflammation (35)(36)(37). Therefore, the presence of H. pylori in the host gastric mucosa motivates the host's immune system to trigger systemic damage (38). Despite this strong inflammatory response, H. pylori's ability to evasion, subversion and manipulation of the host immune responses guarantees the development of persistent infection in the stomach mucosa.…”