Helicobacter pylori infection and eye diseases: a systematic review

Abstract

The connection between Helicobacter pylori (Hp) infection and eye diseases has been increasingly reported in the literature and in active research. The implication of this bacterium in chronic eye diseases, such as blepharitis, glaucoma, central serous chorioretinopathy and others, has been hypothesized. Although the mechanisms by which this association occurs are currently unknown, this review describes shared pathogenetic mechanisms in an attempt to identify a lowest common denominator between eye diseases and Hp infection. The aim of this review is to assess whether different studies could be compared and to establish whether or not Hp infection and Eye diseases share common pathogenetic aspects. In particular, it has been focused on oxidative damage as a possible link between these pathologies. Text word search in Medline from 1998 to July 2014. 152 studies were included in our review. Were taken into considerations only studies that related eye diseases more frequent and/or known. Likely oxidative stress plays a key role. All of the diseases studied seem to follow a common pattern that implicates a cellular response correlated with a sublethal dose of oxidative stress. These alterations seem to be shared by both Hp infections and ocular diseases and include the following: decline in mitochondrial function, increases in the rate of reactive oxygen species production, accumulation of mitochondrial DNA mutations, increases in the levels of oxidative damage to DNA, proteins and lipids, and decreases in the capacity to degrade oxidatively damaged proteins and other macromolecules. This cascade of events appears to repeat itself in different diseases, regardless of the identity of the affected tissue. The trabecular meshwork, conjunctiva, and retina can each show how oxidative stress may acts as a common disease effector as the Helicobacter infection spreads, supported by the increased oxidative damage and other inflammation.

FIGURE 1

Anterior blepharitis of a mixed type of the upper eyelid. This shows a squamous blepharitis-hyperemic. Very evident the presence of collarettes, meibomian secretion around eyelashes (blue arrows) and telangiectasia and very hyperemic vessels of the lid margin (red arrows). Although it is unknown the role of Hp infection in this type of pathology, its eradication leads to an improvement in both subjective and objective symptoms and can, especially in the young, alleviate blepharitis.

FIGURE 2

Glaucoma in oxidative stress plays a key role in mitochondrial dysfunction occurs and consequently the endothelial cells of the trabecular meshwork are not working as they should. There is an alteration of the extracellular matrix is accompanied by the activation of several metabolic pathways that result in an alteration of gene expression, an activation of inflammation and the immune response. This determines the malfunction of the trabecular meshwork and consequently the intraocular pressure increase. All this triggers the apoptosis of retinal ganglion cells.

FIGURE 3

Sequence of the pathogenesis of Hp infection that increases the production of ROS and inflammatory cytokines, sees the recruitment of white blood cells in the presence of a decrease of antioxidant defenses leads to the alteration of gastric mucosa cells and thus of the gastric mucosal barrier.

FIGURE 4

(A) Fluoroangiography of right eye; it shows a central serous chorioretinopathy which highlights the leakage (white) in the retinal pigment epithelium with pooling of the dye in the subretinal space. (B) Indocyanine green angiography shows an area with a late iperfluorescent likeage that suggests as an etiologic factor the choroidal hyperpermeability. (C) The optical coherence tomography (OCT) allows us a qualitative and quantitative assessment of the disease. (D) OCT cross-sectional image of a fovea with central serous chorioretinopathy: The detachment of the neurosensory retina is revealed as optically empty space within the retina. The retinal pigment epithelium remains attached to the choroid and it is evident by OCT as a thin layer (arrow). The retinal layers are intact but detached in the photoreceptors are thicker and a higher reflectivity.

FIGURE 5

Extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma): the lymphoma cells infiltrate around reactive B-cell follicles, external to a preserved follicle mantle, in a marginal zone distribution. Marginal zone B cells have characteristics of small and medium size. The majority of patients present with stage I or II disease. The MALT lymphoma and its natural course is indolent and is slow to disseminate; recurrence may involve other extranodal sites.