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Diagnostic Methods for Helicobacter Pylori Infection: Ideals, Options, and Limitations

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Diagnostic Methods for Helicobacter Pylori Infection: Ideals, Options, and Limitations European Journal of Clinical Microbiology & Infectious Diseases (2019) 38:55–66 https://doi.org/10.1007/s10096-018-3414-4 REVIEW Diagnostic methods for Helicobacter pylori infection: ideals, options, and limitations Parisa Sabbagh1 & Mousa Mohammadnia-Afrouzi1,2 & Mostafa Javanian1 & Arefeh Babazadeh1 & Veerendra Koppolu3 & VeneelaKrishna Rekha Vasigala4 & Hamid Reza Nouri2 & Soheil Ebrahimpour1 Received: 10 October 2018 /Accepted: 26 October 2018 /Published online: 9 November 2018 # Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract Helicobacter pylori (H. pylori) resides in the stomach, colonizes gastric epithelium, and causes several digestive system diseases. Several diagnostic methods utilizing invasive or non-invasive techniques with varying levels of sensitivity and specificity are developed to detect H. pylori infection. Selection of one or more diagnostic tests will depend on the clinical conditions, the experience of the clinician, cost, sensitivity, and specificity. Invasive methods require endoscopy with biopsies of gastric tissues for the histology, culture, and rapid urease test. Among non-invasive tests, urea breath test and fecal antigen tests are a quick diagnostic procedure with comparable accuracy to biopsy-based techniques and are methods of choice in the test and treatment setting. Other techniques such as serological methods to detect immunoglobulin G antibodies to H. pylori can show high accuracy as other non-invasive and invasive biopsies, but do not differentiate between current or past H. pylori infections. Polymerase chain reaction (PCR) is an emerging option that can be categorized as invasive and non-invasive tests. PCR method is beneficial to detect H. pylori from gastric biopsies without the need for the cultures. There is no other chronic gastrointestinal infection such as H. pylori with a set of comparable diagnostic methodologies. Despite the availability of multiple diagnostic methods, it remains unclear on the choice of any one method as the gold standard for detecting H. pylori infection, especially in epidemiological studies. In this work, we review the principal diagnostic methods used to detect H. pylori infection and their advantages and disadvantages, and applications in clinical practice. Keywords Helicobacter pylori . Characteristics of infection . Diagnosis . Invasive tests . Non-invasive tests Introduction during a clinical research project, Barry Marshall and Robin Warren discovered [7]itasCampylobacter pyloridis, which Helicobacter pylori (H. pylori) is a gram-negative bacterium was later changed to H. pylori [8, 9]. that colonizes in gastric epithelium [1–5]. First, this bacterium H. pylori represent one of the most common bacterial in- was misrecognized as Pseudomonas spp. even though [6], fection in humans, which infected about half of the world’s population [10, 11]. Often, H. pylori infection occurs in child- hood and continue throughout life when proper treatment is * Soheil Ebrahimpour not provided [11]. In this regard, some studies suggested that [email protected] the infected mothers are the major source of this infection of their kids, through contact with the contaminated stomach 1 Infectious Diseases and Tropical Medicine Research Center, Health juice from the mother’smouth[12]. Research Institute, Babol University of Medical Sciences, Research indicates that H. pylori spread from East Africa Babol, Islamic Republic of Iran about 58,000 years ago and subsequently developed into 2 Cellular and Molecular Biology Research Center, Health Research many strains with varying degrees of pathogenicity [13]. Institute, Babol University of Medical Sciences, Babol, Islamic Republic of Iran Generally, the prevalence of the bacterium infection varies according to age, region, race, and socioeconomic statuses. 3 Scientist Biopharmaceutical Development Medimmune, Gaithersburg, MD 20878, USA The prevalence of H. pylori infection in the developing coun- tries is 50.8%, whereas the prevalence is 34.7% in the devel- 4 Rangaraya Medical College, NTR University of Health Sciences, Kakinada, India oped countries [14]. Many documents show that humans are 56 Eur J Clin Microbiol Infect Dis (2019) 38:55–66 the primary reservoir of H. pylori. The bacterium can also IL-6, IL-10, IL-12, IL-18, and IL-8 in inflamed mucosa of survive in dental plaques and saliva of a human [15]. The H. pylori–infected individuals [32]. bacterial transmission can be through oral-oral, feco-oral, The Th1/Th2 cell paradigm is an important concept to un- and gastro-oral routes [9, 16]. This bacterium has been found derstand mucosal adaptive immunity and inflammation in- in water, as it is proven that the infection is transmitted duced by H. pylori. Cytokine profiles indicate a Th1- through the water [17]. It is also reported that these bacteria predominant host immune response in the gastric mucosa, can survive in the stomach of animals such as sheep and cats illustrated by IFN-γ production, which is associated with IL- and milk of some others [18]. 12, IL-18, and TNF-α pro-inflammatory cytokines expression Effective treatment of the H. pylori infection is possible by DCs and macrophages [33]. Many studies support the in- through antimicrobial therapy, prescribed to the susceptible volvement of Th17 cells in H. pylori infection by production patients. In order to treat the disease appropriately, suitable of IL-17. IL-17 induces expression of IL-8, as a chemokine diagnostic procedures are necessary. Therefore, in this review, with the strong neutrophil chemoattractive property [34]. we aim to study the invasive and non-invasive diagnostic tests H. pylori can also elicit a strong specific systemic and mucosal for H. pylori infection. IgG and IgA antibody responses. However, the humoral im- mune response is not protective in this infection. Many reports show that H. pylori induces regulatory T cell (Treg) responses Pathogenicity of H. pylori to avoid both innate and adaptive immune defenses and main- tain prolonged colonization of the gastric mucosa (Fig. 1). H. pylori is a gram-negative, helical bacillus, flagellated, slow-growing, microaerophilic, and fastidious bacterium [9, Diseases and clinical manifestation 19–21]. The bacterium isolated from the gastric mucosa is often seen as a spiral and curved in the culture medium [22]. H. pylori is the cause of some gastric disorders (peptic ulcer H. pylori can survive in the gastric tissue, due to the pres- disease (PUD), gastric adenocarcinoma, and gastric mucosa- ence of urease, its mobility, and ability to connect to the gastric associated lymphoid tissue (MALT) lymphoma [7, 35, 36]), epithelium [23, 24]. Some of the factors that provide an ad- which are the results of an interaction between bacterial viru- vantage for the successful bacterial colonization in the gastric lence factors, host, and environmental factors. Several extra- epithelium include the shape of this bacterium, polar-sheathed gastric manifestations have been reported to be linked to flagella, mobility, chemotaxis, adherence, and persistence. H. pylori infection such as neurological, dermatological, he- Pathogenic factors such as cytotoxin-associated gene A matologic, ocular, cardiovascular, metabolic, and allergic dis- (CagA), vacuolating cytotoxin A (VacA), outer inflammatory eases [19]. Most of H. pylori infections usually are without protein A (OipA), duodenal ulcer promoting gene a (dupA), clinical manifestation [37]. However, signs and symptoms sialic acid–binding adhesin (SabA), and blood group antigen– associated with the disease are primarily due to gastric or binding adhesin (BabA) are associated with increased viru- peptic ulcer illness or duodenal inflammation. Furthermore, lence of Hpylori[25–28]. This bacterium, with the help of other symptoms such as abdominal pain, nausea, and the urease enzyme, breaks down urea to carbon dioxide and vomiting may be attributed to other gastrointestinal diseases ammonia [29], through which it can neutralize the gastric acid, [38]. penetrate, and colonize in the gastric epithelium [30]. Peptic ulcer disease Immunopathogenesis of H. pylori–induced Peptic ulcers are usually found in the stomach or proximal infection in gastric mucosa duodenum but can also be found in the esophagus or Meckel’s diverticulum. Peptic ulcer refers to the acid peptic The immune response towards pathogenic agents can be di- injury of the digestive tract, resulting in mucosal break vided into innate and adaptive responses. H. pylori is an acti- reaching the submucosa [39]. The lifetime prevalence of this vator of both the innate and adaptive immune responses. The disease in the general population has been estimated to be colonization of H. pylori in gastric mucosa triggers innate host about 5–10% and incidence 0.1–0.3% per year. Over the past defense mechanisms, including NOD1, TLR2, TLR4, TLR5, two centuries, PUD has been a major threat to the world’s and TLR9, thus stimulating the expression of pro- population [39]. Some studies showed that PUD is at least inflammatory and antimicrobial peptides including defensins fourfold higher in H. pylori–infected individuals than in and cathelicidins by gastric epithelial cells as well as dendritic non-infected individuals [40]. H. pylori alongwithnon- cells (DCs), neutrophils, and macrophages [31]. DCs and steroidal anti-inflammatory drugs (NSAIDs) such as aspirin macrophages are activated and produce cytokines, including is the main cause of gastric and duodenal ulcers (imbalance of Eur J Clin Microbiol Infect
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