In our study, we detected HP colonization in nasal polyps and the prevalence ranged from 25 to 30% depending on the diagnostic method, while higher detection rate was demonstrated using rapid urease test. The frequency rate of HP detection in nasal polyps was similar to many studies (Table 1) [8,9,10,11,12,13,14,15,16,17].

We performed an in-depth review of the literature in PubMed to identify articles about epidemiology of HP in nasal polyps, using the following search string: (“Helicobacter pylori”) AND (“nasal polyps” OR “nasal polyposis” OR “sinusitis”). The frequency rate of HP in nasal polyps is varied depending on method of detection. The prevalence of HP colonization ranges from 0 to 100%. The most studies demonstrated a frequency rate between 25 and 60%, while only one study documented no HP colonization in nasal polyps in patients without GERD symptoms, suggesting a gastro-nasal route of HP [9]. No association between HP colonization in nasal polyps and other factors, such as age, gender, presence of allergy, nasal side or co-existence tonsillar disease has been determined [16]. In addition, a study described that HP sinonasal colonization has no prognostic value for efficacy of functional endoscopic sinus surgery on chronic rhinosinusitis symptoms, but presence of HP was associated with greater improvement of the postoperative endoscopic scores [18]. Furthermore, prevalence seems to be higher using ELISA method for HP detection. In our study, rapid urease test and histochemical examination with Giemsa stain were performed and the most cases of HP colonization demonstrated by urease rapid test. It is worth mentioning, that there are many urease-producing bacteria both in the oral cavity, such as Streptococcus salivarius and Actinomyces naeslundii [19] and urease pathogens in lungs, such as mycobacteria [20], which may colonize the polypoid tissue, producing false positive urease results in urease test and causing higher HP detection rates using CLO test compared to histologic examination with Giemsa stain. However, Giemsa staining is not affected by urease containing organisms.

There are two transmission routes of HP: oral-oral transmission and fecal-oral transmission. The mechanism of transmission and colonization of HP in sinonasal cavity has not been clarified; however, three possible modes have been suggested. First, nasal cavity may be a reservoir of HP. Second, many studies have been described HP colonization in the oral cavity that may be a reservoir of HP [21], which has been detected in dental plaque, tonsillar and adenoid tissue [22, 23]. Therefore, HP may be transmitted to nasal cavity by oronasal reflux. Third, HP colonizes the stomach, which is a reservoir of HP and the bacteria are transmitted to the sinonasal cavity by gastroesophageal reflux [15]. A prospective study documented high rate of HP colonization (75%) in nasal polyp of patients with GERD and gastric HP infection, suggesting a strong association between HP infected nasal polyps and GERD [13]. In our study, all patients with HP in nasal polyps reported GERD symptoms and suffered from gastric HP infection, suggesting transmission of HP from stomach to nasal cavity.

However, it is worth mentioning that HP colonization of nasal polyps in patients with GERD may probably support a reservoir thesis similar to other extragastric sites, because many studies have suggested that gastroesophageal and laryngopharyngeal reflux are linked to nasal disorders and may contribute to chronic rhinosinusitis development via gastric acid exposure and triggering inflammation pathways [24]. A population-based study from Taiwan documented that patients with GERD-related symptoms carry a higher risk of chronic rhinosinusitis development compared with patients without GERD (HR: 2.36; 95% CI  2.08–2.68; P < 0.001) [25]. Moreover, a control study investigated the role of gastroesophageal and laryngopharyngeal reflux on sinusitis and development of nasal polyps, detecting the expression of pepsin in nasal cavity of patients with chronic sinusitis with or without nasal polyps and in patients without sinusitis. They found association between reflux and chronic sinusitis, while laryngopharyngeal reflux was associated with severity of nasal polyps [26].

On the other hand, the role of HP on chronic sinusitis and nasal polyposis development is still unclear. In the stomach, many pathogenic mechanisms have been proposed about HP-induced inflammation. HP may trigger the production of inflammatory cytokines, chymokines and growth factors via different virulence factors, such as, CagA and VacA, leading to recruitment of immune cells to the lamina propria in the stomach [27]. Thus, HP colonization of nasal may be associated with chronic inflammation, contributing to nasal polyposis development; however, the data is limited and several studies have suggested a disputed association between HP and development of nasal polyps. A prospective study demonstrated that HP colonization in nasal cavity was more prevalent in patients with chronic sinusitis compare to control subjects. Furthermore, in this study, the severity of chronic rhinosinusitis was evaluated according to Computer Tomography findings using Lund-MacKay scoring system, demonstrating no association between intranasal HP colonization and severity of rhinosinusitis and concluding no role of HP on pathogenesis of sinusitis and nasal polyposis [28]. Thus, it may be assumed that gastric juice carrying HP refluxes into nasal cavity and not HP itself contributes to rhinosinusitis and nasal polyposis [29]. A recent study investigated the role of gastric HP infection on nasal mucociliary clearance. It demonstrated that patients with gastric infection had increased nasal mucociliary clearance time compared to HP-negative patients, while the nasal mucociliary clearance time was normalized after eradication of gastric HP eradication, proposing that HP infection may have an essential role on the chronic sinusitis development. However, a major limitation of this study was the lack of examination for nasal HP colonization [30]. Consequently, further investigation is needed.

In our study, there were a few of limitations. The sample of patients was small and a control group without nasal polyps did not exist. Also, the gold standard of diagnosis of gastric HP infection is the gastric biopsies and we performed breath test for HP detection in the stomach. Although PCR present more sensitivity and specificity for HP detection, we performed histochemical examination and CLO test.