الفهرس 
Aim of the studyOnly 14 pages are availabe for public view
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Abstract
Summary & Conclusion
H. pylori is one of the most common bacterial infections worldwide. Estimates suggest that more than half of the world’s population is infected by this gastric bacterium. It is associated with chronic gastritis and peptic ulcer diseases and constitutes a major risk factor for gastric adenocarcinoma and gastric mucosa associated lymphoid tissue (MALT) lymphoma.
Although the stomach is the natural reservoir of H. pylori various tissues have been proposed as potential reservoirs of infection such as tonsil, gingiva, dental plate, gallbladder, paranasal sinuses, middle ear cavity, and coronary arteries.
H. pylori is a gram negative microaerophilic, rod-shaped bacteria approximately 0.5nm in diameter and 3-5nm long, it has 4-7 polar-sheathed flagella, which enable the bacterium to move freely in viscous environment such as gastric mucus. This motility is essential for the bacterial colonization of its host. The flagella sheath is a membrane containing protein and lipopolysacharides which probably protects the flagella filaments from gastric acidity.
The precise modes of transmission and extra gastric involvement are still yet to be fully understood yet. Person-to-person transmission occurs through several routes, oral–oral, gastric– oral, and fecal–oral. Transmission may also occur through contaminated water and/or air as well.
H. pylori are able to survive in stomach acid because they produce enzymes (special proteins) that neutralize the acid, This mechanism allows H. pylori bacteria to enter the stomach and make their way to the safe area (the protective mucous lining of the stomach wall).
When H. pylori does cause symptoms, they are usually either symptoms of gastritis or peptic ulcer disease, Other symptoms include: heartburn, increased burping, weight loss, bloating and burping, and less common symptoms include: poor appetite, nausea and vomiting.
There are several methods (invasive and non-invasive) available for detecting H. pylori infection.
1-Invasive methods are based on biopsy specimens as; Rapid urease test, PCR, culture staining biopsy materials with H&E stain, Giemsa stain, Warthin-Stany silver stain.
2-Non-invasive methods as; urea breath test, stool antigen test and the ELISA technique to identify specific immunoglobulin G antibodies against H. pylori in serum.
Gastro esophageal reflux disease (GERD) is a complex disorder defined as a condition that develops when the reflux of stomach contents causes troublesome symptoms and ⁄ or complications.
GERD is the most common upper gastrointestinal problem seen in clinical practice. It is estimated that 10%–20% of adults have symptoms at least once weekly and 15%–40% have symptoms at least once monthly.
GERD, is a very common disorder and occurs when stomach acid refluxes into the lower esophagus through the lower esophageal sphincter (LES). The LES is a band of muscles that act as a protective barrier against reflux material by contracting and relaxing. If this barrier is relaxed at inappropriate times or otherwise compromised, reflux occurs and Abnormalities in the body such as hiatal hernias may also cause GERD.
Other factors that can contribute to GERD include: Obesity, Pregnancy Certain medications, such as asthma medications, calcium channel blockers, and many antihistamines, pain killers, sedatives, and antidepressants, Smoking, or inhaling secondhand smoke, Alcohol and Certain foods: Fatty foods, citrus fruit juices, Spicy foods, aggravate GERD .
The most common symptom of GERD is heartburn, which is a burning sensation in the center of the chest, sometimes spreading to the throat. other common symptoms are: pain in the upper abdomen, chest pain, a sensation of food getting stuck, regurgitation of food/fluid, an acid taste in the throat, and burping. Less common symptoms are: painful swallowing, persistent laryngitis or hoarseness, persistent sore throat, chronic cough and sense of a lump in the throat, dental erosion and bad breath, chronic sinusitis, waking up with a choking sensation .
Specific testing is required for diagnosis: Endoscopy, 24-hour esophageal pH study and Esophageal manometry.
GERD is treated according to its severity:
A- Mild symptoms: Initial treatments for mild acid reflux include dietary changes and using non-prescription medications, including antacids or histamine antagonists.
B-Moderate to severe symptoms: Most patients are treated with a proton pump inhibitor and surgical treatment.
Recently concern regarding gastroesophgeal reflux (GER) or H. pylori as a possible pathologic cause of nasal polyposis chronic rhino sinusitis has been increasing.
The incidence of H. pylori infection in the patients with GERD varies widely in literature from 30% to 90% and is approximately of 35% in most series.
The effects of H. pylori infection on the pathogenesis of GERD have been studied in many reports. Infection with H. pylori produces an increase in basal and stimulated gastric acid output through the secretion of gastrin, somatostatin, and inflammatory mediators, which is a possible cause of GERD.
Some researchers reported the association between H. pylori infection and upper respiratory diseases, including chronic otitis media, and chronic otitis media with effusion.
Mechanism by which H. pylori colonizes nasal cavity could be explained by three possibilities First, the nasal cavity can be H. pylori reservoir .Second, the oral cavity can represent H. pylori reservoir and microorganisms can reach the sinonasal cavity by oronasal reflux . Third, stomach can be the primary infection reservoir and the transmission of H. pylori from stomach to nasal cavity can occur by means of GER.
In the last fifteen years, the number of studies indicating the relation between CRS and GER is increasing, from proving the presence of H. pylori on aspirates and sinus biopsies to pH-metric evidence of increased acidity and pepsin in epipharynx and nasal cavities in some patients with GER.
As overall, there are three hypotheses for presence of H. pylori in sinonasal mucosa:
1. Sinonasal mucosa is the primary source for H. pylori.
2. Oro-nasal reflux transits H. pylori to the nose and middle ear.
3. Gastro-esophageal acidic reflux transport H. pylori to sinonasal area.
There are two possible explanations for why H. pylori has been discovered in the effusion of the middle ear. The first: is that the tonsil, adenoid, and the nasal mucosa act as a storage place for H. pylori. Since the tonsil, adenoid, nasal canal, and Eustachian tube are anatomically close, this can allow for the H. pylori to spread directly.
The second possibility is due to GER, since the gastric fluid can affect the middle ear through the Eustachian tube and the H. pylori that is mixed in with the gastric fluid can then be detected in the middle ear. The gastric fluid can cause inflammation and edema of the mucosa of the Eustachian tube and the bacteria in the nasal cavity can easily enter the middle ear through the Eustachian tube.
Recurrent headache secondary to H. pylori infection has been postulated to be the result of systemic vasospastic effects of pro-inflammatory substances released from infected gastric mucosa.
Several studies concluded that H. pylori should be examined in migranous patients and eradication of the infection may be helpful for the treatment of the disease.
H. pylori has been detected in the oral cavity samples from supragingival plaque, dental plaque and saliva by polymerase chain reaction. And therefore it has a role in recurrent aphthous stomatitis and chronic periodontitis.
More recently, it has also been suggested that adenotonsillar tissues may act as a reservoir for H. pylori, there by several studies evaluated the presence of H. pylori in adenoid and tonsil specimens, and concluded that these result suggest that H. pylori associated with the development of adenotonsillar hypertrophy and chronic nonspecific pharyngitis.
H. pylori eradication was found to decrease globus symptoms, halitosis disappeared with eradication treatment of H. pylori in adult patients with H. pylori infection.
Several studies have been performed to evaluate the association between H. pylori and laryngeal cancer. Some studies have shown that H. pylori is as an etiologic factor for laryngeal carcinoma
Some other studies have investigated the protective effect of H. pylori against laryngeal cancer.
Triple treatment including a proton-pump inhibitor (PPI) and clarithromycin, combined with either amoxicillin or metronidazole, has been recommended for treatment of H. pylori infection.