Abstract:H. pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. Priming effects on mucosal immunology downstream from the foregut may occur after infection with H. pylori.
“…Both whole Helicobacter pylori and lysates induce iNOS mRNA expression, enzymatic activity and nitric oxide release 15 . This association between Helicobacter pylori and iNOS has been demonstrated previously in the foregut 16 and, more recently, by our colleagues in acute appendicitis 17 . In this latter study, the expression of iNOS in mucosal macrophages of appendiceal sections was higher in Helicobacter pylori ‐positive patients.…”
supporting
confidence: 76%
“…Therefore, as the MALT tissue of Waldeyer's ring is the first line of mucosal defence against invading pathogens, it is plausible that Helicobacter pylori induces a pro‐inflammatory reaction that is both local and systemic. Such downstream priming of mucosal immunity by Helicobacter pylori may account for the diverse pathological tissue responses observed in infected patients, which include gastritis, 30 MALTomas of the salivary glands, stomach and rectum 9–11 and a more marked inflammation in appendicitis 17 and Crohn's disease 31…”
Section: Resultsmentioning
confidence: 99%
“…In this study, tissue from patients undergoing tonsillectomy was examined for evidence of the bacterium or the expression of iNOS, as a link has been demonstrated in related MALT sites, i.e. the appendix 17 and the stomach 12,13 …”
Tonsillar tissue is a component of mucosa-associated lymphoid tissue (MALT), which has evolved to protect vulnerable mucosal surfaces. Helicobacter pylori, implicated as an aetiological factor in duodenal ulcers and gastritis, induces the appearance of lymphoid aggregates (MALT) in the stomach. This organism is cytotoxic via a nitric oxide synthase cascade. The possibility that tonsillar tissue processes Helicobacter pylori or that Helicobacter pylori can colonize the palatine tonsils is explored. The study design was that of a prospective study. We determined if Helicobacter pylori (i) forms part of the normal microenvironment of the tonsil, (ii) plays a role in the pathogenesis of tonsillitis and (iii) is associated with increased expression of inducible nitric oxide synthase (iNOS) in macrophages of the tonsil. Serology for Helicobacter pylori was performed on 50 patients undergoing tonsillectomy. Tonsillar specimens were monitored for urease activity by CLO test (a sealed plastic slide holding an agar gel, which contains urea and detects the urease enzyme of Helicobacter pylori), and immunocytochemically probed for Helicobacter pylori and iNOS expression. The mean age of this patient group was 17.2 years (3-36 years). Fourteen (28%) were sero-positive for Helicobacter pylori but no evidence of this pathogen was found in any tonsillar specimen. The number of macrophages staining for iNOS, per field, under a magnification of x40, was increased in sero-positive patients (13.3 +/- 1.3 versus 9.9 +/- 0.7; P = 0.01). Helicobacter pylori does not appear to colonize the tonsil. We believe that Helicobacter pylori primes the tonsils by inducing macrophage iNOS expression. The higher expression in sero-positive patients is a reflection of a pro-inflammatory reaction to Helicobacter pylori that is both local and systemic.
“…Both whole Helicobacter pylori and lysates induce iNOS mRNA expression, enzymatic activity and nitric oxide release 15 . This association between Helicobacter pylori and iNOS has been demonstrated previously in the foregut 16 and, more recently, by our colleagues in acute appendicitis 17 . In this latter study, the expression of iNOS in mucosal macrophages of appendiceal sections was higher in Helicobacter pylori ‐positive patients.…”
supporting
confidence: 76%
“…Therefore, as the MALT tissue of Waldeyer's ring is the first line of mucosal defence against invading pathogens, it is plausible that Helicobacter pylori induces a pro‐inflammatory reaction that is both local and systemic. Such downstream priming of mucosal immunity by Helicobacter pylori may account for the diverse pathological tissue responses observed in infected patients, which include gastritis, 30 MALTomas of the salivary glands, stomach and rectum 9–11 and a more marked inflammation in appendicitis 17 and Crohn's disease 31…”
Section: Resultsmentioning
confidence: 99%
“…In this study, tissue from patients undergoing tonsillectomy was examined for evidence of the bacterium or the expression of iNOS, as a link has been demonstrated in related MALT sites, i.e. the appendix 17 and the stomach 12,13 …”
Tonsillar tissue is a component of mucosa-associated lymphoid tissue (MALT), which has evolved to protect vulnerable mucosal surfaces. Helicobacter pylori, implicated as an aetiological factor in duodenal ulcers and gastritis, induces the appearance of lymphoid aggregates (MALT) in the stomach. This organism is cytotoxic via a nitric oxide synthase cascade. The possibility that tonsillar tissue processes Helicobacter pylori or that Helicobacter pylori can colonize the palatine tonsils is explored. The study design was that of a prospective study. We determined if Helicobacter pylori (i) forms part of the normal microenvironment of the tonsil, (ii) plays a role in the pathogenesis of tonsillitis and (iii) is associated with increased expression of inducible nitric oxide synthase (iNOS) in macrophages of the tonsil. Serology for Helicobacter pylori was performed on 50 patients undergoing tonsillectomy. Tonsillar specimens were monitored for urease activity by CLO test (a sealed plastic slide holding an agar gel, which contains urea and detects the urease enzyme of Helicobacter pylori), and immunocytochemically probed for Helicobacter pylori and iNOS expression. The mean age of this patient group was 17.2 years (3-36 years). Fourteen (28%) were sero-positive for Helicobacter pylori but no evidence of this pathogen was found in any tonsillar specimen. The number of macrophages staining for iNOS, per field, under a magnification of x40, was increased in sero-positive patients (13.3 +/- 1.3 versus 9.9 +/- 0.7; P = 0.01). Helicobacter pylori does not appear to colonize the tonsil. We believe that Helicobacter pylori primes the tonsils by inducing macrophage iNOS expression. The higher expression in sero-positive patients is a reflection of a pro-inflammatory reaction to Helicobacter pylori that is both local and systemic.
“…Diese Befunde unterstützen das Konzept einer Infektionsepidemiologie der Appendizitis [22]. Zwischen Helicobacter pylori und dem Auftreten einer Appendizitis wurde in 2 Studien kein Zusammenhang festgestellt [31,42]. H. pylori kolonisiert nicht im Blinddarm und ist damit höchstwahrscheinlich auch kein pathogener Stimulus für eine Appendizitis.…”
The current incidence of appendicitis is about 100 per 100,000 person-years in Europe/America. Whereas the appendectomy rate is still decreasing, the incidence of appendicitis is now nearly stable. During the last 30 years the incidence of perforated appendicitis has not changed (approximately 20 per 100,000 person-years). Established risk factors for acute appendicitis are age (peak: 10-19 years), sex, and ethnic group/race. Classical theories (diet, hygiene) present illuminating models to explain the rise and fall of incidence in the last century; however, from a contemporary perspective the evidence is insufficient. The study of the epidemiology of appendicitis is complicated by the influence of referral, infrastructure, and surgical treatment strategy on the incidence of acute appendicitis. Therefore, there is a strong need for good prospective studies with high-quality data (e.g., studies directed by a central pathology department).
“…Acute appendicitis is the most common surgical emergency, with 16% of the population undergoing appendicectomy (1). Intraperitoneal culture during appendicectomy is routine practice in some hospitals.…”
Appendicectomy is one of the most common surgical emergency procedures. Intraperitoneal culture during appendicectomy is routine practice in some hospitals, while some surgeons advocate abandoning this routine. The aim of our study is to determine the value of intraoperative abdominal cavity culture and its impact on the patient management. Retrospective analysis was performed on 498 patients who underwent appendicectomy over 2.5-year period. The median of the postoperative hospital stay was 2 days, while the median time taken to receive culture results was 3 days. A positive culture was found in 42.6%. Approximately 42.7% of the patients were discharged from the hospital before receiving the culture results. The culture and sensitivity results altered the antibiotic regimen in one patient (0.85%). Intraoperative abdominal cavity culture results were seldom used for clinical management in patients with acute appendicitis. The traditional surgical practice of routinely culturing peritoneal fluid in these patients should be abandoned.
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