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Helicobacter pylori Specific Antigen (HpSA) Stool Test |
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The inside of the stomach is bathed in about half a gallon of gastric juice every day. Gastric juice is composed of digestive enzymes and concentrated hydrochloric acid, which can readily tear apart the toughest food or microorganism. Bacteria, viruses, and yesterdays steak dinner are all consumed in this deadly bath of chemicals. It used to be thought that the stomach contained no bacteria and was actually sterile, but Helicobacter pylori changed that.
The stomach is protected from its own gastric juice by a thick layer of mucus that covers the stomach lining. Helicobacter pylori takes advantage of this protection by living in the mucus lining. (see image below)
Once H. pylori is safely ensconced in the mucus, it is able to fight the stomach acid that does reach it with an enzyme it possesses called urease. Urease converts urea, of which there is an abundant supply in the stomach (from saliva and gastric juices), into bicarbonate and ammonia, which are strong bases. This creates a cloud of acid neutralizing chemicals around the H. pylori, protecting it from the acid in the stomach.
Another defense H. pylori has is that the body's natural defenses cannot reach the bacterium in the mucus lining of the stomach. The immune system will respond to an H. pylori infection by sending white cells, killer T cells, and other infection fighting agents. However, these potential H. pylori eradicators cannot reach the infection, because they cannot easily get through stomach lining. They do not go away either, though, and the immune response grows and grows. Polymorphs die, and spill their destructive compounds (superoxide radicals) on stomach lining cells. Extra nutrients are sent to reinforce the white cells, and the H. pylori can feed on this. within a few days, gastritis and perhaps eventually a peptic ulcer results. It may not be H. pylori itself which causes peptic ulcer, but the inflammation of the stomach lining; i.e. the response to H. pylori.
 I often find the person who has been infected with the H. pylori organism for years. Not only does the person suffer with multiple digestive complaints, he also has massive amounts of inflammation that then cascade down the digestive system and affect both the large and small intestines.
It is only a mater of time that this person's health becomes severely compromised.
Dr. Gary Farr |
H. pylori is believed to be transmitted orally. Many researchers think that H. pylori is transmitted orally by means of fecal matter through the ingestion of waste tainted food or water. In addition, it is possible that H. pylori could be transmitted from the stomach to the mouth through gastro-esophagal reflux (in which a small amount of the stomach's contents is involuntarily forced up the esophagus) or belching, common symptoms of gastritis. The bacterium could then be transmitted through oral contact. So, yes you can get H. Pylori by kissing your (best) friend.
H. pylori stool antigen (HpSA) testing reveals H. pylori antigens shed directly into the stool2. Helicobacter pylori remains a highly prevalent infection in the United States and throughout the world. Prevalence is highest areas of low socioeconomic status, with infection rates reaching over 80% in middle-aged adults in many developing countries. This compares to infection rates of 20%-50% in most industrialized countries.
Helicobacter pylori infection is associated with gastric cancer.23 H. pylori infection may contribute to DNA damage because of up-regulation of inducible nitric oxide synthetase (iNOS) expression, and thereby radical nitrogen species, in the gastric mucosa. Nitrotyrosine in the gastric mucosa is also significantly higher in H. pyloripositive groups than in H. pylori-negative individuals.24
H. pylori is the major cause of peptic ulcer disease. For those infected, the lifetime risk of developing H. pylori-associated peptic ulcer is estimated at 10%-20%.4 H. pylori infection can lead to gastric adenocarcinoma (with clinical sequelae of gastric atrophy, intestinal metaplasia and, ultimately, gastric carcinoma). Gastric cancer is the second most frequent cause of cancer-related death. H. pylori has been classified as a Type I (definite) carcinogen since 1994. In one Japanese study that tracked patients over 7.8 years, gastric cancer developed in 2.9% of 1246 patients with H. pylori infection, whereas no gastric cancer was observed in 280 non-infected controls.5
Infection with H. pylori can lead to mucosa-associated lymphoid tissue (MALT) lymphoma. As many as 72%-98% of patients with gastric MALT are infected with H. pylori. Eradication of H. pylori induces regression of gastric MALT lymphoma in 70%-80% of cases. Most patients whose lymphomas respond to H. pylori eradication therapy remain in remission for several years. However, evidence concerning long-term outcomes is still limited.6
The relationship between H. pylori infection and non-ulcer dyspepsia and gastroesophageal reflux disease (GERD) is controversial. However, H. pylori eradication therapy appears to result in greater long-term symptom improvement and cost-effectiveness compared with antisecretory therapy. Because of the potential to reduce long-term risk of ulcer disease and possibly gastric cancer, it is widely recommended that patients with GERD and non-ulcer dyspepsia be considered for eradication therapies.7
Patients with duodenal ulcer disease or with a history of duodenal ulcers — Over 90% of patients with duodenal ulcers are infected with H. pylori. Eradication therapy virtually cures the disease, with approximately 5% of patients relapsing after treatment at one year. Without eradication therapy, the relapse rate is 20%-70%, depending on the type of acid suppression therapy used for maintenance.4
Patients with gastric ulcer disease or with a history of peptic ulcers — Although H. pylori is associated with gastric ulcers as well as duodenal ulcer disease, infection should not always be assumed in these patients. Testing should be done to avoid unnecessary therapy.8
Patients using or considering NSAID therapy — Studies have shown that nonsteroidal anti-inflammatory drug (NSAID) use and H. pylori infection are independent risk factors for peptic ulcer disease; when both factors are present, risk increases synergistically.9 Over 16,000 people die every year in the United States due to NSAID therapy. Most of these patients are elderly individuals who are more likely to be infected with H. pylori.
The benefit of diagnosing and eradicating H. pylori infection prior to commencing NSAID therapy was recently confirmed in a randomized trial.10
Patients with GERD — Although this clinical approach is controversial, patients with GERD symptoms should be tested for H. pylori infection and treated, if necessary. One primary justification for this approach is that it may help patients avoid health risks associated with long-term proton pump inhibitor therapies, which can aggravate H. pylori-mediated gastritis and thus increase the risk of gastric cancer.11
Patients with non-ulcer dyspepsia — A number of studies have shown symptomatic improvement (>70%) in this group of patients after eradication therapy for H. pylori. However, there is some evidence that adopting a “test-and-treat” strategy, particularly in the elderly, could be misleading and possibly dangerous if a full diagnostic approach with endoscopy is not adopted.12
Pediatric patients with allergies — Recent studies have demonstrated a significant association between H. pylori, allergic reactions, food allergy and other allergic diseases. 13 When H. pylori colonizes the gastric mucosa, it alters gastric barrier function. This in turn increases the passage of intact molecules across the epithelial barrier with resultant allergies and atopic manifestations.14 Patients previously treated for H. pylori — Because of the high prevalence of metronidazole and clarithromycin resistance, patients who have completed eradication treatments in the past without a confirmatory test for eradication should be tested. Antibiotic-resistance poses a major threat to continued efficacy of the therapeutic regimens.4
Yes. Mastic gum, a resinous exudate from the stem and leaves of Pistacia lentiscus has been reported to be effective in the treatment of benign gastric and duodenal ulcers.16 In vitro studies have demonstrated antibacterial activity against H. pylori, thus explaining the anti-peptic-ulcer properties of mastic gum.17
Zinc carnosine has demonstrated an inhibitory effect on the growth of H. pylori.18 It has been found to inhibit urease activity and superoxide production, stabilize gastric membranes and promote wound healing.19 Research shows that zinc carnosine increases the effectiveness of triple treatment therapy when administered concomitantly.20
In addition, other supplements may also be prescribed if inflammation is present.
Additional testing including the Comprehensive Digestive Stool Analysis may be needed.
H. pylori stool antigen (HpSA) testing provides a simple alternative to urea breath testing. Sensitivity and specificity are both 96%. HpSA testing is appropriate for diagnosis and follow-up of infection, and can be used 2 weeks after discontinuing treatment to verify eradication.21 Because HpSA performs well in children of all ages, it may be the noninvasive test of choice for this group.4
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References
1 Uemura N, et al. Helicobacter pylori infection and the development of gastric cancer. New Engl J Med 2001;345:784-89.
2 Vaira D et al. Noninvasive antigen-based assay for assessing Helicobacter pylori eradication: a European multicenter study. The European Helicobacter pylori HpSA Study Group. Am J Gastroenterol. 2000 Apr;95(4):925-9.
3 Feldman RA. Epidemiologic observations and open questions about disease and infection caused by Helicobacter pylori. In: Achtman M, Suerbaum S, eds. Helicobacter pylori: molecular and cellular biology. Wymondham, United Kingdom: Horizon Scientific Press, 2001:29-51.
4 Duggan A. Helicobacter pylori: when is treatment now indicated? Int Med J 2002;32:465-469.
5 Uemura N, et al. Helicobacter pylori infection and the development of gastric cancer. New Engl J Med 2001;345:784-89.
6 Suerbaum S, Michetti P. Helicobacter pylori infection. New Engl J Med 2002;347(15):1175-86.
7 Katelaris PH, et al. A randomized comparison of quadruple and triple therapies for Helicobacter pylori eradication: the QUADRATE study. Gastroenterology 2002; 123:1763-89.
8 Ong SP, Duggan A. Eradication of Helicobacter pylori in clinical situations. Clin Exp Med. 2004 Sep;4(1):30-8. Review.
9 Huang JQ, Sridhar S, Hunt RM. Role of Helicobacter pylori and nonsteroidal anti-inflammatory drugs in peptic ulcer disease: a metaanalysis. Lancet 2002;359:14-22.
10 Chan FK, et al. Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long-term treatment with non-steroidal anti-inflammatory drugs: a randomized trial. Lancet 2002;359:9-13.
11 Meining A, Kiel G, Stolte M. Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during and after 12 months of treatment with ranitidine and lansoprazole in patients with duodenal ulcer disease. Aliment Pharmacol Ther 1998;12:735-40.
12 Pilotto A, et al. Efficacy of 7 day lansoprazole-based triple therapy for H. pylori infection in elderly patients. J Gastroenterol Hepatol 1999;14:464-71.
13 Corrado G et al. Helicobacter pylori seropositivity in children with atopic dermatitis as sole manifestation of food allergy. Pediatr Allergy Immunol. 2000 May;11(2):101-5.
14 Matysiak-Budnik T, Heyman M. Food allergy and Helicobacter pylori.J Pediatr Gastroenterol Nutr. 2002 Jan;34(1):5-12.
15 Canbaz S et al. Survey of general practitioners' knowledge about Helicobacter pylori infection. BMC Gastroenterol. 2005 Jan 26;5(1):4. 16 Marone P et al. Bactericidal activity of Pistacia lentiscus mastic gum against Helicobacter pylori. J Chemother. 2001 Dec;13(6):611-4.
17 Huwez FU et al. Mastic gum kills Helicobacter pylori.N Engl J Med. 1998 Dec 24;339(26):1946.
18 Matsukura T, Tanaka H. Applicability of zinc complex of L-carnosine for medical use. Biochemistry (Mosc). 2000 Jul;65(7):817-23.
19 Amakawa T. Clinical effect of Z-103 tablets against gastric ulcers: phase III clinical study. Jpn Pharmacol Ther 1992;20:199-223.
20 Kashimura H et al. Polaprezinc, a mucosal protective agent, in combination with lansoprazole, amoxycillin and clarithromycin increases the cure rate of Helicobacter pylori infection. Aliment Pharmacol Ther. 1999 Apr;13(4):483-7.
21 Package insert: Premier Platinum HpSATM (Patent No 5716,971). Enzyme Immunoassay for the Detection of Helicobacter pylori Antigens in Stoll Specimens for Diagnosis and Monitoring.
22 Blanchard TG et al. Helicobacter infection: pathogenesis.
23 Haruma K, Komoto K, Kamada T, et al. Helicobacter pylori infection is a major risk factor for gastric carcinoma in young patients. Scand J Gastroenterol. 2000;35(3):255-259.
24 Goto T, Haruma K, Kitadai Y, et al. Enhanced expression of inducible nitric oxide synthase and nitrotyrosine in gastric mucosa of gastric cancer patients. Clin Cancer Res. 1999;5(6):1411-1415.
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