This article is from the Great Smokies Diagnostic Lab newsletter.
Linda
- H. PYLORI: LIVING UP TO A BAD REPUTATION?
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- THE GROWING BODY OF EVIDENCE AGAINST A PERVASIVE GUT PATHOGEN
Since its discovery just 15 years ago, mounting scientific evidence has
uncovered a powerful role for this gastrointestinal pathogen in a host
of GI disorders, as well as in other disease processes involving the
cardiovascular system and inflammation.
H. pylori is a primary cause of peptic ulcers. In the most recent issue
of Gastroenterology, scientists suggested that H pylori also underlies
gastric injury associated with long-term NSAIDS use. NSAID-induced
ulcers arise with increased neutrophil activity in the gastric mucosa -
particularly the leukocytes that mediate gastrointestinal injury. H.
pylori, it appears, acts as a crucial trigger, encouraging the
infiltration, adhesion and migration of neutrophils in patients
undergoing long-term NSAID therapy. "The strong association between
neutrophils and H. pylori explains...the need to eradicate this
infection to minimize the occurrence of ulcers in long-term users of
NSAIDS," the study concluded.
H. pylori's causative role in gastritis has also been borne out through
a plethora of studies. Most recently, Japanese researchers conducted a
serioepidemiologic nested case-control study on over 1300 adults, the
most statistically rigorous method yet used, and discovered HP infection
associated with a nearly four-fold risk in atrophic gastritis. "The most
important feature of the current study is that HP infection was
established prior to the diagnosis of atrophic gastritis," the authors
observed, supporting a clear causal relationship.
Acting in response to burgeoning evidence linking H. pylori infections
with pre-cancerous lesions and an escalating risk of gastric cancer - an
increase reaching as high as six-fold - the World Health Organization's
International Agency for Research on Cancer (IARC) designated H. pylori
a Class I carcinogen in 1994. While epidemiologists are now carefully
examining the strength of this association, calling for careful
attendance to other environmental and physiological factors involved, a
new study in the American Journal of Gastroenterology reports that
in-vivo inoculation with H. pylori activates telomerase, the enzyme
strongly tied to uncontrolled cancer cell growth and intestinal
metaplasia - an early event in the development of gastric cancer.
The Consortium for Health Outcomes, Innovation, and Cost-Effective
Studies (CHOICE) recently evaluated the cost effectiveness of H. pylori
testing to reduce the incidence of gastric cancer. H. pylori testing,
they concluded, "has the potential to produce important health benefits
at a reasonable cost," particularly for individuals in high risk groups,
such as Japanese men.
Increasingly, investigators are evaluating the possible role of H.
pylori in the etiology of other health conditions, such as
cardiovascular disease. Early this year, the National Public Health
Institute in Finland reported a statistically significant association
between H. pylori infection and elevated serum lipid profiles in men. A
team of Japanese scientists found that H. pylori infection "leads to
the gastric mucosal expression of COX-2," the enzyme that can set off
the destructive inflammatory cascade underlying many chronic and
degenerative disorders.
NOTE: Great Smokies was one the first laboratories in the world to offer
H. pylori testing. The Helicobacter Pylori Test
(http://www.gsdl.com/services/heliobacter.html) examines serum for IgG
antibodies to Helicobacter pylori, the leading cause of peptic ulcers,
chronic gastritis, and increased risk of gastric cancer. Recent studies
in JAMA and Gastrointestinal Endoscopy laud IgG serum antibody testing
for its heightened sensitivity and specificity for detecting H. pylori
infection and evaluating treatment efficacy. Call 800-522-4762 for more
information or send your request for test kits and educational materials
to cs@....
Great Smokies does not endorse commercial products, but several
reputable supplement manufacturers now offer probiotics and combinations
as alternatives to synthetic antimicrobials. The preparations include
such anti-microbial agents as bismuth, citrus seed extract, goldenseal
root, and glycerrhiza, among others. Many suppliers will only offer
these preparations to medical professionals.
Sources:
Aiba Y, Suzuki N, Kabir A, Takagi A, Koga Y. Lactic acid-mediated
suppression of Helicobacter pylori by the oral administration of
Lactobacillus salivarius as a probiotic in a gnotobiotic murine model.
Am J Gastroentol 1998;93(11):2097-2101.
Fendrick AM, Chernew ME, Hirth RA, Bloom BS, Bandekar RR, Scheiman JM.
Clinical and Economic Effects of Population-Based Helicobacter pylori
screening to prevent gastric cancer. Arch Intern Med 1999;159:142-148.
Kameshima H, Yagihashi A, Yajima T, Watanabe N. Helicobacter pylori
infection induces telomerase activity in pre-malignant lesions. Am J
Gastro 1999;4(2):547-548.
Laurila A, Bloigu A, Nayha S, Hassi J, Leinonen M, Saikku P. Association
of Helicobacter pylori infection with elevated serum lipids.
Atherosclerosis 1999;142(1):207-10.
Sawaoka H, Kawano S, Tsuji S, Tsuji M, Sun W, Gunawan ES, Hori M.
Helicobacter pylori infection induces cyclooxygenase-2 expression in
human gastric mucosa. Prostaglandins Leuko Essent Fatty Acids
1998;59(5):313-6.
Taha AS, Dahill S, Morran C, Hudson N, Hawkey CJ, Lee FD, et al.
Neutrophils, Helicobacter pylori and nonsteroidal anti-inflammatory drug
uses. Gastroentrol 1999;116:254-258.
Tien-Chien Tu, Chia-Long Lee, Chi-Hwa Wu, Tzen-Kwan Chen, Chung-Chuan
Chan, Shih-Hung Huang, Shui-Cheng Lee. Comparison of invasive and
noninvasive tests for detecting Helicobacter pylori infection in
bleeding ulcers. Gastrointestinal Endoscop 1999;49(3 Pt 1):302-306.
Ozasa K, Kurata JH, Higashi A, Hayashi K, Inokuchi H, Miki K, et al.
Helicobacter pylori infection and atrophic gastritis: A nested
case-control study. Digestive Diseases and Sciences 1999;44(2):253-56.
Feldman M, Cryer B, Lee E, Peterson WL. Role of seroconversion in
confirming cure of Helicobacter pylori infection. JAMA 1998;280(4):
363-365.