HELICOBACTER PYLORI TESTING - UHCprovider.com
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MEDICAL POLICY
For use with the UnitedHealthcare Laboratory Benefit Management Program, administered by BeaconLBS
HELICOBACTER PYLORI TESTING
Policy Number: CMP - 046
Effective Date: January 1, 2018
Table of Contents Page
BACKGROUND 1
POLICY 4
REFERENCES 6
POLICY HISTORY/REVISION HISTORY 7
INSTRUCTIONS FOR USE
This Medical Policy provides assistance in interpreting UnitedHealthcare benefit plans. When deciding
coverage, the enrollee specific document must be referenced. The terms of an enrollee's document (e.g.,
Certificate of Coverage (COC) or Summary Plan Description (SPD)) may differ greatly. In the event of a
conflict, the enrollee's specific benefit document supersedes this Medical Policy. All reviewers must first
identify enrollee eligibility, any federal or state regulatory requirements and the plan benefit coverage prior
to use of this Medical Policy. Other Policies and Coverage Determination Guidelines may apply.
UnitedHealthcare reserves the right, in its sole discretion, to modify its Policies and Guidelines as necessary.
This Medical Policy is provided for informational purposes. It does not constitute medical advice.
UnitedHealthcare may also use tools developed by third parties, such as the MCG™ Care Guidelines, to assist
us in administering health benefits. The MCG™ Care Guidelines are intended to be used in connection with the
independent professional medical judgment of a qualified health care provider and do not constitute the
practice of medicine or medical advice.
BACKGROUND
Helicobacter pylori (H. pylori) is a gram-negative rod bacteria that is uniquely adapted to survive in the highly
acidic gastric environment. To survive in the harsh, acidic environment of the stomach, H. pylori secretes an
enzyme called urease, which converts the chemical urea to ammonia.1 The production of ammonia around H.
pylori neutralizes the acidity of the stomach, making it more hospitable for the bacterium. In addition, the
shape of H. pylori allows it to burrow into the mucus layer, which is less acidic than the lumen of the stomach.
H. pylori can also attach to the cells that line the inner surface of the stomach.
H. pylori infection with the bacterium is common. The Centers for Disease Control and Prevention (CDC)
estimates that approximately two-thirds of the world’s population harbors the bacterium, with infection rates
much higher in developing countries than in developed nations.1
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CMP-046_Helicobacter Pylori_20171207_v2.4Disease Conditions
Although H. pylori infection does not cause illness in all infected people, it is a major risk factor for the
development of chronic active gastritis, peptic ulcer disease, gastric cancer, and probably some forms of gastric
lymphoma11 Colonization of the stomach with H. pylori has been accepted as an important cause of stomach
cancer and of gastric mucosa-associated lymphoid tissue (MALT) lymphoma.
Gastric Cancer
Infection with H. pylori is the primary identified cause of gastric cancer.1 Other factors that increase the risk for
gastric cancer include chronic gastritis; older age; male sex; a diet high in salted, smoked, or poorly preserved
foods and low in fruits and vegetables; tobacco smoking; pernicious anemia; a history of stomach surgery for
benign conditions; and a family history of stomach cancer.2, 3 Multiple studies have shown that individuals
infected with H. pylori have an increased risk of gastric adenocarcinoma.1, 2, 4-10
Gastric MALT
Gastric MALT lymphoma, a rare type of non-Hodgkin lymphoma, is characterized by the slow multiplication of B
lymphocytes (an immune cell) in the stomach lining.11 In normal circumstances, the stomach lining lacks
lymphoid tissue, but this tissue may be developed in response to H. pylori colonization.12 In rare cases, this
tissue may give rise to MALT. Nearly all patients with gastric MALT lymphoma have signs of H. pylori infection
and the risk of developing this tumor is more than six times higher in infected people than in uninfected
people13, 14.
Diagnosis
According to the American College of Gastroenterology, the established indications for diagnosis and treatment
of H. pylori are:15
Active peptic ulcer disease (gastric or duodenal ulcer)
Confirmed history of peptic ulcer disease (not previously treated for H. pylori infection)
Gastric MALT lymphoma (low grade)
After endoscopic resection of early gastric cancer
Uninvestigated dyspepsia (depending upon H. pylori prevalence) - Test and treat strategy, especially for
those under 55 who have no alarm features.
Alarm features identified by the College of Gastroenterology include bleeding, anemia, early satiety,
unexplained weight loss, progressive dysphagia, odynophagia, recurrent vomiting, family history of GI cancer,
and previous esophagogastric malignancy.15
It is not necessary to perform H. pylori testing in the following situations:
In the absence of documented gastritis or duodenal pathology (i.e. Patients who have had a normal
upper GI endoscopy within the preceding six weeks).
Patients for whom an upper GI endoscopy is planned either for initial diagnosis or follow-up.
Patients who are asymptomatic after treatment of H. pylori infection, unless there is a documented
family history of gastric cancer or it is necessary to resume NSAIDS or ulcerogenic mediations.
Patients with dyspepsia requiring endoscopy and biopsy or to monitor response to therapy.
Patients with new onset, uncomplicated dyspeptic symptoms.
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CMP-046_Helicobacter Pylori_20171207_v2.4Testing
Testing for H. pylori can be divided into invasive specimen collection (biopsy and/or culture), non-invasive
specimen collection (gram stain, rapid urease testing, serologic tests, breath tests) and assay for stool antigens
(HpSA). The choice of specific testing depends on the clinical presentation of the patient and whether or not the
patient requires endoscopy for evaluation. When medically necessary, more than one test may be needed to
achieve the best diagnostic accuracy.
Invasive Tests
Invasive tests for H. pylori detection involve endoscopic biopsies of stomach tissue.
Esophagogastroduodenoscopy (EGD) is used to obtain specimens of gastric mucosa. If endoscopy is indicated
for the clinical evaluation of the patient, collection of biopsy specimens for histologic examination, urease
activity and/or culture may be considered.
Non-Invasive Tests
Non-Invasive Specimen Collection (blood, breath, stool, etc) do not require endoscopy and are generally
serological qualitative or semi-quantitative tests.
The urea breath test or stool test is recommended for initial testing for H. pylori because they are non-invasive,
accurate and cost-effective. Although the serological test for H. pylori antigen is non-invasive and cost-effective,
it is not recommended for initial evaluation or for determination of eradication after treatment for H. pylori
according to the American College of Gastroenterology.15
Serological testing may be appropriate for the patient with non-specific dyspeptic symptoms in order to rule in
or out H. Pylori infection. This test is not appropriate to determine treatment outcome because the test is
limited to the detection of antibodies and therefore cannot accurately detect active infection because high
levels of antibodies persist for months after treatment. Serology is not used for follow-up testing or to
determine cure.
Urea Breath Test
The urea breath test for is a non-invasive diagnostic procedure utilizing analysis of breath samples to determine
the presence of H. pylori in the stomach. The H. pylori breath test consists of analysis of breath samples before
and after ingestion of labeled C-urea. Breath tests can detect the continued presence of H. pylori after
treatment, (which is not the case with serology, where the presence of antibodies can exist for long periods of
time).
Urea Breath Tests are indicated in patients who:
Continue to have symptoms of dyspepsia after completing a treatment regimen which includes
appropriate antibodies and no endoscopy is planned.
Have symptoms that continue four weeks after the treatment regimen has been completed.
Patients that have a history of hemorrhage, or outlet obstruction from peptic ulcer disease.
Patients with a history of ulcer on chronic NSAID or on anticoagulant therapy.
Breath tests are not considered medically necessary for patients who are being screened for H. pylori infection
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CMP-046_Helicobacter Pylori_20171207_v2.4in the absence of documented upper gastrointestinal tract symptoms and/or pathology, patients who have had
upper gastrointestinal endoscopy within the preceding six weeks or for whom an upper gastrointestinal
endoscopy is planned, patients who have non-specific dyspeptic symptoms with a negative H. Pylori serum
antibody test, or patients who are asymptomatic after treatment of an H. pylori infection (either proven or
suspected).
Stool Testing
The stool test describes an in vitro qualitative procedure for the detection of H. pylori antigens in human stool.
A fresh or appropriately stored stool specimen is processed and tested by enzyme immunoassay technique. Test
results can aid in the diagnosis of H. pylori as well as response to therapy. The stool test is appropriate for the
patient with non-specific dyspeptic symptoms. In contrast to the serum antibody test, the stool antigen test
returns to normal (negative) after successful treatment, and may determine treatment outcome.
Indications for stool antigen testing include the initial detection of H. pylori and follow-up of patients who
continue to have symptoms after completing a treatment regimen that includes appropriate antibiotics. The
stool test for H. pylori antigen is also appropriate for the patient with non-specific dyspeptic symptoms. In
contrast to the serum antibody test, the stool antigen test returns to normal (negative) after successful
treatment, and may be used to determine treatment outcome and whether eradication has occurred.
Serological Testing
Serological testing for antibodies to H. pylori is inexpensive, convenient and simple, but, because antibody levels
persist some months after treatment, it is not useful for assessing therapeutic effectiveness.15
Confirmation of successful H pylori cure may be necessary:
In Patients with an H. pylori-associated ulcer
Individuals with persistent dyspeptic symptoms despite the test-and –treat strategy
Those with H. pylori-associated MALT lymphoma
Individuals who have undergone resection of early gastric cancer
POLICY
For the following CPT code(s) in Table 1, the patient should have a diagnosis (ICD-10-CM) code(s) listed in the
attached files below.
Table 1. HCPCS Codes (Alphanumeric, CPT AMA)
HCPCS Code Description
78267 Urea breath test, c-14 (isotopic); acquisition for analysis
78268 Urea breath test, c-14 (isotopic); analysis
83009 Helicobacter pylori, blood test analysis for urease activity, non-radioactive
isotope (eg, C-13)
83013 Helicobacter pylori; breath test analysis for urease activity, non-
radioactive isotope (eg, C-13)
83014 Helicobacter pylori; drug administration
86677 Antibody; Helicobacter pylori
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CMP-046_Helicobacter Pylori_20171207_v2.4HCPCS Code Description
87338 Infectious agent antigen detection by enzyme immunoassay technique,
qualitative or semiquantitative, multiple-step method; Helicobacter
pylori, stool
87339 Infectious agent antigen detection by enzyme immunoassay technique,
qualitative or semiquantitative, multiple-step method; Helicobacter pylori
ICD-10 Diagnosis Codes (Proven)
CMP-046 H Pylori
ICD10_v2.2
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CMP-046_Helicobacter Pylori_20171207_v2.4REFERENCES
1. National I, National Cancer Institute, National Institutes of Health. Fact Sheet Helicobacter pylori and
cancer. Available at: http://www.cancer.gov/cancertopics/factsheet/Risk/h-pylori-cancer (Accessed:
July 17, 2017).
2. Forman D and Burley VJ. Gastric cancer: global pattern of the disease and an overview of environmental
risk factors. Best Pract Res Clin Gastroenterol, 2006. 20(4): p. 633-649.
3. Brenner H, Rothenbacher D and Arndt V. Epidemiology of stomach cancer. Meth Mol Biol, 2009. 472: p.
467-477.
4. Helicobacter and Cancer Collaborative G. Gastric cancer and Helicobacter pylori: a combined analysis of
12 case control studies nested within prospective cohorts. Gut, 2001. 49(3): p. 347-353.
5. Parsonnet J,Friedman GD,Vandersteen DP, et al. Helicobacter pylori infection and the risk of gastric
carcinoma. N Engl J Med, 1991. 325(16): p. 1127-1131.
6. Huang JQ,Sridhar S,Chen Y, et al. Meta-analysis of the relationship between Helicobacter pylori
seropositivity and gastric cancer. Gastroenterol, 1998. 114(6): p. 1169-1179.
7. Eslick GD,Lim LL,Byles JE, et al. Association of Helicobacter pylori infection with gastric carcinoma: a
meta-analysis. Amer J Gastroenterol, 1999. 94(9): p. 2373-2379.
8. Uemura N,Okamoto S,Yamamoto S, et al. Helicobacter pylori infection and the development of gastric
cancer. N Engl J Med, 2001. 345(11): p. 784-789.
9. The ATBC Cancer Prevention Study Group.The alphatocopherol betacarotene lung cancer prevention
study: design methods participant characteristics and compliance. Ann. Epidemiol., 1994. 4(1 ): p. 1-10.
10. Kamangar F,Dawsey SM,Blaser MJ, et al. Opposing risks of gastric cardia and noncardia gastric
adenocarcinomas associated with Helicobacter pylori seropositivity. J. Natl. Cancer Inst., 2006. 98(20): p.
1445-1452.
11. Wu X-C,Andrews P,Chen VW, et al. Incidence of extranodal non-Hodgkin lymphomas among whites,
blacks, and Asians/Pacific Islanders in the United States: anatomic site and histology differences. Cancer
Epidemiol., 2009. 33(5): p. 337-346.
12. Kusters JG, van Vliet AHM and Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin. Microbiol.
Rev., 2006. 19(3): p. 449-490.
13. Parsonnet J,Hansen S,Rodriguez L, et al. Helicobacter pylori infection and gastric lymphoma. N Engl J
Med, 1994. 330(18): p. 1267-1271.
14. Sagaert X,Van Cutsem E,De Hertogh G, et al. Gastric MALT lymphoma: a model of chronic inflammation-
induced tumor development. Nat Rev Gastroenterol Hepatol, 2010. 7(6): p. 336-346.
Proprietary Information of UnitedHealthcare. Copyright 2015 United HealthCare Services, Inc. Page 6
CMP-046_Helicobacter Pylori_20171207_v2.415. Chey WD, Wong BCY and Practice Parameters Committee of the American College of G. American
College of Gastroenterology guideline on the management of Helicobacter pylori infection. Amer J
Gastroenterol, 2007. 102(8): p. 1808-1825.
POLICY HISTORY/REVISION HISTORY
Date Action/Description
12/07/2017 Annual Policy Review Completed – No changes.
01/21/2017 Updated ICD10 codes as per CMS recommendations. Removed ICD9 code file
12/03/2015 Annual Policy Review Completed – changes made:
Added ICD9 diagnosis codes related to malignant neoplasm:
Iron Deficiency- 280.0, 280.1, 280.8, 280.9, 281.0, 281.1
Idiopathic Thrombocytopenic Purpura (ITP)- 287.31
NSAID/Aspirin treatment -V58.69
Added ICD10 diagnosis codes related to:
Iron Deficiency- D50.0,D50.8,D50.1,D50.8,D50.9,D51.0,D51.1,D51.2,D51.3,D51.8,D51.9
Idiopathic Thrombocytopenic Purpura-D69.3
NSAID/Aspirin treatment- Z79.3,Z79.891,Z79.899
10/01/2015 Removed ICD9 table. Embedded ICD9/ ICD10 PDF files.
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