Talicia contains omeprazole, a proton pump inhibitor (PPI), amoxicillin, a penicillin-class antibacterial, and rifabutin, a rifamycin antibacterial. It is contraindicated in patients with known hypersensitivity to any of these medications, any other components of the formulation, any other beta-lactams or any other rifamycins.

Talicia is contraindicated in patients receiving delavirdine, voriconazole or rilpivirine-containing products.

Serious and occasionally fatal hypersensitivity reactions have been reported with omeprazole, amoxicillin and rifabutin.

Acute Tubulointerstitial Nephritis has been observed in patients taking PPIs and penicillins.

Clostridioides difficile-associated diarrhea has been reported with use of nearly all antibacterial agents and may range from mild diarrhea to fatal colitis.

Talicia may cause fetal harm and is not recommended for use in pregnancy. It may also reduce the efficacy of hormonal contraceptives. An additional non-hormonal method of contraception is recommended when taking Talicia.

Talicia should not be used in patients with hepatic impairment or severe renal impairment.

Cutaneous lupus erythematosus and systemic lupus erythematosus have been reported in patients taking PPIs. These events have occurred as both new onset and exacerbation of existing autoimmune disease.

The most common adverse reactions (≥1%) were diarrhea, headache, nausea, abdominal pain, chromaturia, rash, dyspepsia, oropharyngeal pain, vomiting, and vulvovaginal candidiasis.

The Challenge of H. pylori:
The risk of gastric cancer
in the face of increasing resistance
to traditional antibiotics

H. pylori poses a public health threat and can lead to gastric cancer

The Challenge of H. pylori: The risk of gastric cancer in the face of increasing resistance to traditional antibiotics

H. pylori poses a public health threat and can lead to gastric cancer

The Challenge of H. pylori: The risk of gastric cancer in the face of increasing resistance to traditional antibiotics

H. pylori poses a public health threat and can lead to gastric cancer

H. pylori is a Group 1

H. pylori infection has been shown to be the #1 risk factor for the development of gastric cancer.2 If not eradicated, H. pylori infection can cause chronic progressive gastric inflammation which can lead to3
– Atrophic gastritis
– Gastric and duodenal ulcers
– Gastric cancer
In fact, approximately 90% of noncardia gastric cancers are H. pylori-related.4

*A Group 1 carcinogen is one that there is enough evidence to conclude that it can definitely cause cancer in humans according to the International Agency for Research on Cancer (IARC).

The risk of gastric cancer
associated with H. pylori is real.

A recently published analysis done by the University of Pennsylvania of over 370,000 health records from the Veterans Administration database showed that eradication of H. pylori from patients with confirmed infection resulted in a 75% reduction in the risk of developing gastric cancer.5 Statistics from the National Cancer Institute (NCI) show that 27,500 Americans will be diagnosed with and 11,000 will die from gastric cancer in 2019 alone. Further data shows that 1 in 111 Americans will be diagnosed with gastric cancer in their lifetime.2

H. pylori resistance
to clarithromycin is
of great concern.

Due to increasing antibiotic resistance and long-term health consequences, H. pylori is categorized as a public health threat by the FDA.6

H. pylori resistance to clarithromycin has been increasing.

In a studied population of patients in a VA facility with confirmed H. pylori infection, clarithromycin resistance more than doubled from 9.1% in 2009-2010 to 24.2% in 2011-2013.7
In another U.S. multicenter analysis conducted in 2016, greater than 30% of H. pylori strains were found to be resistant to clarithromycin.8

Therapeutic effectiveness of clarithromycin-based triple therapy has been declining.

One study looked at the decline and reported eradication of H. pylori with clarithromycin-based triple therapy dropped from 90% in 1996 to 72% in 2004.7
In fact, multiple studies over time have demonstrated the efficacy of traditional therapies range from 60% to 75% when testing for confirmation of eradication is performed.9-11

Extensive macrolide use and cross resistance are to blame

The problem of H. pylori resistant to clarithromycin has been driven by widespread macrolide use and the tendency for development of cross-resistance within the macrolide class, which has led to declining efficacy rates with clarithromycin-based triple therapy.12

In addition to clarithromycin, other antibiotics in the macrolide class like azithromycin and erythromycin are commonly prescribed for a wide range of conditions. In fact, an analysis published in the New England Journal of Medicine in 2019 found that an estimated 100 million Americans filled a prescription for a macrolide antibiotic in the last 4 years.13

Consistent with prior studies that looked at the ability of clarithromycin-based triple therapy to eradicate H. pylori infection, it should be noted that a U.S. multicenter study conducted in 2017 demonstrated traditional therapies achieved only 63% eradication of H. pylori. In that study, 80% of the traditional therapies used were clarithromycin-based triple therapy. 14

Did you know the American College of Gastroenterology
(ACG) changed its recommendations on
clarithromycin-containing regimens in 2017?

Did you know the American College of Gastroenterology (ACG) changed its recommendations on clarithromycin-containing regimens in 2017?

Use of clarithromycin-containing regimens is not recommended in many cases

Due to long-term health risks of H. pylori and decreasing efficacy of current therapies, the ACG 2017 guideline for H. pylori recommends against using clarithromycin-containing regimens in: patients with any previous macrolide exposure OR in areas where clarithromycin resistance exceeds 15% OR in areas where clarithromycin resistance is unknown.15

In fact, in a 2018 U.S. multicenter study conducted at 55 sites across 20 states, in vitro testing found that of 345 H. pylori isolates taken from patients, 17.4% were resistant to clarithromycin – a resistance rate which already exceeds the 15% threshold in ACG guideline recommendations for clarithromycin use in H. pylori.15,16

Because symptom relief does not correlate with eradication, the ACG 2017 guideline for H. pylori also recommends a “test-treat-confirm” approach.14

Whenever H. pylori infection is identified and treated, testing by urea breath test, fecal antigen test, or biopsy-based testing to prove eradication of H. pylori should be performed. This testing should be performed 4 weeks after the completion of antibiotic therapy and after PPI therapy has been withheld for 2 weeks.

It is important to note that the ACG guidelines generally recommend against using serology for H. pylori testing as it can remain positive even after successful eradication and thus is an inadequate test for active infection.15



  1. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Schistosomes, liver flukes and Helicobacter pylori. Lyon, June 7-14, 1994.
  2. National Cancer Institute: Surveillance, Epidemiology, and End Results Program. Cancer stat facts: stomach cancer. https://seer.cancer.gov/statfacts/html/stomach.html. Accessed February 4, 2020.
  3. Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection-the Maastricht V/Florence Consensus Report. Gut. 2017;66(1):6-30.
  4. Moss S. The clinical evidence linking Helicobacter pylori to gastric cancer. Cell Mol Gastroenterol Hepatol. 2017;3(2):183-191.
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  6. U.S. Food & Drug Administration. CFR–Code of Federal Regulations Title 21. Section 21CFR317.2.
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  8. Park JY, Dunbar KB, Mitui M, et al. Helicobacter pylori clarithromycin resistance and treatment failure are common in the USA. Dig Dis Sci. 2016;61:2373-2380.
  9. Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection–the Maastricht IV/Florence Consensus Report. Gut. 2012;61(5):646-664. Doi:10.1136/gutjnl-2012-302084.
  10. O’Connor A, Gisbert J, O’Morain C, et al. Treatment of Helicobacter pylori infection. Helicobacter. 2015;20(S1):54-61.
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  12. Boltin D, Levi Z, Gingold-Belfer R, et al. Impact of previous exposure to macrolide antibiotics on Helicobacter pylori infection treatment outcomes. Am J Gastroenterol. 2019;114:900-906.
  13. Olesen SW, MacFadden D, Grad YH. Cumulative probability of receiving an antibiotic prescription over time. N Engl J Med. 2019;380(19):1872-1873.
  14. Kalfus IN, Raday G, Graham DY. Randomized placebo controlled Phase III study to assess the safety and efficacy of rifabutin triple therapy (RHB 105) for Helicobacter pylori infection in dyspepsia patients. Gastroenterology. 2017;152(5):S250. doi:10.1016/s0016-5085(17)31130-7.
  15. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG Clinical Guideline: Treatment of Helicobacter pylori infection. Am J Gastroenterol. 2017;112(2):212-239.
  16. Graham DY, Canaan Y, Maher J, Wiener G, Hulten KG, Kalfus IN. Rifabutin-based triple therapy (RHB-105) for Helicobacter pylori eradication: a double-blind, randomized, controlled trial. Ann Intern Med. 2020;172(12):795-802.