Scientifically described 100 years ago, American trypanosomiasis (Chagas disease) is a neglected and often silent disease caused by Trypanosoma cruzi in rural areas, as well as in urban areas of Latin America, where 8–10 million people are infected1. At the chronic stage, 15–20% of infected people develop gastrointestinal disorders2, such as megavisceral gastrointestinal (GI) syndromes due to the degeneration of intramural ganglionic nerve cells and microvasculature3. In the stomach, Chagas disease can induce several motor and secretory disturbances, including hypochlorhydria, which is a well known facilitating factor for Helicobacter pylori infection4,5. H. pylori infection can cause chronic gastritis, peptic ulcer and gastric cancer. It is globally distributed, with a higher prevalence in developing countries, mostly due to poor living conditions and ingestion of contaminated water. As for T. cruzi, H. pylori infection is usually acquired in childhood, but clinical manifestations can appear years later. Currently, and mainly due to the increasing immigration flows from Latin America, Chagas disease is no longer limited to the Americas, and T. cruzi infection is being diagnosed in non-endemic areas, such as Europe and the United States.6
A series of 59 consecutive high-risk Latin American immigrants tested for Chagas disease in Barcelona showed that most presented with upper GI symptoms, mainly epigastric pain (20/59, 34%), atypical chest pain (12/59, 20%), abdominal bloating (11/59, 18.6%), heartburn (7/59, 12%) and dysphagia (5/59, 8.5%). Overall, 49 (83%) were positive for T.cruzi infection (two serological tests as recommended by international guidelines). In 12/49 (24%) of the T.cruzi infected patients, a chronic gastrointestinal form was diagnosed, radiological findings being dolichosigmoid (n=5), dolichocolon (n=3), megacolon (>6cm; n=4) and achalasia level I (n=3). Urea breath test was also positive in 55 cases (45/49 with Chagas disease and 10/10 without T. cruzi infection). H. pylori-positive cases received 7-day clarithromycin-based H. pylori eradication therapy7, with a therapeutic success rate of 81%. After treatment, upper GI tract symptoms completely resolved in 15 patients, all of them with Chagas disease (33%) cases and significantly improved in another 27 patients (23 with Chagas disease) (46%). Co-infection was reported in 45 patients. Clinical controls were regularly performed on 38 patients, and in 36 of them the symptoms improved or were completely resolved.
There are few studies about co-infection with T. cruzi and H. pylori. In Brazil, two short series described a high prevalence of H. pylori infection in individuals with chronic Chagas disease8,9. More recently, a larger series, also from Brazil, confirmed that H. pylori infection was more prevalent in Chagas than in non-Chagas infected individuals10. This association is probably due to common environmental risk factors, but it has been suggested that hypochlorhydria and/or other gastric dysfunctions caused by T. cruzi infection could facilitate H. pylori transmission10.
Irrespective of the mechanisms, our observation confirms the frequent coexistence of both pathogens. Since upper GI symptoms in either Chagas or H. pylori infected individuals are often non-specific, we suggest investigating and treating H. pylori infection in all symptomatic patients with Chagas disease. This is likely to result in an immediate clinical benefit (in our series symptoms improved in more than 70% of treated patients) and a clearer delineation of symptoms induced by T. cruzi infection. Currently, there are only two accepted drugs for antiparasitic treatment, benznidazole (LAFEPE, ex-Roche) and nifurtimox (Bayer), both with a poor side effect profile11 and with extremely variable results of effectiveness depending on the stage of the disease, the dose, the age and the geographic origin of the patient12. Overall, the efficacy of these drugs in chronic stages are 8–20%13.
Moreover, it is plausible that such a strategy could improve patient compliance with the available antiparasitic therapies for Chagas disease (benznidazole, nifurtimox), which is currently highly limited due to their poor GI side effects profile.
