Diarrhea, PPI Use, and Pain in a Restaurant Worker From Mexico

Jaimy Villavicencio Kim, MD; John W. Birk, MD


November 18, 2022


Tropical sprue is a malabsorptive syndrome characterized by steatorrhea that is thought to be caused by a bacterial or viral infection of the small bowel.[1,2] It usually presents with symptoms, such as anorexia, weight loss, glossitis, cheilitis, anemia, and other nutritional deficiencies, which are not present in the patient in this case.[1,2] In addition, although this patient came from Mexico, it is unlikely for the disease to manifest itself 5 years later.

Celiac disease can present with abdominal pain and diarrhea.[3] However, in the absence of serology and any extraintestinal symptoms or signs, such as rash, iron-deficiency anemia, elevated aminotransferase levels, osteopenia/osteoporosis related to calcium or vitamin D deficiency, or skin or neurologic manifestations, it seems unlikely. Inflammatory bowel disease (ulcerative colitis or Crohn's disease) would probably have other signs or symptoms suggestive of an autoimmune inflammatory process, such as positive inflammatory markers in the blood and/or stool. Last, the patient's history, along with a normal CT of the abdomen, is not suggestive of chronic pancreatitis. Consequently, the most likely diagnosis is peptic ulcer disease from the most likely cause, Helicobacter pylori infection.

Dyspepsia is a term that is generally used to encompass variable symptoms associated with upper gastrointestinal tract distress or discomfort. It refers predominantly to epigastric pain, early satiety, postprandial fullness, and/or epigastric burning, in the absence of structural disease that would explain these symptoms.[4] In patients with dyspepsia who are aged 60 years or older, endoscopy is recommended to rule out gastric cancer. In patients who are younger than 60 years, noninvasive testing for H pylori is widely recommended as the first step.[4] If testing is positive, antibiotic therapy is initiated (test and treat strategy). If the results are negative, a trial of PPI therapy can be started. The major caveat here is that serology is not an appropriate test. In this clinical setting, stool or breath testing is required. In addition, if alarm symptoms are present, such as anemia, weight loss, dysphagia, or vomiting, upper endoscopy with biopsies may be warranted.[4]

H pylori was first described in 1983, in association with chronic gastritis.[5] It is a spiral-shaped, microaerophilic, flagellated, gram-negative bacterium that is commonly found in the stomach and duodenum.[6] This microorganism has very high urease activity. Urease hydrolyzes gastric luminal urea into basic ammonia and carbon dioxide, which neutralizes local gastric acid.[6] In addition, carbon dioxide is converted to bicarbonate by an enzyme called alpha-carbonic anhydrase, which further neutralizes gastric acid.[7] These mechanisms all help H pylori to subsist in the acidic environment of the stomach. Moreover, the spiral shape, flagella, and mucolytic enzymes of the bacterium facilitate adhesion and penetration into the gastric viscous mucus layer, where the more pH-neutral environment allows for better bacterial growth.[6] Unfortunately, owing to its activity, H pylori causes cellular injury and inflammation.


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