Peptic ulcer disease (PUD) is an ulceration in the stomach or duodenum that is caused by an imbalance between protective factors of the natural stomach lining and damaging mechanisms that predispose ulceration.
Causes of Peptic Ulcer Disease
Most duodenal ulcers (over 90%) occur in the first portion of the duodenum and gastric ulcers most commonly occur on the lesser gastric curvature near the incisura angularis. Duodenal ulcers are more common than gastric ulcer, occurring 4 times as frequent.
Oftentimes the cause of PUD is multifold. The most common etiology of the damaging mechanisms is Helicobacter pylori infection, which is found in 70% of patients with PUD.
The most common etiology that decreases natural protective factors of the gastric lining is medications such as NSAIDs. These reduce the body’s natural production of prostaglandins.
The leads to an increase in gastric acid secretion, decreased bicarbonate/gastric mucus production, and an overall decreased blood flow to the gastric mucosa. These changes foster the environment for the formation of an ulcer.
Other medications that increase the risk of peptic ulcer formation include aspirin, clopidogrel, and COX-2 inhibitors. Drug interactions between NSAIDs and long term steroids, anticoagulants, SSRIs, and bisphosphonates dramatically increase the risk of ulcer formation as well.
Lower resting tone of the esophageal sphincter, increase bile acid formation, impaired proximal duodenal bicarbonate secretion, cigarette smoking, alcohol abuse, and Zollinger Ellison syndrome have all been linked to increase risk of PUD.
Peptic Ulcer Disease Presentation
Uncomplicated peptic ulcer disease will present with no symptoms around 40% of the time, which is considered a “silent ulcer”.
If symptoms are present they may include epigastric pain, pain that may radiate to the back, thorax, or other parts of the abdomen, in addition to nausea, vomiting, or heartburn.
Textbooks and review courses oftentimes will try to differentiate duodenal versus gastric ulcers on presentation by asking if eating foods aggravates or relieves pain. It is thought that if a person has a gastric ulcer eating food will worsen their symptoms, whereas with a duodenal ulcer, it is thought that food will lessen their pain.
However, this is an unreliable way to diagnose if someone has a gastric versus duodenal ulcer, and I have seen the symptoms flip-flopped in cases of PUD when I was in school, as well as in practice.
Other symptoms may include hematemesis (bright red blood in vomitus), coffee ground emesis, melena (dark-tarry, foul smelling stool), or hematochezia.
How to Workup Peptic Ulcer Disease
Workup includes routine laboratory tests such as a CBC, CMP, PT/INR, and PTT. Anemia may be noted in persons with a significant GI bleed associated with the ulcer or rupture.
At this point, in an outpatient clinic, if I thought the patient had a stable, uncomplicated ulcer, I would refer patient to general surgery or GI for further evaluation and endoscopy.
If any concerning signs such as unstable vital signs, orthostatic hypotension, signs of increased blood loss, abnormal initial lab results (complicated PUD), I would send patient to the emergency room for an urgent endoscopy.
During endoscopy, not only are biopsies done to confirm the potential diagnosis, but if a bleeding ulcer is found thermal coagulation, injection of epinephrine, hemoclips, fibrin sealants, or argon plasma coagulation can be performed.
If hemostasis cannot be obtained with the aforementioned options arteriography with embolization can be performed.
In addition, upper GI barium studies identify approximately 70% to 80% of PUD. This can further be more accurate, approximately 90%, by using double contrast.
As mentioned above, the most common etiology of peptic ulcer disease is a H. pylori infection. This can be determined by endoscopic biopsy during an EGD, stool antigen testing, serum antibody testing, or urea breath test.
Serologic testing for antibodies does not differentiate between past or current H. pylori infection. This means that a positive result might not be a current infection if the patient has had H. pylori infections in the past.
If this is the case you are limited to EGD with biopsy, urea breath testing, or stool antigen for confirmation of infection.
If your patient does have active H. pylori infection contributing to their PUD, therapy must be done to eradicate this infection.
Treating Peptic Ulcer Disease
Current recommendations on first line therapy for H. pylori infection includes the bismuth quadruple therapy. This regimen includes the following medications for 14 days duration:
1) Bismuth subsalicylate, 262 mg, two tablets, four times daily
2) Proton pump inhibitor therapy with:
-Omeprazole, 20 mg, twice daily or,
-Pantoprazole, 40 mg, twice daily or,
-Rabeprazole, 20 mg, twice daily or,
-Lansoprazole, 30 mg, twice daily or,
-Esomeprazole, 20 mg, twice daily
3) Metronidazole, 500 mg, three to four times daily
4) Tetracycline, 500 mg, four times daily
An alternative primary treatment includes the non-bismuth quadruple therapy which replaces the bismuth subsalicylate with amoxicillin, 1000 mg, BID, and Tetracycline, 500 mg, four times daily with Clarithromycin, 500 mg twice daily.
A third primary treatment is the Clarithromycin-based Triple Therapy. This includes a PPI twice daily, Clarithromycin, 500 mg, twice daily, and Amoxicillin, 1000 mg, twice daily, all for 14 days. If a patient has a penicillin allergy, amoxicillin can be replaced with Metronidazole, 500 mg, three times daily.
However, the Sanford Guide to Antimicrobial Therapy and CDC Antibiotic Guidelines only recommend the Bismuth and Non-Bismuth containing regimens as first line therapies. This is due to the Clarithromycin Triple Therapy having a <80% eradication rate in the U.S.
When choosing the initial antimicrobial regimen, you should always take into consideration the presence of risk factors for macrolide resistance and if there is a penicillin allergy.