E-case #13C

Eric Liu, M.D.

June 1014, 2002

Patient is a 52 y.o. male, who presents with a several month history of epigastric burning, odynophagia, and occasional dysphagia.  His symptoms are typically postprandial.  He has rare nausea, but no vomiting, melena, hematochezia or hemetemesis.  He has no history of regurgitation of foods, cough or shortness of breath.  His symptoms are helped minimally by antacids. His past medical history is unremarkable.  He is an occasional drinker, smokes 1 PPD for twenty years, and has coffee throughout his workday.  He has been using NSAIDS for knee tendonitis intermittently the past year.

1. What is the differential diagnosis, and what are the most likely etiologies?

2. What diagnostic tests and therapeutic interventions are indicated?

3. What are the complications of this diagnosis?

His symptom complex is most consistent with dyspepsia and gastroesophageal reflux.  Other possibilities in the workup would include malignancy of the esophagus or proximal gastric carcinoma.  An immunecompromised patient may have fungal or viral causes of esophagitis. Other esophageal abnormalities such trachealesophageal fistula can cause aspiration pneumonia in addition to esophageal symptoms.  Esophageal diverticuli can cause regurgitation of partially digested foods. Achalasia can present with predominately dysphagia, more than reflux.  Atypical presentations of cholelithiasis can present without classic RUQ symptoms.  Pancreatitis can mimic peptic ulcer disease, but is less likely with esophageal complaints.  Acute myocardial ischemia can present nausea and epigastic symptoms as its anginal equivalent.

Most diagnostic algorithims would recommend a diagnostic EGD to document evidence of esophagitis, erosive esophagitis, esophageal ulcer, gastritis or gastric ulcer prior to therapy in patients over the age of 50 (primarily to exclude malignant etiologies).  Patients under 50 may undergo empiric treatment, with endoscope if there is no clinical improvement.  Random biopsies of the mucosa help exclude infection, Barrett's esophagus, malignancy and H. Pylori.  Strictures from chronic inflammation can be dilated for those with significant dysphagia.  Serial hematocrits are useful to monitor for occult blood loss.

1. What is the relative efficacy of H2 antagonists versus proton pump inhibitors (PPI)?

• H2 antagonists have a 60 percent improvement rate in symptomatology and a forty percent efficacy rate in healing esophagitis.

• PPIs have an 8090 percent rate of symptomatic improvement and a similar rate in esophagitis healing

• controversial approaches of a stepapproach (cost effective) versus PPI as first line in uncomplicated GERD (omeprazole becoming generic in near future)

• twenty percent of severe GERD need BID or rarely TID dosing

• PPI first line for healing of erosions/ulcers

• study by Pefghini demonstrates superior nocturnal control of acid secretion by H2 antagonists over PPI by measuring gastric pH in normal subjects (small study/no trials in GERD population) (1)

• evidence for reactive hyperacid secretion after stopping PPI and some advocate weaning to H2 antagonists

2. What is the role of routine endoscopic surveillance of patients with severe GERD for Barrett's esophagus and adenocarcinoma?

• rapid rise of adenocarcinoma of esophagus and GE junction cancer  (24

•  fold)

• Barrett's esophagus is the major risk factor

• two epidemiology studies addressed risk

  • Barrett's seen in 4 - 10 percent of patients with chronic GE reflux

  • risk of adenocarcinoma in Barrett's is 0.5 0.8%/year or 1:150 patient years  (2)

  • overall risk for adenocarcinoma is extremely low and routine surveillance is not indicated for GERD(1:1400 patients per year with adenocarcinoma (3)

  • some groups advocate screening in patients with greater than 10 years of GERD or age>50 and chronic heartburn)

  • patients with documented Barrett's esophagus need screening EGD every 2 - 3 years

3. What is the role of eradication of H. Pylori and nonulcer dyspepsia?

• nonulcer dyspepsia (NUD)is defined as having a negative EGD and symptoms of dyspepsia

• treatment of H. Pylori in NUD results in a 7 - 14% symptomatic improvement of  dyspepsia (4 and 5)

• etiology of NUD is largely functional(dysmotility/increased visceral sensation/psychosocial)

• no proven effective therapy (6)

  • placebo effect 20 - 40 percent

  • H2 antagonist 20 - 24 percent improvement

  • promotility agent 36 - 46 percent improvemen

References

1. Pefghini et al; Gastroenterology 1998;115:1335

2. Lagergren J,et al; NEJM 1999;340:825

3. McColl K et al; NEJM 1998;339:1869

4. Blum A et al; NEJM 1998;339:1875