208 SECTION 3 • MEDICAL PROBLEMS IN THE ATHLETE
will be necessary to confirm GERD and assess for other
esophageal disorders.- More invasive treatments are available for patients with
an established diagnosis of GERD who respond poorly
to PPIs, who are intolerant of medical therapy, or who
desire a permanent solution to potentially eliminate
their need for medication. Laparoscopic antireflux sur-
gery has been shown to provide a 96% improvement in
primary symptoms and 96% long-term satisfaction
rate; however, 2% of patients were worse after surgery
and 14% still required medication (Bammer et al,
2001). Other endoscopic therapies, including suturing,
radiofrequency ablation, injection therapy, and bulking
therapy are currently being investigated.
PEPTIC ULCER DISEASE
- Epigastric pain is the hallmark of PUD. Both gastric
and duodenal ulcers typically present with deep burn-
ing or gnawing pain, sometimes with radiation to the
back. Duodenal ulcer symptoms usually develop 2 to
3 h after meals and are relieved with food or antacids.
Gastric ulcer symptoms develop sooner after meals
but are less consistently relieved with food or
antacids. Food ingestion can actually precipitate gas-
tric ulcer pain in some individuals. Most PUD
patients have associated anorexia and weight loss.
Some patients, particularly with duodenal ulcers,
experience hyperphagia and weight gain, presumably
because of the mitigating effects of food. Not uncom-
monly, the initial presentation of PUD can be life-
threatening upper GI hemorrhage or perforation
(Spechler, 2002). - Peptic ulcers are erosions in the surface of the stom-
ach or duodenum that extend down to the muscularis
mucosa. H. pylori induces ulcers by both direct and
indirect mechanisms. Bacterial phospholipases
weaken the protective mucus barrier, allowing the
toxic compounds created from its breakdown of urea
to directly damage the epithelium. The same urease
enzyme that promotes this direct cell damage acts as
a potent antigenic stimulator of immune cells. By
inciting an exuberant host inflammatory response, H.
pylori produces indirect epithelial damage as well
(Nilius and Malfertheiner, 1996). - NSAID inhibition of prostaglandins affects multiple
layers of the GI tract’s protective barrier. With
increasing concentration, they diminish mucosal
blood flow and penetrate the epithelial cells, eventu-
ally leading to mitochondrial oxidative uncoupling
and cell death (Lichtenstein, Syngal, and Wofe, 1995).
There are no studies directly relating NSAID use to
upper GI symptoms or bleeding specifically in ath-
letes. Nevertheless, the increased mucosal permeabil-
ity and decreased splanchnic blood flow that occurs
with prolonged exercise may magnify the effects of H.
pylori and the NSAIDs.- Athletes should be questioned regarding any relation-
ship of symptom onset with NSAID use. Laboratory
analysis should assess for occult GI bleeding and
anemia. If any alarm signs or symptoms are present,
an individual has new onset dyspepsia after the age of
45, or has a family history of gastric cancer, early gas-
troenterology referral is recommended. - If NSAID use is discovered, it should be discontinued
if possible. If analgesic therapy is crucial, replacing a
nonselective NSAID with acetaminophen or a COX-2
inhibitor would be prudent. Upper GI safety and toler-
ability studies have shown that COX-2 inhibitors have
a 46% lower rate of medication withdrawal for adverse
events, a 71% lower risk of ulcers on endoscopy, and a
39% lower incidence of symptoms because of ulcers,
perforations, bleeding, or obstruction compared to
nonselective NSAIDs (Deeks, Smith, and Bradley,
2002). - If symptoms are not predominantly GERD-related,
there are no markers for severe disease, and medica-
tion-induced disease is eliminated, consensus recom-
mendations support a “test and treat” approach in
adults under the age of 45 with persistent dyspepsia.
These patients should have a noninvasive test for H.
pylori infection. Urea breath analysis is the favored
test with the stool antigen assay as an alternative.
Those who are H. pylori negative, should receive
short term H2RA or PPI therapy (4–6 weeks). If they
fail empiric antisecretory therapy or symptoms recur
upon cessation of treatment, they should have
endoscopy. Symptomatic individuals who test positive
for H. pylori require eradication therapy. PPI or rani-
tidine bismuth citrate along with clarithromycin and
amoxicillin are to be used as first line therapy.
Metronidazole can be substituted for amoxicillin in
penicillin allergic patients. Subsequent second-line
therapy should be with a PPI, bismuth, tetracycline,
and metronidazole (Table 35-2). All patients should
be retested for evidence of a cure no sooner than
4 weeks after therapy. The athlete should be off any
antisecretory medication, especially PPIs, for a mini-
mum of 1 week prior to retesting. Urea breath analy-
sis is the posttreatment diagnostic test of choice. Stool
antigen testing can be used if urea breath testing is
unavailable. Individuals who fail second-line therapy
and those with persistent dyspepsia should be referred to
gastroenterology for further evaluation (Malfertheiner
et al, 2002).