Figure 1. Endoscopy showing: A, antral mucosa is friable, nodular, and has several erosions and small ulcers; B, 2-cm ulcer isseen on the angularis.Figure 2. Endoscopy after 4 days of intramuscular penicillin showing: A, antral mucosa has returned to a nearly normalappearance; B, ulcer on the angularis remains.

been based on radiological, pathological, or gastro­scopic descriptions. In spite of the fact that we wereunable to demonstrate spirochetes in our biopsy spec­imens, we believe that our patient had luetic gastritissince the commonly accepted criteria were all met.1

Whether this patient also had a peptic gastric ulcer inaddition to syphilitic gastritis is uncertain.

REFERENCES1. Bockus HL, ed. Gastroenterology, vol 1, 3rd ed. Philadelphia:

WB Saunders, 1974:1041-58.2. Cooley RN, Childers JH: Acquired syphilis of the stomach.

Gastroenterology 1960:39:201-7.3. Madding GF, Baer LS, Kennedy PA. Gastric syphilis. Ann Surg

1964;159:271-4.4. Mitchell RM, Bralow SP. Acute erosive gastritis due to early

syphilis. Ann Intern Med 1964;61:933-8.5. DeLuca RF, Morton R, Kafka EC, Raskin JB. Early luetic

gastritis presenting as an antral mass. Gastrointest Endosc

Duodenal ulcers associated with salsalatetherapy

Marcos A. Souza Lima, MD

Salsalate (salicylsalicylic acid) is a nonsteroidal,anti-inflammatory agent said to be safe for arthriticpatients with associated peptic ulcer disease becauseof its insolubility in gastric acid medium.1

-3 I report a

From the Gastroenterology Section, Department of Internal Medi­cine, Leesburg Regional Medical Center, Leesburg, Florida. Reprintrequests: Marcos A. Souza Lima, MD, 734 N. 3rd Street, Suite 205,Leesburg, Florida 32748.

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1975;2:95.6. Reisman TN, Leverett FL, Hudson JR, Kaiser MH. Spyphilitic

gastropathy. Am J Dig Dis 1975;20:588-93.7. Morin ME, Tan A. Diffuse enlargement of gastric folds as a

manifestation of secondary syphilis. Am J Gastroenterol1980;74:170-2.

8. Patterson CO, Rouse MO. Description of gastroscopic appear­ance of luetic gastric lesions in late acquired syphilis. Gastro­enterology 1948;10:474-85.

9. Reid AC, Behan PO. Suhacute Wernicke's encepholopathy dueto gastric syphilis. Br J Vener Dis 1981;57:309-11.

10. Vaughan WP, Straus FH, Paloyan D. Squamous carcinoma ofthe stomach after luetic linitis plastica. Gastroenterology1977;72:945-8.

11. Sachar DB, Klein RS, Swerdlow F, et al. Erosive syphiliticgastritis: dark field and immunofluorescent diagnosis from bi­opsy specimen. Ann Intern Med 1974;80:512-5.

12. Butz WC, Watts JC, Rosales-Quintana S, Hicklin MD. Erosivegastritis as a manifestation of secondary syphilis. Am J ClinPathol 1975;63:895-900.

13. Yobs AR, Brown L, Hunter EF. Fluorescent antibody techniquein early syphilis. Arch PathoI1964;77:134-9.

case of multiple small bowel ulcerations related tosalsalate therapy.

CASE REPORTA 47-year-old white woman was admitted to the hospital

with sudden onset of severe epigastric pain. She had beenstarted on salsalate, 750 mg twice a day, for osteoarthritis 2days earlier. Approximately 4 weeks prior to admission shehad documented duodenal bulb ulcer and was given raniti­dine, 150 mg twice daily. Because of severe heartburn, me­toclopramide, 10 mg four times a day, was also prescribed

GASTROINTESTINAL ENDOSCOPY

Figure 1. Ulcerations of the descending duodenum.

with good results. She denied nausea, vomiting, diarrhea,respiratory symptoms, and tinnitus. There was no intake ofother medications or alcohol. She denied previous salsalateexposure or drug allergies.

On examination she appeared moderately distressed. Vitalsigns were normal, but there was marked epigastric tender­ness. Rectal examination revealed guaiac-positive stools.Laboratory studies showed normal complete blood cell countand normal levels of serum glucose, electrolytes, creatinine,transaminases, and bilirubin. Fasting serum gastrin wasnormal at 61 pgjml (normal, <200 pgjml). Antinuclearantibody, rheumatoid factor, serum cryoglobulins, andVDRL were negative. On the second hospital day esopha­gogastroduodenoscopy revealed multiple, well demarcated,linear and oval ulcerations in a circumferential distributionon the folds of the second and third portions of the duo­denum, measuring from 5 to 10 mm in diameter, with smalladherent clots (Fig. 1). There was no evidence of obstruction.Biopsies of the small bowel lesions showed nonspecific in­flammatory infiltrates and ulcer base. Barium enema andflexible sigmoidoscopy were normal. Repeat duodenoscopy1 week later revealed normal duodenal mucosa.

The patient's epigastric pain gradually subsided aftersalsalate withdrawal, resolving within 4 days. Ranitidineand metoclopramide were continued throughout this periodof time.

DISCUSSION

Salsalate is virtually insoluble in gastric acid me­dium, which makes it attractive for patients with

VOLUME 32, NO.5, 1986

associated peptic ulcer disease. However, at the neu­tral pH of the small intestine, salsalate becomes freelysoluble and partly hydrolyzes to salicylic acid, theactive compound.3 Salicylic acid is so irritating in itsfree form that it can only be used externally. Deriva­tives must be synthesized for systemic use.4 The en­doscopic findings reported suggest a direct effect ofthe dissolving tablet on the small bowel in view of therapid resolution following discontinuation of the of­fending agent. Other causes for small bowel ulcerationsuch as enteric-coated potassium chloride tablets, gas­trinoma, and regional enteritis were excluded.5

•6 Dys­

pepsia, heartburn, or epigastric discomfort have beenreported in about 10% of patients receiving salsalate(unpublished data, Riker Laboratories). It is conceiv­able that on occasion these symptoms are harbingersof small bowel injury.

A causal relationship between salsalate and smallbowel ulceration was suggested by the establishedinjury pattern to the drug's active compound and therapid improvement following withdrawal of the drug.?The lack of symptom recurrence over a 6-month fol­low-up period further supports this contention. Thisreport of small bowel ulceration related to the newerforms of salicylates, which bypass the stomach, shouldalert physicians to look for this serious adverse eventin patients receiving these drugs.

ACKNOWLEDGMENTS

The author thanks Kenneth W. Thompson, MD,for referral of this case, and Mrs. Susan F. Souza Limafor secretarial help.

REFERENCES1. Voltin RF. NSAIDs from a G.!. point of view. Pract Gastroen­

terol 1984;8:33-4.2. Aberg G, Larsson KS. Pharmacological properties of some

antirheumatic salicylates. Acta Pharmacol Toxicol1970;28:249-57.

3. Singleton PT Jr. Salsalate: its role in the management ofrheumatic disease. Clin Therap 1980;3:80-102.

4. Flower RJ, Moncada S, Vane JR. Analgesic-antipyretics andanti-inflammatory agents: drugs employed in the treatment ofgout. In: Gilman AG, Goodman LS, Gilman A, eds. The phar­macological basis of therapeutics, 6th ed. New York: Macmillan,1980:682-728.

5. Grendell JH, Ockner RK. Vascular disease of the bowel. In:Sleisenger MG, Fordtran JS, eds. Gastrointestinal disease, 3rded. Philadelphia: WB Saunders, 1983:1543-68.

6. Spiro HM. Ulcerations of the small intestine. In: Spiro HM, ed.Clinical gastroenterology, 3rd ed. New York: Macmillan,1983:548-9.

7. Guideline for use of FDA 1639: drug experience report. Decem­ber 31, 1982. Food and Drug Administration, Rockville, Md.

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