Lung Carcinomas

AJG – July 1998

LETTERS TO THE EDITOR

3. Clark RA, Gallant TE. Acute mesenteric ischemia: Angiographic spectrum. AJR 1984;142:555– 62. 4. Ottinger LW. Mesenteric ischemia. N Engl J Med 1982;307:535–7. 5. Boley SJ, Sprayregen S, Siegelman SS, et al. Initial results from an aggressive roentgenological and surgical approach to acute mesenteric ischemia. Surgery 1977;82:848 –55. 6. Krzewicki J. Disturbances of blood flow in the large bowel during acute pancreatitis. Wiad Lek 1989;42:330 –3. Reprint requests and correspondence: Dr. Deep Narayan Srivastava, Associate Professor, F-97, Ansari Nagar (West), All India Institute of Medical Sciences, New Delhi, 110 029, India. Received Dec. 1, 1997; accepted Apr. 2, 1998.

Should We Still Look for Causes Other Than HP and NSAID for PUD? To the Editor: The association between peptic ulcer disease (PUD) and Helicobacter pylori (HP) has been well established (1). However, in our clinical experience at Our Lady of Mercy Medical center, Bronx, NY, several patients with PUD did not have evidence of HP infection. We reviewed all upper endoscopy reports of patients who underwent the procedure between October 1994 to July 1997. There were a total of 1640 upper endoscopies done during this period of which 251 patients had ulcer disease on endoscopy. A chart review of these 251 patients was done. The following patients were excluded from the ulcer population: 1) those who had insertion of percutaneous endoscopic gastrostomy (PEG) tube; 2) those who underwent a previous Billroth-II resection; and 3) those who were treated with H-2 blockers, proton pump inhibitors, or antibiotics for HP infection 8 wk before the endoscopy. Fifty-six patients met the exclusion criteria mentioned above. One or two biopsies were taken from the antrum using a regular sized forceps (2.3 mm cup size). Testing for HP was done either with rapid urease test (CLO), histopathology, or both. A history of nonsteroidal antiinflammatory drug (NSAID) use was obtained at the time of endoscopy. Of the 110 gastric ulcers, 63 (57%) were negative for HP and history of NSAID use. Similarly, of the 85 duodenal ulcers, 33 (39%) were negative for HP and NSAID use. Both CLO test and histopathology carry a high degree of sensitivity in detecting HP (2) but almost 20% could be missed. If we recalculate the prevalence of HP negative PUD correcting for the above (Table 1 and 2), then the HP negative gastric ulcer prevalence would decrease to 49% and HP negative duodenal ulcer to 25%. The corrected numbers do not agree with current literature on prevalence of HP disease in PUD. Our results show an unusually large percentage of PUD patients who are HP and NSAID negative. Three recent reports from other parts of the country have shown similar findings (3–5). Initially, these observations led to the concern that there is a lack of thoroughness on the part of the endoscopists in testing for HP. However, the CLO test is a simple, highly sensitive test that needs little technical expertise to perform. Moreover, the size and number TABLE 1 Gastric Ulcers* CLO Sensitivity

HP1

HP2NSAID2

100% 80%

37 (34%) 46 (42%)

63 (57%) 54 (49%)

* Eight patients had used NSAIDs, two patients were positive for HP and NSAIDs.

1187

TABLE 2 Duodenal Ulcers* CLO Sensitivity

HP1

HP2NSAID2

100% 80%

48 (56%) 60 (70%)

33 (39%) 21 (25%)

* Four patients had used NSAIDs.

of biopsies do not affect the overall sensitivity of the CLO test (6). Hence, a high percentage of PUD patients having HP negative disease cannot be attributed to ineffective testing. It is our belief that in some parts of the country, at least 50% of gastric ulcers and 25% of duodenal ulcers may have etiological factors other than HP or NSAID use. Our belief, albeit the view of a minority at this stage, needs to be addressed by others. A. Koshy, M.D. C.S. Pitchumoni, M.D. Division of Gastroenterology Our Lady of Mercy Medical Center Bronx, NY REFERENCES 1. Isenberg JI, Thompson JC. Medical progress and ulcer disease: Three key observations that changed the compass. Gastroenterology 1997;113: 1031–3. 2. Cutler AF, Havstad S, Ma CK, Blaser MJ, Perez-Perez GI, Schubert T. Accuracy of invasive and noninvasive tests to diagnose Helicobacter pylori infection. Gastroenterology 1995;109:136 – 41. 3. Maher W, Jyotheeswaran S, Potter G. An epidemiological study of peptic ulcer disease in greater Rochester, New York. Gastroenterology 1997;112:A206 (abstract). 4. Sprung DJ, Apter MN. Low prevalence of Helicobacter pylori in duodenal and gastric ulcers: Results of a prospective community study. Gastroenterology 1997;112;A298 (abstract). 5. IPRO. A quality improvement study. Helicobacter pylori: Diagnostic and treatment patterns in New York state Medicare patients hospitalised for peptic ulcer disease. Dec. 1996. 6. Laine L, Chun D, Stein C. The influence of size or number of biopsies on rapid urease test results: A prospective evaluation. Gastrointest Endosc 1996;43:49 –53. Reprint requests and correspondence: C.S. Pitchumoni, M.D., Division of Gastroenterology, Our Lady of Mercy Medical Center, Bronx, NY 10466. Received Oct. 10, 1997; accepted Apr. 1, 1998.

Acute Hepatitis A Virus Infection-Associated Hemophagocytic Syndrome To the Editor: We read with great interest the case report by Wu et al. (1) entitled “Acute hepatitis A with coexistent hepatitis C virus infection presenting as a virus-associated hemophagocytic syndrome.” We would like to present an additional case of virusassociated hemophagocytic syndrome (VAHS) caused by hepatitis A virus infection. A 40-yr-old man was admitted to our hospital with complaints of fever and anorexia. Physical examination showed slight jaundice and hepatomegaly. Laboratory examinations on admission revealed WBC 5800/ml, hemoglobin 15.9 g/dl, platelets 3.7 3 104/ml, normal coagulation, GOT 2250 IU/I, GPT 2000 IU/I, LDH 3482 IU/I, g-GTP 370 IU/I, total bilirubin 1.65 mg/dl, direct bilirubin 1.17 mg/dl, ferritin 4652 ng/ml. Atypical lymphocytes and giant platelets were seen in the peripheral blood smear. Be-