April 2002
CORRESPONDENCE 1191
consistent associationwas found between antibiotic use and indices of H. pylori in stool samples from 1- to 4-year-old infants.4 YLVA TINDBERG OLOF NYRI~N Department of Medical Epidemiology Karolinska Instituter Stockholm. Sweden MARTA GRANSTROM Department of Clinical Microbiology Karolinska Hospital Stockholm, Sweden
1, Rothenbacher D, Bode G, Adler G, Brenner H. Use of commonly prescribed antibiotics is not associated with prevalence of Helicobacter pylori infection in adults. Scand J Gastroenterol 1997;32: 1096 -1099. 2, Rothenbacher D, Inceoglu J, Bode G, Brenner H. Acquisition of Helicobacter pylori infection in a high risk population occurs within the first 2 years of life. J Pediatrics 2000;136:744-748. 3. Tindberg Y, Bengtsson C, Granath F, Blennow M, Nyr~n O, Granstr6m M. Determinants for Helicobacter pylori infection in Swedish school children: lack of evidence of child-to-child transmission outside the family. Gastroenterology 2001;121:310-316. 4, Rothenbacher D, Bode G, Adler G, Brenner H. History of antibiotic treatment and prevalence of H. pylori infection: results of a population-based study. J Clin Epidemiol 1998;51:267-271.
Correction Gochee PA, Powell LW, Cullen DJ, Du Sart D, Rossi E, and Olynyk JK. A population-based study of the biochemical and clinical expression of the H63D hemochromatosis mutation. Gastroenterology 2002;122:646-651. In reviewing Table 2 from the above article, the authors discovered that the second column heading was incorrect. The corrected Table 2 appears below: Table 2. Transferrin Saturation (TRS) and Serum Ferritin Levels (Ferritin) in Male and Female Subjects Who Were WildType for the C 2 8 2 Y Mutation Male
H63D/H63D
H63D/wild-type
Wild-type/wild-type
Female
TRS
Ferritin
TRS
Ferritin
35.1 4- 1.9 Range, 19-67 (n = 33) 31.5 4- 0.5 Range, 8-74 (n = 356) 28.4 _+ 0.3 b Range, 5-115 (n = 887)
226 4- 25 Range, 21-546 (n = 33) 235 4- 17 Range, 4-5234 (n = 356) 213 4- 7 Range, 8-5233 (n = 887)
29.6 + 1.6 a Range, 11-50 (n = 29) 26.7 4- 0.5 a Range, 5-60 (n = 355) 25.0 4- 0.3 a,b Range, 3-61 (n = 871)
134 4- 26 a Range, 9-492 (n = 29) 94 4- 4 a Range, 3-422 (n = 355) 96 4- 4 a Range, 1-2242 (n = 871)
NOTE. Subjects have been analyzed according to the presence of H63D mutations in the HFE gene.
ap < 0.01 vs. male group of same H63D genotype. bp < 0.01 VS. H63D/H63D and H63D/wild-type of same column.
Image of the Month Answer: Mande Cell Lymphoma Answer to the Image of the Month Question (page 853): The lesion is mantle celt lymphoma involving the terminal ileum. The diagnosis was confirmed by the pathologic specimen of small lymphocytes with irregular nuclei and confirmatory immunohistochemical staining. It presented as a protruding lesion causing traction on the adjacent mucosa, resulting in the appearance noted on barium study and at endoscopy. Watching the lesion in real time, it would repeatedly intussuscept distally and then retract proximally. The barbam study rewealed multiple polypoid lesions of the terminal ileum, a finding that is a common presentation of mantle cell lymphoma involving the gastrointestinal tra,:t. Mantel cell lymphoma is a subset of nodular histiocytic lymphoma that has unique clinical and molecular features. Multiple polypoid lesions in the jejunum and terminal ileum are characteristic. The majority of cases exhibit a balanced translocation between the BCL-1 gene and the immunoglobulin heavy chain gene, which results in cyclin D1 overexpression, and alteration in cell-regulatory gene function. This feature may provide a molecular target for future therapy. Secondary achalasia is a well-documented phenomenon and can be caused by Chagas' disease or a number of malignancies. Tumors that have been reported to produce achalasia include gastric cancer; lung cancer, mesothelioma, lymphoma, hepatocellular carcinoma, and renal cell carcinoma. The onset of achalasia may precede the diagnosis of cancer, with increased age, abrupt onset, and weight loss being possible clues to an underlying malignancy. The parhophysiology of malignancy-associated secondary achalasia may be due to direct invasion of tumor into the muscular and neuroenteric mechanisms of the lower esophageal sphincter (LES). Alternatively, circulating factors may result in a paraneoplastic achalasia syndrome. Treatments directed at both the primary tumor as well as the LES can result in improvement in esophageal symptoms. For submission instructions, please see the C*astroenterolog~t website (http://www.gastrojournal.org).