strong clinical significance for the cause and the mechanism of Crohn’s disease. More and more evidence has suggested that gut bacteria play a critical role in the development of inflammatory bowel disease, and Crohn’s disease seems to develop in the intestine largely as a re- sult of aberrant interaction of gut bacte- ria and their components with the host. If this is true, we would have to answer how Crohn’s disease with the same na- ture occurred in the mouth and esopha- gus, where the amount of bacteria is very limited. Lesions of the intestine can usually be found at the same time or eventually show up in patients with “Crohn’s disease of the esophagus or the mouth.” 5,6 It seems that lesions of the esophagus and mouth are more likely to be manifestations of intestinal Crohn’s disease rather to have originated locally. If this is the case, the lesions of the esophagus and mouth should probably be called oral or esophageal manifesta- tions (or complications) of Crohn’s dis- ease rather Crohn’s disease of the esoph- agus or the mouth, just like the uveitis in Crohn’s patients would be better called a manifestation of Crohn’s disease in the eye rather Crohn’s disease of the eye. Saying that Crohn’s disease can occur anywhere in the digestive tract seems to be a convenient but potentially mislead- ing statement. Xiaofa Qin, MD, PhD Department of Surgery UMDNJ–New Jersey Medical School Newark, New Jersey REFERENCES 1. Isaacs KL. Crohn’s disease of the esophagus. Curr Treat Options Gastroenterol. 2007;10: 61–70. 2. Remes-Troche JM, Martinez-Benitez B, Val- dovinos-Diaz MA. Crohn’s disease of the esophagus. Gastroenterology. 2006;130:1029, 1376. 3. Clayton R, Feiwel M. Crohn’s disease of the mouth. Proc R Soc Med. 1975;68:650 – 651. 4. Fedotin MS, Grimmett GM, Shelburne J. Crohn’s disease of the mouth. Am J Dig Dis. 1974;19:385–388. 5. Decker GA, Loftus EV Jr, Pasha TM, et al. Crohn’s disease of the esophagus: clinical fea- tures and outcomes. Inflamm Bowel Dis. 2001; 7:113–119. 6. Dupuy A, Cosnes J, Revuz J, et al. Oral Crohn disease: clinical characteristics and long-term follow-up of 9 cases. Arch Dermatol. 1999; 135:439 – 442. 7. Jose FA, Heyman MB. Extraintestinal manifes- tations of inflammatory bowel disease. J Pediatr Gastroenterol Nutr. 2008;46:124-133. Guttate Psoriasis Induced by Infliximab in a Child with Crohn’s Disease To the Editor: We read with great interest the article by Angelucci et al 1 regarding the association between new onset of psori- asis in a Crohn’s disease (CD) patient treated with tumor factor necrosis alpha antagonist. Recently, we observed this association in a child with moderate CD who developed guttate psoriasis during infliximab treatment. To the best of our knowledge, this is the first case reported in children. A 14-year-old girl without either personal or familial history of psoria- sis was diagnosed with CD in 2002. Despite having controlled CD with azathioprine (75 mg/day) and amin- osalicylic acid (1 g/day) for 3 years, she had had 3 relapses in the last 6 months. These relapses were treated with corticoids, and as a result she became corticoresistant. Intravenous infliximab (5 mg/kg) was instituted at 0, 2, and 6 weeks following by a main- tenance therapy with infusions every 6 or 8 weeks. Dramatic improvement in her intestinal disease was observed. After the fifth dose of infliximab, her trunk and the proximal part of her ex- tremities were covered in hundreds of small erythematous papules with typi- cal overlying silver scales. An evalu- ation by the dermatology department was requested, and ultimately a clini- cal diagnosis of guttate psoriasis was made. No skin biopsy was performed. Topical treatment with coal tar and prednicarbate was initiated, with the subsequent disappearance of the le- sions in 3 weeks. The discontinuity of infliximab was not necessary. No new lesions developed with the subsequent infusions of infliximab. Neither clini- cal nor serological infections were found. Infliximab is a chimerical IgG1 monoclonal antibody against tumor ne- crosis factor–alpha (TNF-) used for the treatment of different diseases associ- ated with the Th 1 lymphocyte profile such as rheumatoid arthritis, spondylar- thropathies, or psoriasis. 2 A multicenter study of infliximab in pediatric patients with moderate or severe CD carried out in 2006 concluded that infliximab is an effective treatment of moderately to se- vere active CD in children, with a high rate of remission and response. 3 Various adverse cutaneous reac- tions have been reported during anti- TNF- treatment like acute folliculitis, erythema multiforme, hyperhidrosis, ur- ticaria, cutaneous lymphoma, or lupus- like syndrome, with an incidence around 10%. 4,5 New-onset psoriasis has been recently described in adult patients treated with anti TNF- drugs 1,2,4,5 but to the best of our knowledge, not in children. As in the case of our patient, pro- gressive psoriasis lesions usually de- velop a few weeks or months after the onset of infliximab therapy. 2,4 In most of the situations, there is neither personal nor a familial history of psoriasis. The most frequent forms of psoriasis in- duced by infliximab are plaque psoriasis and pustular pattern, 4 but other lesions like palmoplantar guttate psoriasis and change of previous psoriasis morphol- ogy and localization have also been re- ported. 2,6 In most cases, the lesions are self-limited and subsided well with top- ical treatment, 4,6 but in a few patients, discontinuing infliximab is necessary. 6 Recurrence of the eruption is observed after infliximab has been reinstituted or Copyright © 2008 Crohn’s & Colitis Foundation of America, Inc. DOI 10.1002/ibd.20450 Published online 26 March 2008 in Wiley Inter- Science (www.interscience.wiley.com). Costa-Romero et al Inflamm Bowel Dis ● Volume 14, Number 10, October 2008 1462