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To the Editor:

Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized by involvement of rectum and colon. Extraintestinal manifestations are many, and they typically involve the joints, perianal tissues, kidney, liver, skin, and uveal tract.1–6 Oral manifestations, including aphthous stomatitis, are relatively common and have been well described. Nasal disease and septal involvement are, on the other hand, quite rare. Nasal findings, much like oral lesions, can precede the more typical gastroenterologic manifestations of UC.

We present a very interesting case report. The reported patient is the first case of nasal perforation reported in a UC patient in the literature.

A 17-year-old male patient, nonsmoker, nondrug user, was first referred to the hospital in 2009 with bloody diarrhea where he was evaluated and diagnosed as pancolitis UC. The patient recovered with a combination treatment of 5-aminosalicylate (5-ASA), steroid, and azathioprine; upon reoccurrence of symptoms like asthenia and bloody-mucous diarrhea following discontinuation of treatment, he was hospitalized in our clinic for further treatment.

Physical examination revealed conjunctival pallor, mild anemic appearance, and striae on scapula and on both arms due to iatrogenic-steroid use. Intranasal perforation was noticed because the patient spotted the nasal perforation. The patient was consulted by an otolaryngologist due to the nasal perforation. Nasal septal perforation was detected on examination and an image was made (Fig. 1) and biopsy was conducted on the nasal septal perforation site. On the biopsy there was partly dense inflammatory cell infiltration under the stratified squamous epithelium, covered with crust. This finding was interpreted as the nasal septal perforation might be secondary to IBD. The patient had a history of occasional arthralgia. No other extraintestinal complications were determined associated with UC.

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Figure 1. Nasal septal perforation. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

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Laboratory findings were as follows: fecal occult blood (+++) with abundant erythrocytes, leukocytes, and E. histolytica / E. dispar, total protein: 5.3 g/dL (normal: 6.4–8.3 g/dL), albumin 2.6 gr/dL, ferrous <6 μg/dL (normal: 50–150 μg/dL), WBC: 8.16 K/UL, (normal: 4.60–1020), Hgb: 7.88 g/dL (normal: 12.2–18.1), Hct: 24.7 (normal: 37.7–53.7), MCV: 66.8 fl (normal: 80.097.9), MCH: 21.3 pg (normal: 27.0–31.2), RDW: 24.8% (normal: 11.6–16.8), sedimentation 30 mm/s (normal: 8–15), CRP: 1.77 mg/dL (normal: 0–0.5), p-ANCA negative, anti-endomysium antibody and antigliadin antibody: negative, hepatitis markers, HIV negative, EMG and cranial magnetic resonance imaging (MRI) normal. GIS endoscopy showed Hp-positive chronic active gastritis with nonspecific duodenitis in duodenal biopsy and active UC in colonic biopsy.

UC is quite common in our region, although no case of nasal perforation was reported among UC patients up to this date. Our patient is the first nasal perforation case determined in a UC patient in our region. In the literature, nasal perforation was reported in a few Crohn's disease patients but no cases of nasal perforation exist associated with UC patients.

IBD is associated with a variety of extraintestinal manifestations (EIMs) that may produce greater morbidity than the underlying intestinal disease and may even be the initial presenting symptoms of the IBD.2, 6 As many as 36% of patients with IBD have at least one EIM. Some are more commonly related to active colitis (joint, skin, ocular, and oral manifestations). Others are especially seen with small bowel dysfunction (cholelithiasis, nephrolithiasis, and obstructive uropathy), and some are nonspecific disorders (osteoporosis, hepatobiliary disease, and amyloidosis). Development of nasal septal perforation may be due to various causes. Nasal trauma, nasal foreign bodies, a number of infections and chronic diseases, syphilis, Crohn's disease, rheumatoid arthritis, sarcoidosis, cocaine and industrial toxins, or nasal administration of drugs in powdered form may lead to nasal perforation. In the current case, no causal factor (trauma, drugs, chronic disease, etc.) was present to induce nasal septal perforation. The patient stated that he noticed the development of nasal septal perforation around 6 months prior to his referral, i.e., after the development of disease. Besides, findings of inflammation in tissue samples from the margin of nasal septal perforation indicate that nasal septal perforation observed in our UC case is a novel extraintestinal finding of the disease.

UC is common in our country and in our region but no other case of nasal septal perforation was reported in our patients with UC. The reported patient is the first case of nasal perforation reported in a UC patient in our region. In the literature, nasal perforation was reported in a few Crohn's disease patients but no cases of nasal perforation exist associated with UC patients.7 Hence, the case is intriguing in this regard. Therefore, nasal septal perforation should be investigated in patients with UC in the context of extraintestinal involvement and complications. Otolaryngologists should be aware of such an association and consider the diagnosis of UC in atypical cases of nasal disease.

REFERENCES

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Vedat Goral*, * Department of Gastroenterology Dicle University School of Medicine Diyarbakir, Turkey.