Asetil salisilik asit kullanımına bağlı oluşan ileoçekal valv ülserleri ve deformasyonu sonucunda gelişen çekumda çift lümen görünümü

Abstract

The use of non-steroidal anti-inflammatory drugs, especially aspirin, has continued to increase with aging and related cardiovascular diseases. Since their well-known side effect is gastroduodenal mucosal injury, aspirin-induced intestinal damage has also become a growing problem. Herein, we present a case with an advanced anatomical impairment of the ileocecal valve deformation, presumably caused by enteric-coated acetyl salicylic acid induced recurrent ulcers.Keywords: Colonoscopy, intestinal ulcers, enteric-coated acetyl salicylic acid Günümüzde; non steroidal anti-inflamatuvar ilaçlar›n, özellikle aspirinin kullan›m› yafllanma ve yafllanmayla iliflkili kardiyovasküler hastal›klar›n s›kl›¤›n-daki art›flla birlikte giderek artmaktad›r. Aspirinin; gastroduodenal mukozal hasar yap›c› etkisi gibi en iyi bilinen yan etkisinin yan›nda yine aspirin nedeniyle oluflan intestinal hasar da daha s›k karfl›m›za ç›kmaktad›r. Burada muhtemelen enterik-kapl› asetil salisilik asit kullan›m› nedeniyle oluflan rekürran ülserlere ba¤l› geliflen ileoçekal valv deformasyonlu olguyu sunuyoruz.Anahtar kelimeler: Kolonoskopi, intestinal ülserler, enterik-kapl› asetil salisilik asit INTRODUCTIONThe prevalence of non-steroidal anti-inflammatory drugs (NSAIDs) (including aspirin)-induced intestinal injury is higher than had been expected (1). The appearance of NSAIDinduced intestinal injury varies, appearing variously as diaphragm-like strictures, ulcers, erosions, and mucosal redness (2-5). Herein, we present a case with an advanced anatomical impairment of the ileocecal valve deformation, presumably caused by enteric-coated acetyl salicylic acid (EC-ASA)-induced recurrent ulcers. CASE REPORTA 68-year-old male was admitted to the hospital with the complaints of weakness and dyspnea. He had a history of myocardial infarction 12 years ago, and he had been followed until the admission for congestive heart failure. He was still using medications intended for this disease, including 300 mg/day EC-ASA. He did not have any gastrointestinal complaints. On the laboratory examination, deep anemia was determined (hemoglobin: 6.8 g/dl, hematocrit level: 20%, and ferritin level: 2.4 ng/ml). Additionally, occult blood test in the stool examination was found to be positive. Subsequently, upper gastrointestinal endoscopy (revealing pangastritis) and colonoscopy were performed. During colonoscopy, double lumen appearance of the proximal side of the colon was determined ( Figure 1). During the procedure, it was realized that one of the lumens was the base of the cecum (larger arrow #1), and the other was the ileum (larger arrow #2). Both on the mucosa of the terminal ileum and the anatomically disrupted ileocecal valve, multiple ulcers were present (small arrows in Figure 1 and Figure 2). Biopsy specimens taken from the edges of the ulcers were reported as non-specific inflammatory findings. The valve deformation on the cecum resulted in pseudodiverticulum formation (larger arrow #3). Furthermore, two polyps on the cecum determined during colonoscopy we...