Ağustos 2011

65-67

Erkin ÖZTAŞ, Meral AKDOĞAN, Diğdem ÖZER ETİK, İsmail Hakkı KALKAN, Abdurrahim SAYILIR, Sedef KURAN, Burçak KAYHAN

Department of Gastroenterology, Yüksek İhtisas Education and Research Hospital, Ankara

Günümüzde; non steroidal anti-inflamatuvar ilaçların, özellikle aspirinin kullanımı yaşlanma ve yaşlanmayla ilişkili kardiyovasküler hastalıkların sıklığındaki artışla birlikte giderek artmaktadır. Aspirinin; gastroduodenal mukozal hasar yapıcı etkisi gibi en iyi bilinen yan etkisinin yanında yine aspirin nedeniyle oluşan intestinal hasar da daha sık karşımıza çıkmaktadır. Burada muhtemelen enterik-kaplı asetil salisilik asit kullanımı nedeniyle oluşan rekürran ülserlere bağlı gelişen ileoçekal valv deformasyonlu olguyu sunuyoruz.

Kolonoskopi, intestinal ülserler, enterik-kaplı asetil sali silik asit

The 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.

Prostaglandins (PGs) are involved in the regulation of gastrointestinal blood flow and various mucosal functions such as increasing mucus secretion. The decrease in PG production is considered to be the main cause of small bowel injuries due to NSAIDs (6-10). First, NSAIDs solubilize lipids of phospholipids on the mucosal surface, so the epithelial mitochondria are directly damaged. Second, the mitochondrial damage depletes intercellular energy and leads to calcium efflux and induction of free radicals, a disruption of intercellular junctions occurs, and mucosal permeability increases in the small intestinal mucosa. Finally, the mucosal barrier becomes weakened, so bile acid, proteolytic enzymes, intestinal bacteria, or toxins can easily penetrate into the epithelial cells, resulting in mucosal injury (9). EC-ASA has been developed to prevent gastric damage and dissolves in the proximal small intestine, which might allow aspirin to have contact with the intestinal mucosa at a high concentration. Enteric-coated aspirin might injure the small bowel through a topical irritant effect as well as via the inhibitory effect on cyclooxygenase (COX) activity (1).

In our patient, existing congestive heart failure could have aggravated the intestinal toxic effects of EC-ASA due to circulatory disorder. On the other hand, we could not determine any other pathologies causing intestinal ulcers (e.g., Crohn disease, tuberculosis) in spite of detailed immunological, histological and serological evaluation.

Figure 2. Ulcers on the ileocecal valve.

The basic treatment for NSAID-induced injury is discontinuation of the NSAIDs (1). However, even if temporary cessation of the NSAIDs is possible, long-term cessation of NSAIDs is frequently impossible, and long-term administration of prophylactic drugs is needed for chronic users of NSAIDs or aspirin, especially patients who experience small intestinal bleeding. Some trials have shown the efficacy of metronidazole, sulfasalazine and misoprostol for treatment of NSAIDinduced injury (11-13). Clinically, proton pump inhibitors (PPIs) and PG analogs are the first-choice drugs for the prevention of NSAID-induced peptic ulcers and bleeding (14). It is useful to use such drugs to prevent the adverse effects of NSAIDs not only in the stomach but also the small intestine.

In conclusion, to the best of our knowledge, this is the first case of an advanced anatomical impairment of the ileocecal valve deformation presumably occurring due to EC-ASA-induced recurrent ulcers. Thus, routine endoscopic evaluation of the gastrointestinal tract may be beneficial in determining EC-ASA-induced intestinal injury as well as in preventing the associated serious complications, especially in geriatric patients with a history of long-term EC-ASA use.

Acknowledgements: This paper does not present any conflicts of interest.

Prostaglandins (PGs) are involved in the regulation of gastrointestinal blood flow and various mucosal functions such as increasing mucus secretion. The decrease in PG production is considered to be the main cause of small bowel injuries due to NSAIDs (6-10). First, NSAIDs solubilize lipids of phospholipids on the mucosal surface, so the epithelial mitochondria are directly damaged. Second, the mitochondrial damage depletes intercellular energy and leads to calcium efflux and induction of free radicals, a disruption of intercellular junctions occurs, and mucosal permeability increases in the small intestinal mucosa. Finally, the mucosal barrier becomes weakened, so bile acid, proteolytic enzymes, intestinal bacteria, or toxins can easily penetrate into the epithelial cells, resulting in mucosal injury (9). EC-ASA has been developed to prevent gastric damage and dissolves in the proximal small intestine, which might allow aspirin to have contact with the intestinal mucosa at a high concentration. Enteric-coated aspirin might injure the small bowel through a topical irritant effect as well as via the inhibitory effect on cyclooxygenase (COX) activity (1).

In our patient, existing congestive heart failure could have aggravated the intestinal toxic effects of EC-ASA due to circulatory disorder. On the other hand, we could not determine any other pathologies causing intestinal ulcers (e.g., Crohn disease, tuberculosis) in spite of detailed immunological, histological and serological evaluation.

Figure 2. Ulcers on the ileocecal valve.

The basic treatment for NSAID-induced injury is discontinuation of the NSAIDs (1). However, even if temporary cessation of the NSAIDs is possible, long-term cessation of NSAIDs is frequently impossible, and long-term administration of prophylactic drugs is needed for chronic users of NSAIDs or aspirin, especially patients who experience small intestinal bleeding. Some trials have shown the efficacy of metronidazole, sulfasalazine and misoprostol for treatment of NSAIDinduced injury (11-13). Clinically, proton pump inhibitors (PPIs) and PG analogs are the first-choice drugs for the prevention of NSAID-induced peptic ulcers and bleeding (14). It is useful to use such drugs to prevent the adverse effects of NSAIDs not only in the stomach but also the small intestine.

In conclusion, to the best of our knowledge, this is the first case of an advanced anatomical impairment of the ileocecal valve deformation presumably occurring due to EC-ASA-induced recurrent ulcers. Thus, routine endoscopic evaluation of the gastrointestinal tract may be beneficial in determining EC-ASA-induced intestinal injury as well as in preventing the associated serious complications, especially in geriatric patients with a history of long-term EC-ASA use.

Acknowledgements: This paper does not present any conflicts of interest.

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