LAUSR

Due to their anti-inflammatory and analgesic effects, nonsteroidal anti-inflammatory drugs (NSAIDs) are largely used in clinical practice even if they could be associated with severe gastrointestinal adverse effects, such as peptic ulcer disease, bleeding and perforation, especially in elderly patients [1]. Endoscopy remains the gold standard method for studying upper and lower gastrointestinal tracts, whereas video capsule endoscopy and double-balloon enteroscopy are used for studying the small bowel even if all these examinations are burdened by potential complications. Instead, ultrasound is a non-invasive and widely available method that does not require the use of ionizing radiations. For a complete examination of the bowel, mid-frequency range transducers (5–10 MHz) offer the investigator a good compromise between resolution and depth penetration. Intestinal ultrasound (IUS) proved to be effective in distinguishing between inflammatory and non-inflammatory bowel pathologies and in choosing which patients should undergo more invasive examinations becoming a well-defined method in Crohn’s disease and ulcerative colitis. The most prominent parameter used to detect inflammatory activity is the bowel wall thickness that is usually related with the loss of typical wall stratification and an augmented vascularity, with a cutoff of 3 mm even if there is still a lack of standardisation. We herein present a case of NSAID-induced enteropathy in which IUS proved its usefulness in the diagnosis and follow-up. The patient gave approval for anonymous publication of her clinical history [2]. A 65-year-old Caucasian woman suffering from depression, claustrophobia and rheumatoid arthritis treated with low-dose systemic steroid, was referred for anorexia and weight loss (roughly 20 kg over the last year), without fever, abdominal pain, or diarrhoea. She had a history of recurrent abuse of butalbital and propifenazone and a year before she underwent an upper gastrointestinal endoscopy that showed antral hyperaemia and a deformed duodenal bulb with scarring. Upon hospital admission, no trace of butalbital or propifenazone were found in the blood, while further tests revealed anaemia and severe hypoalbuminemia. Three consecutive faecal occult blood tests were positive, along with increased faecal calprotectin (305 mg/kg). There were no signs of renal or hepatic dysfunction, nor urinary protein loss. An IUS was performed, showing some inflammatory lymph nodes at the root of the mesentery and a minimal pelvic effusion with increased bowel wall thickness (up to 5.7 mm) at the terminal ileum and along the entire colon, especially at transverse tract and without evidence of neoplastic lesions (Fig. 1). An upper gastrointestinal endoscopy excluded active bleeding and a lower gastrointestinal endoscopy revealed multiple non-bleeding circumferential ulcers from the transverse colon to the ileocaecal valve; terminal ileum was not evaluated because of a stricture that could not be passed through by a paediatric endoscope or by video capsule endoscopy. Histological examination from biopsies excluded inflammatory bowel disease and stool cultures were negative. She was treated with a 10-day cycle of oral metronidazole (500 mg three times daily) and only later she reported a recent abuse of indomethacin. After 2 months, IUS was repeated and showed an improvement of both bowel wall thickness and vascularity, whilst continuing * Matteo Pistoia [email protected]