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• W2330256723 abstract "Eighty-five to ninety percent of patients with cystic fibrosis (CF) have gastrointestinal complications. The differential diagnosis includes distal intestinal obstruction syndrome, Crohn disease, fibrosing colonopathy, and colonic disease, an entity that Pickhardt et al. (1) described as proximal colonic wall thickening with abdominal pain. Recently Clostridium difficile infections with atypical presentation have been added to this list (2). C. difficile is the primary cause of most cases of pseudomembranous colitis and of many cases of antibiotic-associated colitis (AAC). Carriage rates of C. difficile in patients with CF are high (32%–50%) (3,4) when compared with the normal adult population (2%). Classic symptoms of AAC are rare in patients with CF, whereas patients with atypical presentations (constipation and stool impaction) are often underdiagnosed, or the correct diagnosis is missed and appropriate treatment is delayed. Because the disease can cause quick deterioration, knowledge of the atypical symptoms of AAC should be familiar to physicians treating patients with CF. We report an atypical case of AAC caused by C. difficile in a 28-year-old patient with CF and underlying colonic wall thickening. CASE REPORT Our patient was a 28-year-old white man (weight, 78.5 kg; height, 188 cm; body mass index, 22.2), homozygous for the Δ 508 mutation with severe lung manifestation (vital capacity, 2.69 L, 44% of predicted value; forced expiratory volume in 1 second [FEV1] 1.79 L, 37% of predicted value; maximum expiratory flow at 25% of forced vital capacity [MEF25] 0.28 L/s, 10% of predicted value). Because of chronic Pseudomonas aeruginosa infection, he was regularly treated with intravenous antibiotics every 3 months. He also had allergic bronchopulmonary aspergillosis. This condition was first diagnosed and treated with steroids when the patient was 23 years old. Aspergillus-specific laboratory data at that time follow: total IgE 1,522 kU/L, RAST for Aspergillus fumigatus class 4 (specific IgE 25.3 kU/L), specific IgG 2,350 kU/L, and no evidence of Aspergillus fumigatus in sputum culture or eosinophilia in peripheral blood sample. For pulmonary disease, daily medication consisted of oral prednisolone (10 mg/day), theophylline, mucolytics, leukotriene receptor antagonists, and inhalations with budesonide, ipratropium, formoterol, and tobramycin. Ursodeoxycholic acid was given to protect the liver because of ultrasonographically visible changes. Pancreatic insufficiency was treated with vitamin supplements and Creon 25,000 (lipase 6,700 U/kg daily). In the past (data available since 1990), the patient had been treated with Creon 10,000/ 25,000 (maximum daily lipase 7,812 U/kg). This preparation does not contain the Eudragit enteric coating. Initially, the patient had abdominal pain, right lower abdominal mass, and suspected distal intestinal obstruction syndrome, but ultrasound did not indicate distal intestinal obstruction syndrome. Ultrasound revealed 4-mm colonic thickening. Symptoms resolved with conservative treatment (sorbitol enemas 135 mL/d). Because of concomitant pulmonary exacerbation, antibiotic treatment with fosfomycin and meropenem was given for 14 days. Tobramycin inhalations were started again after ending intravenous antibiotic administration. Four weeks later, severe diarrhea and fever developed. The patient was critically ill with abdominal bloating, sparse bowel sounds, signs of dehydration, tachydyspnea, and cyanosis. Laboratory findings were consistent with severe infection (leukocytosis 45,000/μL; C-reactive protein [CRP], 299 mg/L). Ultrasound and computed tomography (CT) studies (Fig. 1 and 2) revealed a remarkable increase in pancolonic bowel wall thickening (colonic wall thickening assessed by ultrasound was 40 mm). As visible in CT scans of the colon (Fig. 1, longitudinal diameter, and Fig. 2, transverse diameter) bowel wall thickening up to 30 mm totally obstructed the lumen. No fecal material could be seen. Gas was trapped between edematous folds. The contrast-enhancing mucosa was stretched around thickened submucosal folds (accordion sign, see Fig. 2).FIG. 1.: Longitudinal diameter of the colon. Contrast-enhanced helical abdominal computed tomography scan demonstrates thickening of the entire colonic wall.FIG. 2.: Transverse diameter of the colon. The contrast-enhancing mucosa is stretched around thickened submucosal folds (accordion sign).The small bowel was spared, but bowel wall thickening extended to the rectum. Two days later, conventional radiography showed ileus with increasing abdominal distention. Stool cultures were positive for C. difficile. Treatment was started with oral metronidazole and Saccharomyces boulardii. The patient slowly recovered. He was discharged from the hospital after 13 days. He had lost 7 kg. Repeat stool culture was positive for C. difficile. Early follow-up sonographic examinations showed only partial reduction of colonic wall thickening (from 40 to 15 mm) in the asymptomatic patient. Then a course of oral vancomycin for 14 days was given, and stool cultures were negative on day 7 and day 14. However, the patient relapsed 9 days after stopping vancomycin, with loose stool, signs of acute infection (CRP, 120 mg/L), and an increase in colonic wall thickening (30 mm), diagnosed by ultrasound study. After another 21-day course of oral vancomycin, stool cultures were negative for C. difficile and symptoms completely resolved. Two months later, colonic wall thickening (approximately 2 mm) had disappeared. DISCUSSION The hallmark of classic antibiotic-associated colitis is watery diarrhea. But in patients with CF, atypical presentations also are a severe threat. Binkovitz et al. (2) reported unusual presentations of C. difficile colitis with the absence of watery diarrhea. They described patients with abdominal bloating and decreased stooling. In our patient, lack of improvement after standard therapy for stool impaction led us to perform an abdominal ultrasound. Extensive pancolitis and clinical signs of severe infection suggested C. difficile infection before even microbiologic confirmation. With this disease, treatment must be started immediately because severe progression can occur before microbiologic results are available. Our patient already had signs of severe infection at the time of CT, when treatment was started. In accordance with the literature (5,6), we started treatment with metronidazole and Saccharomyces boulardii. Stool cultures cleared only after oral vancomycin was started. Nevertheless, the patient relapsed 5 weeks after discharge. Thus oral vancomycin was given for 21 days. Intestinal obstruction and diarrhea also can be presenting symptoms of fibrosing colonopathy (7–9). Fibrosing colonopathy has been reported rarely in adults (10) and probably is associated with high pancreatin intake and Eudragit preparations (11,12). The older age of our patient, the absence of strictures, no intake of preparations with Eudragit enteric coating, and appropriate dosage of lipase (maximum 7,812 U/kg daily) make this differential diagnosis unlikely. Another detail of our case is the bowel wall thickening that extended to the rectum; case reports also exist of rectal sparing in atypical antibiotic colitis in patients with CF (13). The interesting feature of this case is the persisting colonic wall thickening. In AAC, colonic wall thickening should resolve soon after implementing appropriate treatment. Persistent colonic wall thickening is a finding of another abdominal problem in adult CF patients: colonic disease (1). In this entity, the thickening of the colonic wall may measure 10 mm to 30 mm, resulting from mucosal thickening with histologic signs of acute and chronic inflammation. Patients have abdominal pain, fever, nausea, and vomiting. As the majority of C. difficile colonization in CF is asymptomatic, one could argue that we were dealing with a colonic disease with asymptomatic C. difficile carriage. But according to the data of Pickhardt et al. (1), patients with colonic disease test negative for C. difficile. Two unresolved issues remain in our case: First, at initial presentation, stool cultures for C. difficile were negative, but colonic wall thickening already was evident ultrasonographically. Was the colonic wall thickening true colonic disease or caused by C. difficile infection? Colonic thickening disappeared after appropriate therapy. Second, if we were dealing with colonic disease, why did colonic thickening disappear within weeks? Pickhardt also describes regression, but at 1 year or later. In his study, follow-up data for only three patients are available and regression of colonic wall thickening is described in only one patient. Therefore our case raises the question of whether colonic disease is a true entity or can be mimicked by insufficiently managed C. difficile infection. CONCLUSIONS The clinical presentation of C. difficile colitis in CF can be atypical. To avoid severe progression of disease, if clinical presentation is suspicious and radiologic findings of colitis are evident, anticlostridial treatment should be started before bacteriologic confirmation is available. The differentiation between colonic disease and C. difficile infection can be difficult." @default.
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• W2330256723 title "Severe Antibiotic-Associated Colitis in a Patient With Cystic Fibrosis and Colonic Wall Thickening" @default.
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