Quality of Care and Outcomes Among Hospitalized Inflammatory Bowel Disease Patients: A Multicenter Retrospective Study.

BACKGROUND: Half of patients with inflammatory bowel disease (IBD) require hospitalization. We sought to characterize inpatient quality indicators of care and outcomes during IBD-related hospitalizations at 4 major IBD referral centers in Canada. METHODS: We conducted a multicenter retrospective cohort study of patients with IBD admitted from 2011 to 2013 to tertiary centers in Toronto, Montreal, Ottawa, and Vancouver. We assessed the following inpatient indicators of care: pharmacological venous thromboembolism (VTE) prophylaxis, Clostridium difficile testing, and medical rescue therapy for steroid-refractory ulcerative colitis (UC). We also evaluated rates of VTE, C. difficile infection, and IBD-related surgery. RESULTS: There were 837 patients hospitalized for IBD (Crohn's disease, 59%; UC, 41%). The proportion of patients with IBD who received VTE prophylaxis and C. difficile testing were 77% and 82%, respectively, although these indicators varied significantly by center and admitting specialty. Patients admitted under surgeons were more likely than those admitted under gastroenterologists to receive VTE prophylaxis (84% versus 74%, P = 0.016) but less likely to be tested for C. difficile (41% versus 88%, P < 0.0001). The rate of VTE was the same for those who did and did not receive VTE prophylaxis (2.2 per 1000 hospital-days). Among the 14 VTE events, 79% had received prophylaxis, but only 36% within 24 hours of admission. Among steroid-refractory UC patients, 70% received rescue therapy within 7 days of steroid initiation. The proportion of patients with UC and CD who required respective bowel surgery was 18% and 20%, respectively. CONCLUSIONS: There are opportunities to optimize quality of care among hospitalized patients with IBD.

Time of infliximab therapy initiation and dose escalation in Crohn's disease.

AIM: To determine if early initiation of anti-tumor necrosis factor therapy affects the need for dose escalation. METHODS: This was a retrospective review of patients receiving infliximab therapy for Crohn's disease (CD) at two outpatient gastroenterology clinics during July 2009 to October 2010. All patients included in the study were biologic agent naïve and had moderate to severe CD (Harvey Bradshaw index > 8). Patients were divided into groups based on length of time between diagnosis to therapy initiation and concurrent immunosuppressant therapy. Kaplan-Meier survival analysis was used to compare the time to dose escalation for the four groups. RESULTS: There were 68 patients, 51% female and 49% male, with an average age at diagnosis of 24.7 ± 11.9 years. The average age at infliximab initiation was 34.8 ± 14.8 years. Of the 68 patients, 19% initiated inflixiamb within 2 years of diagnosis, and 51% had concurrent immunosuppressant therapy at the time of therapy initiation. Fifty percent of patients required dose escalation and the median time from therapy initiation to dose escalation was 10 mo (interquartile range: 5.3-14.8). There was a statistically significant higher probability of requiring dose esclataion in patients who initiated biologic therapy within 2 years of diagnosis, without concurrent immunosuppressant therapy (P < 0.01). CONCLUSION: Those who receive infliximab within 2 years of CD diagnosis require more intense immunosuppressant therapy than those who received infliximab later.

Argon plasma coagulation for the treatment of hemorrhagic radiation colitis.

Radiation colitis is a common consequence of pelvic radiation. Its complications may include anemia due to chronic bleeding requiring transfusions. Many of these patients are managed with rectal medications which are often inadequate for control. Argon plasma coagulation (APC) has been well described for its efficacy in treating radiation proctitis. Here we present two cases in whom APC therapy was used to treat severe radiation colitis. We reviewed two cases originally seen at the regional cancer center (Cross Cancer Institute) in Edmonton, Alberta, Canada. Both patients received pelvic radiation for recurrent endometrial cancers and were referred for active bleeding secondary to radiation colitis that had required numerous transfusions. Radiation-induced telangiectasias were found from 10-50 cm in the sigmoid colon. Both patients had significant improvement of symptoms after one session of APC treatment set at 40-60 W and gas flow of 2.0 l/min. There were no complications from the procedures. Neither patient required blood transfusions after the treatment with improvement in their hemoglobin levels and were doing well at 3- and 6-month follow-up. APC can be used effectively to provide immediate and sustained resolution of symptoms in patients with radiation colitis.

Familial hypobetalipoproteinemia-induced nonalcoholic steatohepatitis.

Familial hypobetalipoproteinemia (FHBL) is a rare genetic disorder of lipid metabolism that is associated with abnormally low serum levels of low-density lipoprotein (LDL) cholesterol and apolipoprotein B. It is an autosomal co-dominant disorder, and depending on zygosity, the clinical manifestations may vary from none to neurological, endocrine, hematological or liver dysfunction. Nonalcoholic fatty liver disease is common in persons with FHBL, however progression to nonalcoholic steatohepatitis is unusual. We describe here a patient with a novel APOB mutation, V703I, which appears to contribute to the severity of the FHBL phenotype. He had liver enzyme abnormalities, increased echogenicity of the liver consistent with steatosis, very low LDL cholesterol at 0.24 mmol/l (normal 1.8-3.5 mmol/l) and an extremely low apolipoprotein B level of 0.16 g/l (normal 0.6-1.2 g/l). APOB gene sequencing revealed him to be a compound heterozygote with two mutations (R463W and V703I). APOB R463W has previously been reported to cause FHBL. Genetic sequencing of his first-degree relatives identified the APOB V703I mutation in his normolipidemic brother and father and the APOB R463W mutation in his mother and sister, both of whom have very low LDL cholesterol levels. These results suggest that the APOB V703I mutation alone does not cause the FHBL phenotype. However, it is possible that it has a contributory role to a more aggressive phenotype in the presence of APOB R463W.

Gastric polyps in patients with portal hypertension.

OBJECTIVES: Gastric hyperplastic polyps are usually associated with chronic gastritis including Helicobacter pylori gastritis and postantrectomy stomachs. Here, we report on a series of 12 patients with portal hypertension secondary to liver cirrhosis, who were found to have a unique histological type of gastric polyp on endoscopy. METHODS: Retrospective chart review of 12 patients with portal hypertension, who presented with histologically diagnosed gastric hyperplastic polyps. These polyps were reviewed and compared with hyperplastic polyps from 21 patients who did not have portal hypertension. RESULTS: The endoscopic appearances of portal hypertension-associated polyps varied considerably, with sizes ranging up to 18 mm. They were sessile or pedunculated, singular or multiple, found in the antrum or body of the stomach, and endoscopically appeared to be typical hyperplastic polyps. Histopathological examination, however, showed mucosal hyperplasia and extensive vascular proliferation and granulation tissue formation. CONCLUSION: The unique histological appearance of gastric hyperplastic polyps in patients with portal hypertension polyps is described. The exact pathogenetic mechanism of polyp formation is unclear although it seems possible that the underlying cause is mucosal injury that is vascular in nature rather than being secondary to surface inflammation. Although there is an emerging evidence of the neoplastic potential of usual hyperplastic polyps, the natural history of portal hypertension-associated polyps is unknown. Identification and management of portal hypertension-associated gastric polyps present a particular dilemma, as these patients often have coagulopathies and vascular ectasias. Therefore, the natural history and endoscopic features of gastric polyps arising in portal hypertensive patients warrants further exploration.