Mesenteric vascular thromboembolism in inflammatory bowel disease: a single center experience.

BACKGROUND: Vascular thrombotic complications in inflammatory bowel disease (IBD) are well recognized, although mesenteric vascular thrombotic disease is rare. METHODS: We describe nine patients in a tertiary care center with IBD that developed thrombosis of the mesenteric arterial or venous vasculature (e.g., mesenteric thrombosis, MT). RESULTS: Eight subjects developed mesenteric venous thrombosis (five located in the superior mesenteric vein and three located in a branch of the portal vein) and one had a mesenteric arterial embolus, located in the splenic artery. Five subjects had Crohn's disease (CD), and four had ulcerative colitis. The one subject diagnosed with an arterial thrombosis had CD. Mean time from diagnosis of IBD to diagnosis of thrombosis was 24.6 ± 13.5 years. Five of the nine subjects developed mesenteric venous thrombosis while their IBD was clinically in remission. Seven of nine subjects were symptomatic from the development of MT, including bowel infarction that led to development of short bowel syndrome. CONCLUSION: Mesenteric thrombosis is a rare complication of IBD and may develop during clinical remission, suggesting a potential role for factors other than clinically significant inflammation in its pathogenesis.

An evaluation of the model for end-stage liver disease and serum C-reactive protein as prognostic markers in intestinal failure patients on parenteral nutrition.

BACKGROUND: Intestinal failure (IF) patients require parenteral nutrition (PN) to avoid malnutrition and death. However, they face complications of recurrent sepsis and liver failure. By the time liver failure is discovered, it is often too late for intervention and prognosis on the waiting list is grim. The Model for End-Stage Liver Disease (MELD) has traditionally been used to predict mortality in patients with liver failure but has never been analyzed in IF patients who are at risk for liver complications. C-reactive protein (CRP) is an acute inflammatory marker that has been shown to reflect disease progression in nonalcoholic steatohepatitis, a disease that in many ways resembles PN-associated liver disease. MELD and CRP are promising clinical markers of disease progression in IF patients on PN. METHODS: The authors performed a retrospective, case-control study to compare levels of MELD and CRP within the entire population of 133 adult patients referred to Northwestern Memorial Hospital for IF from 1999 to 2006. RESULTS: Elevated MELD score is strongly predictive of increased mortality over the subsequent 6 months. Elevated CRP is strongly predictive over a smaller 3-month window. One-year mortality was significantly greater in patients who have either elevated MELD scores or serum CRP levels. CONCLUSIONS: In this study, the authors evaluated for the first time use of MELD and serum CRP as predictive markers of mortality in IF patients. Both seem to be promising clinical tools to identify which patients are at highest risk for complication.

Clonidine reduces diarrhea and sodium loss in patients with proximal jejunostomy: a controlled study.

BACKGROUND: Patients with short bowel syndrome have significant fluid losses. This represents a significant management problem, especially in patients with minimal residual intestine. We determined whether clonidine, an alpha2-adrenergic agonist, is effective in decreasing fecal water and sodium (Na) losses in patients with proximal jejunostomy. Eight parenteral nutrition (PN)-dependent subjects (3 men, 5 women), aged 49.9+/-10.2 years, with a residual small bowel length of 71.8+/-152.0 cm that ended in a jejunostomy, were studied. METHODS: Subjects were admitted to the North-western General Clinical Research Center (GCRC) for a 2-day equilibrium period while receiving a self-selected 100 g fat diet with protein 1.5 g/kg/d and 30 kcal/kg/d and 1 L/d of oral rehydration solution. A D-xylose test was performed after an overnight fast. On days 3-5, all stool and urine were collected for volume, weight, fat, nitrogen, energy, sodium, magnesium, potassium, and calcium. Meals were provided in duplicate and the equivalent portions consumed by each patient were analyzed for fluid volume, fat, nitrogen, energy, sodium, magnesium, calcium, and potassium in order to calculate nutrient balances. At the conclusion of the stool and urine collections (day 6), a clonidine (0.3 mg) patch was applied to the shoulder. Subjects were restudied after 1 week. RESULTS: Daily fecal volume and weight were 4.514+/-1.769 L/d and 4394+/-1727 g/d, respectively, at baseline. Five subjects were net "secretors" in that excreted fecal volume exceeded oral intake. Fecal volume decreased by 427+/-562 mL/d (8.9%, p=.07). Fecal weight decreased by 438+/-527 g/d (9.4%, p=.05). Urine volume correspondingly increased by 747+/-1934 mL (18.9%, p=not significant [NS]). The increase in urine output was weakly and negatively correlated with the decrease in fecal volume and weight (r=-0.37 and -0.41, respectively, p=NS). Oral fluid intake decreased slightly from 3.328+/-1.246 L/d baseline to 3.203+/-1.119 L/d with clonidine therapy (-3.8%, p=NS). Fecal Na loss was significantly decreased from baseline (887+/-996 mg/d, 11.2+/-12.3%; p=.036). This was not related to decreased oral Na intake, which actually increased from baseline (3.799+/-2.271 g/d) to 3.933+/-1.314 g/d after clonidine therapy (p=NS). No patient developed hypotension. CONCLUSIONS: Our results show the transdermal administration of clonidine is associated with a modest but clinically significant decrease in fecal output in patients with short bowel syndrome and high-output proximal jejunostomy that require chronic parenteral fluid infusion. This is accompanied by decreased fecal Na loss.