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Biomedical subjects

P Crenn

Publications and source records attributed to P Crenn.

12 recordsLinked to original sources
PubMed2001

[Intestinal failure].

Intestinal failure is defined as the reduction in the functioning gut mass below the minimal amount necessary for the absorption of nutrients and a normal nutritional status. The main cause of chronic intestinal failure in adults is short bowel syndrome secondary to mesenteric ischemia. In short bowel the remnant bowel length is inferior to 200 cm. The two other causes of intestinal failure are extensive small bowel mucosal diseases and chronic intestinal pseudo-obstruction. The reference treatment of severe chronic intestinal failure is home parenteral nutrition. The main alternate for irreversible intestinal failure is small bowel transplantation, isolated or combined to liver transplantation.

Adult↗
PubMed2000

Prevalence of liver disease and contributing factors in patients receiving home parenteral nutrition for permanent intestinal failure.

BACKGROUND: Liver cholestasis can be a life-threatening complication during home parenteral nutrition and may lead to combined liver-intestinal transplantation. OBJECTIVE: To assess the prevalence of home parenteral nutrition-related liver disease and its contributing factors in patients with permanent intestinal failure. DESIGN: Prospective cohort study. SETTING: Two approved home parenteral nutrition centers. PATIENTS: 90 patients with permanent intestinal failure who were receiving home parenteral nutrition were enrolled from 1985 to 1996. INTERVENTION: Clinical, biological, endoscopic, and ultrasonographic follow-up. Histologic examination of the liver was done in 57 patients (112 liver biopsies). MEASUREMENTS: The Kaplan-Meier method was used to determine the actuarial occurrence of chronic cholestasis and complicated home parenteral nutrition-related liver disease (bilirubin level > or =60 micromol/L [3.5 mg/dL], factor V level < or =50%, portal hypertension, encephalopathy, ascites, gastrointestinal bleeding, or histologically proven extensive fibrosis or cirrhosis). Contributing factors were assessed by using univariate and multivariate (Cox model) analysis. RESULTS: 58 patients (65%) developed chronic cholestasis after a median of 6 months (range, 3 to 132 months), and 37 (41.5%) developed complicated home parenteral nutrition-related liver disease after a median of 17 months (range, 2 to 155 months). Of these patients, 17 showed extensive fibrosis after 26 months (range, 2 to 148 months) and 5 had cirrhosis after 37 months (range, 26 to 77 months). The prevalence of complicated home parenteral nutrition-related liver disease was 26%+/-9% at 2 years and 50%+/-13% at 6 years. Six patients died of liver disease (22% of all deaths). In multivariate analysis, chronic cholestasis was significantly associated with a parenteral nutrition-independent risk for liver disease, a bowel remnant shorter than 50 cm in length, and a parenteral lipid intake of 1 g/kg of body weight per day or more (omega-6-rich long-chain triglycerides), whereas complicated home parenteral nutrition-related liver disease was significantly associated with chronic cholestasis and lipid parenteral intake of 1 g/kg per day or more. CONCLUSION: The prevalence of complicated home parenteral nutrition-related liver disease increased with longer duration of parenteral nutrition. This condition was one of the main causes of death in patients with permanent intestinal failure. Parenteral intake of omega-6-rich long-chain triglycerides lipid emulsion consisting of less than 1 g/kg per day is recommended in these patients.

Adolescent↗
PubMed2000

Postabsorptive plasma citrulline concentration is a marker of absorptive enterocyte mass and intestinal failure in humans.

BACKGROUND & AIMS: No blood marker assessing the functional absorptive bowel length has been identified. Plasma citrulline, a nonprotein amino acid produced by intestinal mucosa, is one candidate. We tested this hypothesis in adult patients with the short-bowel syndrome, whose condition can lead to intestinal failure. METHODS: In 57 patients, after a minimal follow-up of 2 years subsequent to final digestive circuit modification, postabsorptive citrulline concentration was measured and parenteral nutrition dependence was used to define permanent (n = 37) and transient (n = 20) intestinal failure. Absorptive function, studied over a 3-day period, was evaluated by net digestive absorption for protein and fat (n = 51). Relations between quantitative values were assessed by linear regression analysis and cutoff citrulline threshold, for a diagnosis of intestinal failure by linear discriminant analysis. Cox model was used to compare citrulline threshold and anatomic variables of the short bowel as indicators of transient as opposed to permanent intestinal failure. RESULTS: In patients with short-bowel syndrome, citrulline levels were lower than in controls (n = 51): 20 +/- 13 vs. 40 +/- 10 micromol/L (mean +/- SD), respectively (P < 0.001). After multivariate analysis, citrullinemia was correlated to small bowel length (P < 0.0001, r = 0.86) and to net digestive absorption of fat, but to neither body mass index nor creatinine clearance. A 20-micromol/L threshold citrullinemia, (1) classified short bowel patients with permanent intestinal failure with high sensitivity (92%), specificity (90%), positive predictive value (95%), and negative value (86%); and (2) was a more reliable indicator (odds ratio, 20.0; 95% confidence interval, 1.9-206.1) than anatomic variables (odds ratio, 2.9; 95% confidence interval, 0. 5-15.8) to separate transient as opposed to permanent intestinal failure. CONCLUSIONS: In patients with short-bowel syndrome, postabsorptive plasma citrulline concentration is a marker of functional absorptive bowel length and, past the 2-year adaptive period, a powerful independent indicator allowing distinction of transient from permanent intestinal failure.

Absorption↗
PubMed2000

Duodenal vs. gastric administration of labeled leucine for the study of splanchnic metabolism in humans.

Low-rate (6 ml/h) intragastric infusion of stable, isotope-labeled amino acids is commonly used to assess the splanchnic handling of amino acids in humans. However, when used in the postabsorptive state, this method yields unreliable plasma isotopic enrichments, with a coefficient of variation >10%. In this metabolic condition, we confirmed in six subjects that an intragastric infusion of L-[(2)H(3)]leucine at 6 ml/h yields an unreliable isotopic steady state in plasma amino acids with a coefficient of variation of 43 +/- 12% (mean +/- SD). In five additional subjects, we assessed the effects of 1) increasing the rate of delivery of a leucine tracer in an isotonic plasmalike solution at 240 ml/h into the gastric site, and 2) changing the site of infusion from gastric to duodenal with this same high rate of delivery. In contrast to the gastric route, and regardless of the rate of delivery, only the intraduodenal route allowed 1) isotopic plasma steady state (i.e., coefficients of variation were <10%: 5 +/- 3%), and 2) reproducible leucine extraction coefficients (22 +/- 5%). We conclude that an infusion site that bypasses the gastric emptying process, i.e., the duodenal route, along with delivery of a plasmalike solution, is necessary to reach isotopic steady state in plasma when labeled leucine is infused into the gastrointestinal tract in the postabsorptive state.

Adult↗
PubMed1999

Long-term survival and parenteral nutrition dependence in adult patients with the short bowel syndrome.

BACKGROUND & AIMS: The short bowel syndrome (SBS) may be associated with either transient or permanent intestinal failure, presently treated by parenteral nutrition (PN). Survival and PN-dependence probabilities, taking into account both small bowel remnant length and the type of the digestive circuit of anastomosis, are not known in adult SBS patients. The aim of this study was to assess such prognostic factors. METHODS: A total of 124 consecutive adults with nonmalignant SBS were enrolled from 1980 to 1992 at 2 home PN centers. They were analyzed for survival and PN-dependence probabilities using the Cox model and for PN dependence using linear discriminant analysis. Data were updated in April 1996. RESULTS: Survival and PN-dependence probabilities were 86% and 49% and 75% and 45% at 2 and 5 years, respectively. In multivariate analysis, survival was related negatively to end-enterostomy, to small bowel length of <50 cm, and to arterial infarction as a cause of SBS, but not to PN dependence. The latter was related negatively to postduodenal small bowel lengths of <50 and 50-99 cm and to absence of terminal ileum and/or colon in continuity. Cutoff values of small bowel lengths separating transient and permanent intestinal failure were 100, 65, and 30 cm in end-enterostomy, jejunocolic, and jejunoileocolic type of anastomosis, respectively. CONCLUSIONS: In adult SBS patients, small bowel length of <100 cm is highly predictive of permanent intestinal failure. Presence of terminal ileum and/or colon in continuity enhances both weaning off PN and survival probabilities. After 2 years of PN, probability of permanent intestinal failure is 94%. These rates may lead to selection of other treatments, especially intestinal transplantation, instead of PN, for permanent intestinal failure caused by SBS.

Adolescent↗
PubMed1997

Leiden factor V mutation in four patients with small bowel infarctions.

The Leiden factor V mutation is observed in 20% of unexplained lower limb venous thromboses and involves substitution of the arginine residue at position 506 by glutamine (R506Q). It is known to decrease the anticoagulant activity of activated protein C. This case report describes 4 cases of small bowel infarction (SBI) associated with the presence of this mutation. Two cases of arterial and 2 cases of venous SBI were observed. Extensive assessment excluded the usual causes of SBI and plasma hypercoagulation syndrome (antithrombin III, protein C, and protein S deficiency and myeloproliferative syndrome). An abnormal resistance to activated protein C was observed. Molecular analysis consisting of polymerase chain reaction amplification and digestion with MnlI showed that 2 patients were heterozygous and 2 were homozygous for the R506Q mutation. Despite familial history of thrombosis in only 1 patient, first- and second-degree relatives of 2 patients also had the presence of the mutation. Examination for the presence of abnormal resistance to activated protein C should be part of the etiological assessment of SBI. Its presence may warrant consideration of long-term anticoagulant therapy, especially for patients with shortened small bowel who are treated by home parenteral nutrition with deep venous access.

Adult↗