Impact of the Crohn's disease digestive damage score (Lémann Index) on the perioperative course in patients with Crohn's disease and ileocolic anastomosis.

BACKGROUND: Risk factors influencing the high postoperative morbidity in Crohn`s disease are controversially discussed but the role of cumulative structural bowel damage, as assessed by the Crohn's disease digestive damage score (Lémann Index), has been neglected so far. Our aim was evaluating the influence of the Lémann Index on postoperative complications and investigating its suitability for surgical decision making. METHODS: A single-center, retrospective cohort study was conducted including Crohn`s disease patients who underwent ileocolic anastomosis. Lémann Indices were calculated and, additionally, categorized into three groups [0-3; 3-10; >10] due to the strong influence of previous bowel resections on high indices. A multivariate regression model was used to analyze the index`s influence on postoperative complications. RESULTS: Patients with higher Lémann Index were more likely to need open surgery (p < .001) or stoma creation (p = .03). Overall, of the 103 patients enrolled, 18 (17.5%) showed postoperative complications Clavien-Dindo > 2. The Lémann Index was higher in patients with complications compared to those without (median 6.15 [IQR 4.16-11.98] vs. 3.88 [1.63-12.63]), but not linearly associated with postoperative complications. After categorization, patients with Lémann Index 3-10 had an 8.42 (95% CI 1.8-54.55) times higher chance to develop a complication compared to patients with Lémann Index 0-3 (p = .01). CONCLUSIONS: The Lémann Index might affect surgical decision making but is not linearly associated with postoperative morbidity. However, medium indices (3-10) - mainly accounted for by high amounts of intraabdominal active Crohn`s lesions - showed significantly higher rates of complications, potentially defining a group at risk.

Brain serotonin deficiency affects female aggression.

The neurotransmitter serotonin plays a key role in the control of aggressive behaviour. While so far most studies have investigated variation in serotonin levels, a recently created tryptophan hydroxylase 2 (Tph2) knockout mouse model allows studying effects of complete brain serotonin deficiency. First studies revealed increased aggressiveness in homozygous Tph2 knockout mice in the context of a resident-intruder paradigm. Focussing on females, this study aimed to elucidate effects of serotonin deficiency on aggressive and non-aggressive social behaviours not in a test situation but a natural setting. For this purpose, female Tph2 wildtype (n = 40) and homozygous knockout mice (n = 40) were housed with a same-sex conspecific of either the same or the other genotype in large terraria. The main findings were: knockout females displayed untypically high levels of aggressive behaviour even after several days of co-housing. Notably, in response to aggressive knockout partners, they showed increased levels of defensive behaviours. While most studies on aggression in rodents have focussed on males, this study suggests a significant involvement of serotonin also in the control of female aggression. Future research will show, whether the observed behavioural effects are directly caused by the lack of serotonin or by potential compensatory mechanisms.