Correlation of postoperative splenic volume increase with prognosis of hepatocellular carcinoma after curative hepatectomy

Background: Previous studies have reported a close connection between the spleen and hepatic tumours. We investigated the prognostic value of postoperative splenic volume increase (PSVI) in patients with hepatocellular carcinoma after curative hepatectomy. Methods: This was a retrospective study of adult patients with hepatocellular carcinoma who underwent hepatectomy between January 2007 and May 2013. We categorized patients into 2 groups according to the cut-off value of the receiver operating characteristic curve: group A (PSVI < 19.0%) and group B (PSVI ≥ 19.0%). We compared the clinicopathological data, overall survival and disease-free survival between the 2 groups. We performed univariate and multivariate analyses to identify factors associated with disease-free and overall survival. Results: There were 275 patients in group A and 196 patients in group B. The 1-, 3- and 5-year overall survival rates were 98.9%, 74.9% and 63.6%, respectively, for patients in group A, and 97.4%, 65.3% and 49.8%, respectively, for patients in group B (p = 0.004). The corresponding disease-free survival rates were 69.5%, 48.0% and 40.3%, and 58.1%, 36.5%, and 29.8% (p = 0.01). On multivariate analysis, PSVI was an independent predictor of overall (p = 0.01) and disease-free (p = 0.03) survival. Conclusion: Postoperative splenic volume increase correlates with poor prognosis of patients with hepatocellular carcinoma after curative hepatectomy.

Contexte: Des études antérieures faisaient état d'un lien étroit entre la rate et les tumeurs hépatiques. Nous avons étudié la valeur pronostique de l'augmentation postopératoire du volume de la rate (APVR) chez les patients ayant subi une hépatectomie curative en raison d'un carcinome hépatocellulaire. Méthodes: Il s'agit d'une étude rétrospective portant sur des adultes qui ont subi une hépatectomie entre janvier 2007 et mai 2013 pour cause de carcinome hépatocellulaire. Nous avons classé les patients en 2 groupes, selon un seuil sur la courbe ROC : le groupe A (APVR : < 19,0 %) et le groupe B (APVR : ≥ 19,0 %). Nous avons ensuite comparé les données clinicopathologiques, le taux de survie globale et le taux de survie sans récidive des 2 groupes, et avons effectué des analyses univariées et multivariées pour repérer les facteurs associés à la survie sans récidive et à la survie globale. Résultats: Le groupe A comptait 275 patients, tandis que le groupe B en comptait 196. Les taux de survie globale à 1 an, à 3 ans et à 5 ans étaient de 98,9 %, de 74,9 % et de 63,6 %, respectivement, dans le groupe A, et de 97,4 %, de 65,3 % et de 49,8 %, respectivement, dans le groupe B (p = 0,004). Les taux de survie sans récidive à 1 an, à 3 ans et à 5 ans étaient de 69,5 %, de 48,0 % et de 40,3 %, respectivement, dans le groupe A, et de 58,1 %, de 36,5 % et de 29,8 %, respectivement, dans le groupe B (p = 0,01). Selon l'analyse multivariée, l'APVR était un prédicteur indépendant de survie globale (p = 0,01) et de survie sans récidive (p = 0,03). Conclusion: L'augmentation postopératoire du volume de la rate est corrélée à un mauvais pronostic chez les patients ayant subi une hépatectomie curative en raison d'un carcinome hépatocellulaire.

Effects of Duodenal-Jejunal Exclusion and New Bilio-Pancreatic Diversion on Blood Glucose in Rats with Type 2 Diabetes Mellitus.

OBJECTIVE: The current study aimed to investigate the effects of duodenal-jejunal bypass (DJB), new bilio-pancreatic diversion (NBPD), and duodenal-jejunal exclusion (DJE) on blood glucose in rats with type 2 diabetes mellitus (T2DM). METHODS: Male Sprague Dawley rats were fed with high glucose, high fat food, and intraperitoneally injected with streptozotocin to establish a T2DM animal model. T2DM rats were randomly assigned into 4 groups: a sham group (n = 8), DJB group (n = 9), NBPD group (n = 10), and DJE group (n = 10). Body weight, 2-h postprandial glucose, oral glucose tolerance, fasting serum bile acid, 2-h postprandial serum bile acid, fasting insulin, 2-h postprandial insulin (INS), fasting glucagon-like peptide-1 (GLP-1), and 2-h postprandial GLP-1 were measured before and after surgery. RESULTS: Six weeks after surgery, the 2-h postprandial glucose in the DJB (16.1 ± 6.7 mmol/L) and NBPD (19.5 ± 5.7 mmol/L) groups decreased significantly compared to the sham group (25.8 ± 4.9 mmol/L) (P < 0.05). There was no significant difference between the DJE (25.0 ± 5.0 mmol/L) and sham groups (P > 0.05). Four weeks after surgery, fasting serum bile acid in the DJB group (60.6 ± 11.4 µmol/L) and NBPD group (54.4 ± 7.64 µmol/L) was significantly higher than that in the sham group (34.3 ± 6.98 µmol/L; P < 0.05). However, fasting GLP-1, 2-h postprandial GLP-1, and insulin remained unchanged at different time points after surgery (P > 0.05). Body weight remained stable after surgery in all 4 groups (P > 0.05). CONCLUSION: NBPD plays a major role in the therapy of T2DM with DJB. NBPD may significantly increase fasting serum bile acid in T2DM rats, an action that may be one of the mechanisms underlying the therapeutic effects of DJB on T2DM.

Effects of 5-hydroxytamine and its antagonists on hepatic stellate cells.

BACKGROUND: Hepatic stellate cell (HSC) plays a key role in hepatic fibrosis. This study was undertaken to investigate the expression of 5-hydroxytamine receptors in HSC and the effect of 5-hydroxytamine on biological characteristics of HSC. METHODS: Liver ex vivo perfusion of collagenase and density gradient centrifugation were used to isolate HSCs. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression of 5-hydroxytamine receptor subtypes 1A, 2A, 2B and 3. Western blot hybridization was used to elucidate the effect of 5-hydroxytamine and its 2A receptor antagonist ketanserin and 3 receptor antagonist ondanosetron on the expression of transforming growth factor-beta1 (TGF-beta1) and Smad4 in HSC. RESULTS: HSC expressed 5-hydroxytamine receptor subtypes 1A, 2A and 2B. 5-hydroxytamine significantly increased the expression of TGF-beta1 and Smad4 in HSC (P<0.05). This action can be antagonized by ketanserin, not by ondanosetron. CONCLUSIONS: HSC expresses 5-hydroxytamine receptors. 5-Hydroxytamine could effect the biological characteristics of HSC through its receptor mediation, and may play a role in the pathogenesis of liver cirrhosis and portal hypertension.

[Expression of 5-hydroxytamine receptors in hepatic stellate cell and action of 5-hydroxytamine on biological characteristics of hepatic stellate cell].

OBJECTIVE: To investigate the expression of 5-hydroxytamine receptors in hepatic stellate cells HSCs and action of 5-hydroxytamine on biological characteristics of HSC. METHODS: Liver ex vivo perfusion of collagenase and density gradient centrifugation were used to isolate hepatic stellate cell. RT-PCR was used to detect the expression of 5-hydroxytamine receptor subtypes 1A, 2A, 2B and 3. Western blot hybridization was used to elucidate the effect of 5-hydroxytamine and its 2A receptor antagonist ketanserin and 3 receptor antagonist ondanosetron on expression of transforming growth factor-beta1 (TGF-beta1) and Smad4 in HSC. HSCs were cultured on silicone membrane. The effect of 5-hydroxytamine, ketanserin and ondanosetron on cell contraction were studied. RESULTS: HSC expressed 5-hydroxytamine receptors subtypes 1A, 2A and 2B. 5-hydroxytamine significantly increased the expression of TGF-beta1 and Smad4 in HSC (P < 0.05). This was antagonized by ketanserin, not by ondanosetron. 5-hydroxytamine induced cell contraction in a dose-dependant manner. Ketanserin antagonized this action, but ondanosetron did not. CONCLUSIONS: HSCs express 5-hydroxytamine receptors. 5-hydroxytamine could affect the biological characteristics of HSC through its receptor mediation, and may play a role in the pathogenesis of liver cirrhosis and portal hypertension.

Effects of modified biliopancreatic diversion on glucose tolerance of GK rats.

BACKGROUND: The purpose of this study was to investigate the hypoglycemic effect of new biliopancreatic diversion and duodenal-jejunal bypass in Goto-Kakizaki rats and observe effects of the new surgical procedure on the glucose tolerance of GK rats. METHODS: Twenty-four 10-week-old rats (SPF grade) were randomly divided into groups A, B, and C, each with eight rats. Group A underwent duodenal-jejunal bypass, group B underwent modified biliopancreatic diversion, and group C underwent a sham operation. Median rat body weight, fasting blood glucose, OGTT, and blood lipids were measured in fasting 1 week before surgery and 1, 2, 4, and 8 weeks after surgery. Changes in gastric inhibitory polypeptide, glucagon P-like peptide-1, and insulin levels were measured by ELISA 1 week before surgery and 8 weeks after surgery. RESULTS: Rats' mean body weight in groups A and B decreased significantly from 368.025 ± 11.726 and 373.100 ± 9.859 g preoperatively to 345.750 ± 11.403 and 343.260 ± 12.399 g at the early postoperative stage (P < 0.05), and with statistically significant differences compared to the weight of rats in group C (P < 0.05). Comparisons between fasting blood glucose before surgery and 8 weeks after surgery revealed no significant differences between all three groups (P > 0.05). Glucose tolerance in groups A and B decreased from preoperative 21.175 ± 3.684 and 20.820 ± 1.671 mmol/L to postoperative 8.950 ± 0.580 and 10.500 ± 1.509 mmol/L, and both were better than that of group C (P < 0.001). CONCLUSIONS: Both new biliopancreatic diversion and duodenal-jejunal bypass improve glucose tolerance of Goto-Kakizaki rats.