[Preoperative workup to assess indication for laparoscopic treatment in gastroesophageal reflux disease].

INTRODUCTION AND OBJECTIVES: antireflux surgery performed by an experienced surgeon is a maintenance option for patients with well-documented gastroesophageal reflux disease (GERD). Well-documented GERD is difficult to find, as GERD is a multifactorial disease in which the gastroesophageal junction, with its special anatomical and functional components, is important. In order to examine patient preoperative workups, and their indication for surgical treatment in GERD, we retrospectively studied patients who underwent a laparoscopic antireflux procedure. METHODS: preoperative workups in patients from our health care area who underwent a laparoscopic antireflux procedure from December 1997 to February 2007 were retrospectively analyzed. Data related to epidemiological findings, symptoms, morphologic and functional evaluation, medical therapy, and indication for surgical treatment were recorded and statistically analyzed by means of a bivariate test. Differences were significant when the p value was equal to or less than 0.05. RESULTS: 100 patients (50 % female, 51.31 +/- 13.53 years of age) underwent a laparoscopic antireflux surgery after 56.47 +/- 61.33 months with symptoms. Ninety-five percent of patients had an anatomical abnormality. The pH monitoring test diagnosed three quarters of cases. The most frequent indication for GERD treatment was persistent or recurrent esophagitis despite adequate medical treatment (52 cases). CONCLUSIONS: based on our preoperative workup, as described, 100 percent of subjects were well documented and diagnosed with GERD (both non-erosive reflux disease and erosive reflux disease), and their indication for laparoscopic treatment was retrospectively assessed in 94% of cases.

[Effect of ursodeoxycholic acid in an experimental colon cancer model]. / Efecto del ácido ursodeoxicólico en un modelo experimental de cáncer de colon.

AIMS: The present study was designed to examine the effect of ursodeoxycholic acid as chemoprotective agent in experimental colon carcinogenesis in rats. MATERIAL AND METHODS: One hundred and ten 10-week-old, Sprague-Dawley rats were divided into five groups: group A (20), no treatment. Group B (20), receiving daily both ursodeoxycholic acid (UDCA) 4 mg/kg of body weight and ethanol 1.23 g/kg of body weight added to the drinking water from the beginning of the study through 24 weeks. Group C (30), receiving 18 weekly doses of dimethylhydrazine (DMH) 21 mg/kg of body weight subcutaneously from the beginning of the study, with the same doses of UDCA and ethanol as in group B. Group D (20), ethylen-diamin-tetracetic acid solution alone for 18 weeks. Group E (20), receiving the same doses of ethanol plus DMH injections as in group C. All experimental animals were sacrificed after 25-27 weeks. RESULTS: No tumors developed in dimethylhydrazine-free groups. No significant differences in number of tumor-free animals, number of tumors per rat, and macro-microscopic tumor findings were seen between animals in group C and animals in group E. CONCLUSIONS: We concluded that such an ursodeoxycholic acid supplementation did not modify colorectal carcinogenesis using a dynamic DMH-induced model in rats.

Effect of defunctionalization on colon carcinogenesis in the rat.

OBJECTIVE: to examine the effect of fecal absence on experimental colon carcinogenesis in both male and female rats. MATERIAL AND METHODS: a total of 138 10-week-old Sprague-Dawley, male and female rats were divided into five groups: A) 20 rats, no treatment; B) 26 rats, colonic defunctionalization; C) 30 rats, 18 weekly doses of dimethylhydrazine (DMH), 21 mg/kg body weight each, from the beginning of the study; D) 20 rats, ethylen-diamine-tetraacetic acid for 18 weeks; and E) 42 rats, same surgical procedure as rats in group B plus DMH injections at the same doses as rats in group C. Animals were sacrificed after 25-27 weeks. Number of tumors, their location, and pathological findings were all compared between groups. RESULTS: no tumors developed in the dimethylhydrazine-free groups. No differences were obtained either in number of tumors or tumors per rat for group C as compared to group E. Fecal absence was associated with smaller-sized tumors (p = 0.007), greater numbers of non-mucinous tumors (p = 0.00009), better differentiation (p = 0.0054), and lesser penetration into the wall (p = 0.015) for group E as compared to group C. In the dimethylhydrazine group, fecal absence altered the number of tumors developing in males as compared to female rats (p = 0.025). Moreover, this fecal absence showed no inhibitory effect on right colonic tumors (p = 0.0065). CONCLUSIONS: fecal absence alters the DMH-carcinogenic pattern in the defunctionalized colon when using an experimental model in both male and female rats.

Effect of ethanol consumption on colon cancer in an experimental model.

AIMS: The present study was designed to examine the effect of an ethanol supplement on experimental colon carcinogenesis. MATERIAL AND METHODS: One hundred and ten 10-week-old Sprague-Dawley rats were divided into five groups: group A (20 rats) received no treatment. Group B (20 rats) received a supplement of ethanol at 1.23 g/kg of body weight per day added to their drinking water for 24 weeks. Group C (30 rats) received 18 weekly doses of dimethylhydrazine (DMH) at 21 mg/kg of body weight from the beginning of the study. Group D (20 rats) received ethylen-diamin-tetracetic acid (EDTA) solution only for 18 weeks. Group E (20 rats) received ethanol at the same dose as group B plus DMH injections at the same dose as the rats in group C from the beginning of the study. All experimental animals were sacrificed after 25-27 weeks. RESULTS: No significant differences in the number of rats that developed tumors, number of tumor-free animals, and number of tumors per rat, as well as in macro-microscopic tumoral findings were observed for animals in group C compared to animals in group E. CONCLUSIONS: We concluded that the addition of an ethanol supplement does not modify colorectal carcinogenesis using a dynamic model of tumor induction with DMH.

Calcium inhibits colon carcinogenesis in an experimental model in the rat.

Different dietary factors can affect colorectal cancer incidence. However, the effect of increased levels of dietary calcium on neoplasms is unclear. The present study was designed to examine the effect of a low calcium supplement on experimental colon carcinogenesis induced by parenteral administration of dimethylhydrazine (DMH). One hundred and twenty 10-week-old Sprague-Dawley rats were divided into five groups of equal sex distribution. The 10 rats in group A (control group) received no treatment; the 30 rats in group B (DMH group) were injected subcutaneously with 18 weekly doses of 21 mg/kg DMH; the 20 rats in group C (EDTA control group) received EDTA solution only; the 30 rats in group D (calcium group) received calcium at 3.2 g/l by adding calcium lactate to the drinking water from the start until the conclusion of the experiment; and the 30 rats in group E (DMH + calcium group) received oral calcium supplements at the same dose as the rats in group D (calcium group) and the same DMH injections as the rats in group B (DMH group). The rats were sacrificed at 25-34 weeks. In group E, we observed a significant diminution in the number of tumours (P = 0.01); an increase in the number of tumour-free animals (P = 0.006); a change in tumour location towards the distal colon (P < 0.025); more adenomas (P = 0.02); and a diminution of adenocarcinomas and mucinous carcinomas, although this was not significant. We conclude that a low dietary calcium supplement in rats inhibits colon cancer carcinogenesis induced by DMH, and changes tumour location towards the distal colon.

Repetitive mucosal trauma promotes colon cancer in experimental rat model.

OBJECTIVE: To investigate the effect of repetitive mucosal trauma, anastomosis and intestinal content on experimental colonic carcinogenesis as there is the possibility than non-specific colon lesions can promote cancer. MATERIAL AND METHOD: We performed to sixty female Sprague-Dawley rats a 4 cm colon loop defunctionalization with double colostomy (traumatic site). Intestinal continuity was restored with an end-to-end colo-colic silk anastomosis. The surviving 47 rats were divided in 3 groups: Group A: 27 rats treated with DMH. Group B: 10 rats treated with EDTA and Group C: Control of 10 rats. Animals were sacrificed 31-32 weeks after surgery for macro and micropathological studies. RESULTS: In group A appeared 60 tumours: 44 in the functional colon, 20 of them in the anastomotic site; 8 in the non traumatised defunctionalized segment and 18 in the traumatised segment (p < 0.05). CONCLUSIONS: a) Continuous microtraumas on colonic mucosa in rats are cancer promotional factors; b) silk suture in anastomosis promotes cancer.