Biomedical subjects

G Caderni

Publications and source records attributed to G Caderni.

At least 37 records · Page 2Linked to original sources

PubMed1998

A dietary trial with a short-term low-sucrose diet in an Italian population: effects on colorectal mucosal proliferation.

Colorectal mucosal proliferation is supposed to predict colon cancer risk. We investigated whether a low-sucrose diet might reduce colorectal mucosal proliferation in a group of patients at higher risk of colorectal cancer after at least two colon adenoma resections. In a pilot phase, 14 patients [12 men and 2 women, 60.3 +/- 5 (SD) yr] were instructed to adopt a low-sucrose diet for one month. Colorectal biopsies were taken twice in the same patients, at the start and the end of the intervention period, and mucosal proliferation was measured by [3H]thymidine uptake in vitro and autoradiography. Although compliance of study participants to dietary modification was high, only a few agreed to two consecutive endoscopies; thus we carried out a randomized study, and 107 patients were assigned to a low-sucrose diet (50 treated patients: 31 men and 19 women, 59.7 +/- 7.5 yr) or instructed to continue their usual diet for one month (55 control patients: 32 men and 23 women, 59.6 +/- 7.7 yr). At the end of this period, colorectal biopsies were obtained. The results of the pilot phase and the randomized study showed that a low-sucrose diet for one-month did not affect proliferation or the distribution of proliferation activity along the crypt. The food-frequency questionnaires indicated that treated patients consumed significantly less sucrose (and fewer total calories) during the dietary modification. Urinary fructose, a measure of dietary sucrose intake, was also reduced at the end of the intervention period. In conclusion, we found no evidence that a low-sucrose diet for one month influences colorectal mucosal proliferation.

Adult↗

PubMed1997

In vivo studies on genotoxicity of pure and commercial linuron.

The ureic herbicide linuron [3-(3, 4-dichlorophenyl)-1-methoxy-1-methylurea] (CAS 330-55-2) was investigated for genotoxicity in a series of in vivo experiments. Since human exposure to herbicides is not only to the active principles, but also to all the chemicals present in the commercial formulation, we tested both pure and commercial linuron. Groups of rats were treated with gavage containing different doses of the herbicide (pure compound or commercial formulation) for 14 days. The doses were 150, 300 and 450 mg/kg b.wt. for the pure compound and 315.8, 631.6 and 947.4 mg/kg b.wt. for the commercial formulation (47.5% of linuron). Faeces and urine were collected at regular intervals. Urine specimens were analysed for their mutagenic metabolites, thioethers and D-glucaric acid content. Faeces extracts were tested for mutagenicity. Linuron's ability to cause DNA damage and cytogenetic effects was also investigated after treating groups of rats once with different doses of pure or commercial linuron. DNA single-strand breaks were assessed in rat liver using the alkaline elution technique and the single-cell microgel electrophoresis assay (SCGE: 'comet' assay), and in rat testes cells with the SCGE assay. Micronuclei induction was analysed in rat bone marrow erythrocytes. Results obtained were mainly negative when the excretion of mutagenic metabolites in urine and faeces of animals treated with the pure compound or with the linuron-based commercial formulation were monitored, whereas an increase in the urinary excretion of thioethers and D-glucaric acid was observed in rats treated with the commercial formulation. No increase in the frequency of micronucleated polychromatic erythrocytes was observed in the treated animals. However, linuron affected the viability of hepatocytes isolated from animals treated with higher doses. This cytotoxicity was accompanied by the induction of DNA single-strand breaks in the liver, as seen by the alkaline elution assay. The potential of pure linuron to induce in vivo DNA damage was confirmed with the microgel-electrophoresis technique ('comet' assay). Cytotoxicity was also seen in rat testes cells. However, no indication of DNA damage was visible.

Administration, Oral↗

PubMed1997

Dietary sucrose and starch affect dysplastic characteristics in carcinogen-induced aberrant crypt foci in rat colon.

To study whether dietary carbohydrates affect dysplasia in aberrant crypt foci (ACF), rats treated with 1,2-dimethilhydrazine (DMH) were fed for three months with diets containing 46% sucrose or corn starch. The number of ACF/colon in the two dietary groups was similar (P = 0.58), but ACF were smaller in the starch than in sucrose group (P < 0.05). ACF in the starch group also showed less severe goblet cell dysplasia, more sulphomucins and less sialomucins than in the sucrose group (P < 0.05), indicating that corn starch protects against colon carcinogenesis while sucrose in the diet is detrimental, promoting the dysplasia of preneoplastic lesions like ACF.

1,2-Dimethylhydrazine↗

PubMed1997

Modification of azoxymethane intestinal carcinogenesis in rats by feeding sucrose boluses, pasta, and glucose.

We studied whether repeated boluses of sucrose or diets containing carbohydrates with a variable glycemic index (GI) affect intestinal carcinogenesis in rats. Male F344 rats were treated twice (1 wk apart) with 15 mg/kg sc azoxymethane (AOM) and then divided into four experimental dietary groups with different carbohydrate composition and administration schedules: the sucrose group was fed 44% (wt/wt) sucrose (GI = 65), the bolus group was fed sucrose as carbohydrate and 43 boluses of sucrose (10-15 g/kg) at various time intervals, the pasta group was fed pasta [77% (wt/wt) cooked pasta, GI = 55], and the glucose group was fed 44% (wt/wt) glucose (GI = 97). All nutrients, including carbohydrates, were provided in similar amount to the different groups. The experiment was terminated between Day 230 and Day 245 after AOM administration. At this time the pasta group had significantly higher cecal short-chain fatty acids than the other groups. Intestinal adenomas and cancers occurred with the same frequency in the bolus, sucrose, and glucose groups. On the contrary, we observed a significant decrease (p = 0.03) in the cumulative incidence of intestinal adenomas, but not adenocarcinomas, in the pasta group compared with the sucrose group (intestinal adenoma incidence in the pasta group was 31% compared with 63% in the sucrose group, 46% in the bolus group, and 37% in the glucose group). In conclusion, these results do not support the hypothesis that sucrose boluses or carbohydrates with a high GI stimulate colon carcinogenesis, but they indicate that foods such as pasta may exert a protective effect.

Adenoma↗

PubMed1997

Aberrant crypt foci in human colon carcinogenesis.

We developed a procedure for the endoscopic visualization in humans of aberrant crypt foci (ACF), preneoplastic lesions of the colon mucosa, and we determined the frequency of ACF in resected sections of human colon. For the endoscopy we studied 12 consenting adults (6 controls and 6 colon cancer cases) by dyeing colon mucosa with 0.5% methylene blue and searching ACF with a magnifying endoscope. ACF of varying dimensions were visualized in all subjects. We also studied colon surgical specimens from patients with colon cancer or diverticulitis. After staining the mucosa with 2% methylene blue, we found approximately the same density of ACF in the colon mucosa of the patients with colon cancer as in that of patients with diverticulitis (ACF/cm2 were 0.124 +/- 0.143 [N = 14] and 0.108 +/- 0.210 [N = 4], respectively [mean +/- SD]). In conclusion, the visualization of ACF with methylene blue in humans does not identify groups at low and high risk of colon cancer.

Adult↗

PubMed1996

Dietary sucrose, glucose, fructose, and starches affect colonic functions in rats.

To study the effect of dietary sugars and starches on parameters linked to colon carcinogenesis, female Sprague-Dawley rats were fed for one month five different diets containing sucrose, glucose, fructose, cornstarch, or Hylon 7, a starch with a high amylose content. After this period, colon proliferation, assessed by [3H] thymidine incorporation in vitro, was higher (p < 0.05) in rats fed sucrose than in rats fed glucose, fructose, or cornstarch [labeling index was 7.17 +/- 0.75, 5.03 +/- 0.07, 4.55 +/- 0.72, 4.00 +/- 0.70, and 5.89 +/- 1.05 (SE) in sucrose, glucose, fructose, cornstarch, and Hylon 7 diets, respectively]. Cecal pH was lower in rats fed cornstarch and Hylon 7 than in rats fed sucrose, glucose, or fructose. Content of short-chain fatty acids (SCFAs) in the cecum was higher in rats fed Hylon 7 than in those fed glucose and fructose. In conclusion, glucose and fructose, compared with sucrose, decrease mucosal proliferation and may be considered protective factors in colon carcinogenesis, although they do not affect SCFA production and cecal pH. On the contrary, Hylon 7 does not change mucosal proliferation but increases SCFAs and lowers cecal pH, two conditions associated with a lower risk of colon cancer.

Amylose↗

PubMed1996

Effects of repeated boluses of sucrose on proliferation and on AOM-induced aberrant crypt foci in rat colon.

Colonic mucosal proliferation, aberrant crypt foci (ACF) induction, and fecal bile acids, parameters connected to the risk of colon cancer development, were studied in female F344 rats treated with starch or sucrose boluses or with a sucrose diet. Cell proliferation was higher in animals treated with a single sucrose bolus than in those given a starch bolus (15 g/kg body wt), with 4.3 +/- 0.64 and 2.17 +/- 0.57 (SE) mitotic figures (MF) per crypt in the sucrose and starch bolus groups, respectively (p < 0.01). When azoxymethane (AOM, 20 mg/kg) was administered 24 hours after a single sucrose or starch bolus, the number of ACF per colon after 30 days was higher in the sucrose bolus group [107.5 +/- 9.5 (SE)] than in the starch bolus group (67.8 +/- 0.9, p < 0.01). In additional experiments, colon cell proliferation (MF/crypt) was higher in rats given boluses of sucrose three times per week for 40 days after AOM (20 mg/kg) [5.9 +/- 0.7 (SE)] than in rats given starch boluses (2.96 +/- 0.4) or fed sucrose continuously (3.6 +/- 0.5). On the contrary, after 40 days of dietary treatment, the number, dimension, and percentage of ACF secreting sulfomucins and sialomucins were not varied among these three groups. However, the percentage of "large ACF" (ACF with > or = 4 crypts) secreting sialomucins or predominantly sialomucins was higher (p < 0.05) in the sucrose bolus group than in the starch group. The concentration of fecal bile acids and long-chain fatty acids was the same in the sucrose and starch groups, but the concentrations of deoxycholic and oleic acid were significantly higher in the sucrose bolus group. In conclusion, the administration of sucrose as a bolus had a stronger effect than continuous sucrose feeding on some parameters related to colon carcinogenesis and might be considered a risk factor in colon carcinogenesis.

Animals↗

PubMed1996

Urinary excretion of sucrose and fructose as a predictor of sucrose intake in dietary intervention studies.

The urinary excretion of sucrose, glucose, and fructose was measured in 9 healthy subjects consuming a common Italian diet and after 3 days of a low sucrose diet, in which the intake of sucrose was restricted but the other main nutrients were unmodified. After the low sucrose diet, we observed a significant drop in the average urinary excretion of sucrose, glucose, and fructose determined at four different times (8:00 and 10:00 a.m.; 3:00 and 10:00 p.m.). The average urinary excretion of fructose in the four urine samples was significantly correlated with dietary sucrose intake. We also found a significant correlation between the average urinary excretion of sucrose and dietary sucrose intake. Urinary fructose can be used as a marker of sucrose intake in dietary intervention studies aimed at studying the effect of variation of carbohydrate intake on specific cancers.

Adult↗

PubMed1995

Effects of short chain fatty acids on mucosal proliferation and inflammation of ileal pouches in patients with ulcerative colitis and familial polyposis.

PURPOSE: To verify whether short chain fatty acids (SCFA) alter the proliferative and endoscopic pattern of the mucosa in ileal pouches of ulcerative colitis (UC) or familial adenomatous polyposis (FAP) patients. METHODS: We studied patients after proctocolectomy carrying a pelvic ileal pouch for FAP or UC (noncanalized pouches in 10 UC and 4 FAP patients and canalized pouches in 6 UC and 5 FAP patients). Patients with noncanalized pouches were treated twice daily for one week with 30 ml of a SCFA solution (60 mM sodium acetate, 30 mM sodium propionate, 40 mM sodium butyrate, and 22 mM sodium chloride, pH 7); patients with canalized pouches were treated with the same solution twice daily for two weeks. Pouch mucosal biopsies were collected before and after SCFA. Mucosal proliferation was assessed by incorporation of [3H]thymidine in vitro and autoradiography. RESULTS: In UC patients proliferation did not vary in noncanalized pouches but was significantly reduced in canalized pouches after SCFA. In FAP patients SCFA did not alter proliferation. No significant effects of SCFA were observed on daily defecation frequency, endoscopic appearance, or histopathology of the pouches. CONCLUSIONS: SCFA do not control inflammation and clinical functions but reduce cell proliferation in UC patients. On the contrary, FAP patients are refractory to SCFA.

Adenomatous Polyposis Coli↗

PubMed1995

Characterisation of aberrant crypt foci in carcinogen-treated rats: association with intestinal carcinogenesis.

Carcinogen-treated rats develop foci of aberrant crypts in the colon (ACFs) that have been interpreted as preneoplastic lesions. To characterise ACFs further, we studied in the unsectioned colon of rats the number, multiplicity, some morphological characteristics and the type of mucin production in ACFs. In ACFs observed 115 days after the administration of 50 mg kg-1 1,2-dimethylhydrazine (DMH), crypt multiplicity [number of aberrant crypts (AC) per focus] was positively correlated (P < 0.0001) with the reduction of goblet cells, and with luminal and nuclear alterations in the cells surrounding the lumen of the ACs. We studied mucin production in the unsectioned colon, demonstrating that ACFs producing sulphomucins (like the normal distal rat colon) were progressively reduced when ACF multiplicity increased, whereas ACFs containing sialomucins (correlated with an increased risk of colon cancer) or both sulphomucins and sialomucins increased with crypt multiplicity. We also studied ACFs in the colon and the occurrence of intestinal tumours in rats treated with azoxymethane (AOM; 64 mg kg-1). A significant association was found (P = 0.04) between tumours and the presence of 'large' ACFs (AC/ACF > 14 crypts) and a borderline significant association (P = 0.057) between the presence of tumours and sialomucin-producing ACFs. We found no association between the number of ACFs, ACF multiplicity and the presence of tumours.

1,2-Dimethylhydrazine↗

PubMed1994

Rectal proliferation and polyp occurrence in patients with familial adenomatous polyposis after sulindac treatment.

BACKGROUND/AIMS: Sulindac, a nonsteroidal anti-inflammatory drug (NSAID), decreases the occurrence of polyps in patients with familial adenomatous polyposis (FAP). The effects of colectomy with ileorectal anastomosis (IRA) and sulindac treatment on rectal mucosa proliferation and polyp occurrence were examined in patients with FAP. METHODS: The number and size of rectal polyps were measured with colonoscopy. The labeling index, the percentage of labeled cells per crypt compartment, was assessed in rectal biopsy specimens with [3H]thymidine incorporation and autoradiography in 6 non-IRA and 14 IRA patients before and after treatment with 200 mg of sulindac/day for 60 days. RESULTS: The IRA patients had a lower labeling index and a decrease in the percentage of labeled cells in the upper compartment of the crypt (P < 0.01) relative to non-IRA subjects. Sulindac did not influence the labeling index and the distribution of labeled cells along the crypt. On the contrary, a dramatic decrease in the size and number of polyps was observed after sulindac treatment (P < 0.001). CONCLUSIONS: The persistence of a abnormal mucosal proliferation after sulindac therapy, in spite of the reduction of polyp number, suggests caution in assuming a lower risk of rectal cancer in patients with FAP.

Adenomatous Polyposis Coli↗

PubMed1994

Dietary carbohydrates modify azoxymethane-induced intestinal carcinogenesis in rats.

The effect of different dietary carbohydrates (sucrose, cornstarch and high amylose cornstarch) on intestinal carcinogenesis was studied in male Sprague-Dawley rats treated subcutaneously with azoxymethane (AOM) at a weekly dose of 8 mg/kg body wt for 8 wk. The diets, high in fat and low in calcium and fiber, were fed during and after AOM treatment. The number of colonic adenomas per rat in the groups fed either starch was lower (P < 0.05) than the number in the sucrose-fed rats [1.06 +/- 0.38, 0.30 +/- 0.10 and 0.41 +/- 0.22 (mean +/- SEM), in the sucrose-, cornstarch- and high amylose cornstarch-fed groups, respectively]. The incidence of total intestinal tumors (adenomas + adenocarcinomas) was not affected by dietary treatment. However, the incidence of tumors in the small intestine of the rats fed the two cornstarch diets tended to be slightly lower than for rats fed the sucrose diet (P = 0.075). Adenoma dysplasia and adenocarcinoma differentiation were similar among the rats fed the three diets. However, the adenocarcinomas in the rats fed the cornstarch diet were significantly smaller than those in the rats fed sucrose [0.99 +/- 0.14 cm2 (n = 13), 0.56 +/- 0.14 cm2 (n = 13) and 0.55 +/- 0.17 cm2 (n = 9) in rats fed the sucrose, cornstarch and high amylose starch diets, respectively]. Moreover, in the rats fed the cornstarch diet, the adenocarcinomas showed lower invasive potential than those in rats fed the sucrose diet. The results suggest an overall inhibition of AOM-induced carcinogenesis in rats fed the cornstarch diets.

Adenocarcinoma↗

PubMed1993

The growth of preneoplastic lesions by 1,2-dimethylhydrazine in rat colon is inhibited by dietary starch.

The effect of dietary starch and sucrose on colon proliferation and the growth of foci of dysplastic crypts in the colon (FDC) were studied in female Sprague-Dawley rats, treated p.o. with 1,2-dimethylhydrazine (DMH). The animals were fed for 30 and 105 days with high fat (23% w/w corn oil) diets in which carbohydrates were represented by corn starch (starch diet) or sucrose (sucrose diet) (46% w/w). After 105 days of feeding, proliferation was markedly reduced in animals fed the starch diet. The number of FDC was not significantly affected by dietary treatments. However, after 30 and 105 days the percent of small FDC (formed by one-two dysplastic crypts) was higher in the animals fed the starch diet when compared to the sucrose diet. In the cecum of the animals fed the starch diet the percent of butyrate, propionic, isovaleric, and valeric over total short-chain fatty acids (SCFA) was increased, whereas the percent of acetic acid was decreased. Cecal pH was also decreased in the animals fed starch. The results suggest that starch diets have a protective role against DMH-colon carcinogenesis in the rat, mediated by a drop in cecal pH and an increased concentration of some SCFA.

1,2-Dimethylhydrazine↗

PubMed1993

Mitotic activity in colorectal mucosa of healthy subjects in two Italian areas with different dietary habits.

The proliferative activity was evaluated in colorectal biopsies of 39 healthy subjects living in two distinct geographical areas, Trieste in northern and Florence in central Italy. Subjects living in Trieste had a significantly higher mitotic activity compared with subjects living in Florence (mitoses/cells counted x 100 were 0.17 +/- 0.04 in Trieste and 0.089 +/- 0.02 in Florence). The results of a dietary questionnaire also showed that subjects in Trieste consumed significantly fewer starches, fibers, nitrites, and proteins. However, no correlation was evident between the consumption of these nutrients and intestinal proliferation.

Adult↗

PubMed1993

Rats fed high starch diets have lower colonic proliferation and fecal bile acids than high sucrose-fed controls.

We studied the effects of sucrose or starch in the diet (460 g/kg diet) on fecal bile acid concentrations in Sprague Dawley rats after 4 wk of feeding. Total bile acid concentration in the feces was significantly lower in the rats fed the starch diet than in those fed the sucrose diet (4.56 +/- 0.47 mg/g dry weight and 8.03 +/- 0.94, respectively, SEM), due to a reduction of deoxycholic, alpha-muricholic and beta-muricholic acids. Fecal and cecal pH values were significantly lower in the rats fed the starch diet compared to those fed the sucrose diet (6.79 +/- 0.08 and 7.15 +/- 0.09 for fecal pH and 7.02 +/- 0.05 and 7.2 +/- 0.04 for cecal pH in the two diet groups, respectively). Colon proliferation was also significantly lower in the starch-fed rats compared to those fed sucrose (labeling index 3.51 +/- 0.6 and 5.69 +/- 0.74, respectively), and the reduction was apparent in the middle and upper compartments of the colon crypts. The mucosal proliferation, expressed as percentage of labeled cells in the upper compartment of the colon crypts, was positively correlated with the concentration of deoxycholic, lithocholic, alpha-muricholic, beta-muricholic, cholic and total bile acids in the feces (per gram wet weight). The results indicate a protective effect of starch versus sucrose diets on colon mucosa.

Administration, Oral↗

PubMed1992

Profile of short-chain fatty acids and rectal proliferation in rats fed sucrose or cornstarch diets.

Rats were fed high fat (231 g/kg diet), low calcium (1.3 g/kg diet), low cellulose (20 g/kg diet) diets in which carbohydrates were represented by sucrose or starch (460 g/kg diet). A subgroup of animals was treated with 1,2-dimethylhydrazine (DMH) twice, 4 and 8 d before the beginning of the dietary treatments. Animals fed the starch diet, compared with those fed the sucrose diet, had higher concentrations of cecal and fecal short-chain fatty acids and a significantly lower acetic acid:butyric acid ratio in the cecal contents at d 105. Ratios were 14.7 +/- 1.7 and 6.8 +/- 0.4 for rats fed the sucrose and starch diets, respectively (P less than 0.01). Cecal pH was significantly lower in animals fed the starch diet for 105 d. At d 105, rectal proliferation was lower in rats fed the starch diet (labeled cells/crypt were 7.89 +/- 0.56 and 3.57 +/- 0.40 for rats fed the sucrose and starch diets, respectively, P less than 0.01); at d 30 the effect of starch on proliferation was evident in controls but not in DMH-treated rats. Rectal proliferation data were negatively correlated with the concentration and percentage of butyric acid and positively correlated with the percentage of acetic acid, the acetic acid:butyric acid ratio and cecal pH. These results suggest that low rectal proliferation in animals fed a high fat, high starch diet might be associated with a lower relative concentration of butyric acid in the cecal contents.

1,2-Dimethylhydrazine↗

PubMed1991

Effect of dietary carbohydrates on the growth of dysplastic crypt foci in the colon of rats treated with 1,2-dimethylhydrazine.

The effect of dietary starch and sucrose on the growth of foci of dysplastic crypts in the colon (FDC) was studied in female Sprague Dawley rats treated twice p.o. with 25 mg/kg of 1,2-dimethylhydrazine (DMH). After DMH administration, the animals were fed high-fat (23% corn oil, w/w)/low-calcium (0.1%, w/w)/low-cellulose (2%, w/w) diets in which carbohydrates were represented by corn starch (starch diet) or sucrose (sucrose diet) (46%, w/w). The animals were fed for either 30 or 105 days with the experimental diets. The number of FDC was not significantly affected by diet. However, after 30 days the percentage of small FDC (formed by 1-2 dysplastic crypts) was higher in the animals fed the starch diet compared to the animals fed the sucrose diet [90.3 +/- 1.1% (SE) and 82.6 +/- 3.1%, respectively; P less than 0.05]. In contrast, foci formed by 3-4 dysplastic crypts were decreased by the starch diet (P less than 0.05). After 105 days of feeding, the starch diet induced a number of dysplastic crypts/focus lower than that induced by the sucrose diet (2.6 +/- 0.1 and 2.9 +/- 0.1, respectively; P less than 0.05). The percentage of small FDC was also higher in the animals fed the starch diet compared to animals fed the sucrose diet (P less than 0.01). After 30 days of feeding, DMH treatment increased colon proliferative activity in both dietary groups (P less than 0.05). But after 105 days of feeding, proliferation was similar in controls and DMH-treated rats and markedly reduced in animals fed the starch diet (mean labeling index values for both controls and DMH-treated rats were 10.4 +/- 0.8 and 4.4 +/- 0.5 in the sucrose and starch diets, respectively; P less than 0.001). The overall results suggest that starch in high-fat/low-calcium/low-cellulose diets has a protective role against DMH-colon carcinogensis in the rat.

1,2-Dimethylhydrazine↗

PubMed1991

Mucosal cell proliferation of the rectal stump in ulcerative colitis patients after ileorectal anastomosis.

The proliferative activity and polyamine levels of the rectal epithelium in unoperated ulcerative colitis patients and in ulcerative colitis patients after total colectomy and ileorectal anastomosis were determined and compared with control subjects. Cell proliferation was evaluated in rectal biopsies by in vitro 3H thymidine incorporation by measuring the labeling index and the position of labeled cells along the crypt; polyamines were determined with a chromatographic method. In ulcerative colitis patients the labeling index was significantly increased, and labeled cells were shifted toward the upper part of the crypt when compared with controls. Ileorectal anastomosis patients showed a normalization of the labeling index and a distribution of labeled cells similar to controls. Polyamine levels were also increased in ulcerative colitis patients; in ileorectal anastomosis patients, the level of polyamines was decreased in respect to unoperated patients and return to normal values except for spermine. Because the increased proliferation and higher polyamine levels are related to increased colon cancer risk, our results confirm that ulcerative colitis is a risk factor for the development of carcinoma. Ileorectal anastomosis may reduce this risk through a normalization of mucosal cell proliferative activity and of some polyamine levels.

Adolescent↗