Infección crónica por el virus de la hepatitis C: un factor de riesgo independiente para la ateromatosis subclínica / Chronic hepatitis C infection: an independent risk factor for subclinical atheromatosis

Introducción: Se desconoce la asociación entre ateromatosis subclínica e infección crónica por el virus de la hepatitis C (VHC), relevante ahora que los antivirales mejoran la supervivencia en los pacientes infectados. Objetivos: Conocer si el VHC es factor de riesgo independiente de ateromatosis subclínica y analizar las modificaciones del perfil lipídico según niveles de ARN viral y fibrosis hepática. Pacientes y métodos: Estudio observacional y transversal; incluye 102 pacientes VHC positivos y 102 sujetos VHC negativos con paridad de sexo y edad, sin antecedentes de enfermedad cardiovascular, renal ni diabetes. La ateromatosis (presencia de placas de ateroma) y el grosor íntima-media carotídeo (GIMc) se evaluó mediante ecografía de arterias carótidas y femorales. Resultados: La presencia de ateromatosis en cualquier territorio vascular fue mayor en pacientes VHC que en sujetos no infectados (58,8% frente a 28,4%, p<0,001). En el análisis multivariante, los factores significativamente asociados con ateromatosis incluyeron infección por VHC (OR=14,37 [5,5-37,3]; p<0,001), edad (OR=1,12 [1,1-1,2]; p<0,001), sexo masculino (OR=4,32 [1,9-9,5]; p<0,001) y el coeficiente triglicéridos/colesterol HDL (TG/HDL-indicador indirecto de insulinorresistencia) (OR=1,34 [1,1-1,6]; p=0,007). Los pacientes VHC con placas de ateroma presentaban mayor coeficiente TG/HDL, sin diferencias significativas en cuanto a la carga viral ni grado de fibrosis hepática con un perfil lipídico de «bajo riesgo». Conclusiones: La infección VHC es factor de riesgo independiente de ateromatosis subclínica. La ecografía arterial sistémica en esta población mejora la evaluación del riesgo cardiovascular más allá de las alteraciones del perfil lipídico y del cálculo de riesgo por tablas SCORE

Background: The association between subclinical atheromatosis and chronic hepatitis C virus (HCV) infection is unknown but is relevant now that antivirals are improving the survival of patients with the infection. Objectives: To determine whether HCV is an independent risk factor for subclinical atheromatosis and to analyse the changes in lipid profiles according to viral RNA levels and hepatic fibrosis. Patients and methods: We conducted an observational, cross-sectional study that included 102 HCV-positive patients and 102 HCV-negative patients with parity in terms of sex and age, with no history of cardiovascular or kidney disease or diabetes. Atheromatosis (the presence of atheromatous plaques) and the carotid intima-media thickness (CIMT) were assessed using ultrasonography of the carotid and femoral arteries. Results: There was a greater presence of atheromatosis in any vascular territory in HCV-positive patients than in the patients without infection (58.8% vs. 28.4%, p<.0001). In the multivariate analysis, the factors significantly associated with atheromatosis included HCV infection (OR, 14.37 [5.5-37.3]; p<.001), age (OR, 1.12 [1.1-1.2]; p<.001), male sex (OR, 4.32 [1.9-9.5]; p<.001) and the triglyceride/HDL cholesterol coefficient (TG/HDL-indirect indicator of insulin resistance) (OR, 1.34 [1.1-1.6]; p=.007). The HCV-positive patients with atheromatous plaques had a higher TG/HDL coefficient but no significant differences in terms of the viral load or degree of hepatic fibrosis and with a 'low risk' lipid profile. Conclusions: HCV infection is an independent risk factor for subclinical atheromatosis. Systemic arterial ultrasonography for this population improves the cardiovascular risk assessment beyond lipid profile abnormalities and the risk calculation using SCORE tables

Chronic hepatitis C infection: An independent risk factor for subclinical atheromatosis. / Infección crónica por el virus de la hepatitis C: un factor de riesgo independiente para la ateromatosis subclínica.

BACKGROUND: The association between subclinical atheromatosis and chronic hepatitis C virus (HCV) infection is unknown but is relevant now that antivirals are improving the survival of patients with the infection. OBJECTIVES: To determine whether HCV is an independent risk factor for subclinical atheromatosis and to analyse the changes in lipid profiles according to viral RNA levels and hepatic fibrosis. PATIENTS AND METHODS: We conducted an observational, cross-sectional study that included 102 HCV-positive patients and 102 HCV-negative patients with parity in terms of sex and age, with no history of cardiovascular or kidney disease or diabetes. Atheromatosis (the presence of atheromatous plaques) and the carotid intima-media thickness (CIMT) were assessed using ultrasonography of the carotid and femoral arteries. RESULTS: There was a greater presence of atheromatosis in any vascular territory in HCV-positive patients than in the patients without infection (58.8% vs. 28.4%, p<.0001). In the multivariate analysis, the factors significantly associated with atheromatosis included HCV infection (OR, 14.37 [5.5-37.3]; p<.001), age (OR, 1.12 [1.1-1.2]; p<.001), male sex (OR, 4.32 [1.9-9.5]; p<.001) and the triglyceride/HDL cholesterol coefficient (TG/HDL-indirect indicator of insulin resistance) (OR, 1.34 [1.1-1.6]; p=.007). The HCV-positive patients with atheromatous plaques had a higher TG/HDL coefficient but no significant differences in terms of the viral load or degree of hepatic fibrosis and with a 'low risk' lipid profile. CONCLUSIONS: HCV infection is an independent risk factor for subclinical atheromatosis. Systemic arterial ultrasonography for this population improves the cardiovascular risk assessment beyond lipid profile abnormalities and the risk calculation using SCORE tables.

Telomeres and telomerase in the clinical management of colorectal cancer

Colorectal cancer (CRC) is the third most common cancer worldwide. Our aim is to describe the state of the art about the role of telomeres and telomerase in the clinical management of CRC and its potential utility as prognostic and diagnostic biomarkers and targets of new treatments. Telomere length could be a new diagnostic marker as an anomalous behavior is observed in peripheral blood cells when CRC patients and healthy people are compared. Moreover, telomeres and telomerase may be used as diagnostic markers considering that universal changes appear along the CRC process. Currently, new therapeutic cancer approaches are focused on inhibiting the maintenance of telomere length, choosing as targets telomerase -or its subunits- or the Shelterin complex. The goal of these therapies is the shortening of telomeres and the induction of cell senescence. Telomeres and telomerase emerge as useful molecular tools in the clinical management of CRC (AU)

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Telomeres and telomerase in the clinical management of colorectal cancer.

Colorectal cancer (CRC) is the third most common cancer worldwide. Our aim is to describe the state of the art about the role of telomeres and telomerase in the clinical management of CRC and its potential utility as prognostic and diagnostic biomarkers and targets of new treatments. Telomere length could be a new diagnostic marker as an anomalous behavior is observed in peripheral blood cells when CRC patients and healthy people are compared. Moreover, telomeres and telomerase may be used as diagnostic markers considering that universal changes appear along the CRC process. Currently, new therapeutic cancer approaches are focused on inhibiting the maintenance of telomere length, choosing as targets telomerase -or its subunits- or the Shelterin complex. The goal of these therapies is the shortening of telomeres and the induction of cell senescence. Telomeres and telomerase emerge as useful molecular tools in the clinical management of CRC.

Telomeric repeat factor 1 protein levels correlates with telomere length in colorectal cancer.

BACKGROUND: colorectal cancer is the third cancer cause of death in Spain. It is important to investigate new tumoral markers for early diagnosis, disease monitoring and prevention strategies. Telomeres protect the chromosome from degradation by nucleases and endto-end fusion. The progressive loss of the telomeric ends of chromosomes is an important mechanism in the timing of human cellular aging. Telomeric Repeat Factor 1 (TRF1) is a protein that binds at telomere ends. PURPOSE: to measure the concentrations of TRF1 and the relationships among telomere length, telomerase activity, and TRF1 levels in tumor and normal colorectal mucosa. METHOD: from normal and tumoral samples of 83 patients who underwent surgery for colorectal cancer we analyzed TRF1 protein concentration by Western Blot, telomerase activity, by the fluorescent-telomeric repeat amplification protocol assay and telomere length by Southern Blot. RESULTS: high levels of TRF1 were observed in 68.7% of tumor samples, while the majority of normal samples (59%) showed negative or weak TRF1 concentrations. Among the tumor samples, telomere length was significantly associated with TRF1 protein levels (p = 0.023). CONCLUSIONS: a relationship was found between telomere length and TRF1 abundance protein in tumor samples, which means that TRF1 is an important factor in the tumor progression and maybe a diagnostic factor.

Telomerase activity and telomere length in the colorectal polyp-carcinoma sequence.

OBJECTIVE: The role of telomerase activity and telomere length in the adenoma-carcinoma sequence of colon carcinogenesis has not been well established. The objective of this study was to determine telomerase activity and telomere length patterns in patients with adenomatous polyps either associated or not with colorectal cancer, as well as the role of telomeric instability in the adenoma-carcinoma sequence. PATIENTS AND METHODS: We included in the study 14 patients who underwent surgery for colorectal cancer and/or polyps. In 6 of these patients fresh samples of tumor tissue, polyps, and normal mucosa were obtained; in the 8 remaining cases, we collected only polyps and normal mucosa. We used the fluorescent-telomeric repeat amplification protocol assay (TRAP-F) to determine telomerase activity and telomere length using Southern-blot testing. RESULTS: Telomerase activity was detected in 86% of polyps and 50% of associated normal mucosa. Mean telomerase activity in polyp tissue was 5.85; in the normal mucosa it was 0.58 TPG. Mean telomere length was 6.78 Kbp and 7.78, respectively. Polyps in patients without synchronous cancer had a telomerase activity that was significantly higher (9.4) than in those with cancer (1.1). CONCLUSIONS: Telomerase activity increases in the colorectal adenoma-carcinoma sequence, concurrently with a decrease in telomere length. The presence of synchronous cancer modifies telomerase activity in polyps.

Actividad de la telomerasa y longitud del telómero en la secuencia pólipo-carcinoma colorrectal / Telomerase activity and telomere length in the colorectal polyp-carcinoma sequence

Objetivo: el papel de la actividad de la telomerasa y la longitud del telómero en la secuencia adenoma-carcinoma de la carcinogénesis colónica no ha sido bien establecido. El objetivo fue determinar el comportamiento de la actividad de la telomerasa y la longitud del telómero en pacientes con pólipos adenomatosos asociados o no a cáncer colorrectal y conocer el papel de la inestabilidad telomérica en la secuencia adenoma-carcinoma. Pacientes y métodos: se estudiaron 14 pacientes intervenidos de cáncer colorrectal y/o pólipos. En 6 de ellos se recogieron muestra colónica tumoral, pólipo y muestra de mucosa colónica normal, mientras que en los 8 restantes se tomaron muestras de pólipos y mucosa normal. Se determinó la actividad de la telomerasa mediante el protocolo de amplificación de repeticiones teloméricas (TRAP-F) y la longitud del telómero por Southern-blot. Resultados: se detectó actividad de la telomerasa en un 86% de los pólipos y en un 50% de sus correspondientes mucosas normales. La actividad de la telomerasa en los pólipos fue de 5,85 y en la mucosa normal 0,58 TPG. La longitud del telómero fue 6,78 kbp y 7,78 respectivamente. Se observó que los pólipos de pacientes que no presentaban cáncer sincrónico mostraban una actividad de telomerasa significativamente superior (9,4) a aquellos con cáncer (1,1) (p = 0,02). Conclusiones: existe una actividad de la telomerasa creciente en la secuencia adenoma-carcinoma en la mucosa colónica así como una disminución de la longitud del telómero. La presencia de cáncer sincrónico modifica la actividad de telomerasa del pólipo(AU)

Objective: the role of telomerase activity and telomere length in the adenoma-carcinoma sequence of colon carcinogenesis has not been well established. The objective of this study was to determine telomerase activity and telomere length patterns in patients with adenomatous polyps either associated or not with colorectal cancer, as well as the role of telomeric instability in the adenoma-carcinoma sequence. Patients and methods: we included in the study 14 patients who underwent surgery for colorectal cancer and/or polyps. In 6 of these patients fresh samples of tumor tissue, polyps, and normal mucosa were obtained; in the 8 remaining cases, we collected only polyps and normal mucosa. We used the fluorescent-telomeric repeat amplification protocol assay (TRAP-F) to determine telomerase activity and telomere length using Southern-blot testing. Results: telomerase activity was detected in 86% of polyps and 50% of associated normal mucosa. Mean telomerase activity in polyp tissue was 5.85; in the normal mucosa it was 0.58 TPG. Mean telomere length was 6.78 Kbp and 7.78, respectively. Polyps in patients without synchronous cancer had a telomerase activity that was significantly higher (9.4) than in those with cancer (1.1). Conclusions: telomerase activity increases in the colorectal adenoma-carcinoma sequence, concurrently with a decrease in telomere length. The presence of synchronous cancer modifies telomerase activity in polyps(AU)

[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.

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

Objetivos: analizar si la administración oral del ácido urso -deo xi cólico previene la aparición y desarrollo de carcinogénesiscolónica en ratas.Material y métodos: ciento diez ratas de la raza “Sprague-Dawley” de 10 semanas de vida, de ambos sexos, fueron divididasen 5 grupos: a) 20 ratas control, sin tratamiento; b) 20 ratas, tratadascon ácido ursodeoxicólico (AUDC), a 4 mg/kg/día, juntocon etanol, a 1,23 g/kg peso al día, añadidos al agua de bebida,desde el principio del estudio y durante 24 semanas; c) 30 ratas,18 dosis semanales, de 21 mg/kg peso de dimetilhidracina(DMH) subcutánea, desde el principio del estudio, junto con lasmismas dosis de etanol y AUDC, que en el grupo B; d) 20 ratas,18 dosis semanales subcutáneas de ácido etilen-diamino-tetracético;y e) 20 ratas, tratadas con las mismas dosis de etanol y lasmismas inyecciones de DMH, que el grupo C. El sacrificio de todoslos animales, se llevó a cabo en las semanas 25-27.Resultados: no aparecieron tumores en ausencia de DMH.No se observaron diferencias significativas en el número de ratasque desarrollaron cáncer de colon, ni en el número de neoplasiaspor rata, ni en los hallazgos macro-microscópicos de los tumores,entre los animales del grupo C y del grupo E.Conclusiones: la administración de ácido ursodeoxicólico, enla dosis y tiempo utilizados no modificó la carcinogénesis colónica,usando un modelo dinámico de administración concomitantede inducción tumoral con DMH en ratas

Aims: the present study was designed to examine the effect ofursodeoxycholic acid as chemoprotective agent in experimentalcolon 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 ursodeoxycholicacid (UDCA) 4 mg/kg of body weight and ethanol 1.23 g/kg ofbody weight added to the drinking water from the beginning ofthe study through 24 weeks. Group C (30), receiving 18 weeklydoses of dimethylhydrazine (DMH) 21 mg/kg of body weight subcutaneouslyfrom the beginning of the study, with the same dosesof 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 ingroup C. All experimental animals were sacrificed after 25-27weeks.Results: no tumors developed in dimethylhydrazine-freegroups. No significant differences in number of tumor-free animals,number of tumors per rat, and macro-microscopic tumorfindings were seen between animals in group C and animals ingroup E.Conclusions: we concluded that such an ursodeoxycholicacid supplementation did not modify colorectal carcinogenesis usinga 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.

Efecto de la desfuncionalización colónica en un modelo experimental de cáncer de colon / Effect of defunctionalization on colon carcinogenesis in the rat

Objetivo: examinar el efecto de la ausencia fecal en la aparicióny desarrollo de la carcinogénesis colónica en ratas de ambossexos.Material y métodos: ciento treinta y ocho ratas “Sprague-Dawley” de 10 semanas de vida, de ambos sexos, divididas en5 grupos: A) 20 ratas, sin tratamiento; B) 26 ratas, con una desfuncionalizacióncolónica; C) 30 ratas, 18 dosis semanales de 21mg/kg peso de dimetilhidracina (DMH) desde el principio del estudio;D) 20 ratas, 18 semanas con ácido etilen-diamino-tetracético;y E) 42 ratas, igual técnica quirúrgica que B, y las mismas inyeccionesque C. El sacrificio tuvo lugar a las 25-27 semanas. Se estudióla incidencia de tumores colorrectales, su localización y loshallazgos anátomo-patológicos, comparando entre grupos.Resultados: la ausencia de carcinógeno no desarrolló tumores.No hubo diferencias significativas entre el número total de tumoresinducidos ni en el promedio de tumores por rata entre lasratas C y las E. La ausencia fecal provocó unos tumores de menortamaño (p = 0,007), los cuales presentaron estirpes más glandulares(p = 0,00009), mejor diferenciadas (p = 0,0054) y menos invasivas(p = 0,015). Así mismo, la ausencia fecal modificó tanto elpredominio natural de los machos sobre las hembras para desarrollarun mayor número de tumores colónicos DMH-inducidos(p = 0,025), como el predominio en el colon derecho de los carcinomasmucinosos DMH-inducidos (p = 0,0065).Conclusiones: la desfuncionalización colónica en ratas provocaen los segmentos desfuncionalizados una alteración de lospatrones de la carcinogénesis DMH-inducida

Objective: to examine the effect of fecal absence on experimentalcolon 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) 20rats, no treatment; B) 26 rats, colonic defunctionalization; C) 30rats, 18 weekly doses of dimethylhydrazine (DMH), 21 mg/kgbody 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 atthe same doses as rats in group C. Animals were sacrificed after25-27 weeks. Number of tumors, their location, and pathologicalfindings were all compared between groups.Results: no tumors developed in the dimethylhydrazine-freegroups. No differences were obtained either in number of tumorsor tumors per rat for group C as compared to group E. Fecal absencewas associated with smaller-sized tumors (p = 0.007),greater numbers of non-mucinous tumors (p = 0.00009), betterdifferentiation (p = 0.0054), and lesser penetration into the wall(p = 0.015) for group E as compared to group C. In the dimethylhydrazinegroup, fecal absence altered the number of tumors developingin males as compared to female rats (p = 0.025). Moreover,this fecal absence showed no inhibitory effect on rightcolonic tumors (p = 0.0065).Conclusions: fecal absence alters the DMH-carcinogenic patternin the defunctionalized colon when using an experimentalmodel 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.

Modelo experimental de cáncer colorrectal / Experimental colorectal cancer model

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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.

Traumatismos repetitivos sobre la mucosa promueven cáncer / Repetitive mucosal trauma promotes cancer in experimental rat model of colonic carcinogenesis

Objetivo: investigar el efecto de traumatismos repetitivos sobre la mucosa del colon en un modelo de carcinogénesis colónica experimental, ya que es posible que lesiones colónicas inespecíficas sean promotoras de cáncer. Material y método: a 60 ratas hembra Sprague-Dawley les realizamos una desfuncionalización colónica de 4 cm con doble colostomía, restableciendo la continuidad intestinal con sutura término-terminal de seda. Las 47 ratas supervivientes se dividieron aleatoriamente en 3 grupos: Grupo A: 27 ratas tratadas con dimetilhidracina (DMH). Grupo B: 10 ratas tratadas con EDTA y Grupo C: Control de 10 ratas. Se sacrificaron los animales a las 31-32 semanas después de la cirugía para estudio macro y microscópico. Resultados: en el grupo A aparecieron 70 tumores: 44 en colon funcional, 20 de ellos en el lugar de la anastomosis. 26 tumores en el segmento desfuncionalizado, 18 de ellos en su zona traumatizada (p< 0,05). No hubo tumores en los otros grupos. Conclusiones: a) los microtraumatismos continuos en la mucosa del colon son factores promotores de cáncer en la rata; b) la sutura de seda en la anastómosis es un factor promotor de cáncer (AU)

[Obstructive colitis: analysis of 7 patients]. / Colitis obstructiva: un análisis de 7 enfermos.

The term "obstructive colitis" is defined by the presence of ulcero-inflammatory lesions in a colonic area proximal to a potentially obstructive lesion. Seven cases retrospectively identified during a 5-year period are here reported. They illustrate the clinico-pathological spectrum of this entity. Most patients were women, with a mean age of 66 years and with history of chronic underlying disease (diabetes mellitus and arterial hypertension). Abdominal distension and pain, as well as acute constipation were the main clinical symptoms. An adenocarcinoma predominantly located at the rectosigmoidal region accounted for the obstructive nature in 100% of cases. Macroscopically the colitis area was moderately dilated and there were single or confluent ulcers in the luminal surface. Characteristically, there was always a transitional preserved area between the obstruction and the colitis area. Microscopically, the mucosa was totally replaced by a granulation tissue with a relevant inflammatory infiltrate involving up to the muscularis propria. The cytometric study revealed and increase in the cell cycle (S-phase) and proliferation index, at the level of the obstructive lesion, with marked aneuploidy in cases with advanced neoplastic invasion. The role of mural hypoperfusion with localized ischemia in the pathogenesis is discussed. The similarities with other colonic inflammatory diseases are emphasized.

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.