Helicobacter pylori: efectividad del tratamiento secuencial vs tratamiento convencional / Helicobacter pylori: effectiveness of conventional treatment versus sequential treatment

Helicobacter pylori (Helicobacter p.) es una bacteria que se aloja a nivel de la mucosa gástrica la cual presenta una prevalencia variable y está asociada al desarrollo de úlceras pépticas, linfomas y cáncer gástrico. Aproximadamente el 40% de los individuos en países desarrollados están afectados y hasta un 85%, en los países subdesarrollados, por ello, se asocia con un bajo nivel socioeconómico. Recientemente se ha propuesto el uso de una terapia secuencial con el objetivo de erradicar la infección por Helicobacter p. El objetivo de este estudio consiste en comparar la efectividad de ambos tratamientos en la consulta del Servicio de Gastroenterología del Hospital “Carlos J. Bello” en el período de febrero 2008 a octubre 2009, en un total de 83 pacientes, 77,1% de sexo femenino, y 22,9% de sexo masculino. El grupo que recibió tratamiento convencional representó el 57,83%, del total de pacientes estudiados, y el grupo que recibió tratamiento secuencial, representó el 42,17%. En cuanto a la efectividad, el tratamiento convencional fue efectivo en un 46,99%, y el secuencial en un 32,53%, dentro de su propio grupo de pacientes. La prueba X2 no representó diferencia significativa entre la efectividad de ambos tratamientos.

Helicobacter pylori (Helicobacter p. ) Its a bacteria that lives in the gastric mucosa and its prevalence is variable and it is associated to the development of peptic ulcer, lymphoma, and gastric cancer. Approximately 40% of individuals in developed countries are affected and 85% in undeveloped countries in which are related to low socioeconomics level. Recently its been proposed the use of a sequential therapy to eradicate the infection by Helicobacter p. The objective of this study consist in to compare the effectiveness between both treatments (Sequential and conventional) in the consult from the Gastroenterology Service of the Carlos J. Bello Hospital in a period of time between February 2008 to October 2009 in a total of 83 patients, 77,1% feminine, 22,9% masculine. The group that received conventional treatment represented 57,83% and sequential 42,17%. In regard to the effectiveness the conventional group presented 46, 99% and sequential group 32, 53%. The X2 test it didn’t present significative difference of effectiveness between both treatments.

Decrease of cyclin D1 in the human lung adenocarcinoma cell line A-427 by 7-hydroxycoumarin.

Coumarin in vivo has antitumor activity in various types of cancer. In vitro, coumarin and 7-hydroxycoumarin, its major biotransformation product in humans, inhibit the proliferation of several human tumor cell lines. The molecular mechanisms of these effects are unknown. To gain information about these mechanisms, we studied the effects of coumarin and 7-hydroxycoumarin in the human lung adenocarcinoma cell line A-427 on the inhibition of: (i) cell proliferation; (ii) cell cycle progression; and (iii) expression of cyclins D1, E and A. The inhibitory concentrations 50 (IC(50)) of both compounds were estimated by cytostatic assays of tetrazolium (MTT) reduction. The effects on cell cycle progression were assayed with propidium iodide and BrdU using DNA histograms and multiparametric flow cytometry. The percentages of cells expressing cyclins D1, E, and A were estimated by means of bivariate flow cytometry using propidium iodide, and FITC-conjugated monoclonal antibodies for each cyclin. The IC(50) (+/-S.E.M. n=3) of 7-hydroxycoumarin and coumarin at 72 h exposure, were 100+/-4.8 and 257+/-8.8 microg/ml, respectively. 7-Hydroxycoumarin at the concentration of 160 microg/ml (1 mM), inhibited the G(1)/S transition of the cell cycle, an action consistent with the cytostatic effect. No significant decreases of cyclins E and A were observed. In contrast, cyclin D1 significantly decreased, which appears to indicate an action of 7-hydroxycoumarin in early events of phase G(1). However, messenger RNA of cyclin D1, assayed by RT-PCR, did not change. This suggests a posttranscriptional effect. The effects of coumarin were not significant. Cyclin D1 is overexpressed in many types of cancer, and its inhibition has been proposed as a pharmacological and therapeutic target for novel antitumor agents. Knowledge of the decrease of cyclin D1 by 7-hydroxycoumarin may lead to its use in cancer therapy, as well as to the development of more active compounds.

Cytostatic activity of coumarin metabolites and derivatives in the B16-F10 murine melanoma cell line.

Coumarin has antitumour effects in vivo and cytostatic effects in vitro. Its half-life in humans is short (1-1.5 h) and the monohydroxylated biotransformation products have significantly longer half-lives. One or several of these products may thus be responsible for the antitumoral effects. We have assayed the in vitro cytostatic activity of five monohydroxylated coumarins (3-, 4-, 6-, 7- and 8-monohydroxycoumarin), their acetates and methyl-ethers. Murine melanoma cells (cell line B16-F10) and murine fibroblasts (B82) were exposed to the test compounds at concentrations between 10 and 160 microg/ml. The cytostatic effects were estimated by reduction of the tetrazolium dye MTT. In the melanoma cells, some of the compounds inhibited growth after exposure for 1 day. In contrast, coumarin inhibited growth to a smaller extent, and only after exposure for 3 days. The most active compounds (3-acetoxycoumarin, 4-methoxycoumarin and 6-hydroxycoumarin), as well as coumarin, were also assayed in murine fibroblasts. The cytostatic effects of 4-methoxycoumarin and 6-hydroxycoumarin were less pronounced in fibroblasts than in melanoma cells. Our observations suggest that these compounds may have a greater therapeutic margin.