COXIB frente a AINE no específico + gastroprotector. La mejor opción es un COXIB / Coxibs vs nonspecific NSAID plus a gastroprotective agent. The best option is a coxib

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[Effect of exogenous administration of platelet-derived growth factor and epidermal growth factor on duodenal ulcer healing in rats treated with indomethacin]. / Efecto de la administración exógena de PDGF y EGF en la cicatrización de la úlcera duodenal en ratas tratadas con indometacina.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) delay peptic ulcer healing through mechanisms that are still not entirely understood. Growth factors play a significant role in healing. AIM: To evaluate whether exogenous administration of platelet-derived growth factor (PDGF) reverses the effect of indomethacin in experimental duodenal ulcers in rats and to define the potential mechanisms involved in this process. METHOD: Duodenal ulcer was induced in male Wistar rats with acetic acid. The rats were then administered indomethacin (2 mg/kg/day), PDGF-BB (30 ng/100 g/day), epidermal growth factor (EGF) (50 /kg/day) or famotidine (positive control) or the possible combinations of these. Macroscopic area, reduction in microscopic diameter, epithelial and granulation tissue proliferation, collagen secretion by granulation tissue, and gastric acid secretion were analyzed. RESULTS: Indomethacin delayed duodenal ulcer healing by decreasing cellular proliferation and inhibiting collagen secretion. PDGF and EGF accelerated healing and reversed the effects of indomethacin. The mechanisms involved were associated with an increase in collagen proliferation and secretion without affecting gastric acid secretion. Famotidine also accelerated healing and reversed the effect of indomethacin, and these effects were associated with a marked inhibition of gastric acid secretion and increase in collagen secretion by granulation tissue. CONCLUSIONS: Exogenous administration of PDGF and EGF accelerated healing and reversed the harmful effects of indomethacin in an experimental model of duodenal ulcer.

Prevención de la gastropatía por antiinflamatorios

Los antiinflamatorios no esteroides (AINE) se encuentran entre los fármacos más prescritos y utilizados en el mundo, debido a que poseen propiedades antiinflamatorias y análgésicas, además de por su tolerancia y su rapidez de acción. Sin embargo, es su acción analgésica la que determina la mayor parte de las prescripciones y, por tanto, una utilización indiscriminada que no está exenta de efectos secundarios.El tratamiento de la gastropatía por AINE sigue siendo uno de los problemas principales a los que nos enfrentamos en la práctica clínica diaria. Al evidente problema clínico que supone el tratamiento de esta afección por la frecuencia de utilización de estos fármacos, se le une un aspecto no menos importante hoy día como es el económico.Por todo ello, es evidente que aunque el tratamiento profiláctico es importante, no lo es menos la utilización adecuada de los recursos terapéuticos que se disponen (AU)

Tratamiento y prevención de la gastropatía por antiinflamatorios no esteroideos

El término gastropatía por antiinflamatorios no esteroideos hace referencia a las lesiones que la utilización de éstos origina en la mucosa gastroduodenal, pero se debe recordar que originan también lesiones y complicaciones en el esófago, intestino delgado y grueso. La correcta valoración de estas lesiones es clave a la hora de determinar el manejo de los pacientes que las padecen (AU)

Effects of long-term treatment with lansoprazole and omeprazole on serum gastrin and the fundic mucosa.

OBJECTIVE: To compare the effects of long-term lansoprazole and omeprazole treatment (6 months) on serum gastrin levels. PATIENTS: Forty duodenal ulcer patients without previous treatment with proton pump inhibitors were randomized to receive either 20 mg/day or omeprazole or 30 mg/day of lansoprazole. Serum gastrin levels were determined on entry and every 2 months. On finalizing the study antral and fundic biopsies were obtained for immunohistochemical analysis of the enterochromaffin-like cell population. RESULTS: Before starting the treatment fasting serum gastrin was similar in both groups (108.7 +/- 60.9 pg/mL omeprazole; 102.7 +/- 56.9 pg/mL lansoprazole). The treatment with either omeprazole or lansoprazole increased serum gastrin levels, but the increase was mild, maximal at 2 months and similar between omeprazole and lansoprazole (113.44 +/- 114.9 pg/mL omeprazole vs 166.1 +/- 117.9 pg/mL lansoprazole; p > 0.05). When serum gastrin levels were individually analyzed by patient, most were below 200 pg/mL and only 3 patients (1 omeprazole/2 lansoprazole) had levels near 500 pg/mL which were not correlated with enterochromaffin-like cell hyperplasia. CONCLUSIONS: Long-term treatment with either omeprazole or lansoprazole is safe, at least during 6 months, and results in mild hypergastrinemia. No differences between these two drugs were observed.

[Effect of indomethacin on the secretion of pepsinogen in isolated human cells in vitro]. / Efecto de la indometacina sobre la secreción de pepsinógeno en células humanas aisladas in vitro.

The effects of indomethacin on pepsinogen secretion were studied in isolated human peptic cells prepared from endoscopically obtained biopsies after collagenase digestion, mechanical disruption and percoll gradient centrifugation. Low concentrations of indomethacin (10(-8)-10(-10) M) stimulated basal pepsinogen secretion. Higher doses of indomethacin (10(-5)-10(-6) M) potentiated histamine (10(-4) M) and db-cAMP (10(-4) M)-stimulated pepsinogen secretion without affecting acetylcholine (10(-6) M) and CCK-8-stimulated pepsinogen secretion or cell vitality. Increase of pepsinogen secretion was dependent on extracellular calcium because potentiation was abolished by calcium depletion of the medium. We conclude that indomethacin potentiates basal and secretagogue-stimulated pepsinogen secretion by dispersed human peptic cells and this might be an additional mechanism of NSAID-induced gastric injury. This potentiation effect is regulated by calcium and independent of endogenous prostaglandin inhibition.

[Refractory peptic ulcer: the pathogenic mechanisms]. / Ulcera péptica refractaria: mecanismos patogénicos.

The vast majority of peptic ulcers heal after treatment with either H2 receptor antagonists or omeprazole at standard doses. However, it is also recognized that a 5-10% of peptic ulcers will not heal. The possibility of identifying the factors associated with refractory ulcers would have important repercussions. Several retrospective and prospective studies have pointed out a number of clinical, environmental or intrinsic factors. In recent years 2 factors have emerged as the main cause of peptic ulcer. Helicobacter pylori infection and NSAID use, and these two factors might be involved in the pathogenesis of refractory ulcer.

[A iatrogenic pathology study in an internal medicine service]. / Estudio de la patología iatrógena en un servicio de Medicina Interna.

BASIS: It's obvious that the current medicine practice generates iatrogenesis . However, we are unaware about its magnitude and severity, specially in Spain, where this item has been scarcely studied. METHODS: All the patients admitted to the Department of Internal Medicine were prospectively studied during a 13 months period, selecting among the patients those fulfilling criteria for an iatrogenic problem both of pharmacological origin and not pharmacological. The kind of iatrogenesis, its severity, related mortality, gravity of the basic illness, affected organ and avoidability of the iatrogenesis were evaluated. Infusion phlebitis were recorded only during 6 months. RESULTS: Iatrogenic pathology was found in 228 cases over 1.549 patients admissions, accounting for 14.7% of incidence. Iatrogenic pathology was the reason for admission in 65 cases. The average stay was significantly increased in patients with iatrogenic pathology (p < 0.01). Adverse reactions to drugs accounted for 62% of the total account with 141 cases. The non-steroids antiinflammatory (NSA) drugs were the most frequently troublesome pharmacological agents. The GI tract was the more affected system (84 cases). Infusion phlebitis are not included in the total account of cases. CONCLUSIONS: a) iatrogenic pathology is an illness of very high incidence in our surroundings; b) NSA is a group of drugs generating frequently adverse reactions in off-hospital environment; c) GI hemorrhage is an iatrogenic illness accounting for high percentage of cases; d) many of the iatrogenic events can be catalogued as avoidable and with more accurate attention to some factors the more of them could be prevented.