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Biomedical subjects

A Lanas Arbeloa

Publications and source records attributed to A Lanas Arbeloa.

17 recordsLinked to original sources
PubMed2002

[Effect of exogenous administration of platelet-derived growth factor and epidermal growth factor on duodenal ulcer healing in rats treated with indomethacin].

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.

Acetic Acid↗
PubMed1997

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.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

[Refractory peptic ulcer: the pathogenic mechanisms].

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.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1994

[A iatrogenic pathology study in an internal medicine service].

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.

Age Distribution↗