Eicosapentaenoic acid in cystic fibrosis: evidence of a pathogenetic role for leukotriene B4
Lawrence R, Sorrell T
Lancet (London, England) · 79 citas
Etiquetas de revisión
Financiación no declaradaDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 1993-08-01 · Lancet · vol. 342 · número 8869 · págs. 465–469
- Editorial
- Elsevier BV
- Citado
- 117 citas · más que el 98% de estudios similares · 8.1× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 30 trabajos
- Acceso
- De pago
- Áreas de investigación
- Cystic Fibrosis Research Advances · Fatty Acid Research and Health · Asthma and respiratory diseases
- Palabras clave
- cystic fibrosis, eicosapentaenoic acid, leukotriene B4, Pseudomonas aeruginosa, neutrophil chemotaxis, lung inflammation, omega-3 fatty acids, dietary supplementation, lung function, sputum volume, neutrophil function
- MeSH
- neutrophils, sputum, humans, pseudomonas aeruginosa, cystic fibrosis, dietary fats, eicosapentaenoic acid, leukotriene b4, placebos, vital capacity, forced expiratory volume, leukocyte count, pilot projects, double-blind method, chemotaxis, leukocyte, adolescent, adult, child, female, male
2 autores
- R. Lawrence🇦🇺The University of Sydney; Westmead Hospital
- Tania Christine Sorrell🇦🇺The University of Sydney; Westmead Hospital
Resumen
El texto original del estudio, en el idioma en que se publicó.
Much of the lung damage that limits the life of young adults with cystic fibrosis is due to proteases and oxygen metabolites generated by neutrophils, which are recruited into the airway by the interaction between Pseudomonas aeruginosa and pulmonary macrophages. Leukotriene B4 (LTB4) has been proposed as a local mediator of this process; its production is susceptible to specific modulation with dietary eicosapentaenoic acid (EPA). We carried out a placebo-controlled trial of EPA (2.7 g daily for 6 weeks) to assess its effects on markers of clinical state, peripheral neutrophil function, and lung inflammation in sixteen patients with cystic fibrosis colonised with P aeruginosa. EPA was well tolerated and resulted in a significant reduction in sputum volume (median change with EPA -10 mL/day, placebo 0; p = 0.015), and improvements in Schwachman score (EPA 5%, placebo 0; p = 0.034), forced expiratory volume in 1 s (EPA 0.25 L, placebo -0.1 L; p = 0.006), and vital capacity (EPA 0.6 L, placebo 0; p = 0.011). Relative chemotaxis of circulating neutrophils to LTB4 increased from a subnormal baseline of 4 (median; range 0-10) microns/30 min before treatment, to a near normal value of 11 (5-18) microns/30 min after EPA. Relative chemotaxis to LTB4 of patients taking placebo did not change: the difference in response was highly significant (p = 0.001). Specific reduction of neutrophil chemotaxis to LTB4 is a sensitive assay of chronic in-vivo exposure to LTB4. Our results suggest that LTB4 has a pathogenetic role in the lung damage of cystic fibrosis. Longer-term clinical trials of EPA are warranted in a larger number of cystic fibrosis patients.
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