Conceptos Categóricos

SINDROME DE ANOREXIA-CAQUEXIA ASOCIADO AL CANCER: PATOGENESIS, CARACTERISTICAS CLINICAS Y ENFOQUES TERAPEUTICOS

SINDROME DE ANOREXIA-CAQUEXIA ASOCIADO AL CANCER: PATOGENESIS, CARACTERISTICAS CLINICAS Y ENFOQUES TERAPEUTICOS

(especial para SIIC © Derechos reservados)
El síndrome de anorexia y caquexia se observa frecuentemente en las personas con cáncer. Es importante reconocer y tratar este síndrome lo más tempranamente posible para prolongar la supervivencia y mejorar la calidad de vida.
laviano9.jpg Autor:
Alessandro Laviano
Columnista Experto de SIIC

Institución:
Department of Clinical Medicine, University La Sapienza


Artículos publicados por Alessandro Laviano
Coautores
Alessio Molfino*  Filippo Rossi-Fanelli** 
MD, Department of Clinical Medicine, University La Sapienza*
MD, Full Professor of Medicine, Chairman of the Department of Clinical Medicine, University La Sapienza**
Recepción del artículo
12 de Julio, 2005
Aprobación
15 de Julio, 2005
Primera edición
15 de Febrero, 2006
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
El síndrome de anorexia-caquexia es muy prevalente en los pacientes con cáncer, repercute sobre la morbimortalidad y altera la calidad de vida. La anorexia se define como la pérdida del deseo de comer; mientras que se considera caquexia la consumición progresiva de la masa muscular esquelética y del tejido adiposo. La patogénesis del síndrome de anorexia-caquexia es multifactorial, pero los factores tumorales y las citoquinas parecen cumplir un papel significativo y representan un objetivo terapéutico adecuado. En los músculos, el incremento de la proteólisis y la disminución de la síntesis de proteínas llevan al deterioro muscular esquelético; mientras que el aumento de la lipólisis y la disminución de la lipogénesis producen la consunción del tejido adiposo. Las alteraciones neuroquímicas parecen representar el mecanismo patogénico de la anorexia y de la reducción de la ingesta alimentaria. El enfoque terapéutico del síndrome de anorexia-caquexia asociado al cáncer debe centrarse en los mecanismos patogénicos. De este modo, la estrategia terapéutica óptima debe dirigirse a contrarrestar los cambios en los hábitos alimentarios y las alteraciones metabólicas relacionadas con el tumor.

Palabras clave
Anorexia, caquexia, cáncer, patogénesis, terapia


Artículo completo

(castellano)
Extensión:  +/-8.68 páginas impresas en papel A4
Exclusivo para suscriptores/assinantes

Abstract
Anorexia-cachexia syndrome is highly prevalent among cancer patients, it impacts on morbidity and mortality, and impinges on quality of life. Anorexia is defined as the loss of the desire to, while cachexia defines the progressive wasting of skeletal muscle mass and adipose tissue. The pathogenesis of anorexia-cachexia is multifactorial, but tumour-derived factors and cytokines appear to play a significant role, representing a suitable therapeutic target. In muscles, increased proteolysis and reduced protein synthesis yield to skeletal muscle wasting. Increased lipolysis and depressed lipogenesis result in adipose tissues wasting. Neurochemical perturbations appear to represent the pathogenic mechanism of anorexia and reduced food intake. Cancer anorexia-cachexia syndrome should be therapeutically approached by targeting the pathogenic mechanisms. Thus, the optimal therapeutic approach should be aimed at counteracting both changes in dietary habits and tumour-related metabolic perturbations.

Key words
Anorexia, cachexia, cancer, pathogenesis, therapy


Full text
(english)
para suscriptores/ assinantes

Clasificación en siicsalud
Artículos originales > Expertos del Mundo >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Oncología, Salud Mental
Relacionadas: Farmacología, Medicina Farmacéutica, Medicina Interna



Comprar este artículo
Extensión: 8.68 páginas impresas en papel A4

file05.gif (1491 bytes) Artículos seleccionados para su compra



Bibliografía del artículo
  1. Laviano A, Meguid MM, Inui A, et al. Therapy insight: cancer anorexia-cachexia syndrome – when all you can eat is yourself. Nature Clin Pract Oncol 2005; 2:158-165.
  2. Tisdale MJ. Cachexia in cancer patients. Nat Rev Cancer 2002;2:862-871.
  3. Bossola M, Muscaritoli M, Costelli P, et al. Increased muscle ubiquitin mRNA levels in gastric cancer patients. Am J Physiol 2001; 280:R1518-R1523.
  4. Bozzetti F, Gavazzi C, Mariani L, et al. Artificial nutrition in cancer patients: which route, what composition World J Surg 1999; 23:577-583.
  5. Norton JA, Stein TP, Brennan MF. Whole body protein synthesis and turnover in normal man and malnourished patients with and without cancer. Ann Surg 1981; 194 :123-128.
  6. Lundholm K, Bennegard K, Eden E, et al. Efflux of 3-methylhistidine from the leg of cancer patients who experience weight loss. Cancer Res 1982; 42:4802-4818.
  7. Lundholm K, Bylund AC, Holm J, et al. Skeletal muscle metabolism in patients with malignant tumour. Eur J Cancer 1976; 12:465-473.
  8. Warren RS, Jeevanandam M, Brennan MF. Protein synthesis in the tumor-influenced hepatocyte. Surgery 1981; 98:275-281.
  9. Lecker SV, Solomon V, Mitch WE, et al. Muscle protein breakdown and critical role of the ubiquitin-proteasome pathway in normal and disease states. J Nutr 1999; 129:227S-237S.
  10. Goll DE, Thompson VF, Taylor RG, et al. Role of the calpain system in muscle growth. Biochimie 1992; 74:225-237.
  11. Drott C, Persson H, Lundholm K. Cardiovascular and metabolic response to adrenaline infusion in weight-losing patients with and without cancer. Clin Physiol 1989; 9:427-439.
  12. Bing C, Brown M, King P, et al. Increased gene expression of brown fat uncoupling protein (UCP)1 and skeletal muscle UCP2 and UCP3 in MAC16-induced cancer cachexia. Cancer Res 2000; 60:2405-2410.
  13. Russell ST, Hirai K, Tisdale MJ. Role of β3-adrenergic receptors in the action of a tumour lipid mobilizing factor. Br J Cancer 2002; 86:424-428.
  14. Todorov P, Cariuk P, McDevitt T, et al. Characterization of a cancer cachectic factor. Nature 1996; 379:739-742.
  15. Ramos EJ, Suzuki S, Marks D, et al. Cancer anorexia-cachexia syndrome: cytokines and neuropeptides. Curr Opin Clin Nutr Metab Care 2004; 7:427-434.
  16. Schwartz MW, Woods SC, Porte D Jr, et al. Central nervous system control of food intake. Nature 2000; 404:661-671.
  17. Laviano A, Meguid MM, Rossi-Fanelli F. Cancer anorexia: clinical implications, pathogenesis, and therapeutic strategies. Lancet Oncol 2003; 4:686-694.
  18. Stubbs RJ, Hughes DA, Johnstone AM, et al. The use of visual analogue scales to assess motivation to eat in human subjects: a review of their reliability and validity with an evaluation of new hand-held computerized systems for temporal tracking of appetite ratings. Br J Nutr 2000; 84 :405-415.
  19. Rossi Fanelli F, Cangiano C, Ceci F, et al. Plasma tryptophan and anorexia in human cancer. Eur J Cancer Clin Oncol 1986; 22:89-95.
  20. Laviano A, Meguid MM. Nutritional issues in cancer management. Nutrition 1996; 12:358-371.
  21. Geels P, Eisenhauer E, Bezjak A, et al. Palliative effect of chemotherapy: objective tumor response is associated with symptom improvement in patients with metastatic breast cancer. J Clin Oncol 2000; 18:2395-2405.
  22. Sutton LM, Demark-Wahnefried W, Clipp EC. Management of terminal cancer in elderly patients. Lancet Oncol 2003; 4:149-157.
  23. Walsh D, Donnelly S, Rybicki L. The symptoms of advanced cancer: relationship to age, gender, and performance status in 1,000 patients. Support. Care Cancer 2000; 8:175-179.
  24. DeWys WD, Begg C, Lavin PT, et al. Prognostic effect of weight loss prior to chemotherapy in cancer patients. Eastern Cooperative Oncology Group Am J Med 1980; 69:491-497.
  25. Walsh D, Rybicki L, Nelson KA, et al. Symptoms and prognosis in advanced cancer. Support Care Cancer 2002; 10:385-388.
  26. Ravasco P, Monteiro-Grillo I, Vidal PM, et al. Cancer: disease and nutrition are key determinants of patients’ quality of life. Support Care Cancer 2004; 12:246-252.
  27. Cherny NI, Catane R. Attitudes of medical oncologists toward palliative care for patients with advanced and incurable cancer. Cancer 2003; 98:2502-2510.
  28. Isenring EA, Capra S, Bauer JD. Nutrition intervention is beneficial in oncology outpatients receiving radiotherapy to the gastrointestinal or head and neck area. Br J Cancer 2004; 91:447-452.
  29. Inui A. Cancer anorexia-cachexia syndrome: current issues in research and management. CA Cancer J Clin 2002; 52 :72-91.
  30. Pascual Lopez A, Roque I Figuls M, et al. Systematic review of megestrol acetate in the treatment of anorexia-cachexia syndrome. J Pain Symptom Manage 2004; 27:360-369.
  31. Calder PC. Dietary modifications of inflammation with lipids. Proc Nutr Soc 2002; 61:345-358.
  32. Fearon KC, von Meyenfeldt MF, Moses AG, et al. Effect of a protein and energy dense N-3 fatty acid enriched oral supplement on loss of weight and lean tissue in cancer cachexia: a randomised double blind trial. Gut 2003; 52:1479-1486.
  33. Moses AW, Slater C, Preston T, et al. Reduced total energy expenditure and physical activity in cachectic patients with pancreatic cancer can be modulated by an energy and protein dense oral supplement enriched with n-3 fatty acids. Br J Cancer 2004; 90:996-1002.
  34. Jatoi A, Rowland K, Loprinzi CL, et al. An eicosapentaenoic acid supplement versus megestrol acetate versus both for patients with cancer-associated wasting: a North Central Cancer Treatment Group and National Cancer Institute of Canada collaborative effort. J Clin Oncol 2004; 22:2469-2476.
  35. Burns CP, Halabi S, Clamon G, et al. Phase II study of high-dose fish oil capsules for patients with cancer-related cachexia. Cancer 2004; 101:370-378.
  36. Diksic M, Young SN. Study of the brain serotonergic system with labelled α-methyl-L-tryptophan. J Neurochem 2000; 78:1185-1200.
  37. Cangiano C, Laviano A, Meguid MM, et al. Effects of administration of oral branched-chain amino acids on anorexia and caloric intake in cancer patients. J Natl Cancer Inst 1996; 88:550-552.
  38. Heisler LK, Cowley MA, Tecott LH, et al. Activation of central melanocortin pathways by fenfluramine. Science 2002; 297:609-611.
  39. Marks DL, Butler AA, Turner R, et al. Differential role of melanocortin receptor subtypes in cachexia. Endocrinology 2003; 144:1513-1523.
  40. Smith HJ, Greenberg NA, Tisdale MJ. Effect of eicosapentaenoic acid, protein and amino acids on protein synthesis and degradation in skeletal muscle of cachectic mice. Br J Cancer 2004; 91:408-412.
  41. Torelli GF, Meguid MM, Moldawer LL, et al. Use of recombinant human soluble TNF receptor in anorectic tumour-bearing rats. Am J Physiol 1999; 277:R850-R855.
  42. Eichorst ST, Krueger A, Muerkoster S, et al. Suramin inhibits death receptor-induced apoptosis in vitro and fulminant apoptotic liver damage in mice. Nat Med 2004; 10:602-609.
  43. Cahlin C, Gelin J, Delbro D, et al. Effect of cyclooxigenase and nitric oxide synthase inhibitors on tumor growth in mouse tumor models with and without cachexia related to prostanoids. Cancer Res 2000; 60:1742-1749.
  44. Lundholm K, Daneryd P, Bosaeus I, et al. Palliative nutritional intervention in addition to cyclooxigenase and erythropoietin treatment for patients with malignant disease: effects on survival. Metabolism, and function. Cancer 2004; 100:1967-1977.
  45. Inui A, Asakawa A, Bowers CY, et al. Ghrelin, appetite, and gastric motility: the emerging role of the stomach as an endocrine organ. FASEB J 2004; 18:439-456.
  46. Neary NM, Small CJ, Alison MW, et al. Ghrelin increases energy intake in cancer patients with impaired appetite: acute, randomized, placebo-controlled trial. J Clin Endocrinol Metab 2004; 89:2832-2836.
  47. Inui A. Cancer anorexia-cachexia syndrome: are neuropeptides the key Cancer Res 1999; 59:4493-4501.

Título español
Resumen
 Palabras clave
 Bibliografía
 Artículo completo
(exclusivo a suscriptores)
 Autoevaluación
  Tema principal en SIIC Data Bases
 Especialidades

 English title
 Abstract
 Key words
Full text
(exclusivo a suscriptores)

Autor 
Artículos
Correspondencia

Patrocinio y reconocimiento
Imprimir esta página
 
 
 
 
 
 
 
 
 
 
 
 
Está expresamente prohibida la redistribución y la redifusión de todo o parte de los contenidos de la Sociedad Iberoamericana de Información Científica (SIIC) S.A. sin previo y expreso consentimiento de SIIC.
ua31618
-->