Malnutrition and cachexia in ovarian cancer patients: pathophysiology and management.
In ovarian cancer patients the poor nutritional status and cachexia are caused by the metabolic effects of the enlarging tumor masses and bowel obstruction. These patients may have a high resting energy expenditure due to increase in Cori cycle activity, glucose and triglyceride-fatty acid cycling and gluconeogenesis. Biochemical mediators of cachexia include cytokines, such as tumor necrosis factor and interleukin-6, and tumor-produced catabolic factors, such as lipid-mobilizing factor, proteolysis-inducing factor, and anemia-inducing factor. Mechanisms involved in the pathogenesis of obstruction may include extrinsic occlusion of the bowel due to pelvic, mesenteric omental masses, or intestinal motility disorders due to infilor tration of the mesentery or bowel muscle and nerves. The relief of malnutrition and cachexia may be attempted through nutritional support, pharmacological approach (megestrol acetate, cyclooxygenase inhibitors) and palliative treatment of bowel obstruction. Very few agents have been demonstrated to have true anticachectic activity, so future research should be addressed to the identification of drugs able to block the activity of tumor-produced catabolic factors. The decision regarding optimum management of bowel obstruction should be individualized. Krebs' and Goplerud's score (based on age, nutritional status, tumor status, ascites, previous chemotherapy and irradiation) seems to offer reliable eligibility criteria for those patients who can benefit from surgery.
Gadducci
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Department of Procreative Medicine, University of Pisa, Italy. a.gadducci@obgyn.med.unipi.it
Cosio
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Fanucchi
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Genazzani
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AR
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000693:Anaerobiosis; D000818:Animals; D000855:Anorexia / Q000209:etiology; D001201:Ascites / Q000378:metabolism; D016466:CHO Cells; D002100:Cachexia / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D050260:Carbohydrate Metabolism; D006224:Cricetinae; D003412:Cricetulus; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use; D016207:Cytokines / Q000502:physiology; D015118:Eicosapentaenoic Acid / Q000627:therapeutic use; D004734:Energy Metabolism / Q000187:drug effects; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D005467:Floxuridine / Q000627:therapeutic use; D006019:Glycolysis; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics / Q000502:physiology; D007415:Intestinal Obstruction / Q000209:etiology / Q000601:surgery / Q000628:therapy; D007441:Intubation, Gastrointestinal; D019787:Linoleic Acid / Q000378:metabolism; D008066:Lipolysis / Q000187:drug effects; D008071:Lipoprotein Lipase / Q000037:antagonists & inhibitors; D019290:Megestrol Acetate / Q000494:pharmacology; D051379:Mice; D008819:Mice, Nude; D009325:Nausea / Q000209:etiology; D009748:Nutrition Disorders / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D010051:Ovarian Neoplasms / Q000150:complications* / Q000378:metabolism; D010166:Palliative Care; D010289:Parenteral Nutrition, Total / Q000009:adverse effects; D011506:Proteins / Q000378:metabolism; D011788:Quality of Life; D014162:Transfection; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000502:physiology
D000319:Adrenergic beta-Antagonists; D016861:Cyclooxygenase Inhibitors; D016207:Cytokines; D005227:Fatty Acids; D015850:Interleukin-6; D011506:Proteins; D014409:Tumor Necrosis Factor-alpha; D005467:Floxuridine; D019787:Linoleic Acid; D015118:Eicosapentaenoic Acid; D008071:Lipoprotein Lipase; D019290:Megestrol Acetate; C025034:doxifluridine