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Weight loss, weakness, and wasting of the body encountered in certain diseases or in terminal illnesses.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.



a state of profound wasting and physical debility manifested by severe emaciation, weight loss, dry and flabby skin, loss of hair, disappearance of subcutaneous fat, atrophy of muscles and viscera, and low serum protein level. Edema, hemorrhages, and sometimes mental derangement can occur with cachexia. It results from prolonged malnutrition or starvation, severe metabolic disorders, chronic arsenic, lead, mercury, or fluorine poisoning, and severe lesions of the digestive tract (atrophy of the intestinal mucosa, condition after resection of the stomach and intestines). Cachexia may occur in severe cases of tuberculosis or other chronic infections, some lesions of the endocrine glands, (hypophysis, thyroid, adrenals, pancreas), large slow-healing wounds, abscesses, and malignant tumors (especially of the esophagus and stomach).

The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.
References in periodicals archive ?
Leptin, insulin sensitivity and growth hormone binding protein in chronic heart failure with and without cardiac cachexia. Eur J Endocrinol 2001; 145: 727-35.
Gastro-intestinal protein loss is likely to be rare in patients with cardiac cachexia and is therefore not a significant factor in its production.
Considering the hypertrophic effects of chronic [beta]-AR activation, some authors have suggested [beta]-AR agonists as a pharmacologic therapy in counteracting cardiac cachexia in late 80's decade onwards.
An understanding of the underlying mechanisms of cardiac cachexia may allow the treatment of CHF and undernutrition independently thereby reducing the excessive morbidity and mortality associated with this condition.
Fat malabsorption has been implicated in the development of cardiac cachexia [12-14] but the relevant studies were poorly designed and uncertainty still exists about the role of fat malabsorption in cardiac cachexia.
Clinical characteristics of patients with heart failure CC NON-CC (n = 29) (n = 14) Severity of heart failure NYHA II 9 8 III 15 6 IV 5 0 Rhythm SR 9 5 AF 20 9 Orthopnoea(*) Yes 27 4 No 2 10 Early satiety(**) Yes 20 2 No 9 12 Anorexia(***) Yes 13 1 No 16 13 CC = cardiac cachexia group; NON-CC = patients without cachexia.
Cumulative [sup.14] CO[.sub.2] exhalations (%) in the triolein (TBT) and glycocholic acid (GABT) breath tests [mean (SD)] in controls, and heart failure patients with (CC) and without (NON-CC) cardiac cachexia Controls CC NON-CC (n = 29) (n = 29) (n = 14) TBT(**) 12.84(7.22) 7.25(3.61) 10.85(4.71) GABT(*) 3.9 (2.69) 3.34 (2.96) 6.49 (4.60) Analysis of variance: (**) p = 0.001; (*) p = 0.02.
Fat malabsorption has previously been described as one of the underlying mechanisms in cardiac cachexia [12-14].
Other experimental studies have also shown that mice bearing Walker 256 and MAC13/16 tumors developed cardiac cachexia in response to DNA and/or protein oxidative damage in heart tissues [20,36].
Cecchini, "Oxidative and proteolytic profiles of the right and left heart in a model of cancer-induced cardiac cachexia," Pathophysiology, vol.