Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006625 (cachexia)
 5,650 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein-energy malnutrition (PEM) is common in cancer patients and may develop into the syndrome known as 'cancer cachexia'. This is characterised by complex disturbances in carbohydrate, lipid, protein, and electrolyte metabolism. The aetiology is equally complex, with host and therapeutic factors contributing to the reduced food intake and effects on host tissues. Anorexia is of prime importance, differing in its cause from one patient to another and often presenting a barrier to successful nutritional support. Further research is necessary to elucidate the interaction of central and peripheral factors that may be involved in the aetiology of anorexia. Because of the interplay of biochemical, physiological, and psychological consequences of cancer, the nutritional support of the patient presents a considerable challenge to the caring professions.
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PMID:Malignant disease: nutritional implications of disease and treatment. 312 Dec 1

Cancer cachexia is a complex syndrome that includes host tissue wasting, anorexia, asthenia, and abnormal host intermediary metabolism. It is present in approximately 50% of cancer patients during treatment and nearly 100% of treated cancer patients at death. Cachexia has a detrimental impact on cancer therapy. The central problem of cancer cachexia is that energy balance is not maintained, and the host has a relative hypophagia which results in host tissue wasting. The tumor by its nature and obligate growth can continue to consume glucose, amino acids, and lipids at the expense of the host. This produces abnormal host intermediary metabolism including elevated glucose production and recycling, decreased muscle protein synthesis, and increased muscle and fat breakdown. The exact mechanisms of cancer cachexia have been only partially elucidated. The identification of signal molecules like cachectin which mediate these changes may be on the horizon. Nutritional support can reverse some of the derangements seen with cachexia, and there is evidence that functional lean body mass or body cell mass can be restored in some (but not all) patients. However, nutritional support has not yet improved response to chemotherapy or radiation therapy, nor has it improved host tolerance of chemotherapy. It has improved operative mortality and morbidity in cachectic cancer patients undergoing major surgical procedures. Optimum host nutritional support appears to be dependent on high insulin concentrations in both humans and rats. Insulin and exercise may be methods to preserve host lean tissue and feed the host rather than the tumor. Future studies depend on better definition of tumor-bearing host metabolism, altering the relationship between neoplasm and host to preferentially feed the host, and making the neoplasm more susceptible to effective treatment.
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PMID:Cancer cachexia. 312 81

The nutritional status of a tumor patient can be negatively influenced by the local and systemic effects of the malignant tumor (tumor cachexia, anorexia, difficult oral food intake), by the effects of the various antitumoral therapy modalities (surgery, radiotherapy, chemotherapy), and by the complications associated with such modalities (anorexia, nausea, vomiting, mucositis, xerostomia, alterations of the smell and taste sensations, odynophagia, dysphagia, maldigestion, malabsorption, diarrhea, steatorrhea, conditioned aversions, radiogenic late effects), as well as by the psychological reactions of the patient to the real or feared existence of his tumor. The radiation-induced nutritional disorders depend on the tumor localization, the region irradiated, the dose and length of radiotherapy, the fractionation, the volume irradiated, and the combination with other therapeutic modalities ("combined modality therapy"). The acute radiation-induced reactions are usually of limited duration and for this reason tend to interfere with the nutritional status to a lesser extent than the permanent chronic consequences of irradiation. Weight loss and malnutrition tend to develop particularly in patients in whom segments of the gastrointestinal tract are subjected to irradiation. The incidence and severity of deficient nutrition depend not only on the region irradiated (head-neck region, thorax, abdomen, pelvis) but also, and most particularly, on the volume of the digestive tract irradiated. Chemotherapy and radiotherapy combined act very strongly on rapidly proliferating cell populations (skin, mucosa, epithelium of the gastrointestinal tract). In this context, actinomycin D and adriamycin act like real sensitizers, whereas the majority of the other drugs are likely to produce only an additive effect. The first named cytostatics give rise to the so-called recall phenomenon, i.e., the reactivation of latent radiation effects in response to the subsequent administration of the drug. Malnutrition impairs organ function and ultimately results in increased morbidity and mortality. For this reason it has proven mandatory and reasonable that the organism of all tumor patients suffering from malnutrition is provided with the missing essential nutrients (especially amino acids for protein synthesis). This tends to clearly improve the Karnofsky performance status, with a positive effect on response rates, toxicity, and survival rates in retrospective studies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Malnutrition and the role of nutritional support for radiation therapy patients. 314 Mar 23

Cholecystokinin octapeptide (CCK-8, 5 micrograms/kg) was injected i.p. into male Sprague-Dawley rats bearing the Walker 256-carcinosarcoma, or into non-tumour bearing controls, on a 20-h food deprivation schedule. Food and water intake and body weight maintenance were monitored for 15 days after tumour implantation and compared to that of tumour-bearing animals not injected with CCK-8. Food intake was significantly reduced for the duration of the two 4-day periods of CCK-8 injection, indicating that behavioural tolerance to this peptide did not occur. The severity of anorexia and body weight loss in tumour-bearing animals was significantly greater than that observed in non-tumour bearing controls, for the first 13 days of observation. These results indicate that endogenous peptides, such as CCK, may function in tumour-bearing animals to enhance the anorexia and wasting which typifies the anorexia cachexia syndrome.
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PMID:Facilitation of cancer-associated anorexia by cholecystokinin. 316 58

Cachectin/tumor necrosis factor (TNF) is a macrophage product which may have a role in cancer cachexia. Recombinant human cachectin/TNF (Cetus Corporation) was administered i.p. twice daily to male F344 rats at varying, nonlethal dosages for either 5 or 10 days, and daily rat food intake and body weight were measured. There was a dose-dependent cachectin/TNF-induced decline in food intake and body weight gain over the treatment period. However, after 1 day rats became tolerant to these effects and increased food intake and gained body weight despite receiving cachectin/TNF. Rats were subsequently inoculated with a transplantable methylcholanthrene-induced sarcoma, and survival was measured. Rats previously treated with high-dose (either 100 or 200 micrograms/kg/day) cachectin/TNF survived significantly longer following tumor inoculation than did control rats given saline or rats given 10 micrograms/kg/day of cachectin/TNF. Analysis of tumor growth curves and tumor weight indicated that high-dose cachectin pretreatment did not retard tumor growth. Analysis of food intake and tumor burden following tumor inoculation indicated that high-dose cachectin pretreatment decreased the reduction in food intake associated with progressive tumor growth and allowed rats to withstand a greater tumor burden at death. Rats immunized with low-dose human cachectin/TNF developed high IgG titers against human TNF, but failed to demonstrate the same protection against a methylcholanthrene-induced tumor challenge as rats made tolerant with repetitive twice daily high-dose cachectin/TNF. The observation of reduced cancer-associated anorexia and increased survival of tumor-bearing rats associated with previous tolerance to exogenous cachectin/TNF strengthens the contention that endogenously produced cachectin may be a factor in the pathogenesis of cancer anorexia in the tumor-bearing rat. The mechanism of this tolerance is unclear but does not appear to be a humoral immune response.
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PMID:Cachectin/tumor necrosis factor: a possible mediator of cancer anorexia in the rat. 316 53

Five cases of carcinoma and one case of lymphosarcoma of the pancreas in cats are reported. Duration of clinical signs ranged between three days and ten weeks, the mean age was 10.2 years. Anorexia, depression, and cachexia were the mean symptoms, in four animals a palpable mass in the cranial abdomen was noted. Laboratory evaluation was unspecific, in all cases diagnosis was performed by necropsy. Further diagnostical and therapeutical possibilities are discussed critically.
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PMID:[Tumors of the exocrine pancreas in the cat]. 318

Cachexia can be a severe problem in the management of patients with cancer and other illnesses because it produces an ever-increasing spiral of anorexia, undernutrition, loss of tissue mass, muscle wasting, and increased susceptibility to infection and treatment toxicity. Megestrol acetate has been observed to produce weight gain in patients with hormone-sensitive tumors and has recently been noted to produce a similar degree of weight gain in those with hormone insensitive tumors. A review of our experience in a phase I-II study of escalating doses of megestrol acetate for advanced breast cancer revealed that weight gain occurred in more than 80% of all treated patients and in 90% of those patients who received treatment for 6 or more weeks. The median maximum weight gain was 5.5 kg, with a range of -5.6 to 44 kg. Subjective improvement in appetite occurred in most patients. These data provided the impetus for a series of further studies of the role of megestrol acetate in the control of cachexia, including a randomized study in cancer cachexia, AIDS cachexia, and anorexia nervosa. In addition, a number of laboratory trials seeking the mechanism of action have been initiated, as well as whole-animal studies to define the compartment of increased weight. Our data and the preliminary observation of weight gain in patients with hormone insensitive tumors suggest that megestrol acetate has a potential role in producing a possibly dose-related subjective improvement and an increase in appetite and weight. Further research is necessary to understand the mechanism of appetite stimulation and anabolic effect.
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PMID:Studies of high-dose megestrol acetate: potential applications in cachexia. 328 86

Cancer cachexia describes a syndrome of progressive weight loss, anorexia, and persistent erosion of host body cell mass in response to a malignant growth. Although often associated with preterminal patients bearing disseminated disease, cachexia may be present in the early stages of tumor growth before any signs or symptoms of malignancy. A decline in food intake relative to energy expenditure (which may be increased, normal, or decreased) is the fundamental physiologic derangement leading to cancer-associated weight loss. In addition, abnormalities of host carbohydrate, protein, and fat metabolism lead to continued mobilization and ineffective repletion of host tissue, despite adequate nutritional support. Mediators of cancer anorexia and associated abnormalities are unknown. Cachectin/TNF or other host-derived cytokines (produced as a defense against malignancy) have been implicated as signal molecules in cachexia, based upon similar metabolic derangements produced by these cytokines in other chronic wasting illnesses. Nutritional support is effective in maintaining body weight of cachectic cancer patients, but ineffective in maintaining lean body mass. Although in one study parenteral nutritional support has improved operative morbidity and mortality in cancer patients, it has not yet improved response to chemotherapy or radiation therapy. Because of metabolic derangements seen in cancer cachexia, effective nutritional treatment regimens will probably require manipulation of host intermediary metabolism in addition to feeding. Insulin therapy or exercise are two such methods which appear to preserve host composition by preferential feeding of the host at the expense of the tumor. Future studies which more clearly define the role of signal molecules in producing cancer cachexia syndrome may lead to new treatment strategies, possibly involving modulation of the effects of such molecules on host metabolism.
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PMID:Cancer cachexia. 329 98

A decline in nutritional status is seen in many, but not all cancer patients. The factors leading to this decline are complex and include anorexia, malabsorption and alterations in energy expenditure. The end result of this decline is cachexia, but it is questionable whether this syndrome differs materially from that seen in severe undernutrition arising from other causes. Of the measurable changes in body composition taking place in cancer patients those of most importance are losses of lean tissue, which result in a reduced functional capacity for organ systems. Such losses are difficult to detect because accumulated water may mask many of the early changes in composition and make conventional assessment of nutritional status unreliable. Nutritional support should be provided for undernourished patients, irrespective of the primary cause of their poor nutrition, but there is no convincing evidence that the treatment of nutritional deficiencies alone improves the outcome in cancer patients.
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PMID:Nutritional status in cancer. 329 41

Soluble proteins synthesized and released by phagocytic cells may be responsible for the protein and energy wasting frequently observed during catabolic states, including cancer cachexia. This hypothesis is based upon the observation that many of the hosts's metabolic responses to infection, inflammation, accidental trauma and some forms of cancer are remarkably similar. Anorexia and degradation of skeletal and connective tissue protein, as well as increases in hepatic protein synthesis and energy expenditure, can all be reproduced by the administration of activated macrophage products. During inflammatory states, including active tumour growth, increased production of some cytokines, including interleukin 1 and tumour necrosis factor-alpha (cachectin), have been observed. If these monokines serve as metabolic inducers, then efforts to block therapeutically the actions of macrophage-secreted substances may play a role in slowing the progression of tissue-wasting associated with catabolic states, particularly due to malignant tumours.
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PMID:Interleukin 1, tumour necrosis factor-alpha (cachectin) and the pathogenesis of cancer cachexia. 330 9


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