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)

The aim of this study was to evaluate whether spontaneous physical exercise can modify cancer anorexia and cachexia in tumour-bearing rats. Two transplantable experimental tumours were evaluated. Tumour-bearing Wistar Furth rats fed ad libitum and with free access to a running wheel had a delayed onset of anorexia compared with their non-exercised tumour-bearing controls, retained normal behaviour and were able to run the same daily distance as non-tumour controls until the onset of cachexia. Exercise resulted in a decreased carcass wet weight and lipid stores but in an increased carcass dry weight in the tumour-bearing animals. Despite increased food intake, physical exercise resulted in a reduced final tumour weight without any change in water content. Skeletal and cardiac muscle tissue did not show any difference in water content but there was an increased RNA/protein quotient in the exercising tumour-bearing animals. Thus the deleterious alterations induced by the malignancy on tumour host metabolism are not inevitable but can be modified by spontaneous physical exercise.
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PMID:Effects of spontaneous physical exercise on experimental cancer anorexia and cachexia. 170 20

The cachexia associated with cancer and AIDS appears to result from a number of processes, most of which impair caloric intake. Although past attempts to reverse anorexia-cachexia have generally been disappointing, several promising new pharmacologic approaches are currently being evaluated, including megestrol acetate, hydrazine sulfate, metoclopramide, and dronabinol.
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PMID:Management of anorexia-cachexia associated with cancer and HIV infection. 172 21

Growth hormone (hGH) has been reported to improve nitrogen balances and accrue lean mass tissue in stable subjects. However, the ability of hGH to positively influence host preservation in stressed catabolic states such as cancer-induced cachexia remains unproven. Thirty-seven sham or tumor implanted Fischer 344 rats were randomized to receive either 0.5 mg/kg/day hGH or saline (SAL) subcutaneously from Days 14 to 23 postimplantation. Plasma levels of hGh and somatomedin C/insulin-like growth factor I (IGF I) as well as IGF I bioactivity were determined at sacrifice. Gastrocnemius muscle protein content was used as a index of host lean tissue mass and the tumor response was evaluated via flow cytometry for analysis of cell-cycle distribution. Host cachexia was not attenuated by hGH as muscle protein content was similar in hGH and saline-treated groups. Despite elevated hGH levels (range, 77-222 ng/ml (GH) vs less than 2 ng/ml (SAL], IGF I levels and bioactivity were not elevated in GH-treated groups. In contrast, cancer-induced anorexia markedly decreased IGF I levels (4 U/ml vs 9 U/ml, NTB; P less than 0.01) and this response remained refractory to hGH administration. While final tumor weights were similar between GH- and SAL-treated groups, hGH treatment caused a twofold increase in the proportion of aneuploid cells (P less than 0.05). In conclusion, hGH failed to attenuate lean mass dissolution in the tumor bearing host and this response may be related to the failure of IGF I induction. Conversely, the altered proportion of tumor aneuploid cells suggests a direct influence on tumor cell-cycling populations.
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PMID:Impact of exogenous growth hormone on host preservation and tumor cell-cycle distribution in a rat sarcoma model. 186 78

The literature contains about 500 cases of equine leucosis, though the reports are deposited in a great number of journals and vary considerably concerning particular topics. During the last years there has been a remarkable increase of publications about this syndrome in the equine. The clinical leucosis key recommended by us has been confirmed in principle considering the latest literature. In about 70 individual symptoms which can be clinically observed in equine with leucosis 11 can be considered as main symptoms because of their frequency; they are again classified in primary (lymph node tumours including splenomegaly--loss of condition, weakness--cachexia, weight loss, periphery oedema), secondary (anorexia, inappetence--fever--paleness of mucous membrane--anaemia--tachycardia) and accessory (incoordination--tachypnoea, dyspnoea--apathy, lethargy) main symptoms. Furthermore in future it will be necessary to take into more consideration the symptoms "recurrent colic" and "hydrothorax" within differential diagnosis. The main symptom "incoordination" (ataxia, asynergy, paresis, paralysis) is used by us more precisely only in case of impairment of nervous system by neoplastic infiltrations and does not signify as possible symptoms of general physical weakness, for example faltering, staggering, tumbling or lameness. The morphological classification follows further on our previous recommendation. There exist generalized forms with tumour infiltrations in abdominal and in thoracic cavity as well as especially in peripheral lymph nodes. On the other hand there are characteristic manifestations in certain regions of the body, which establish distinctly the clinical symptomatology. They are marked as regional multicentric forms with the main localizations "mediastinal", "splenic", "mesenteric" or "intestinal".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical diagnostic keys and special manifestations in equine leukosis]. 195 30

This randomized, controlled trial assessed the activity, tolerance, and degree of weight gain and anorexia of two doses of megestrol acetate in patients with advanced cancer and cachexia. Patients received either 480 mg/d or 960 mg/d megestrol acetate or placebo for 8 weeks. As of June 1990, 55 patients had been randomized; 16 died during the 8-week study, and it was too early to evaluate another 5 patients. The remaining 34 patients were included in analyses. The median initial weight loss ranged from 15% to 22% of usual body weight, which shows the severe degree of malnutrition. Further weight loss was seen in 6 of 8 patients in the placebo group compared with only 5 of 15 and 3 of 11 patients in the low-dose and high-dose megestrol acetate groups, respectively. The median further weight loss was comparable in all groups. Six of 15 and 6 of 11 patients in the low-dose and high-dose groups, respectively, gained weight with a median of 3 kg and 4 kg, respectively. A trend showed beneficial effects of megestrol acetate. Appetite improvement was similar in all groups. Due to the small sample size, however, there were no statistically significant differences among the three groups. Side effects of megestrol acetate were mild. In a subgroup of 15 patients, measurement of body water content indicated a decrease of body fat after 8 weeks in the placebo and low-dose groups. Only the high-dose megestrol acetate group showed an increase in both fat and lean body mass, suggesting a positive effect.
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PMID:Megestrol acetate in cancer cachexia. 199 34

Tumor necrosis factor (TNF) or cachectin has been proposed as an important mediator of cancer anorexia and cachexia. The present studies examined the extent to which TNF administration generates symptoms similar to those produced by tumor growth. Like the growth of certain tumors, TNF administration was found to be associated with the development of strong aversions to a novel diet. Area postrema lesions were found to significantly attenuate the effects of TNF on intake of a novel diet, a finding previously reported for tumor anorexia. In addition, the anorexic effects of TNF differed considerably as a function of the novelty of the diet. When the available diet was novel, effects of TNF in lowering food intake were substantial, whereas more modest effects were seen when the diet was familiar. These findings provide evidence for parallels between TNF- and tumor-induced anorexias. Nonetheless, these studies also confirm previous observations of the rapid development of tolerance to the anorexic effects of TNF, a finding that is not consistent with a role for TNF as a critical mediator of tumor anorexia.
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PMID:TNF-induced anorexia and learned food aversions are attenuated by area postrema lesions. 203 2

Chronic undernutrition and high-dose daily corticosteroid therapy are well-accepted causes of growth failure in children with inflammatory bowel disease. Occasionally, children are seen with minimal gastrointestinal symptoms but in whom severe anorexia and profound growth impairment are evident. Recent observations that elevated serum levels of tumor necrosis factor-alpha (TNF) in cachexia associated with a number of disease states have suggested a similar possible role in inflammatory bowel disease. Accordingly, we determined TNF levels in 45 children and adolescents with inflammatory bowel disease (18 ulcerative colitis, 27 Crohn's disease) at varying times during their clinical course and compared them to values obtained from a group of 25 children with functional bowel disease. No differences were noted in serum TNF levels between the children with inflammatory bowel disease and the control population. Values were generally within the range of the lower limit of detection of the assay. In the children with inflammatory bowel disease, there was no significant correlation between TNF levels and disease activity or growth parameters. Our observations suggest that elevated TNF levels are not associated with inflammatory bowel disease in children.
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PMID:Tumor necrosis factor-alpha is not elevated in children with inflammatory bowel disease. 205 Dec 74

Anorexia, cachexia, and resultant weight loss are major clinical problems in a substantial proportion of patients with advanced cancer. Effective means of alleviating these problematic symptoms are lacking. Extensive clinical data demonstrate a weight enhancing effect for the serotonin antagonist, cyproheptadine, in several clinical situations. In addition, sound basic research suggests that cyproheptadine may be helpful in patients with cancer anorexia/cachexia. Because of this, the authors performed a randomized, placebo-controlled, double-blinded clinical trial using cyproheptadine, 8 mg orally three times a day in 295 patients with advanced malignant disease. Patients assigned to cyproheptadine had less nausea (P = 0.02), less emesis (P = 0.11), more sedation (P = 0.07), and more dizziness (P = 0.01) than placebo patients. Patients' appetites, measured by serial patient-completed questionnaires, appeared to be mildly enhanced by cyproheptadine. Unfortunately, cyproheptadine did not significantly abate progressive weight loss in these patients with advanced malignant disease; patients assigned to cyproheptadine lost an average of 4.5 pounds per month compared to 4.9 pounds per month for patients assigned to a placebo (P = 0.72).
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PMID:A controlled trial of cyproheptadine in cancer patients with anorexia and/or cachexia. 218 85

Preliminary information has suggested that megestrol acetate leads to appetite stimulation and nonfluid weight gain in patients with breast cancer, other cancers, and AIDS. Pursuant to this, we developed a randomized, double-blind, placebo-controlled trial of megestrol acetate in patients with cancer-associated anorexia and cachexia. We randomly assigned 133 eligible patients to receive 800 mg of megestrol acetate per day or a placebo. Patients assigned to megestrol acetate more frequently reported improved appetite (P = .003) and food intake (P = .009) when compared with patients receiving the placebo. A weight gain of 15 lb or more over baseline was seen in 11 of 67 (16%) patients receiving megestrol acetate compared with one of 66 (2%) given the placebo (P = .003). Patients receiving megestrol acetate reported significantly less nausea (13% vs. 38%; P = .001) and emesis (8% vs. 25%, P = .009). No clinically or statistically significant toxic reactions were ascribed to megestrol acetate, with the exception of mild edema. This study convincingly demonstrated that megestrol acetate can stimulate appetite and food intake in patients with anorexia and cachexia associated with cancer, leading to significant weight gain in a proportion of such patients.
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PMID:Controlled trial of megestrol acetate for the treatment of cancer anorexia and cachexia. 199 53

Cachectin/tumor necrosis factor (TNF-alpha) is a macrophage-secreted cytokine initially found to be a lipoprotein lipase-suppressing serum factor in cachectic, parasite-infected animals. Cloning of the cDNA encoding the gene for cachectin enabled biosynthesis of recombinant human cachectin and proof that the protein is identical to TNF-alpha. Numerous biological activities have subsequently been attributed to this pluripotent cytokine. In addition to suppressing LPL, cachectin/TNF mediates decreased lipogenic enzyme synthesis in adipocytes, causing a state of "cellular cachexia" in vitro. Similarly, catabolic cellular energy responses are induced by cachectin/TNF in cultured skeletal muscle cells which exhibit accelerated glycogenolysis, enhanced lactate production, and increased expression of hexose transporters. Persistent cachectin/TNF production occurs in chronic infection and malignancy, and chronic exposure induces a cachexia syndrome characterized by anorexia, weight loss, and anemia. Acute systemic appearance of cachectin/TNF is capable of inducing a state of lethal shock, disseminated hemorrhagic necrosis, catabolic hormone release, and multiple organ injury. Inhibiting the toxic effects of cachectin/TNF with monoclonal anti-cachectin antibodies during overwhelming Gram-negative bacteremia confers protection against septic shock. In these studies, the unprotected controls succumbed within hours, but baboons immunized against cachectin/TNF did not develop the characteristic increases of IL-1, IL-6, or catabolic stress hormones and did not die, suggesting that cachectin/TNF is a pivotal, proximal factor in the humoral cascade mediating septic shock syndrome. Recent evidence indicates that when produced in lesser quantities, cachectin/TNF may participate in the degradative and reparative mechanisms of physiological tissue remodelling and homeostasis. Future studies of the immunological and metabolic effects of cachectin/TNF should lead to a better understanding of the pathogenesis of infection and inflammation.
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PMID:Metabolic responses to cachectin/TNF. A brief review. 219 78


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