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 medical records of 32 cats with small intestinal adenocarcinoma were reviewed. Common clinical signs included vomiting, dehydration, weight loss, cachexia, anorexia, and lethargy. In 50% of the cats, an abdominal mass was palpated, and in 38%, a mass was seen on radiographs. Biopsy of the tumor without resection was performed in 9 cats; 8 cats were euthanatized at the time of surgery, 7 because of metastases, and 1 cat died 1 day after surgery. In 23 cats, resection was performed. Eleven of these died within 2 weeks after surgery (mean survival time, 2.6 days); 8 had lymph node metastasis. Twelve cats survived greater than 2 weeks after surgery. The mean survival of 11 of these cats was 15 months. Six cats were euthanatized because of recurrent signs; 5 of the 6 had a recurrent abdominal mass. One cat was alive 2 years after surgery. Results of this study indicated that cats with adenocarcinoma, even those cats with advanced disease, can have long-term survival after surgery.
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PMID:Small intestinal adenocarcinoma in cats: 32 cases (1978-1985). 335 Jul 52

Cachexia is a potentially lethal syndrome of unknown etiology characterized by anorexia, weight loss, and protein wasting that frequently complicates the treatment of chronic inflammation and cancer. Cachectin/TNF was isolated during the search for a humoral mediator of cachexia and found to stimulate the breakdown of energy stores from adipocytes and myocytes in vitro, but the chronic effects of the monokine in vivo are not known. Sublethal doses of recombinant human cachectin administered twice daily for 7-10 d caused cachexia in rats, as evidenced by reduced food intake, weight loss, and depletion of whole-body lipid and protein stores. Significant anemia is also observed and found to be the result of decreased red blood cell mass, not expanded plasma volume. Leukocytosis and histopathological evidence of tissue injury and inflammation are observed in several organs, including omentum, liver, spleen, and heart. These data suggests that the exposure of the normal host to cachectin is capable of inducing a pathophysiological syndrome of cachexia, anemia, and inflammation similar to that observed during inflammatory states or malignancy.
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PMID:Cachectin/tumor necrosis factor induces cachexia, anemia, and inflammation. 335 36

Autonomic dysfunction was diagnosed in a 2.5-year-old spayed domestic shorthair cat. The cat had an 8-day history of progressive anorexia, signs of depression, constipation, weight loss, and intermittent regurgitation. Physical examination findings were signs of depression, dehydration, cachexia, bradycardia, bilateral nonresponsive mydriasis, prolapse of both nictitating membranes, dry oral and nasal mucous membranes, and urinary bladder atony. Thoracic radiography revealed megaesophagus. The cat lacked esophageal motility and had a decreased gastric emptying rate. Providing adequate fluid intake, electrolyte balance, and nutrition is a major problem in the management of dysautonomic cats. We were able to provide adequate nutritional support for this patient, using total parenteral feeding and, later, enteral nutrition using a nasogastric tube. Results of an ocular pharmacologic study indicated that the mydriasis and prolapse of the nictitating membrane were attributable to complete autonomic denervation of the eye. Using the method described, topical, autonomic-stimulating agents may assist the clinician in diagnosing dysautonomia in the feline. This report describes a syndrome that is well recognized in the United Kingdom and has the potential to develop in the United States.
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PMID:Dysautonomia in a cat. 339 54

A 5-year-old intact male llama (Llama glama) with gastric squamous cell carcinoma and generalized metastasis is presented. Weight loss, anorexia and cachexia were the presenting clinical signs. Abnormal laboratory findings included neutrophilia, lymphopenia, increased serum activity of hepatic enzymes, mildly increased serum urea nitrogen concentration and elevated protein concentration and nucleated cell count in the peritoneal fluid. Fasciola hepatica ova were identified by fecal sedimentation examination. The presence of flukes, as well as carcinoma metastasis, probably contributed to the increased serum hepatic enzyme activity. Similarities to gastric squamous cell carcinoma in the equine and bovine species are discussed. This case suggests that neoplasia, although rarely reported in the llama, must be considered in the differential diagnostic list for anorexia and weight loss in the llama.
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PMID:Gastric squamous cell carcinoma and fascioliasis in a llama. 340 19

The results of 24 h food preference tests have suggested that learned food aversions may be involved in the development of anorexia in tumour bearing rats and in patients with cancer. We have performed similar tests over longer periods, up to 10 days, in male rats implanted with Leydig cell tumours, using semisynthetic diets containing differing proportions of fat, protein and carbohydrate. Tumour growth caused anorexia (16-30% decrease in food intake) and cachexia (78% decrease in body fat and 18% decrease in body protein, but 16% increase in body water). Both tumour bearing and control rats preferred a high carbohydrate diet to a high fat diet regardless of their previous diet: tumour bearing rats showed no evidence of a learned food aversion in these experiments. Tumour bearing rats did show an initial preference for a novel high protein diet when this was offered as an alternative to the normal protein diet they had previously been consuming, but this apparent learned food aversion disappeared on the second day of the test and was in fact reversed on all the subsequent days of the test. However, tumour bearing rats did show a sustained preference for a novel low protein diet when this was offered as an alternative to the normal protein diet they had previously been consuming. These results suggest that anorexia in the tumour bearing rats was not caused by a learned food aversion. However the results do indicate that the tumour bearing rats may have developed a specific aversion to protein in the diet. Leydig cell tumours are known to secrete large amounts of oestradiol. However injections of oestradiol in normal male rats caused an increase in body fat content and had no effect on the rats' preference for dietary protein. Clearly hypersecretion of oestradiol was not responsible for the loss of body fat, the fluid retention and the aversion to dietary protein which characterised the tumour bearing rats. The mechanisms by which tumour growth causes anorexia and cachexia in these rats remains obscure.
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PMID:The significance of learned food aversions in the aetiology of anorexia associated with cancer. 347 46

Progressive weight loss and anorexia are frequent phenomena in cancer patients. Although cachexia is an expected occurrence in the terminal stages of nearly all malignancies, it may be a presenting sign when the tumor burden is quite small. Lipid depletion occurs out of proportion to the protein loss and accounts for most of the weight loss in cancer. Lipids, more specifically fatty acids, are the major source of fuel in mammals and may also be used in the synthesis of new cell products. Lipolysis and lipogenesis are under the influence of several important enzymes and peptide hormones that may be modulated by a variety of exogenous factors. There is evidence that cancer patients have lost the normal homeostatic responses to decreased energy intake or starvation that allow a decrease in oxygen consumption and protein sparing. An increase in Cori cycle activity or futile recycling of metabolic products occurs with a net energy expenditure rather than energy production. Clinical studies have shown that the body lipid depletion accompanying tumor progression is not solely secondary to decreased food intake and may be reproduced by the transplantation of certain noninvasive tumors to normal hosts. Elevated basal lipolysis has occasionally been seen early in tumor growth. Such findings suggest the presence of a tumor-associated factor responsible for this increase in lipid mobilization. Some of the potential mechanisms for the altered lipid metabolism seen in cancer have been discussed. Metabolic substrates may be remodeled and directed away from fuel-efficient into energy-requiring pathways. An increased energy expenditure may occur as a result of the energy costs of tumor synthesis, an uncoupling of oxidative phosphorylation, or energy-requiring futile cycling. An overall depletion of lipid may be the final outcome of the inhibition of lipid deposition. TNF/cachectin has recently been found to suppress the activity and synthesis of several key lipogenic enzymes, including lipoprotein lipase. Abnormalities in insulin secretion or sensitivity may be involved in the decrease of fat storage in malignancy. Insulin also exerts a significant antilipolytic effect by its antagonism of hormone-sensitive lipase. Mediators of lipolysis and abnormal lipid metabolism may occur in a number of clinical conditions and include ectopic hormone production, growth factors, and tumor-associated lipolytic factors (lipid mobilizing factor, toxohormone).
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PMID:Fat metabolism and cancer. 353 75

Cancer cachexia is a chronic wasting illness directly associated with the presence of uncontrolled malignancy. The authors discuss the various causes of inadequate nutrient intake, including the known data on anorexia, and outline the potential role of humoral factors as mediators of cachexia.
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PMID:General metabolic abnormalities in cancer patients: anorexia and cachexia. 353 80

Anorexia and weight loss are serious complications that adversely effect the prognosis of cancer patients. It has been suggested that TNF/cachectin may cause cachexia. To determine if TNF/cachectin can induce progressive weight loss in tumor-bearing animals, a clone of the human TNF/cachectin gene was isolated and inserted into a mammalian expression vector. This construct was transfected into CHO cells, and a cell line (CHO/TNF-20) that secretes TNF/cachectin was isolated. A cell line (CHO/CMV-Neo) that contains the same expression vector without the TNF/cachectin gene was also isolated. Nude mice injected intraperitoneally with CHO/TNF-20 cells died more quickly than mice injected with CHO/CMV-Neo cells. Eighty-seven percent of mice inoculated intramuscularly with CHO/TNF-20 cells developed severe cachexia and weight loss. All mice bearing CHO/CMV-Neo tumors maintained or increased their body weight. We conclude that mice bearing tumors that secrete TNF/cachectin develop progressive wasting and die more quickly than mice bearing control tumors.
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PMID:Tumors secreting human TNF/cachectin induce cachexia in mice. 360 79

Two closely related lines of the same Walker 256 carcinoma in Crl-CD/COBS rats, described as behaving differently as regards tumor growth and host reaction, show different chemotherapeutic sensitivity to cyclophosphamide (CPA). Line B, which induces early cachexia with marked anorexia, is only moderately sensitive to CPA, while line A, which causes mild anorexia and only terminal cachexia, shows marked responsiveness to CPA, cure being attained in 75% of animals treated with a single dose of 120 mg/kg and in 90-100% of those given 20 mg/kg every other day. Comparative studies in both tumor lines on the distribution of CPA in vivo and on its metabolism by the liver perfusion technique showed no appreciable differences between the two lines in the pharmacokinetics of the compound, but indicate a much greater metabolizing capacity of CPA in the Walker 256/A animals. In vitro metabolic and covalent binding studies confirm that the liver of the Walker 256/A group metabolizes and covalently binds twice as much CPA as the liver of the Walker 256/B group. Conversely to Walker B, microsomal preparations of the Walker tumor line A are able to metabolize CPA to intermediates which irreversibly bind to tissue macromolecules, suggesting an in situ activation of the compound in the sensitive Walker tumor.
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PMID:Different sensitivity of two Walker 256 carcinoma lines to cyclophosphamide: correlation with drug distribution, biotransformation and macromolecule binding. 372 87

Weight loss and anorexia are significant complications of a variety of disorders and add morbidity to the underlying process. We observed marked weight gain (median, 5.1 kg; range, 0.9 to 20.1 kg) and appetite enhancement in 27 of the 28 patients with breast cancer receiving treatment consisting of high doses of oral megestrol acetate (480 to 1600 mg/d). Weight gain occurred regardless of pretreatment weight, extent of metastases, or response to therapy. Our results suggest a possible role for megestrol acetate in reversing anorexia and weight loss, thereby improving the quality of life of patients with cachexia. Further research is needed to establish the mechanism of weight gain and potential clinical applications.
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PMID:High-dose megestrol acetate. A possible treatment for cachexia. 380 18


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