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)

Based on promising preliminary information obtained from uncontrolled pilot studies, several randomized, placebo-controlled, double-blind clinical trials have been launched to evaluate the effectiveness of megestrol acetate for the treatment of patients with anorexia and/or cachexia. The results of these studies have demonstrated that megestrol acetate can improve patients' appetites and promote nonfluid weight gain in some. They also suggest that megestrol acetate has antiemetic properties. Ongoing clinical trials are evaluating the dose-response relationship of megestrol acetate for these clinical problems and whether megestrol acetate will improve the survival of patients at risk for developing cancer anorexia/cachexia.
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PMID:Megestrol acetate for anorexia and cachexia. 146 28

Involuntary weight loss or wasting indicative of severe protein energy malnutrition is a frequent complication of acquired immune deficiency syndrome (AIDS). Malnutrition, with its associated adverse effects on immunocompetence, may contribute to the progression of AIDS itself. Since death from wasting is ultimately related to the magnitude of tissue depletion, restoration of body cell mass may enhance survival. The mechanism of weight loss in AIDS has not been clearly elucidated. The etiology is likely to be multifactorial, the result of interactions between decreased caloric intake, malabsorption, and alterations in energy expenditure secondary to hormonal and/or metabolic abnormalities. Although weight loss is occasionally reversible with treatment of underlying infections and/or easily identifiable and reversible causes, the majority of patients are not this fortunate. Enteral and parenteral nutrition, which are expensive, cumbersome, and potentially morbid, have been suggested by some as therapeutic options. Megestrol acetate, a synthetic, orally active progestational agent, has been reported to stimulate appetite and weight gain. Data regarding the use of megestrol acetate for the treatment of cachexia related to human immunodeficiency virus (HIV) infection demonstrate convincingly its effectiveness in treating many patients with HIV-related anorexia and cachexia.
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PMID:HIV-related cachexia: potential mechanisms and treatment. 146 29

Thirty-five 6-week-old guinea fowl keets, seronegative for maternal antibodies to Newcastle disease virus, were infected with Herts strain (33/56) and Kumarov strain of Newcastle disease virus intramucularly (IM) or intranasally (IN). Clinical signs were first noticed four days post infection (PI) in the group infected IM but five days PI in the group infected IN with Herts strain of Newcastle disease virus. These clinical signs were similar in both groups and included anorexia, droopiness, huddling together, greenish diarrhoea and marked cachexia. Prominent nervous signs, including spasms of the head and neck, were observed in groups infected with Herts strain. The major gross lesions observed were emaciation with prominent keel bone, empty intestinal tract and distended gall bladder in most keets. The histological lesions were characterised by meningoencephalitis, necrosis and loss of lymphocytes from splenic and lymphoid aggregates. There was muscular degeneration and necrosis in the gizzard and mild pulmonary congestion and oedema in some keets. Neither gross or microscopic lesions were observed in keets that had received the Kumarov strain.
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PMID:Pathogenicity of two strains of Newcastle disease virus in the grey-breasted helmet guinea fowl. 150 75

Cancer cachexia is one of the most prevalent and devastating syndromes associated with advanced cancer. Its main clinical manifestation is profound anorexia. Progestational drugs have shown meaningful effects on appetite, food intake, and nutritional status in patients with advanced cancer and AIDS, and could be useful in managing anorexia. Corticosteroids also seem to produce increased appetite, but these effects are short-lived. Cyproheptadine, hydrazine sulfate, and cannabinoids also are being studied in the management of cancer-induced anorexia, but their role has not yet been clearly established. Future research should evaluate how the different drugs affect specific symptoms associated with cachexia.
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PMID:Current pharmacological management of anorexia in cancer patients. 153 97

Diabetic neuropathic cachexia is characterized by neuropathic pain and severe weight loss of unknown aetiology. We describe four patients with diabetic neuropathic cachexia who were found to have malabsorption. Four diabetic patients presented with neuropathic pain, anorexia, depression and weight loss of 16 (range 10-21) kg. None complained of diarrhoea. There were three males and one female, median age 54 (46-67) years. A butterfat test showed a serum turbidity difference of 9 (6-10) light scattering units (normal greater than 60 units). The median serum xylose was low and there was delayed urinary xylose excretion. Urinary indicans, small bowel histology, liver function tests, and thyroid and renal function were normal. Ultrasound scans of liver, gall bladder and pancreas, and endoscopic retrograde cholangiopancreatogram were normal. The patients were treated with pancreatic supplements and a high calorie diet. Three have completely recovered and the other patient is improving. Thus these cases of diabetic neuropathic cachexia appeared to be associated with malabsorption which may be due to pancreatic dysfunction. It is suggested that the management of diabetic neuropathic cachexia should include the investigation and treatment of malabsorption.
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PMID:Diabetic neuropathic cachexia associated with malabsorption. 156 56

In this report we describe an experimental model of cachexia that fulfills the criteria of an early effect with a small tumor mass not related to the growth rate of the tumor, and progressive wasting of muscle and fat without a detectable loss of appetite. C-26.IVX is a cell line derived from murine colon-26 adenocarcinoma which retains the transplantability of the original tumor and induces true cachexia in syngeneic hosts. Evidence is presented to support a role for interleukin (IL-6) as a cachectic factor in the development of cancer cachexia in this model system. Thus, increasing levels of IL-6 in C-26.IVX-bearing mice correlate with the development of cachexia. If the primary tumors were resected, mice gained weight and the levels of IL-6 in the serum were reduced significantly. Moreover, monoclonal antibody to murine IL-6 (but not anti-tumor necrosis factor antibody) was able to significantly suppress the development of key parameters of cachexia in tumor bearing mice.
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PMID:Evidence for the involvement of interleukin 6 in experimental cancer cachexia. 156 7

Tumor necrosis factor (TNF), a pleiotropic cytokine, is produced by macrophages and other cells in a variety of infectious and noninfectious diseases. Ultimately, the net biological effects of TNF may be either beneficial or injurious to the host. For instance, during overwhelming bacterial infection, the acute overproduction of TNF causes septic shock syndrome characterized by hypotension, organ failure, and death. Antibodies against TNF prevent and reverse these sequelae in animal models of septic shock, and their use in humans is currently under investigation in clinical trials. In another instance, TNF has been implicated as an injurious mediator in the state of malnutrition that complicates the course of chronic infection and cancer. Termed cachexia, this chronic syndrome inevitably causes the afflicted host to succumb from weight loss, anorexia, and catabolism of protein and lipid. Experimental studies of animals exposed to TNF for protracted periods indicate that this cytokine is capable of causing cachexia, and the biochemical basis for these catabolic changes has been identified. More recent data indicate that the detrimental metabolic effects of TNF are not dependent upon its circulating levels in the bloodstream, but rather are dependent upon its actions locally in vital organs (e.g., brain). Thus, the metabolic basis for cachexia in infection may be largely dependent upon the amount of cytokine produced in metabolically important tissues. As a result, circulating TNF levels in cachectic patients may not accurately reflect the metabolic state of the host, and do not correlate to weight loss.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tumor necrosis factor and regulation of metabolism in infection: role of systemic versus tissue levels. 157 88

The cause of cancer cachexia is unclear. Tumors may be competing with the host for ingested nutrients or may be releasing some factor that actively inhibits energy utilization. To explore these questions, plasma was sterilely collected and pooled from 103 terminally cachectic Fischer 344 rats implanted with an experimental sarcoma. Control plasma was collected in similar fashion from 138 nontumor-bearing rats (NTBP). Plasma from tumor-bearing rats (TBP) or NTBP was continuously infused in a randomized, blinded fashion for 4 days into 20 normal rats. During infusion, food intake and nitrogen excretion were measured daily. At sacrifice, body weight and organ masses were determined. Rats receiving TBP demonstrated an immediate and profound anorexia compared with those receiving NTBP. Total food intake during treatment was 31.2 +/- 3.3 (g +/- SEM) in the TBP group versus 48.2 +/- 2.8 in the NTBP group (P less than 0.001 by t test). Likewise, the total decline in body weight was greater in the TBP group as compared with the NTBP group (-35.2 +/- 3.4 versus -14.6 +/- 4.0, P less than 0.001). Mean daily nitrogen balance during treatment was negative in the rats receiving TBP (-14.5 +/- 20.1 mg +/- SEM) while remaining highly positive in the rats receiving NTBP (110.7 +/- 19.3, P less than 0.002). Finally, cardiac and gastrocnemius muscle masses were decreased, while hepatic mass was unaffected. These data demonstrate that the syndrome of cancer-associated cachexia is transmissible in plasma and therefore may be mediated by a circulating molecule or molecules. Identification and purification of the molecule(s) responsible for this effect would have obvious clinical benefits.
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PMID:Cancer cachexia is transmissible in plasma. 159 73

Two adult Hampshire rams, unrelated and from separate farms, were examined for the cause of intermittent bloat and, or anorexia which lasted for three to six weeks and caused depression and cachexia. The rumen of each ram was hypermotile and ballottement of the ventral abdomen of each animal revealed an enlarged doughy viscus. Mild prerenal azotaemia, hypokalaemia with metabolic alkalosis, and high rumen chloride concentrations were evident. One ram died during the induction of anaesthesia for an abomasotomy and the other was euthanased after unsuccessful medical therapy. The abomasum of each ram was four to six times larger than that of a normal adult ram and filled with coarse, semi-moist, impacted ingesta. This abnormality was clinically identical to the abomasal emptying syndrome which has been described only in the Suffolk breed.
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PMID:Abomasal dilatation and impaction in two Hampshire rams. 162 57

Although cachexia is a common feature of cytomegalovirus infection, little is known about its cause. To explore any contributory role that tumour necrosis factor-alpha (TNF) might have the serum concentrations of TNF in eight patients who developed CMV disease after liver transplantation were investigated. All patients exhibited pronounced and long lasting increases in TNF serum concentrations. Increased endogenous TNF concentrations were associated with weight loss and anorexia. In contrast, liver transplant recipients without CMV disease showed no weight loss.
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PMID:Cachexia and tumour necrosis factor-alpha in cytomegalovirus infection. 164 79


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