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At least 451 records · Page 25Linked to original sources
PubMed1984

Contribution of inert mass to experimental cancer cachexia in rats.

An inert artificial tumor (AFT) was inflated in male F344 rats to simulate, experimentally, the growth in mass of large transplantable tumors that produce cachexia. The AFT depressed host weight gain and skeletal muscle mass up to 30% and food intake up to 20% of the depression induced by tumors of comparable size. When the growth rate of the AFT was low, there was no depression of food intake. Work-induced hypertrophy of skeletal muscles, as assessed by a gastrocnemius tenotomy model, was approximately equal to that of normal, tumor-bearing, and AFT-bearing animals. The AFT elevated host total energy expenditure by 12.5% and compartment-of-energy expenditure attributable to motor activity by 10.5%. The elevation of energy expenditure accounted for most of the depression of weight gain of AFT-bearing animals below that of intact animals. The large mass of most transplantable tumors leads to an overestimate of the malignant tissue-depletive effects of tumor and an under-estimate of the asthenic effects.

Animals↗
PubMedDate not supplied

[Echographic diagnosis of a cachexia-inducing diencephalic tumor].

In a 2 month-old girl presenting with severe cachexia, ultrasonography of the brain through the fontanella showed a diencephalic tumor. Ultrasonographic pictures were compared with those obtained with CT scan. This report emphasizes the value of ultrasonography in such a syndrome with little neurologic symptoms.

Brain Neoplasms↗
PubMed1981

Carbohydrate metabolism in cancer cachexia.

A profound loss of body mass and energy reserves is a characteristic feature of cancer cachexia. Because glucose is a major energy-yielding fuel, abnormalities of carbohydrate metabolism may prove to be important in the development or end-result of this common syndrome. In this paper, we review the known alterations of glucose and lactate metabolism that occur in patients with malignant tumors.

Blood Glucose↗
PubMed1983

Effect of cancer cachexia and amiloride treatment on the intracellular sodium content in tissue cells.

This study was designed to investigate the effects of a growing H6 hepatoma on the intracellular element content in three distinctly different tissue cell populations of the mouse host (hepatocytes, fibroblasts, and crystal enterocytes). X-ray microanalysis measurements of the intranuclear concentrations of several elements (sodium, magnesium, phosphorus, sulfur, chlorine, and potassium) were made. Briefly, the tumor presence significantly increased intranuclear sodium concentration but not the concentration of magnesium, phosphorus, sulfur, chlorine, or potassium in three tissue cell types of mice that were anorectic and cachectic. A second aim of the study was to see if injections of the diuretic amiloride, a drug reported to block passive influx of sodium into mammalian cells, would counteract the effect of the tumor presence and lower the intranuclear concentration of sodium towards that of a non-tumor-bearing host. Amiloride did significantly lower the intranuclear level of sodium in the host tissues to that of non-tumor-bearing mice. The amiloride-caused decrease on intracellular sodium was correlated to a decreased cell proliferation activity in the tumor cells and duodenal enterocytes. A possible relationship between the intracellular concentration of sodium in tissue cells and cancer cachexia is discussed.

Amiloride↗
PubMed1982

[Cryptosporidium in veal calves affected with cachexia].

Coccidia of the genus Cryptosporidium were detected in histological sections of the small intestine of three veal calves. Autopsy was performed on these calves as part of a study of the aetiology of the syndrome "cachexia" in veal calves. In addition, typical 4 mu cryptosporidium oocysts were observed in the bowel contents of one of two histologically positive calves examined and seven out of eight other cachectic calves in which coccidia had not been detected on histological examination. The changes of the mucosa of the small intestine observed are described and the possible role of cryptosporidiosis in the pathogenesis of these lesions is discussed.

Animals↗
PubMed1995

The role of restricted food intake in the pathogenesis of cachexia in severe combined immunodeficient beige mice infected with Mycobacterium paratuberculosis.

A paired feeding experiment was conducted to investigate if reduced food intake is a reason for the body weight loss previously observed in severe combined immunodeficient beige (SCID bg) mice infected with Mycobacterium paratuberculosis. Mice were paired on the basis of age, litter and sex. One of each pair was injected intraperitoneally with 10(5) viable M. paratuberculosis organisms. The remainder served as uninfected pairfed mates. Each uninfected mouse was restricted to the amount of food (per gram body weight) that its infected paired mate ate in the previous 24 hour period starting at four weeks postinfection until 12 weeks postinfection when the mice were necropsied. The mean body weights of the two groups were not significantly different (p < 0.05) at the start of the experiment (infected 27.6 +/- 2.1 g, pairfed 27.3 +/- 3.4 g) but the pairfed group weighed less after 12 weeks of restricted food intake. Mycobacterium paratuberculosis was isolated from the spleen, liver, gut and fecal pellets of the infected but not the uninfected mice. Acid-fast bacilli were seen histologically in the liver, spleen and intestines of the infected mice only. Analysis of carcass compositions indicated that both infected and pairfed mice lost dry matter. Despite the loss in dry matter, the infected mice appeared to have maintained their body weights due to an increased retention of body water (presumably due to edema of inflammation). These results suggest that infection of SCID bg mice with M. paratuberculosis causes a reduction in their food intake (presumably due to reduced appetite) which, in turn, contributes to a loss in dry matter. We suggest that this loss in dry matter is one of the initial events that eventually lead to cachexia, and that it precedes the body weight loss that inevitably occurs in SCID bg mice chronically affected with M. paratuberculosis.

Animals↗
PubMed1994

[A case report of surgical repair of a ruptured aneurysm of the sinus Valsalva in an aged person with cardiac cachexia].

A 71-year-old woman underwent surgical repair of a ruptured aneurysm of the sinus Valsalva. She had an aneurysm of the right coronary sinus ruptured into the right atrium. There was no VSD. The patient suffered from heart failure for 38 years and went into cardiac cachexia. Direct closure from the right atrium was performed and the patient has resumed full physical activities. As far as we know, this is one of the oldest patients who underwent successful surgery for this disease in this country.

Aged↗
PubMed1993

Galloway Memorial Lecture. Protein engineering of tumor necrosis factor-beta and its applications in cancer, septicaemia and cachexia.

The tumour necrosis factors (TNFs) are cytokines, small proteins produced by cells as part of the intercellular signalling network. The exact physiological role of TNFs is unknown, but interest in them focused on three of their capabilities: as potential anti-tumour agents, as humoral mediators of an organism's response to injury and as effector molecules in cachexia. The first TNF to be described, now known as TNF-alpha, has been relatively well studied because the recombinant protein was easily produced since it was cloned in 1984. Studies on TNF-beta or lymphotoxin were hampered by the inability of most groups to express the recombinant protein. This paper describes the expression and purification of recombinant TNF-beta in Escherichia coli, followed by studies to localise the receptor binding site of the molecule through site-directed mutagenesis. Mutants with single amino acid changes at either of two distinct loop regions, at positions aspartic acid-50 or tyrosine-108, were found to have greatly reduced receptor binding and cytotoxic activity. These two regions in TNF-beta correspond to known loop regions where mutations also result in loss of biological activity of TNF-alpha, a related cytokine which shares the same cellular receptors with TNF-beta. This provides evidence for a new hypothesis that both the TNFs bind to their receptors as trimers, each of which is capable of binding simultaneously to three receptors. This leads further to the intriguing possibility of a new mechanism of receptor clustering through simultaneous binding to a single ligand.

Cachexia↗
PubMed1993

[Surgical treatment of cardiac cachexia with mitral valve disease: the effect of preoperative IVH and left atrial plication on postoperative respiratory condition].

Twenty-four patients with cardiac cachexia associated with mitral valve disease were evaluated from the point of postoperative respiratory management. Our previous study suggested that preoperative intravenous hyperalimentation (IVH) had just a effect on postoperative respiratory management, but another study suggested that left atrial plication (LAP) for giant left atrium might improve the postoperative respiratory function. Therefore, four groups could be identified: (1) IVH group (17 patients), (2) No-IVH group (7 patients), (3) LAP group (6 patients), (4) No-LAP group (18 patients). The hospital mortality was 18% in IVH group and was not related to the postoperative respiratory distress. On the contrary, the mortality in No-IVH group was 57%, related to the postoperative respiratory distress. The mortality of LAP group was 67%, and was related to the respiratory distress except one patient. In No-LAP group which had undertaken preoperative IVH, the mortality was 17%. As a result, preoperative IVH therapy may consider to be a favorite procedure in order to get the good postoperative respiratory condition, but LAP itself would be suspicious for this purpose.

Adult↗
PubMed1994

Anorexia and cachexia in advanced cancer patients.

Cachexia is a frequent and devastating complication of advanced cancer. Current understanding of the pathophysiology of this syndrome implicates tumour induced metabolic changes and immune responses. Clinical manifestation include anorexia, chronic nausea, asthenia and change in body image. Aggressive nutritional intervention has not been shown to be of benefit. Patients and families should be counselled about the goals of nutritional intake. In selected cases, enteral nutrition may be appropriate. Pharmacological management should first be directed at correcting nausea. Agents of potential usefulness in the treatment of anorexia include corticosteroids, megestrol acetate, cyproheptadine, hydrazine sulphate and dronabinol. Future research should further address pathophysiology, symptomatic and metabolic effects of interventions and interactions with other syndromes of terminal cancer.

Adrenal Cortex Hormones↗
PubMed1996

Muscle wasting and dedifferentiation induced by oxidative stress in a murine model of cachexia is prevented by inhibitors of nitric oxide synthesis and antioxidants.

Muscle wasting is a critical feature of patients afflicted by AIDS or cancer. In a murine model of muscle wasting, tumor necrosis factor alpha (TNF alpha) induces oxidative stress and nitric oxide synthase (NOS) in skeletal muscle, leading to decreased myosin creatinine phosphokinase (MCK) expression and binding activities. The impaired MCK-E box binding activities resulted from abnormal myogenin-Jun-D complexes, and were normalized by the addition of Jun-D, dithiothreitol or Ref-1, a nuclear redox protein. Treatment of skeletal muscle cells with a phorbol ester, a superoxide-generating system, an NO donor or a Jun-D antisense oligonucleotide decreased Jun-D activity and transcription from the MCK-E box, which were prevented by antioxidants, a scavenger of reducing equivalents, a NOS inhibitor and/or overexpression of Jun-D. The decreased body weight, muscle wasting and skeletal muscle molecular abnormalities of cachexia were prevented by treatment of TNF alpha mice with the antioxidants D-alpha-tocopherol of BW755c, or the NOS inhibitor nitro-L-arginine.

Animals↗
PubMed1977

Uncomplicated starvation versus cancer cachexia.

Host starvation is a common accompaniment to the presence of cancer. Diminished intake is a major contributor to this starvation and does not require that the oropharynx or gastrointestinal tract be the primary site. There is suggestive evidence that the normal adaptive mechanisms of the nontumor-bearing host to starvation that result in body protein conservation are not functioning in the tumor-bearing host. Cancer cachexia has some similarity to the metabolic disturbances of host metabolism that are seen in major injury or sepsis. The growing tumor shows little respect for normal constraints of host tissue growth. With the widespread availability of methods of total parenteral nutrition, the interrelationship of nutrition and host-tumor growth assumes greater importance.

Animals↗
PubMedDate not supplied

The effect of megestrol acetate on anorexia, weight loss and cachexia in cancer and AIDS patients (review).

Weight gain is a well-known side-effect of megestrol acetate (MA) treatment. This effect has been studied systematically in cancer and AIDS patients with involuntary weight loss, anorexia or manifest cachexia, situations in which weight gain is desirable. Significant, positive effects on weight gain and on certain quality of life aspects, such as appetite, nausea, body image and mood have been reported for cancer patients treated with 160 mg to 1.600 mg daily and similar effects have been registered in AIDS patients if doses of about 400-800 mg are used. Maximal weight gain is normally achieved within 8 weeks. The weight gain is, unfortunately, mainly due to an increase in fat mass and partly due to edema and, therefore, no significant effects are reported as regards the Karnovsky index. If anorexia, nausea and a negative body image are major concerns and if the patient has a life expectancy of more than 3 months, MA is a reasonable treatment option. However, if the central problem is fatigue and a low Karnovsky index, especially in a patient with a short expected survival, MA, which is not inexpensive, is not likely to be of significant help.

Acquired Immunodeficiency Syndrome↗
PubMed1997

IL-4 protects against TNF-alpha-mediated cachexia and death during acute schistosomiasis.

To examine the role of the Th2-type response during schistosomiasis mansoni we compared disease progression in wild type (wt), and Th2-response deficient IL-4(-/-) mice. Whereas wt C57BL/6 mice tolerate infection and develop chronic disease, IL-4(-/-) C57BL/6 animals are highly susceptible, exhibiting severe acute cachexia followed by death. Data point toward morbidity in the IL-4(-/-) C57BL/6 mice being mediated by TNF-alpha, possibly through the uncontrolled production of nitric oxide in target organs such as the ileum. We propose that IL-4 prevents severe disease during schistosomiasis by regulating macrophage activation.

Animals↗
PubMed1998

Human immunodeficiency virus-associated wasting and mechanisms of cachexia associated with inflammation.

Profound weight loss and progressive depletion of muscle mass is a common sequela of chronic diseases such as cancer, tuberculosis, and human immunodeficiency virus (HIV) infection. Studies of HIV-associated wasting have revealed several possible mechanisms. Alterations in anabolic hormones, energy intake, energy expenditure, and production of proinflammatory cytokines, which cause cachexia, may contribute to wasting in HIV-infected patients. These studies have revealed the complexity of the interactions between cytokines and the hormones that typically regulate catabolic-anabolic homeostasis. Despite this complexity, HIV-associated wasting should be manageable. Several strategies are currently under investigation, including anabolic steroid and human growth hormone therapy, appetite stimulants, nutritional supplementation, and cytokine antagonists. Some of these approaches have shown early promise. Further research in these areas should facilitate development of effective intervention strategies and lead to improvements in quality of life for patients suffering from wasting syndromes.

Cachexia↗
PubMed1998

Effects of plasmapheresis in a rabbit model of cancer cachexia.

We developed a model of cancer cachexia by transplanting VX2 tumors into rabbits and investigated the effects of plasmapheresis in this model. AIS activity was identified in supernatants obtained from VX2 tumor by phenyl Sepharose chromatography. Fractions eluted with 0.5 M NaCl showed the ability to damage the red blood cell membrane and suppress immunity. Rabbits exhibited marked weight loss, anemia and immunodeficiency 40 days after transplantation of VX2 tumors. Plasmapheresis inhibited plasma-induced damage of the red blood cell membrane and suppression of immunity. Twice-weekly plasmapheresis resulted in gradual normalization of cellular immunity. Weight loss and survival were also improved. No side effects were observed.

Animals↗
PubMed1998

Lipoprotein lipase expression exclusively in liver. A mouse model for metabolism in the neonatal period and during cachexia.

Lipoprotein lipase (LPL), the rate-limiting enzyme in triglyceride hydrolysis, is normally not expressed in the liver of adult humans and animals. However, liver LPL is found in the perinatal period, and in adults it can be induced by cytokines. To study the metabolic consequences of liver LPL expression, transgenic mice producing human LPL specifically in the liver were generated and crossed onto the LPL knockout (LPL0) background. LPL expression exclusively in liver rescued LPL0 mice from neonatal death. The mice developed a severe cachexia during high fat suckling, but caught up in weight after switching to a chow diet. At 18 h of age, compared with LPL0 mice, liver-only LPL-expressing mice had equally elevated triglycerides (10,700 vs. 14,800 mg/dl, P = NS), increased plasma ketones (4.3 vs. 1.7 mg/dl, P < 0.05) and glucose (28 vs. 15 mg/dl, P < 0.05), and excessive amounts of intracellular liver lipid droplets. Adult mice expressing LPL exclusively in liver had slower VLDL turnover than wild-type mice, but greater VLDL mass clearance, increased VLDL triglyceride production, and three- to fourfold more plasma ketones. In summary, it appears that liver LPL shunts circulating triglycerides to the liver, which results in a futile cycle of enhanced VLDL production and increased ketone production, and subsequently spares glucose. This may be important to sustain brain and muscle function at times of metabolic stress with limited glucose availability.

Age Factors↗