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PubMed1993

[2 cases report of open heart surgery with non-blood transfusion in severe valvular heart disease with cardiac cachexia--the efficacy of recombinant human erythropoietin].

Open heart surgery with non-blood transfusion was performed in 2 cases of severe mitral valve disease with cardiac cachexia by administering recombinant human erythropoietin (EPO). Case 1 was a 72-year-old and case 2 was a 66-year-old woman whose % usual body weight was 71-79% and Ht value on admission was 28.5-30%. Both patients were administered 9000-18000 U/week of EPO and ferrous sulfate pre- and postoperatively. In each case 800-1200 ml of autologous blood was drawn within 3 weeks preoperatively without hemodynamic change or decrease of Ht value. Both patients were received mitral valve replacement with non-blood transfusion. Preoperative administration of EPO and autologous blood preservation allowed open heart surgery with non-blood transfusion even in such a serious case as cardiac cachexia.

Aged↗

PubMed1996

Tumor necrosis factor-alpha inhibits collagen alpha1(I) gene expression and wound healing in a murine model of cachexia.

The mechanisms responsible for impaired wound healing in patients with cachexia-associated infection, inflammation, and cancer are unknown. As tumor necrosis factor (TNF)-alpha is elevated in these diseases, and TNF-alpha inhibits collagen alpha1(I) gene expression in cultured fibroblasts, we analyzed whether chronically elevated serum TNF-alpha affects collagen metabolism in vivo by inoculating nude mice with Chinese hamster ovary cells secreting TNF-alpha (TNF-alpha mice) or control Chinese hamster ovary cells (control mice). Before the onset of weight loss, TNF-alpha mice had a selective decrease in collagen synthesis and collagen alpha1(I) mRNA in the skin. In addition, TNF-alpha mice displayed impaired healing of incisional and excisional skin wounds, compared with control animals, before the onset of cachexia. The expression of transforming growth factor-beta1, a potent fibrogenic factor, was inhibited by TNF-alpha in the skin. In studies with transgenic mice expressing the human growth hormone under the direction of 5' regulatory regions of the human collagen alpha1(I) gene, TNF-alpha treatment inhibited the expression of the collagen alpha1(I) human growth hormone transgene containing -2.3 kb of the 5' region, whereas transgene expression directed by -0.44 kb of the 5' region was not affected. These experiments suggest that TNF-alpha may play an important role in the impaired wound healing of chronic diseases that are characterized by a high production of this cytokine and provide insights for potential therapeutic approaches.

Animals↗

PubMed1997

The cancer cachexia syndrome.

The cancer cachexia syndrome is clinically characterized by anorexia, wasting, weight loss, weakness, fatigue, poor performance status, and impaired immune function, which are unresolved by forced caloric intake. Diminished nutritional intake, maladaptive metabolic processes, and increased metabolic expenditure all play roles in the development of this syndrome. Multiple mediators of both tumor and host cell origin are mechanistic in its etiology. Treatment is not entirely satisfactory and should be directed toward improvement in the quality of life of the patient and should often include nutritional counseling. It should take into consideration both disease and treatment related factors as well as the cachexia syndrome itself. Use of progestogens (megesterol acetate, medroxyprogesterone), corticosteroids (decadron, prednisone), metoclopramide, tetrahydrocannabinol (dronabinol), and possibly anabolic steroids (nandrolone decanoate, oxandrolone), melatonin, and eicosapentaenoic acid, may yield therapeutic benefit.

Anorexia↗

PubMed1998

Association between tumor necrosis factor in serum and cachexia in patients with prostate cancer.

The present study was undertaken to evaluate the relationship between serum tumor necrosis factor (TNF) and cachexia in patients with prostate cancer. TNF levels were determined in 110 serum samples from prostate cancer patients by an enzyme immunoassay. Serum TNF activity was positive in 76% of the patients with relapsed disease, whereas only 11% of the untreated patients and 0% of the patients in remission as a result of endocrine therapy were positive. The serum total protein and albumin levels, hemoglobin levels, and body mass index of the patients with elevated serum TNF levels were significantly lower (P < 0.05) than the corresponding values in patients with undetectable serum TNF levels. The serum TNF levels of patients with serum albumin levels of <3.5 g/dl, serum total protein levels of <7.0 g/dl, hemoglobin levels of <11.0 g/dl, and a body mass index of <21 kg/m2 were significantly higher (P < 0.05) than the values in their respective counterparts. There was a significant correlation between the detectability of serum TNF and performance status (P < 0.05). Patients with elevated serum TNF levels had a significantly higher mortality rate (P < 0.05) than those with undetectable serum TNF levels. These findings suggest that TNF may be one of the factors contributing to the complex syndrome of cachexia in patients with prostate cancer.

Adenocarcinoma↗

PubMed1983

Cancer cachexia--a clinical entity?

A number of metabolic abnormalities associated with cancer may interfere with normal starvation-adaption to alter the pattern of tissue loss in individuals with cancer. The cachexia thus produced is said to differ from simple under-nutrition and may therefore be detectable using simple clinical methods. Seven measurements commonly used for nutritional assessment were made before treatment in 72 patients with cancer and 89 patients who were undernourished but cancer-free. Body weight as a percentage of ideal weight, arm muscle circumference, triceps skinfold thickness, plasma protein, albumin and transferrin and the peripheral blood lymphocyte count did not differ significantly between the groups. If body composition in cancer cachexia differs from that found in comparable simple undernutrition then such variations are not detectable by a standard nutritional assessment.

Journal Article↗

PubMed1996

Involvement of human interleukin 6 in experimental cachexia induced by a human uterine cervical carcinoma xenograft.

In this experimental study, the authors examined the role of various cytokines in the development of cancer cachexia. After in vitro culture and selection of a single clone of tumor cells, a growing uterine cervical carcinoma from human origin was implanted subcutaneously in nude mice. Body weight and tumor volume were measured throughout the study period; tissue wasting was assessed by weighing the gastrocnemius muscle and the peri-ovarian white adipose tissue. Serum and tumor cytokine concentrations, including human G-CSF, murine and human tumor necrosis factor (TNF)- proportional, variant, IFN-gamma, interleukin (IL)-1 proportional, variant and IL-6, were determined by ELISA at the end of the study. Two months after implantation, the tumor (4% of carcass weight) induced severe loss of adipose tissue (-95%) and muscle mass (-49%). Human IL-6 (0.38 +/- 0.19 ng/ml) and human G-CSF were detected in the serum and the tumor tissue of these animals; none of the cytokines of murine origin was detected in the serum, except IL-6 (0.14 +/- 0.05 ng/ml). Treatment with neutralizing anti-human IL-6 antibodies reduced plasma IL-6 and G-CSF levels and significantly increased host carcass weight (16%) and fat mass (353%). The authors conclude that human IL-6 produced by tumor cells is an essential mediator of cachexia in this model.

Journal Article↗

PubMed1992

Interleukin 6 reduces lipoprotein lipase activity in adipose tissue of mice in vivo and in 3T3-L1 adipocytes: a possible role for interleukin 6 in cancer cachexia.

To investigate whether interleukin 6 (IL-6) might be a potential mediator of the depleted fat reserves observed in malignancy-associated cachexia, we measured lipoprotein lipase (LPL) activity in adipose tissue of mice after administration of IL-6 or tumor necrosis factor and in cultured adipocytes after addition of these cytokines. Injection of IL-6 i.p. reduced adipose tissue LPL activity by 53% within 4.5 to 5.5 h. Injection of tumor necrosis factor elevated serum IL-6 levels and reduced adipose tissue LPL activity by 70%. Both human and murine IL-6 reduced heparin-releasable LPL activity in 3T3-L1 adipocytes in a dose-dependent manner; half-maximal inhibition of LPL activity was achieved with 5000 hybridoma growth factor units/ml. Thus, IL-6 reduces adipose LPL activity and may contribute to the loss of body fat stores associated with some cases of cancer cachexia. Since tumor necrosis factor increases circulating IL-6, some of its effects may be mediated or potentiated by IL-6.

3T3 Cells↗

PubMed1998

[Megestrol in the treatment of AIDS associated cachexia. Evaluation by bioelectric impedance analysis of body composition].

OBJECTIVE: To value the effects of megestrol acetate wer the weight and the body composition (fat, lean and body water) in patients with AIDS associated cachexia, by bioelectric impedance analysis. SUBJECTS: 25 patients between 23 and 57 years of age, with confirmed HIV infection and prior weight lost of 7.96 +/- 4.6 kg in relation to their habitual weight in the previous months. All the patients were under antiretroviral therapy. METHOD: Basal determination, before the beginning of the antianorexic treatment and at the end of it, using bioelectric impedance analysis by Maltron BF 905 analyzer, calculating fat, lean and total body water in relation to weight, height, age and sex. Oral administration of 320 mg/day megestrol acetate for three consecutive months. Statistical comparation (RSIGMA and SPSS) by paired t-test of the mean weight, body mass index, fat, lean and total body water. RESULTS: During the three months treatment the mean basal body weight of the patients increased 3.54 Kg (p < 0.001) at the expense of an increase of 2.24 kg in the total body lean (p < 0.01), while the increment of the body fat (1.2 kg) was not statistically significant. The total body water increased 1.48 L (p < 0.001) and the body mass index in 1.22 kg/m2 (p < 0.001). CONCLUSION: Treatment with megestrol acetate results in a substained and very significant increase of the weight and body mass index in patients with AIDS related cachexia. This increment in weight is at the expense of body lean.

Adult↗

PubMed1983

Diabetic neuropathic cachexia. Report of a woman with this syndrome and review of the literature.

A 64-year-old woman was admitted to the neurology service complaining of lower extremity weakness and pain. She was found to have lost more than 180 kg in a 2 1/2-year period. In addition, she had mild diabetes. A diagnosis of diabetic neuropathic cachexia was made. Not only is this case remarkable for the massive weight loss, but, to our knowledge, this is the first report of this syndrome in a woman.

Body Weight↗

PubMed1999

The effect of adrenaline and Walker-256 tumour-induced cachexia upon Kupffer cell metabolism.

Kupffer cells (KC), the liver macrophages, are able to produce PGE(2), which is involved in immune suppression and in the aggravation of cancer cachexia due to interference with lipid metabolism in the liver. Since tumour-bearing (TB) rats present high plasma epinephrine levels, and this hormone is able to affect macrophage metabolism and function, we have assessed the effect of epinephrine (5 nM) upon Kupffer cell PGE(2) production. Epinephrine induced increased production of PGE(2) both by control (3.5-fold) and TB rats (27 per cent) KC, an effect blocked by propranolol. Enhancement of cAMP content in the cells by addition of isoproterenol (0.1 microM) to the incubations, however, failed to induce the same response in the cells. Nevertheless, when phenylephrine (1 microM) was added to the incubation, a similar pattern of PGE(2) production to that observed for epinephrine was found for control and TB rat KC. We propose that the effect of epinephrine upon KC PGE(2) production is mediated by alpha-adrenergic receptors and that Ca(2+) is involved in the response, since increasing concentrations of the ion added to the incubation medium (0.25, 0.5 and 1.0 mM) enhanced the eicosanoid production, while EDTA abolished the response.

Adrenergic alpha-Agonists↗

PubMed1979

Cancer cachexia.

Cancer cachexia is characterized clinically by anorexia, early satiety, weight loss. anemia, and marked asthenia. The syndrome is not the result of semistarvation alone but it represents a complex metabolic problem. In the host there are abnormalities in metabolism of energy, carbohydrate, lipid and protein, in water content, in acid-base balance, in electrolyte, mineral and vitamin concentrations, alterations in the activity of host tissue enzymes and changes in endocrine homeostasis and immunologic mechanisms. The cancer initiates and contributes to the genesis of the syndrome but complications of the disease and the treatment may also play a role. Only the control of the cancer can reverse completely the syndrome. It was proposed that cancer peptides throw the host metabolism into a chaotic biochemical state by activating and inactivating host enzymes. This results in increased energy expenditure; the released host metabolites and trapped by the growing cancer.

Animals↗

PubMed1986

Improved protein kinetics and albumin synthesis by branched chain amino acid-enriched total parenteral nutrition in cancer cachexia. A prospective randomized crossover trial.

A prospective randomized crossover trial was conducted to determine the effect of a branched chain amino acid (BCAA)-enriched solution on whole body leucine kinetics and fractional rates of albumin synthesis in patients with intra-abdominal metastatic adenocarcinoma. Ten malnourished cancer patients were provided isonitrogenous amounts of both a conventional total parenteral nutrition (TPN) formula containing 19% BCAA and a BCAA-enriched TPN formula containing 50% of the amino acids as BCAA in a random order. Whole body protein turnover was determined by a 10 hour continuous infusion of leucine 14C. Increased whole body leucine flux (68 +/- 5 mumols/kg BW/hr versus 145 +/- 11; mean +/- SEM; P less than 0.001) and oxidation (13 +/- 2 mumols/kg BW/hr to 46 +/- 5; P less than 0.001) were determined on the BCAA-enriched TPN. Increased whole body protein synthesis (2.2 +/- 0.2 g protein/kg BW/day versus 3.9 +/- 0.3; P less than 0.005) and leucine balance (2.5 +/- 0.4 g leucine/d versus 6.5 +/- 0.6; P less than 0.001) were also observed in patients receiving the BCAA-enriched TPN solution. Leucine release from protein breakdown was not statistically elevated (1.65 +/- 0.18 g protein/kg BW/d versus 2.48 +/- 0.40; P greater than 0.05) but, incorporation of leucine 14C into plasma albumin was significantly elevated (2.37 +/- 0.23 mumols/g/hr to 4.21 +/- 0.33; P less than 0.001) when the patients received BCAA-enriched TPN. Despite the better leucine balance, the improvement in the 24-hour urinary nitrogen balance was not statistically significant (6.6 +/- 3.9 g protein/d versus 11.4 +/- 2.9; control versus BCAA-enriched; P = 0.15). BCAA-enriched formulas improve whole body leucine kinetics, fractional rates of albumin synthesis, and leucine balance, and thus may favorably influence protein metabolism in cancer cachexia.

Abdominal Neoplasms↗

PubMed1990

A controlled trial of cyproheptadine in cancer patients with anorexia and/or cachexia.

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).

Adult↗

PubMed1998

Role of cysteine and glutathione in signal transduction, immunopathology and cachexia.

Abnormally low plasma cystine levels have been found in the late asymptomatic stage of HIV infection and several other diseases associated with progressive loss of skeletal muscle mass. The phenomenon is commonly associated with a low NK cell activity, skeletal muscle wasting or muscle fatigue and increased rates of urea production. In its extreme form, the negative nitrogen balance leads to overt cachexia and is associated with severe debilitation and psychological stress. The low NK cell activity is in most cases not life-threatening but may be disasterous in HIV infection, because it may compromise the initially stable balance between immune system and virus and trigger disease progression. This review summarizes briefly (i) the role of cysteine in the physiological regulation of body cell mass and the development of skeletal muscle wasting, and (ii) the role of glutathione in the immune system.

Animals↗

PubMed1989

Branched chain amino acids as the protein component of parenteral nutrition in cancer cachexia.

A prospective randomized trial was conducted to determine the effects of branched chain amino acids (BCAA) as the protein component of total parenteral nutrition (TPN) on protein kinetics in patients with intraabdominal adenocarcinoma. Nine malnourished patients were given both conventional TPN containing 19 per cent BCAA (AA) and isocaloric, isonitrogenous TPN containing 50 per cent BCAA (BCAA-TPN), in random order. Both [13C]leucine and [14C]tyrosine were employed as tracers to avoid the potential bias due to the different amino acid composition of the two TPN solutions. With BCAA-TPN, leucine and tyrosine flux increased significantly from (mean +/- s.d.) 158.0 +/- 37.2 to 243.5 +/- 75.8 mumol kg-1 h-1 (P less than 0.025) and from 35.0 +/- 8.4 to 42.6 +/- 11.0 mumol kg-1 h-1 (P less than 0.05) respectively. Leucine oxidation was significantly higher on BCAA-TPN (24.1 +/- 6.3 on AA versus 68.3 +/- 37.1 mumol kg-1 h-1, P less than 0.025) while tyrosine oxidation was significantly lower (3.7 +/- 1.8 mumol kg-1 h-1 on AA versus 2.5 +/- 2.0 mumol kg-1 h-1 on BCAA-TPN, P less than 0.05). Whole body protein synthesis and breakdown was significantly higher on BCAA-TPN by the tyrosine tracer (31.3 +/- 7.3 on AA versus 40.1 +/- 9.3 mumol kg-1 h-1, P less than 0.025 and 33.0 +/- 8.4 on AA versus 41.3 +/- 11.1 mumol kg-1 h-1, P less than 0.05) respectively. Using the leucine tracers both synthesis and breakdown were increased, but not significantly, from 133.8 +/- 40.0 to 175.3 +/- 65.1 mumol kg-1 h-1 and from 127.9 +/- 33.6 to 167.7 +/- 71.2 mumol kg-1 h-1 respectively. The fractional albumin synthetic rate increased significantly on BCAA-TPN from 4.3 +/- 2.9 on AA to 8.0 +/- 5.1 per cent per day (P less than 0.05). The reduction in tyrosine oxidation, suggesting improved protein utilization, coupled with an increase in protein and albumin synthesis, strongly support a positive benefit from BCAA-TPN in cancer cachexia.

Abdominal Neoplasms↗

PubMed2004

Phase II study of high-dose fish oil capsules for patients with cancer-related cachexia.

BACKGROUND: The authors undertook a multiinstitutional Phase II cooperative group study to examine the potential of oral fish oil fatty acid supplements administered at high doses to slow weight loss and to improve quality of life in patients with malignancy-related cachexia. METHODS: Patients with advanced malignancy and weight loss > or = 2% of body weight in the preceding month took concentrated, high-dose omega-3 fatty acid capsules (7.5 g eicosapentaenoic acid plus docosahexaenoic acid for a 70 kg individual) that were supplied by the National Institutes of Health. RESULTS: Forty-three patients with moderate or severe malnutrition were enrolled. The median time receiving treatment was 1.2 months. For the 36 patients who took at least 1 capsule and did not have edema, there was a weight change ranging from -6.2 kg to +3.5 kg and an overall median weight loss of 0.8 kg. Twenty-four patients had weight stabilization (a gain of < or = 5% or a loss of < 5%), 6 patients gained > 5% of their body weight, and 6 patients lost > or = 5% of their body weight. There was marked variability in the tolerability of the capsules, and many patients had gastrointestinal side effects. There was a correlation between time receiving treatment and weight gain for the 22 patients who were able to tolerate the capsules for at least 1 month. Quality-of-life scores were superior for patients who gained weight. CONCLUSIONS: A majority of patients did not gain weight, and in that sense, the results of the study were unfavorable. However, a small but definite subset of patients had weight stabilization or weight gain. This suggests that omega-3 fatty acids have potential utility at the study doses, which were more than twice the doses used in published Phase III studies.

Adult↗

PubMed2007

The 'natural' endpoint of dementia: death from cachexia or dehydration following palliative care?

OBJECTIVES: To investigate the causes of death in nursing home patients with dementia, and to compare causes of death in patients who survive until the final phase of dementia with those who die before reaching that phase, adjusted for potential confounders. DESIGN: Observational analysis of a cohort of patients with a prospective follow-up. SETTING: Psychogeriatric nursing home 'Joachim en Anna' in Nijmegen, the Netherlands. PARTICIPANTS: Eight hundred and ninety dementia patients admitted between 1980 and 1989. All patients were followed until death. MEASUREMENTS: The final phase of dementia was defined as total impairment on 20 items of a functional status questionnaire. Immediate causes of death (part 1a of the Dutch death certificate) were classified by the International Classification of Health Problems in Primary Care. RESULTS: The three most important reported immediate causes of death were cachexia/dehydration (35.2%), cardio-vascular disorders (20.9%) and acute pulmonary diseases (20.1%), mainly pneumonia. Cachexia/dehydration was particularly common as a cause of death of patients who survived to the final phase (53.2%); survival to the final phase of dementia was an independent predictor of cachexia/dehydration as an immediate cause of death with reference to cardiovascular disorders in multinomial regression adjusted for age at death, gender, and type of dementia. CONCLUSION: Patients who survive to the final phase of dementia are more likely to die from cachexia or dehydration than those who die before. The findings contribute to a debate on what should be reported as the immediate cause of death in dementia including perspectives from a palliative care viewpoint.

Activities of Daily Living↗

PubMed1986

Metabolic and morphologic changes in brown adipose tissue from non-growing mice with an isogeneic sarcoma. Evaluation with respect to development of cachexia.

Brown adipose tissue plays a thermoregulatory role influencing energy balance in experimental animals and possibly also in humans. In the present study we have reevaluated whether brown adipose tissue may contribute to the development of cancer cachexia in non-growing mice bearing an isogeneic tumor. Interscapular brown adipose tissue mass decreased by 20% in freely-fed sarcoma-bearing mice housed at room temperature. Increased mitochondrial density and increased oxidation rate of acetate at low acetate concentrations were found in brown fat from sarcoma-bearing mice, while the oxidation capacity was unchanged compared with that of freely-fed controls. Metabolic and morphologic changes in brown fat from sarcoma-bearing mice were similar to those found in weight-paired controls, which had experienced the same loss of body weight as the tumor-bearing mice. Selective and non-selective B-receptor blockade and surgical removal of interscapular brown fat before tumor implantation did not influence the nutritional state of freely-fed tumor-bearing mice. Injections of noradrenaline caused a proportionately lower increase in oxygen uptake in tumor-bearing animals than in freely-fed controls. Exposure to cold (+5 degrees C) doubled food intake and led to hypertrophy of brown fat in both sarcoma-bearing mice and control animals. Tumor growth was lower although not statistically different in animals housed at +5 degrees C compared with animals housed at +25 degrees C. It is concluded that brown adipose tissue from sarcoma-bearing mice could not account quantitatively for the host wasting in tumor-bearing mice housed at room temperature.

Acetates↗