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PubMed2005

Anorexia/cachexia-related quality of life for children with cancer.

BACKGROUND: Anorexia is a common symptom in patients with cancer, which can lead to poor tolerance of treatment and can contribute to cachexia in extreme cases. Children with advanced-stage cancer are especially vulnerable to malnutrition resulting from anorexia and cachexia. Currently, there are no instruments that measure common concerns specifically associated with anorexia and cachexia in children with cancer. The purpose of the current article was to test the psychometric properties of a newly developed pediatric Functional Assessment of Anorexia and Cachexia Therapy (peds-FAACT) for children with cancer. METHODS: Ninety-six patients (ages 7-17 yrs) receiving cancer treatment and their parents were asked to complete the 12-item peds-FAACT. The authors implemented both classical test theory and item response theory to evaluate the agreement between parents and patients, internal consistency and unidimensionality of the scale, and stability of items across subgroups. RESULTS: As a result, a patient-reported six-item scale was recommended as the core measure for all pediatric patients with cancer and four additional peripheral items were recommended for adolescent patients. CONCLUSIONS: The peds-FAACT demonstrated good psychometric properties, differentiated patients with different functional performance status, and was determined to be a useful tool for future clinical trials.

Adolescent↗
PubMed2004

Tumor-host interactions.

A number of malignant tumors interact with the host to cause a syndrome of cachexia, characterized by extensive loss of adipose tissue and skeletal muscle mass, but with preservation of proteins in visceral tissues. Although anorexia is frequently present, the body composition changes in cancer cachexia cannot be explained by nutritional deprivation alone. Loss of skeletal muscle mass is a result of depression in protein synthesis and an increase in protein degradation. The main degradative pathway that has been found to have increased expression and activity in the skeletal muscle of cachectic patients is the ubiquitin-proteasome proteolytic pathway. Cachexia-inducing tumors produce catabolic factors such as proteolysis-inducing factor (PIF), a 24 kDa sulfated glycoprotein, which inhibit protein synthesis and stimulate degradation of intracellular proteins in skeletal muscle by inducing an increased expression of regulatory components of the ubiquitin-proteasome proteolytic pathway. While the oligosaccharide chains in PIF are required to initiate protein degradation the central polypeptide core may act as a growth and survival factor. Only cachexia-inducing tumors are capable of elaborating fully glycosylated PIF, and the selectivity of production possibly rests with the acquisition of the necessary glycosylating enzymes, rather than expressing the gene for the polypeptide core. Loss of adipose tissue is probably the result of an increase in catabolism rather than a defect in anabolism. A lipid mobilizing factor (LMF), identical with the plasma protein Zn-alpha2-glycoprotein (ZAG) is found in the urine of cachectic cancer patients and is produced by tumors causing a decrease in carcass lipid. LMF causes triglyceride hydrolysis in adipose tissue through a cyclic AMP-mediated process by interaction with a beta3-adrenoreceptor. Thus, by producing circulating factors certain malignant tumors are able to interfere with host metabolism even without metastasis to that particular site.

Adipose Tissue↗
PubMed2000

Heavy metals contamination and body condition of wintering guillemots (Uria aalge) at the Belgian coast from 1993 to 1998.

A sample of 166 common guillemots (Uria aalge) recovered from Belgian beaches during five wintering seasons, from 1993-1994 to 1997-1998, were examined. At necropsy, postmortem examination including body mass, fat reserves, presence or not of intestinal contents, eventual status of oiling, and pathological changes (cachexia, acute hemorrhagic gastroenteropathy (GEAH)) was attributed to each individual. Mild to severe cachexia, a pathology characterized by moderate to severe atrophy of the pectoral muscle as well as reduced amounts or absence of subcutaneous and/or abdominal fat, was observed for most specimens (85.8%). Heavy metal analyses (Cu, Zn, Fe, Cd, Ni, Cr, and Pb) of the tissues (typically liver, kidney, and pectoral muscle) were performed, and total lipids were determined (liver and pectoral muscle). The guillemots collected at the Belgian coast exhibited higher Cu and Zn concentrations compared to individuals collected in more preserved areas of the North Sea such as the northern colonies. A general decrease of their total body mass as well as liver, kidney, and pectoral muscle mass was associated to increasing cachexia severity. Moreover, significantly increasing heavy metal levels (Cu and Zn) in the tissues as well as depleted muscle lipid contents were observed parallel to increasing cachexia severity. On the contrary the organs' total metal burden barely correlates to this status. These observations tend to indicate a general redistribution of heavy metals within the organs as a result of prolonged starvation and protein catabolism (cachectic status). Such a redistribution could well be an additional stress to birds already experiencing stressfull conditions (starvation, oiling).

Animals↗
PubMed1995

Splenectomy before tumor inoculation prolongs the survival time of cachectic mice.

The effects of splenectomy on the development of cachexia, tumor growth and animal survival were studied in tumor-bearing CDF1 mice. Mice were inoculated with two subclones of colon 26 adenocarcinoma, clone 20 (with a potent capacity to induce cachexia) and clone 5 (without such activity), and underwent splenectomy before or after tumor inoculation. Splenectomy significantly prolonged the survival of mice bearing clone 20 when it was performed prior to tumor inoculation, although the progression of cachexia and tumor growth were not affected. The survival rate was higher in splenectomized than it was in nonsplenectomized mice 20-40 days after tumor inoculation. Such effects on survival were not observed, however, in mice splenectomized after inoculation with clone 20 or in mice that underwent splenectomy either before or after inoculation with clone 5. The decrease of peripheral blood lymphocyte count observed in mice bearing clone 20 was magnified when splenectomy was performed before tumor inoculation, but the serum levels of tumor necrosis factor and interleukin-6 were comparable. These results indicate that cancer death from cachexia is not directly attributable to enhanced catabolism. The mechanism by which splenectomy ameliorates the survival of cachectic mice remains to be studied, although several changes observed in the splenectomized mice after inoculation, including decreases in the peripheral blood L3T4+ cells and Lyt-2+ cells on the 9th day and 15th day respectively, and increase in the L3T4+/Lyt-2+ cell ratio on the 15th day suggest the involvement of the modified host's immune response.

Adenocarcinoma↗
PubMed2004

Heat shock protein 70 in patients with chronic heart failure: relation to disease severity and survival.

BACKGROUND: Heat shock protein 70 (Hsp70) is essential for cellular recovery, survival and maintenance of cellular function. Research into the possible use of Hsp70 as a cytoprotective therapeutic agent is ongoing. Chronic heart failure (CHF) is a state associated with systemic inflammation, particularly in patients with cardiac cachexia. We hypothesised that circulating Hsp70 levels are elevated in patients with CHF, more so in cachechtic patients, and that Hsp70 levels would relate to mortality. METHODS AND RESULTS: We studied 107 patients (28 female, age 67+/-1 years, NYHA class 2.6+/-0.6 and LVEF 29+/-1%, mean+/-SEM) and 21 controls. Cardiac cachexia was present in 32 patients. Hsp70 was detectable in 41% of CHF patients and in only 10% of controls. Overall serum levels were significantly higher in CHF patients vs. controls (7.13+/-1.34 vs. 0.38+/-0.26 ng/ml, p=0.004). Hsp70 levels were also higher in patients with advanced CHF according to NYHA class or the presence of cachexia (all p<0.05). There was no relation between Hsp70 and left ventricular ejection fraction, maximal oxygen consumption and several inflammatory cytokines (all p>0.05). During a median follow-up of 208 days (range 4-2745 days) 38 patients died. Cox proportional hazards analysis showed that increased Hsp70 did not predict survival (p=0.17). CONCLUSION: Hsp70 levels are elevated in CHF patients, particularly in those with cardiac cachexia and Hsp70 relates to disease severity but not to survival. The significance of the relationship of Hsp70 expression and morbidity in CHF needs further evaluation.

Aged↗
PubMed2002

Pathophysiologic quantities of endotoxin-induced tumor necrosis factor-alpha release in whole blood from patients with chronic heart failure.

Bacterial endotoxin activity is elevated in patients with decompensated chronic heart failure (HF) and acts as a potent stimulus for immune activation. We sought to determine whether endotoxin, at an activity level seen in vivo (around 0.6 EU/ml), is sufficient to stimulate the secretion of tumor necrosis factor-alpha (TNF-alpha) and TNF-alpha soluble receptor (sTNFR2) in ex vivo whole blood from patients with HF. We studied 15 patients with HF (aged 65 +/- 1.9 years, New York Heart Association class 2.1 +/- 0.3, left ventricular ejection fraction 31 +/- 5%; mean +/- SEM), of whom 5 had cardiac cachexia, and 7 healthy control subjects (59 +/- 5 years, p = NS). Reference endotoxin was added to venous blood at concentrations of 0.6, 1.0, and 3.0 EU/ml, and was incubated for 6 hours. Endotoxin induced a dose-dependent increase in TNF-alpha release (p <0.05 in all groups). Patients with noncachectic HF produced significantly more TNF-alpha compared with controls after stimulation with 0.6, 1.0, and 3.0 EU/ml of endotoxin (113 +/- 46 vs 22 +/- 4 [p = 0.009], 149 +/- 48 vs 34 +/- 4 [p = 0.002], and 328 +/- 88 vs 89 +/- 16 pg/ml [p = 0.002], respectively; mean +/- SEM). Patients with cardiac cachexia produced significantly less TNF-alpha compared with patients without cardiac cachexia for all given concentrations (all p <0.05, analysis of variance p = 0.02). Production of sTNFR2 was greater at all concentrations of endotoxin versus controls (all p <0.05, analysis of variance p = 0.002). Plasma endotoxin levels were higher in patients with cardiac cachexia (4.3 times higher than in control subjects, p <0.005). Thus, low endotoxin activity, at levels seen in vivo in patients with HF, induces significant TNF-alpha and sTNFR2 production ex vivo. These results suggest that elevated plasma endotoxin activity observed in patients with HF is of pathophysiologic relevance.

Adult↗
PubMed2001

Do patients with nonmetastatic non-small cell lung cancer demonstrate altered resting energy expenditure?

BACKGROUND: The cancer cachexia syndrome occurs in patients with non-small cell lung cancer (NSCLC) and includes elevated resting energy expenditure (REE). This increase in REE leads to weight loss, which in turn confers a poor prognosis. This study was undertaken to determine whether the cancer cachexia syndrome occurs in patients with nonmetastatic NSCLC. METHODS: In this case-control study, 18 patients with nonmetastatic NSCLC (stages IA to IIIB) were matched to healthy controls on age (+/- 5 years), gender, and body mass index (+/- 3 kg/m2). Only 4 cancer patients had experienced > 5% weight loss. Cancer patients and controls were compared on the basis of: (1) unadjusted REE, as measured by indirect calorimetry; (2) REE adjusted for lean body mass, as measured by dual x-ray absorptiometry; (3) REE adjusted for body cell mass, as measured by potassium-40 measurement; and (4) REE adjusted for total body water, as measured by tritiated water dilution. RESULTS: We observed no significant difference in unadjusted REE or in REE adjusted for total body water. However, with separate adjustments for lean body mass and body cell mass, cancer patients manifested an increase in REE: mean difference +/- standard error of the mean: 140+/-35 kcal/day (p = 0.001) and 173+/-65 kcal/day (p = 0.032), respectively. Further adjustment for weight loss yielded similarly significant results. CONCLUSIONS: These results suggest that the cancer cachexia syndrome occurs in patients with nonmetastatic NSCLC and raise the question of whether clinical trials that target cancer cachexia should be initiated before weight loss.

Aged↗
PubMed1996

A new cancer hypothesis.

Despite intensive efforts to cure breast cancer, treatment generally fails, as evidenced by the age-adjusted mortality rate for breast cancer. For 60 years, breast cancer mortality remained virtually constant. As treatment failed to improve the life prospect of the average patient, it is based on false premises, e.g. Halsted's hypothesis, according to which the tumor is the only threat to the patient. Yet there is more to cancer than just the tumor. Two hallmarks of cancer, cachexia, and paraneoplasia, are usually ignored, since it is assumed that they are caused by the tumor. But what if it is the other way round, and cancer is first of all a cachexia accompanied by a tumor? At least this could explain why, in most cancers, treatment fails. Cancer is a chronic systemic disease with local manifestations like arteriosclerosis, which is also systemic and manifested solely by its local manifestations, e.g. stroke and myocardial infarction. In the same way as treatment of an ailing heart does not cure the underlying arteriosclerosis, tumor removal does not cure cancer, as it is 'metabolically' systemic. It is proposed here that carcinogens deplete a vital substance and induce a metabolic deficiency that ends in cachexia. In order to survive, the organism grows a protective organ-the tumor-that replenishes the missing substance. During the preclinical phase of cancer, deficiency is slight and compensated only by a minute tumor. With time, it gets worse and the tumor has to grow more and more in order to make up for the loss, causing pain and secondary damage to vital functions. The patient seeks help and the disease starts its clinical course. When deficiency worsens, the patient becomes cachectic and dies. Such a metabolic relationship exists in pernicious anemia, which illustrates how a tumor might be protective. Cancer is viewed here as pernicious cachexia induced by the loss of a vital metabolite and compensated by the tumor. Until the discovery of the missing substance, treatment ought to preserve the tumor and alleviate its secondary manifestations.

Breast Neoplasms↗
PubMed1996

Anorexia during acute and chronic disease.

Anorexia is associated with disorders of all systems. Anorexia represents a consistent clinical manifestation during acute and chronic pathophysiological processes (infection, inflammation, injury, toxins, immunological reactions, malignancy and necrosis). Anorexia during disease can be beneficial or deleterious depending on the timing and duration. Temporary anorexia during acute disease may be beneficial to an organism since a restriction in the intake of micro- and macro-nutrients will inhibit bacterial growth. Long-term anorexia during chronic disease, however, is deleterious to an organism and may be associated with cachexia, which can ultimately result in death. Various mechanisms participate in the anorexia observed during disease, including cytokine action. Anorexia induced by cytokines is proposed to involve modulation of hypothalamic-feeding associated sites, prostaglandin-dependent mechanisms, modifications of neurotransmitter systems, gastrointestinal, metabolic, and endocrine factors. In addition, the anorexia-cachexia syndrome is multifactorial and may involve chronic pain, depression or anxiety, hypogeusia and hyposmia, chronic nausea, early satiety, malfunction of the gastrointestinal system, metabolic alterations, cytokine action, production of other anorexigenic substances and/or iatrogenic causes (chemotherapy, radiotherapy). Cachexia may result not only from anorexia and a decreased caloric intake, but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions), or a change in body metabolism. Research has focused on potential interventions to modify anorexia during disease and the anorexia-cachexia syndrome. Nutritional modifications and the use of specific steroids (such as megestrol acetate) are being tested in the clinical setting. Understanding the specific mechanisms responsible for anorexia during disease as well as their interactions is essential to develop interventions for the control of anorexia (during a critical time in a specific disease), and to devise less toxic immunotherapeutic regimens using cytokines.

Acute Disease↗
PubMed2006

Inhibition of tumor progression and paraneoplastic syndrome development in a murine lung adenocarcinoma by medroxyprogesterone acetate and indomethacin.

Mice bearing LP07 lung adenocarcinoma present some characteristics similar to those shown in patients with several malignant diseases. LP07 tumor bearers develop paraneoplastic syndromes such as cachexia, leukocytosis, and hypercalcemia, partly due to a systemic inflammatory response. We analyzed some of the mechanisms involved in the effectiveness of the association of the appetite-stimulant medroxiprogesterone acetate (MPA) and the nonselective cyclooxigenase (COX) inhibitor indomethacin (INDO) in LP07 tumor bearing mice. INDO and INDO plus MPA treatments significantly inhibited tumor growth, which was not inhibited by MPA. The number of lung metastatic nodules was decreased with all treatments, being most effective INDO alone and INDO plus MPA. A significant decrease of plasmatic levels of the matrix metalloproteinases MMP-9 and MMP-2 correlated with these results. Paraneoplastic syndromes, leukocytosis, and cachexia were abolished by all treatments. We determined effects of the treatments on circulating cytokines shown to regulate cachexia and inflammation. Both treatments alone, and INDO plus MPA, reduced circulating IL-6 throughout tumor evolution. A pronounced increase in serum IL-1ss levels was detected in untreated tumor bearers. These levels decreased and were closer to normal serum values when LP07 mice were treated with INDO plus MPA. The combination of a nonsteroidal antiinflammatory drug as INDO and MPA showed to be effective in inhibiting tumor and metastatic growth and diminishing paraneoplastic symptoms and SIR. A variety of specific molecules are implicated as playing a role in cancer-induced cachexia and hematological alterations.

Adenocarcinoma↗
PubMed1999

The pathophysiology of wasting in the elderly.

Aging is associated with changes in body composition and energy and protein metabolism that are due both to the direct effects of aging and to the effect of age-related diseases. We have recently differentiated these changes under three categories: wasting, cachexia, and sarcopenia. We have defined wasting as unintentional loss of weight, including both fat and fat-free compartments. Experience in the HIV epidemic suggests that wasting is driven largely by inadequate dietary intake. Cachexia, on the other hand, refers to loss of fat-free mass, and especially body cell mass, but with little or no weight loss. The metabolic hallmarks of cachexia are hypermetabolism and hypercatabolism, driven by inflammatory cytokine-mediated acute phase responses. Finally, sarcopenia refers to loss of muscle mass specifically, and seems to be an intrinsic age-related condition. In the elderly, wasting as defined here is at the extreme end of the spectrum, but generally develops in the setting of pre-existing sarcopenia and cachexia. The challenges before us now are to better define these conditions, establish guidelines for their recognition, and develop better methods for intervening when appropriate.

Aged↗
PubMed1991

Risk of death from Alzheimer's disease in a community population of older persons.

A random sample of 467 persons over age 65 years from the population of an urban US community, stratified by age, sex, and performance on a brief memory test, underwent clinical evaluation for dementing illness in 1982-1984. Of these persons, 134 had probable Alzheimer's disease, 166 had possible Alzheimer's disease, and 167 had no evidence of Alzheimer's disease. Over a median follow-up period of 4.9 years following evaluation, 165 (35%) died. Overall, persons with probable Alzheimer's disease had a relative risk of death 1.44 (95% confidence interval (Cl) 1.05-1.96) times that of the unaffected. Level of cognitive impairment and the presence of cachexia upon physical examination both strongly and independently modified risk of death. Among those with probable Alzheimer's disease, mortality for those with mild or moderate cognitive impairment and no evidence of cachexia was comparable to that of the unaffected. However, among those with probable Alzheimer's disease and either severe cognitive impairment or cachexia, the risk of death was substantially higher. Persons with probable Alzheimer's disease who had both severe cognitive impairment and clear cachexia had a risk of death 4.60 (95% Cl 1.63-13.1) times that of unaffected persons.

Aged↗
PubMed2004

Therapy of muscle wasting in cancer: what is the future?

PURPOSE OF REVIEW: The aim of the present review is to provide insights into the future therapeutic approaches to cancer-related muscle wasting that flow from the progressive knowledge of mechanisms regulating muscle mass in health and disease. RECENT FINDINGS: Cancer cachexia is a severely debilitating and life-threatening paraneoplastic syndrome accounting for approximately 20% of cancer deaths. The prominent clinical feature of cancer cachexia is the progressive loss of muscle mass, which is substantially not reversible with any of the currently available nutritional, metabolic or pharmacological approaches. Cancer cachexia has long been considered a late event in the natural history of cancer patients, thus condemning them to merely palliative interventions. The accumulating evidence that the metabolic and molecular derangements ultimately leading to muscle wasting are operating early after tumour onset, even when weight loss is minimal or absent, is strengthening the view that cancer cachexia should be considered an early phenomenon. SUMMARY: Currently, despite scientific and economic efforts, the therapy of cancer-related muscle wasting has a poor success rate. Present knowledge of the intracellular mechanisms involved in muscle homeoastasis is prompting continuous research aimed at developing more effective and selective therapeutic tools for the prevention and treatment of muscle loss in cancer.

Cachexia↗
PubMed2006

Anticatabolic properties of melanocortin-4 receptor antagonists.

PURPOSE OF REVIEW: Health problems related to weight regulation are increasingly common in the USA and around the world. Although obesity and associated complications garner the most attention in the media, clinical problems at the opposite end of the spectrum, such as involuntary disease-associated weight loss or cachexia, are equally devastating. This review focuses on the role of the central melanocortin system in body weight regulation, and specifically on the anticatabolic properties of antagonists of the melanocortin-4 receptor. RECENT FINDINGS: Over the past several years, the central melanocortin system has emerged as a major contributor to the body weight regulatory system in both animals and humans. In particular, the melanocortin-4 receptor, its endogenous agonist alpha-melanocyte stimulating hormone, and its endogenous antagonist agouti-related protein have been shown to be vital to the maintenance of normal body weight in both genetic and physiologic experiments. This system is now the target of multiple drug discovery endeavors, as the search continues for effective treatments for both obesity and cachexia. Several investigators have recently shown that selective synthetic antagonists of the melanocortin-4 receptor can prevent or attenuate the development of cachexia in animal models of acute and chronic disease. SUMMARY: An understanding of the biology of weight regulation, including both appetite regulation and energy metabolism, is vital if we are to unravel the etiology of and develop effective treatment for obesity and cachexia. The data reviewed here supporting a role for melanocortin-4 receptor antagonists in the treatment of catabolism represent an important advance in this field.

Animals↗
PubMedDate not supplied

Nutritional alterations and the effect of fish oil supplementation in dogs with heart failure.

Alterations in body composition and nutritional status are common in humans with heart failure and are related, in part, to increases in cytokine concentrations. Cytokines have not been studied previously in dogs with naturally occurring cardiac disease nor has fish oil administration been used in this population to decrease cytokine production. The purposes of this study were to characterize nutritional and cytokine alterations in dogs with heart failure and to test the ability of fish oil to reduce cytokines and improve clinical outcome. Body composition, insulinlike growth factor-1, fatty acids, and cytokines were measured in 28 dogs with heart failure and in 5 healthy controls. Dogs with heart failure then were randomized to receive either fish oil or placebo for 8 weeks. All parameters were measured again at the end of the study period. At baseline, 54% of dogs with heart failure were cachectic and the severity of cachexia correlated with circulating tumor necrosis factor-alpha concentrations (P = .05). Cytokine concentrations at baseline, however, were not significantly increased in dogs with heart failure compared to controls. Baseline plasma arachidonic acid (P = .02), eicosapentaenoic acid (P = .03), and docosahexaenoic acid (P = .004) concentrations were lower in dogs with heart failure than in controls. Fish oil supplementation decreased interleukin-1 beta (IL-1) concentrations (P = .02) and improved cachexia (P = .01) compared to the placebo group. The mean caloric intake of the heart failure dogs as a group was below the maintenance energy requirement (P < .001), but no difference was found in food intake between the fish oil and placebo groups. Insulinlike growth factor-1 concentrations (P = .01) and reductions in circulating IL-1 concentrations over the study period (P = .02) correlated with survival. These data demonstrate that canine heart failure is associated with cachexia, alterations in fatty acids, and reduced caloric intake. Fish oil supplementation decreased IL-1 concentrations and improved cachexia. In addition, reductions in IL-1 predicted survival, suggesting that anticytokine strategies may benefit patients with heart failure.

Animals↗
PubMed2005

Myofiber degeneration/regeneration is induced in the cachectic ApcMin/+ mouse.

Cachexia is characterized as an inflammatory state induced by the cancer environment, which is accompanied by the loss of muscle and fat mass. Well-investigated mechanisms of cachexia include the suppression of myofiber protein synthesis and the induction of the protein degradation. However, it is not well characterized whether chronic inflammation during cachexia induces myofiber degeneration, which contributes to muscle mass loss and decreased functional capacity. The purpose of this study was to determine whether Apc(Min/+) mice, which demonstrate a chronic systemic inflammatory state due to an intestinal tumor burden, undergo cachexia and whether the myofibers exhibit signs of degeneration and/or regeneration. Six-month-old female Apc(Min/+) body weight decreased 21% compared with C57BL/6 mice and was not the result of blunted growth. Apc(Min/+) gastrocnemius muscle was reduced 45%, and soleus mean fiber cross-sectional area decreased 24% vs. C57BL/6 mice. Soleus muscle morphology demonstrated pathology of myofibers undergoing degeneration and/or regeneration. These data demonstrate that the Apc(Min/+) mouse becomes cachectic by 6 mo of age and that skeletal muscle degeneration and regeneration may be related to the muscle loss.

Adenomatous Polyposis Coli↗
PubMed2005

Treatment of unintentional weight loss in patients with cancer.

Malnutrition from anorexia and reduced nutrient intake is common in patients with cancer. Abnormalities in gastrointestinal function caused by the tumor or treatment of the tumor may be direct causes for nutrition challenges. However, other patients may present with cancer cachexia, a wasting syndrome characterized by weight loss, anorexia, early satiety, progressive debilitation, and malnutrition that results in a greater risk of organ dysfunction and death. Changes in host metabolism and energy expenditure are thought to contribute to the development of cachexia, although this relationship is not clear. There is evidence that the etiology of these metabolic changes may be mediated by a neurohormonal response stimulated by the tumor. Because a single cause for these metabolic abnormalities has not been identified, several approaches to treatment of cancer cachexia have been reported. After correction of any underlying gastrointestinal abnormalities, single nutrients or other pharmacologic agents have been used in an attempt to favorably affect appetite or counter metabolic abnormalities that cause inefficient nutrient use. A variety of agents have been studied for their positive effects on appetite, including progestational agents, glucocorticoids, cannabinoids, cyproheptadine, olanzapine, and mirtazapine. Other agents have been investigated for their anti-inflammatory properties, including thalidomide, pentoxyphylline, melatonin, and omega-3 fatty acids. Anabolic agents such as testosterone derivatives have been investigated as well. The decision to treat symptoms of cancer cachexia should be based on the patient's desires and current medical condition. Choice of the most appropriate agent to treat unintentional weight loss in patients with cancer should include consideration of effects on appetite, weight, quality of life, and risk of adverse effects according to current evidence-based medicine, and cost and availability of the agent.

Appetite Stimulants↗
PubMed1996

Hormonal treatment in advanced non-small cell lung cancer: fact or fiction?

In patients with advanced non-small cell lung cancer, cachexia is an important cause of morbidity and mortality. The pathogenic mechanism of this finding, usually referred to as "cancer anorexia and cachexia syndrome" (CACS), is complex and far from completely understood, but a disturbed equilibrium between possible food intake and metabolic needs seems to be fundamental. The literature data on the treatment options in advanced non-small cell lung cancer (NSCLC) with cachexia are reviewed. Based on the clinical studies on cancer cachexia, some recommendations for the therapeutic approach of this disorder in patients with advanced NSCLC can be given. Metoclopramide is easily administered, can alleviate gastric disturbances, but probably does not correct the catabolic spiral of CACS. There are not enough data to advise the use of parenteral nutritional support, hydrazine, cyproheptadine, tetrahydrocannabinol or nandrolone decanoate. Corticosteroids are useful in additional analgesia and fast palliation of very weak and debilitated patients in the final episode of their disease. Recent data in non-small cell lung cancer patients are in favour of the use of high-dose progestagens to improve both appetite and weight.

Cachexia↗