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The evaluation of quality of life (QoL) assesses patients' well-being by taking into account physical, psychological and social conditions. Cancer and its treatment result in severe biochemical and physiological alterations associated with a deterioration of QoL. These metabolic changes lead to decreased food intake and promote wasting. Cancer-related malnutrition can evolve to cancer cachexia due to complex interactions between pro-inflammatory cytokines and host metabolism. Beside and beyond the physical and the metabolic effects of cancer, patients often suffer as well from psychological distress, including depression. Depending on the type of cancer treatment (either curative or palliative) and on patients' clinical conditions and nutritional status, adequate and patient-tailored nutritional intervention should be prescribed (diet counselling, oral supplementation, enteral or total parenteral nutrition). Such an approach, which should be started as early as possible, can reduce or even reverse their poor nutritional status, improve their performance status and consequently their QoL. Nutritional intervention accompanying curative treatment has an additional and specific role, which is to increase the tolerance and response to the oncology treatment, decrease the rate of complications and possibly reduce morbidity by optimizing the balance between energy expenditure and food intake. In palliative care, nutritional support aims at improving patient's QoL by controlling symptoms such as nausea, vomiting and pain related to food intake and postponing loss of autonomy. The literature review supports that nutritional care should be integrated into the global oncology care because of its significant contribution to QoL. Furthermore, the assessment of QoL should be part of the evaluation of any nutritional support to optimize its adequacy to the patient's needs and expectations.
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PMID:Nutritional intervention and quality of life in adult oncology patients. 1736 56

Atrophy of skeletal muscle is due to a depression in protein synthesis and an increase in degradation. Studies in vitro have suggested that activation of the dsRNA-dependent protein kinase (PKR) may be responsible for these changes in protein synthesis and degradation. In order to evaluate whether this is also applicable to cancer cachexia the action of a PKR inhibitor on the development of cachexia has been studied in mice bearing the MAC16 tumour. Treatment of animals with the PKR inhibitor (5 mg kg(-1)) significantly reduced levels of phospho-PKR in muscle down to that found in non-tumour-bearing mice, and effectively attenuated the depression of body weight, with increased muscle mass, and also inhibited tumour growth. There was an increase in protein synthesis in skeletal muscle, which paralleled a decrease in eukaryotic initiation factor 2alpha phosphorylation. Protein degradation rates in skeletal muscle were also significantly decreased, as was proteasome activity levels and expression. Myosin levels were increased up to values found in non-tumour-bearing animals. Proteasome expression correlated with a decreased nuclear accumulation of nuclear factor-kappaB (NF-kappaB). The PKR inhibitor also significantly inhibited tumour growth, although this appeared to be a separate event from the effect on muscle wasting. These results suggest that inhibition of the autophosphorylation of PKR may represent an appropriate target for the attenuation of muscle atrophy in cancer cachexia.
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PMID:Attenuation of muscle atrophy in a murine model of cachexia by inhibition of the dsRNA-dependent protein kinase. 1738 45

Severe or chronic disease can lead to cachexia which involves weight loss and muscle wasting. Cancer cachexia contributes significantly to disease morbidity and mortality. Multiple studies have shown that the metabolic changes that occur with cancer cachexia are unique compared to that of starvation. Specifically, cancer patients seem to lose a larger proportion of skeletal muscle mass. There are three pathways that contribute to muscle protein degradation: the lysosomal system, cytosolic proteases and the ubiquitin (Ub)-proteasome pathway. The Ub-proteasome pathway seems to account for the majority of skeletal muscle degradation in cancer cachexia and is stimulated by several cytokines including tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interferon-gamma and proteolysis-inducing factor. Cachexia is particularly severe in pancreatic cancer and contributes significantly to the quality of life and mortality of these patients. Several factors contribute to weight loss in these patients, including alimentary obstruction, pain, depression, side effects of therapy and a high catabolic state. Although no single agent has proven to halt cachexia in these patients there has been some progress in the areas of nutrition with supplementation and pharmacological agents such as megesterol acetate, steroids and experimental trials targeting cytokines that stimulate the Ub-proteasome pathway.
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PMID:Mechanisms of skeletal muscle degradation and its therapy in cancer cachexia. 1745 54

Cancer-related fatigue (CRF) is one of the most prevalent symptoms patients with cancer experience, both during and after treatment. CRF is pervasive and affects patients' quality of life considerably. It is important, therefore, to understand the underlying pathophysiology of CRF in order to develop useful strategies for prevention and treatment. At present, the etiology of CRF is poorly understood and the relative contributions of the neoplastic disease, various forms of cancer therapy, and comorbid conditions (e.g., anemia, cachexia, sleep disorders, depression) remain unclear. In any individual, the etiology of CRF probably involves the dysregulation of several physiological and biochemical systems. Mechanisms proposed as underlying CRF include 5-HT neurotransmitter dysregulation, vagal afferent activation, alterations in muscle and ATP metabolism, hypothalamic-pituitary-adrenal axis dysfunction, circadian rhythm disruption, and cytokine dysregulation. Currently, these hypotheses are largely based on evidence from other conditions in which fatigue is a characteristic, in particular chronic fatigue syndrome and exercise-induced fatigue. The mechanisms that lead to fatigue in these conditions provide a theoretical basis for future research into the complex etiology of this distressing and debilitating symptom. An understanding of relevant mechanisms may offer potential routes for its prevention and treatment in patients with cancer.Disclosure of potential conflicts of interest is found at the end of this article.
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PMID:Mechanisms of cancer-related fatigue. 1757 53

Quality of life (QOL) is a concept assessing physical, psychological and social factors which are influencing the patients' well being. Cancer and its therapy induce severe metabolic changes associated with QOL impairment. These alterations contribute to an increased energy wasting and a decreased food intake. Besides, it may lead to tumoral cachexia due to the complex interactions between pro-inflammatory cytokines and the host metabolism. On the other hand, and beyond physical impairments and metabolic effects from cancer, patients often suffer from psychological stress, such as depression. A nutritional intervention should be implemented as soon as cancer is diagnosed. It should be appropriate to the individual needs of the patient, considering the type of oncologic treatment (whether it is curative or palliative), the clinical conditions and the nutritional status. The aim is to reduce or even revert nutritional status impairment, improve the general condition, and subsequently improve quality of life. The primary focus of nutritional intervention accompanying oncologic treatment intended to cure is on the optimization of the balance between energy waste and food intake. Thus trying to achieve further specific purposes such as a decrease of rate of complications and an amelioration of the response and tolerance to the oncologic therapy. The purpose of nutritional support in palliative care is controlling the symptoms related to food intake and delaying the loss of autonomy. And by this means maintaining or improving patients' QOL. It is corraborated by a literature review, that nutritional therapy should form part of the integral oncological support since it contributes considerably to a QOL improvement. Because of the possibility to identify the patients' needs and expectations by assessing their QOL it should be generally included into their nutritional evaluation to be able to tailor the adequate nutritional support.
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PMID:[Relationship between nutritional intervention and quality of life in cancer patients]. 1972 35

Corticosteroids have been used extensively since cortisone was first synthesized in the 1950s. Glucocorticoids are derived from cortisone and are used in treatments for inflammation, dermatitis, allergic reactions, asthma, hepatitis, lupus erythematosus, nausea, vomiting and inflammatory bowel diseases. In the setting of palliative care, glucocorticoids have many uses, including many symptoms of malignancy, nausea, vomiting, depression, fatigue, anorexia and cachexia.
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PMID:Role of corticosteroids in palliative care. 1803 21

HIV/AIDS affects the heart through different mechanisms. Before the advent of HIV/AIDS, cachexia had been established as a cause of cardiac morbidity. Interestingly when HIV/AIDS affects the heart, not much role is ascribed to cachexia; one of the major criteria for diagnosis. As most electrocardiographic (ECG) changes in HIV/AIDS are also seen in cachexia, it became necessary to look at the ECG changes in HIV/AIDS in relation to body mass index (BMI). This was to see if any relationship existed. One hundred, 78 and 80 full blown AIDS, HIV positive asymptomatic and HIV negative subjects underwent 12 lead resting ECG respectively. Their BMI were determined from the heights and weights. BMI was least in the first group and highest in the last group. The mean differences achieved statistical significance. Systolic and diastolic blood pressures significantly fell from HIV negative to the AIDS patients. This was as BMI fell. Systolic and diastolic blood pressures fall significantly with cachexia. The following indices on ECG: heart rate, corrected QT interval, ST segment depression and T wave inversion increased from the HIV negative to the full blown AIDS patients. This was also the direction of reduction in BMI. Since these ECG changes have long been known with cachexia, it is being suggested that the cachexia associated with HIV/AIDS contributes to the heart disease in them.
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PMID:Heart disease in HIV/AIDS. How much is due to cachexia? 1805 Jul 81

This article describes the research strategy for the development of a computerized assessment tool as part of a European Union (EU)-funded project, the European Palliative Care Research Collaborative (EPCRC). The EPCRC is funded through the Sixth Framework Program of the EU with major objectives to develop a computer-based assessment and classification tool for pain, depression, and cachexia. A systematic approach will be applied for the tool development with emphasis on multicultural and multilanguage challenges across Europe. The EPCRC is based on a long lasting collaboration within the European Association for Palliative Care Research Network. The ongoing change in society towards greatly increased use of communication as well as information transfer via digital systems will rapidly change the health care system. Therefore, patient-centered outcome assessment tools applicable for both clinic and research should be developed. Report of symptoms via digital media provides a start for face-to-face communication, treatment decisions, and assessment of treatment effects. The increased use of electronic media for exchange of information may facilitate the development and use of electronic assessment tools and decision-making systems in oncology. In the future, patients may find that a combination of a face-to-face interview plus a transfer of information of subjective symptoms by electronic means will optimize treatment.
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PMID:Symptom assessment in palliative care: a need for international collaboration. 1868 54

On December 13th and 14th a group of scientists and clinicians met in Washington, DC, for the cachexia consensus conference. At the present time, there is no widely agreed upon operational definition of cachexia. The lack of a definition accepted by clinician and researchers has limited identification and treatment of cachectic patient as well as the development and approval of potential therapeutic agents. The definition that emerged is: "cachexia, is a complex metabolic syndrome associated with underlying illness and characterized by loss of muscle with or without loss of fat mass. The prominent clinical feature of cachexia is weight loss in adults (corrected for fluid retention) or growth failure in children (excluding endocrine disorders). Anorexia, inflammation, insulin resistance and increased muscle protein breakdown are frequently associated with cachexia. Cachexia is distinct from starvation, age-related loss of muscle mass, primary depression, malabsorption and hyperthyroidism and is associated with increased morbidity. While this definition has not been tested in epidemiological or intervention studies, a consensus operational definition provides an opportunity for increased research.
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PMID:Cachexia: a new definition. 1871 96

Tumours contain immune cells and a network of pro- and anti-inflammatory cytokines, which collaborate in the development and progression of cancer. Cytokine profiles might prove to be prognostic. The systemic effects of pro-inflammatory cytokines are associated with fatigue, depression and cognitive impairment, and can affect quality of life before, during and after treatment. In people with advanced cancer, pro-inflammatory cytokines are additionally associated with anorexia and cachexia, pain, toxicity of treatment and resistance to treatment. However, physical activity might modify cytokine levels and decrease fatigue in patients with cancer, and might also improve their prognosis.
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PMID:Cytokines and their relationship to the symptoms and outcome of cancer. 1919 83


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