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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anx/anx mouse displays poor appetite and lean appearance and is considered a good model for the study of anorexia nervosa. To identify new genes involved in feeding behavior and body weight regulation we performed an expression profiling in the hypothalamus of the anx/anx mice. Using commercial microarrays we detected 156 differentially expressed genes and validated 92 of those using TaqMan low-density arrays. The expression of a set of 87 candidate genes selected based on literature evidences was also quantified by TaqMan low-density arrays. Our results showed enrichment in deregulated genes involved in cell death, cell morphology, and cancer, as well as an alteration of several signaling circuits involved in energy balance including neuropeptide Y and melanocortin signaling. The expression profile along with the phenotype led us to conclude that anx/anx mice resemble the anorexia-cachexia syndrome typically observed in cancer, infection with human immunodeficiency virus or chronic diseases, rather than starvation, and that anx/anx mice could be considered a good model for the treatment and investigation of this condition.
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PMID:Hypothalamus transcriptome profile suggests an anorexia-cachexia syndrome in the anx/anx mouse model. 1881 57

The cachexia-anorexia syndrome (CACS) is common and important implication of cancer. It occurs in 30% to 80% cancer patients. At the time of diagnosis of lung cancer CACS is not yet very important problem, but the weight loss increases with progression of the cancer. CACS is characterized by anorexia, weight loss, weakness, impaired immune system and metabolic dysfunction. Weight loss is a potent stimulus to food intake in normal humans. The persistence of anorexia in cancer patients, therefore, implies a failure of this adaptive feeding response. The weight loss in patients with CACS differs from that in simple starvation or anorexia nervosa. Most research effort has focused on the role of cytokines as mediators of CACS. The role of TNF-alpha, IL-1 and IL-6 in CACS development has been evaluated and confirmed in many research, but some investigators suggest that the changes in cytokines' levels could be the result rather than the cause of CACS. A few of the latest studies concentrate on the role of nuclear factor kappa B and prevention of CACS by its inhibitors. CACS is an independent predictor of shorter survival and increases the risk of treatment failure and toxicity.
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PMID:[The incidence and pathogenesis of cancer anorexia-cachexia syndrome in lung cancer]. 1900 67

Approximately two thirds of cancer patients at advanced stages of the disease suffer from anorexia, which leads to significant weight loss and progressive cachexia, an important factor that contributes to death. It has been observed that cancer cachexia differs from simple starvation, although the exact mechanisms associated with cancer cachexia are not well known. Several theories regarding its pathogenesis point to a complex mixture of tumor, host and treatment variables. Unfortunately, the wasting syndrome also constitutes for the patient, a progression of the cancer process, significantly affecting quality of life and social interactions. Treatable causes should be identified and treated. Knowledge of the mechanisms underlying the effects of caquexia on the patient may play a role in identifying treatment measures targetted to muscle wasting and to maintain body strength. In this article we review the main features and mechanisms of the anorexia-cachexia syndrome in patients with cancer.
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PMID:[The cachexia-anorexia syndrome among oncological patients]. 1904 64

Reports on the clinico-pathology and mechanisms of trypanosomosis in free-living and captive wild animals showed that clinical disease and outbreaks occur more commonly among captive than free-living wild animals. This is because the free-living wild animals co-exist with the disease until subjected to captivity. In exceptional cases however, draught, starvation and intercurrent diseases often compromised trypanotolerance leading to overt trypanosomosis in free-living wild animals. Meanwhile, in captivity, space restriction, reduced social interactions, change in social herd structure, reduced specie-to-specie specific behaviors, altered habitat and translocation were the major stressors that precipitated the disease. The cumulative effect of these factors produced severe physiological and somatic stress leading to diminished immune response due to increased blood cortisol output from adrenal cortex. The major symptoms manifested were pyrexia, innapetence, increased respiration, anaemia, cachexia and death. At necropsy, pulmonary oedema, splenomegally, hepatomegally, lympadenopathy and atrophy of body fats were the gross changes encountered. At the ultra-structural level, the tissues manifested degenerative changes, haemorghages, necrosis and mononuclear cellular infiltrations. The mechanisms of cellular and tissue injuries were primarily associated with physical and metabolic activities of the organisms. From the foregoing, it is evident that stress is the underlying mechanism that compromises trypanotolerance in wild animals leading to severe clinico-pathological effects.
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PMID:The clinico-pathology and mechanisms of trypanosomosis in captive and free-living wild animals: a review. 1934 Jun

Parenteral nutrition offers the possibility of increasing or ensuring nutrient intake in patients in whom normal food intake is inadequate and enteral nutrition is not feasible, is contraindicated or is not accepted by the patient. These guidelines are intended to provide evidence-based recommendations for the use of parenteral nutrition in cancer patients. They were developed by an interdisciplinary expert group in accordance with accepted standards, are based on the most relevant publications of the last 30 years and share many of the conclusions of the ESPEN guidelines on enteral nutrition in oncology. Under-nutrition and cachexia occur frequently in cancer patients and are indicators of poor prognosis and, per se, responsible for excess morbidity and mortality. Many indications for parenteral nutrition parallel those for enteral nutrition (weight loss or reduction in food intake for more than 7-10 days), but only those who, for whatever reason cannot be fed orally or enterally, are candidates to receive parenteral nutrition. A standard nutritional regimen may be recommended for short-term parenteral nutrition, while in cachectic patients receiving intravenous feeding for several weeks a high fat-to-glucose ratio may be advised because these patients maintain a high capacity to metabolize fats. The limited nutritional response to the parenteral nutrition reflects more the presence of metabolic derangements which are characteristic of the cachexia syndrome (or merely the short duration of the nutritional support) rather than the inadequacy of the nutritional regimen. Perioperative parenteral nutrition is only recommended in malnourished patients if enteral nutrition is not feasible. In non-surgical well-nourished oncologic patients routine parenteral nutrition is not recommended because it has proved to offer no advantage and is associated with increased morbidity. A benefit, however, is reported in patients undergoing hematopoietic stem cell transplantation. Short-term parenteral nutrition is however commonly accepted in patients with acute gastrointestinal complications from chemotherapy and radiotherapy, and long-term (home) parenteral nutrition will sometimes be a life-saving maneuver in patients with sub acute/chronic radiation enteropathy. In incurable cancer patients home parenteral nutrition may be recommended in hypophagic/(sub)obstructed patients (if there is an acceptable performance status) if they are expected to die from starvation/under nutrition prior to tumor spread.
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PMID:ESPEN Guidelines on Parenteral Nutrition: non-surgical oncology. 1947 52

The discovery of ghrelin has resulted in the development of approaches to appetite, enabling a better understanding of the mechanisms regulating appetite through molecular analyses. Ghrelin is a 28-amino acid peptide that was isolated from the stomach only a decade ago, and has recently been investigated as a potential therapeutic endogenous agent. This peptide increases appetite, adjusts energy balance, suppresses inflammation, and enhances the release of growth hormone from the pituitary gland. Although many bioactive substances such as peptide YY, leptin, adiponectin and obestatin are involved in appetite control, ghrelin is the only known peptide to signal starvation information from a peripheral organ to the central nervous system, contributing to an increase in appetite. Clinical trials have revealed the effectiveness of ghrelin in increasing lean body mass and activity in cachectic patients. As shown in clinical research on humans and basic research using animal models, cachexia often occurs in response to excess release of proinflammatory cytokines and induces further appetite loss, which aggravates the physiological status of underlying diseases. Ghrelin functions as a protector against the vicious cycle of the cachectic paradigm through orexigenic, anabolic and anti-inflammatory effects, so administration of ghrelin may be able to improve quality of life in cachectic patients. We show here a significant role of ghrelin in the pathophysiology of cachectic diseases and the possibility of clinical applications.
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PMID:Ghrelin and its therapeutic potential for cachectic patients. 1959 27

Cancer-induced cachexia (CIC) is a paraneoplastic syndrome that may account for up to 20% of deaths in cancer patients. Cachexia includes distinct metabolic changes that are the result of an acute-phase response (APR) mounted by the host as a reaction to tumor cells. These changes include increased muscle proteolysis, increased fat lipolysis, and increased hepatic production of acute-phase proteins such as C-reactive protein and fibrinogen. This APR pathogenesis is an important consideration in trying to treat cachectic patients as most therapies do not target the APR and its subsequent metabolic effects. Although there is currently no cure for CIC, the oncologist frequently encounters cachectic patients in practice, and evidence-based management is needed. We review the current data for assessment of starvation and cachexia, providing guidelines for management that include serum markers and functional assessment. In addition, a review of current therapies is provided, including hypercaloric feeding and nutritional intervention to address starvation, as well as data on appetite stimulants such as corticosteroids and megestrol acetate. Experimental therapies are also discussed, including nonsteroidal antiinflammatory drugs, tumor necrosis factor alpha antagonists, tetrahydrocannabinol, growth hormone, ghrelin, oxandrolone, and omega-3 fatty acids.
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PMID:Cancer-induced cachexia: a guide for the oncologist. 1988 31

Eating disorders are typical diseases of adolescence and early adulthood. About 1-3% of female juveniles suffer from anorexia nervosa (AN) or bulimia nervosa (BN). Today AN is still the psychiatric disease with the highest mortality rate. The peri-operative mortality rate of patients suffering from AN is in the range up to 15%. The beginning of AN is a lingering process and the majority of patients show increasingly restrictive eating habits ending in cachexia. Patients are obsessed by the predominant idea of being obese in spite of having a significant underweight. Patients suffering from bulimia break the strict regimen by eating enormous amounts of high calorie food. Such eating attacks are followed by weight reducing measures, mostly vomiting. Most of the physical changes caused by AN are due to starvation and loss of weight. The most significant medical complications are alterations of the cardiovascular system accompanied by decreasing contractility of the heart, bradycardia, electrocardiographic changes as well as disequilibrium of electrolytic and water balance. Most of these symptoms can be reversed by putting on weight.
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PMID:[Anesthesia in patients with anorexia nervosa and bulimia nervosa]. 2013 84

Cancer anorexia-cachexia syndrome (CACS) is a lethal but poorly defined involuntary wasting disorder. Loss of skeletal muscle and fat distinguishes it from starvation. Cachexia has been described as a clinical syndrome since ancient times, and the poor prognosis has long been acknowledged. In this article we have reviewed historical perspectives on cancer cachexia, and commented on modern definitions. In cancer cachexia, most historical descriptions included anorexia, wasting and a pale complexion. Other associated symptoms, such as fatigue, early satiety and taste changes, were inconsistently described. Newer descriptions have not significantly expanded the clinical picture.Today, there is still no consensus definition, hindering research on early diagnosis and effective therapy. The language descriptors used to characterise the syndrome are important. For example, the word 'cachexia' itself may mislead; perhaps cancer-related wasting syndrome is more accurate. Cancer anorexia-cachexia syndrome is a disorder associated with high morbidity and mortality, and deserves greater attention in both clinical and translational research.
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PMID:What is cancer anorexia-cachexia syndrome? A historical perspective. 2060 45

Geriatric patients are not defined by their age but by their general profile. Ageing is characterized by loss of organ function together with a reduced capability for adapting to changes in the environment (loss of homeostatic mechanisms) leading to frailty. In the older patient with cancer, there can be problems of dietary intake next to the effects of ageing per se. On top of this situation, the deleterious effects of the inflammatory processes induced by the tumour are superimposed. When these changes are translated into nutritional concepts, it is clear that, in the older cancer patient, there is a strong overlap of starvation, sarcopenia, and cachexia. Nutritional assessment should be part of the routine preliminary evaluation of the older oncology patient. Difference should be made between assessment of risk and actual nutritional status, which should be assessed with specific malnutrition indices. Body weight assessment with specific attention to unintended weight loss is essential in this evaluation. One should recognise the fact that body mass index (BMI) should be interpreted with caution, but that a low value for BMI still heralds an increased malnutrition risk. This increased alertness for nutritional problems has a lot to offer in the willingness for early intervention. The nutritional assessment, however, must be framed in a larger comprehensive geriatric assessment addressing several functional domains.
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PMID:[Nutritional assessment in oncogeriatrics]. 2111 57


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