General ill health, malnutrition, and weight loss, usually associated with chronic disease.
The lack or loss of APPETITE accompanied by an aversion to food and the inability to eat. It is the defining characteristic of the disorder ANOREXIA NERVOSA.
Agents that are used to stimulate appetite. These drugs are frequently used to treat anorexia associated with cancer and AIDS.
A condition of involuntary weight loss of greater then 10% of baseline body weight. It is characterized by atrophy of muscles and depletion of lean body mass. Wasting is a sign of MALNUTRITION as a result of inadequate dietary intake, malabsorption, or hypermetabolism.
Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation.
Megestrol acetate is a progestogen with actions and uses similar to those of the progestogens in general. It also has anti-androgenic properties. It is given by mouth in the palliative treatment or as an adjunct to other therapy in endometrial carcinoma and in breast cancer. Megestrol acetate has been approved to treat anorexia and cachexia. (From Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
Decrease in existing BODY WEIGHT.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
A melanocortin receptor subtype found primarily in BRAIN. It shows specificity for ALPHA-MSH; BETA-MSH and ADRENOCORTICOTROPIC HORMONE.
A 28-amino acid, acylated, orexigenic peptide that is a ligand for GROWTH HORMONE SECRETAGOGUE RECEPTORS. Ghrelin is widely expressed but primarily in the stomach in the adults. Ghrelin acts centrally to stimulate growth hormone secretion and food intake, and peripherally to regulate energy homeostasis. Its large precursor protein, known as appetite-regulating hormone or motilin-related peptide, contains ghrelin and obestatin.
The administration of nutrients for assimilation and utilization by a patient by means other than normal eating. It does not include FLUID THERAPY which normalizes body fluids to restore WATER-ELECTROLYTE BALANCE.
A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.
The consumption of edible substances.
Peptides derived from pro-opiomelanocortin (POMC) which can stimulate MELANOCYTES or CORTICOTROPHS. Melanocortins include ACTH; ALPHA-MSH; and other peptides such as BETA-MSH and GAMMA-MSH, derived from other fragments of POMC. These peptides act through a variety of MELANOCORTIN RECEPTORS to control different functions including steroidogenesis, energy homeostasis, feeding, and skin pigmentation.
Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.
Inflammation of a DIVERTICULUM or diverticula.
Inflammation of the COLONIC DIVERTICULA, generally with abscess formation and subsequent perforation.
Abnormally high level of calcium in the blood.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.
The terms, expressions, designations, or symbols used in a particular science, discipline, or specialized subject area.

Medroxyprogesterone acetate inhibits interleukin 6 secretion from KPL-4 human breast cancer cells both in vitro and in vivo: a possible mechanism of the anticachectic effect. (1/649)

Interleukin 6 (IL-6) is a multifunctional cytokine. Recent reports suggest that circulating IL-6 secreted from tumour cells plays an important role in cancer-induced cachexia. Medroxyprogesterone acetate (MPA) has been used as an endocrine therapeutic agent for patients with breast cancer. It has been suggested that MPA decreases serum IL-6 levels and preserves the bodyweight of patients with advanced breast cancer. However, the mechanisms of action responsible for the anticachectic effect of MPA have not been elucidated. Therefore, the effects of MPA on IL-6 secretion were studied both in vitro and in vivo using a human breast cancer cell line, KPL-4, which secretes IL-6 into medium and induces cachexia when injected into female nude mice. MPA (10-1000 nM) dose-dependently decreased basal IL-6 secretion into medium, and also suppressed tumour necrosis factor (TNF-alpha)-induced IL-6 secretion. Both basal and TNF-alpha-induced IL-6 mRNA levels were dose-dependently lowered by MPA. Moreover, intramuscular injections of MPA (100 mg kg(-1) twice a week) into nude mice bearing KPL-4 transplanted tumours significantly decreased serum IL-6 levels without affecting tumour growth and preserved the bodyweight of recipient mice. These findings suggest that suppression of IL-6 secretion from tumour cells, at least in part, causes the anticachectic effect of MPA.  (+info)

Tumour inoculation site-dependent induction of cachexia in mice bearing colon 26 carcinoma. (2/649)

Murine colon 26 carcinoma growing at either subcutaneous (s.c.) or intramuscular (i.m.) inoculation sites causes cachexia in mice. Such animals show extensive loss of body weight, wasting of the muscle and adipose tissues, hypoglycaemia, and hypercalcaemia, even when the tumour weight comprises only about 1.9% of carcass weight. In contrast, the same tumour when inoculated into the liver does not cause any sign of tumour-related cachexia even when the tumour becomes much larger (6.6% of carcass weight). Interleukin 6 (IL-6), a mediator associated with cachexia in this tumour model, is detected at high levels both in the tumour tissues and in the circulating blood of mice bearing colon 26 tumour at the s.c. inoculation site. In contrast, only minute levels of IL-6 are detected in the tumour grown in the liver. The colon 26 tumour grown in the liver does not lose its ability to cause cachexia, because the tumour when re-inoculated s.c. is able to cause extensive weight loss and produce IL-6 as did the original colon 26 cell line. Histological studies revealed differences in the composition of tumour tissues: the tumours grown in the subcutis consist of many polygonal tumour cells, extended-intercellular space, and high vascular density, whereas those grown in the liver consist of spindle-shaped tumour cells. Thus, the environment where tumour cells grow would be a critical factor in determining the cachectic phenotype of cancer cells, including their ability to produce IL-6.  (+info)

Alterations of lipid and cholesterol metabolism in cachectic tumor-bearing rats are prevented by insulin. (3/649)

The ascites hepatoma Yoshida AH130 causes in the host a rapid and progressive body weight loss, associated with reduced food intake, and protein and lipid hypercatabolism. Because insulin regulates glucose as well as lipid and protein metabolism, we suggest that the observed alterations are at least in part secondary to hypoinsulinemia and/or to the increase of counterregulatory hormones in AH130-bearing rats. To verify this hypothesis, controls with free access to food (n = 4), controls with free access to food plus insulin (107 micromol. kg body wt-1. d-1) (n = 4), controls pair-fed to the tumor-bearing rats (n = 4), pair-fed controls treated with insulin (n= 4), tumor hosts (n = 9), and tumor hosts treated with insulin (n = 6) were used. The Yoshida ascites hepatoma cells ( approximately 10(8) cells/rat) were inoculated intraperitoneally. Daily food intake and body weight were measured; insulin was injected starting the day of tumor implantation for 6 d. The metabolism of both cholesterol and lipids was investigated in tumor cells, and ascitic fluid and blood serum were investigated at the end of treatment. Insulin prevented the reduction of food intake (19 +/- 0.6 vs. 13 +/- 0.4 g/d, P < 0.01; AH130 hosts treated and not treated with insulin, respectively), the loss of body weight (202 +/- 12 vs. 135 +/- 9 g, P < 0.01), lowered the circulating triglycerides (48.3 +/- 4.9 vs. 84.5 +/- 7.1 mmol/L, P < 0.01), and free fatty acids (561 +/- 47 vs. 989 +/- 54 mmol/L (P < 0.01), while corrected the decrease of adipose lipoprotein lipase activity (1,240 +/- vs. 300 +/- pmol FA, P < 0.01) observed in AH130 hosts. Moreover, insulin prevented the decrease in HDL cholesterol (13.2 +/- 0.8 vs. 9.3. +/- 0.7 mmol/L, P < 0.01) and significantly increased hepatic cholesterol synthesis as evaluated by 14C-acetate incorporation into cholesterol, in both liver (3,337 +/- 245 vs. 830 +/- 115 Bq/g, P < 0.01) and AH130 cells (11,676 +/- 1,693 vs. 4,196 +/- 527 Bq/10(6) cells, P < 0.01). Thus insulin treatment ameliorated many metabolic derangements, with a lengthening of rats survival time (7 +/- 1 vs. 11 +/- 1 d, P < 0.05) without significantly stimulating tumor growth. These data, together with our previous observations on the effectiveness of insulin on protein turnover perturbations, suggest that many metabolic alterations occurring during cancer cachexia can be avoided by the administration of this hormone.  (+info)

Inhibition of prostate cancer metastasis in vivo: a comparison of 1,23-dihydroxyvitamin D (calcitriol) and EB1089. (4/649)

The steroid hormone 1,25-dihydroxyvitamin D [1,25(OH)2D, also known as calcitriol] is known to inhibit the proliferation and to promote the differentiation of human prostate cancer cells. Additionally, we showed that 1,25(OH)2D markedly inhibits the invasiveness of human prostate cancer cells in vitro (G. G. Schwartz et al., Cancer Epidemiol. Biomark. Prev., 6: 727-732, 1997). These properties support the use of 1,25(OH)2D as differentiation therapy in prostate cancer. However, the use of 1,25(OH)2D in vivo is limited by the risk of hypercalcemia. We therefore compared the effects of 1,25(OH)2D and of EB1089, an analogue of 1,25(OH)2D with reduced calcemic effects, in an in vivo model of androgen-insensitive metastatic prostate cancer, the rat Dunning MAT LyLu prostate cancer model. Tumor growth and metastasis were studied using Copenhagen rats given s.c. injections of MAT LyLu cells. Fifty male rats were divided into five groups of 10 rats each. Four experimental groups received i.p. injections of low and high doses of 1,25(OH)2D and EB1089 (0.5 and 1.0 microg/kg, low and high, respectively). A control group received injections of vehicle only. Tumor volumes were measured three times per week. Rats were weighed weekly. The number of metastases to the lungs and the extent of hypercalcemia were evaluated. Compared with controls, tumor volumes were significantly smaller in all experimental groups. Similarly, the number of lung metastases (number of foci/lung) was reduced markedly by both 1,25(OH)2D and EB1089. Control rats developed 22.7 (+/- 1.98 SE) tumor foci per lung. Rats treated with 1,25(OH)2D and with EB1089 (1.0 microg/kg) developed 10.4 (+/- 2.81) and 7.70 (+/- 1.29) tumor foci, respectively (P < 0.001 and P < 0.0001, respectively; drug versus control). Compared with controls (10.79 +/- 0.1 mg/dl), serum calcium levels were significantly elevated in both 1,25(OH)2D and EB1089-treated rats (P < 0.01). However, EB1089 was significantly less calcemic than 1,25(OH)2D (12.59 +/- 0.21 mg/dl versus 14.47 +/- 0.46 mg/dl; 1.0 microg/kg; P < 0.001). Rats treated with 1,25(OH)2D showed marked weight loss: 20.0 +/- 1.9% and 26.3 +/- 1.7% of their initial weight (low and high doses, respectively, P < 0.001). Weight loss was significantly lower in rats treated with EB1089 at the high dose 8.4 (+/- 2.9) %. Moreover, rats treated with low-dose EB1089 gained 5.2 (+/- 3.7) % of their initial weight. In conclusion, 1,25(OH)2D and EB1089 showed marked and equivalent inhibition of prostate cancer metastasis in vivo. EB1089 was significantly less calcemic than 1,25(OH)2D and did not induce severe weight loss. This is the first report of a vitamin D analogue that significantly inhibits prostate cancer metastasis in vivo and that does so without producing cachexia or unacceptable hypercalcemia.  (+info)

Intratumoral injection of oligonucleotides to the NF kappa B binding site inhibits cachexia in a mouse tumor model. (5/649)

Cancer cachexia, characterized by anorexia, weight loss and progressive tissue wasting, has been postulated to be mediated by various cytokines. However, the precise mechanism of cachexia induction is not fully explained. We have developed synthetic double-stranded oligodeoxynucleotides (ODN) as 'decoy' cis-elements that block the binding of nuclear factors to promoter regions of targeted genes, resulting in the inhibition of gene transactivation in vivo as well as in vitro. This novel molecular strategy could be useful for treating a broad range of human diseases including cancer. In this study, we injected decoy ODN targeting the transcriptional factor, NF-kappa B (NF kappa B) binding cis-elements, which are essential for transactivation of gene expression of cytokines, directly into tumors of adenocarcinoma colon26 in mice, in order to examine whether or not cachexia is alleviated by inhibiting the action of cytokines. Tumor growth was not affected by transfection of NF kappa B decoy ODN as compared with scrambled decoy ODN. Nevertheless, transfection of NF kappa B decoy, but not scrambled decoy, ODN resulted in attenuation of the reductions in body weight, epididymal fat, gastrocnemius muscle mass and food intake, which were induced by the tumor presence. Interleukin 6 mRNA in the tumor was also markedly decreased by the transfection of NF kappa B decoy ODN. It is known that the transcriptional factor E2F plays a pivotal role in the coordinated transactivation of cell cycle regulatory genes. Therefore, we hypothesized that the introduction of synthetic double-stranded DNA with high affinity for E2F in vivo as 'decoy' cis-elements might inhibit the tumor growth of colon26, resulting in turn in inhibition of cachexia induction. However, injection of E2F decoy ODN failed to inhibit tumor growth and cachexia induction, as compared with mismatched decoy ODN. Overall, the present study demonstrated that cachexia induced by adenocarcinoma colon26 was inhibited by blocking of NF kappa B, using a novel molecular decoy strategy, without an effect on tumor growth, and also that tumor growth and cachexia induction in the colon26 model were not affected by E2F decoy ODN. These results suggest that cytokines regulated by NF kappa B may play a pivotal role in the induction of cachexia by colon26, providing a new therapeutic strategy for cancer cachexia.  (+info)

Effect of a cachectic factor on carbohydrate metabolism and attenuation by eicosapentaenoic acid. (6/649)

The effect of a proteolysis-inducing factor (PIF), produced by cachexia-inducing tumours on glucose utilization by different tissues and the effect of pretreatment with the polyunsaturated fatty acid eicosapentaenoic acid (EPA), has been determined using the 2-deoxyglucose tracer technique. Mice receiving PIF showed a profound depression of body weight (2.3 g) over a 24-h period, which was completely abolished by pretreatment with a monoclonal antibody to PIF or by 3 days pretreatment with EPA at 500 mg kg(-1). Animals receiving PIF exhibited a marked hypoglycaemia, which was effectively reversed by both antibody and EPA pretreatment. There was an increase in glucose utilization by brain, heart and brown fat, but a decrease by kidney, white fat, diaphragm and gastrocnemius muscle after administration of PIF. Changes in organ glucose consumption were attenuated by either monoclonal antibody, EPA, or both. There was a decrease in 2-deoxyglucose uptake by C2C12 myoblasts in vitro, which was attenuated by EPA. This suggests a direct effect of PIF on glucose uptake by skeletal muscle. These results suggest that in addition to a direct catabolic effect on skeletal muscle PIF has a profound effect on glucose utilization during cachexia.  (+info)

Weight loss and low body cell mass in males with lung cancer: relationship with systemic inflammation, acute-phase response, resting energy expenditure, and catabolic and anabolic hormones. (7/649)

The aim of the present study was to investigate, in human lung cancer, the relationship between weight loss and the existence of a low body cell mass (BCM) on the one hand, and the putative presence of systemic inflammation, an increased acute-phase response, anorexia, hypermetabolism and changes in circulating levels of several anabolic and catabolic hormones on the other. In 20 male lung cancer patients, pre-stratified by weight loss of >/=10% (n=10) or of <10% (n=10), the following measurements were performed: BCM (by dual-energy X-ray absorptiometry/bromide dilution), circulating levels of sTNF-R55 and sTNF-R75 (soluble tumour necrosis factor receptors of molecular masses 55 and 75 kDa respectively), interleukin-6, lipopolysaccharide-binding protein, albumin, appetite (scale of 0-10), resting energy expenditure (by indirect calorimetry) and circulating levels of catabolic (cortisol) and anabolic [testosterone, insulin-like growth factor-I (IGF-I)] hormones. Compared with the patients with a weight loss of <10%, those with a weight loss of >/=10% were characterized by higher levels of sTNF-R55 (trend towards significance; P=0.06), and lower levels of albumin (27.4 compared with 34.4 mmol/l; P=0.02), testosterone (13.2 compared with 21.5 nmol/l; P=0.01) and IGF-I (119 compared with 184 ng/ml; P=0.004). In the patient group as a whole, the percentage weight loss was significantly correlated with sTNF-R55 (r=0.59, P=0.02), albumin (r=-0.63, P=0.006) and IGF-I (r=-0.50, P=0.02) levels. Height-adjusted BCM was significantly correlated with sTNF-R55 (r=-0.57, P=0.03), sTNF-R75 (r=-0.50, P=0. 04), lipopolysaccharide-binding protein (r=-0.50, P=0.04), albumin (r=0.56, P=0.02) and resting energy expenditure/BCM (r=-0.54, P=0. 03), and there was a trend towards a correlation with IGF-I concentration (r=0.44, P=0.06). We conclude that, in human lung cancer, weight loss and the presence of a low BCM are associated with systemic inflammation, an increased acute-phase response and decreased levels of IGF-I. In addition, a decreased BCM is associated with hypermetabolism.  (+info)

Differential reconstitution of mitochondrial respiratory chain activity and plasma redox state by cysteine and ornithine in a model of cancer cachexia. (8/649)

The mechanism of wasting, as it occurs in malignant diseases and various etiologically unrelated conditions, is still poorly understood. We have, therefore, studied putative cause/effect relationships in a murine model of cancer cachexia, C57BL/6 mice bearing the fibrosarcoma MCA-105. The plasma of these mice showed decreased albumin and increased glutamate levels, which are typically found in practically all catabolic conditions. Skeletal muscles from tumor-bearing mice were found to have an abnormally low mitochondrial respiratory chain activity (mito.RCA) and significantly decreased glutathione (GSH) levels. The decrease in mito.RCA was correlated with an increase in the i.m. GSH disulfide/GSH ratio, the plasma cystine/thiol ratio, and the GSH disulfide/GSH ratio in the bile. This is indicative of a generalized shift in the redox state extending through different body fluids. Treatment of tumor-bearing mice with ornithine, a precursor of the radical scavenger spermine, reversed both the decrease in mito.RCA and the change in the redox state, whereas treatment with cysteine, a GSH precursor, normalized only the redox state. Treatment of normal mice with difluoromethyl-ornithine, a specific inhibitor of ornithine decarboxylase and spermine biosynthesis, inhibited the mito.RCA in the skeletal muscle tissue, thus illustrating the importance of the putrescine/spermine pathway in the maintenance of mito.RCA. Ornithine, cysteine, and N-acetyl-cysteine (NAC) also reconstituted the abnormally low concentrations of the GSH precursor glutamate in the skeletal muscle tissue of tumor-bearing mice. Higher doses, however, enhanced tumor growth and increased the plasma glucose level in normal mice. In the latter, cysteine and NAC also decreased i.m. catalase and GSH peroxidase activities. Taken together, our studies on the effects of ornithine, cysteine, and NAC illuminate some of the mechanistic pathways involved in cachexia and suggest targets for therapeutic intervention.  (+info)

Cachexia is a complex metabolic disorder characterized by severe weight loss, muscle wasting, and weakness. It is often associated with chronic diseases such as cancer, HIV/AIDS, heart failure, kidney disease, and chronic obstructive pulmonary disease (COPD). Cachexia differs from simple malnutrition or starvation in that it involves a significant loss of muscle mass and an imbalance in energy metabolism, even when adequate calories are consumed.

The hallmark features of cachexia include:

1. Weight loss: Unintentional loss of more than 5% of body weight over 12 months or less, or more than 2% in individuals already underweight.
2. Muscle wasting: Reduction in skeletal muscle mass and strength, leading to weakness and functional impairment.
3. Fatigue and anorexia: Decreased appetite and reduced food intake due to various factors such as inflammation, hormonal imbalances, and psychological distress.
4. Inflammation: Elevated levels of pro-inflammatory cytokines (e.g., TNF-α, IL-1, IL-6) that contribute to metabolic dysregulation and muscle wasting.
5. Insulin resistance: Impaired glucose uptake and utilization by cells, leading to increased blood glucose levels and altered energy metabolism.
6. Altered protein metabolism: Increased protein breakdown and decreased protein synthesis in skeletal muscles, contributing to muscle wasting.
7. Altered lipid metabolism: Increased lipolysis (breakdown of fat) and impaired lipogenesis (formation of fat), leading to loss of adipose tissue and altered energy storage.

Cachexia significantly impacts patients' quality of life, treatment outcomes, and overall survival. Currently, there is no single effective treatment for cachexia, and management typically involves addressing the underlying disease, nutritional support, exercise interventions, and pharmacological therapies to target specific aspects of the metabolic dysregulation associated with this condition.

Anorexia is a medical condition defined as a loss of appetite or aversion to food, leading to significant weight loss. It can be a symptom of various underlying causes, such as mental health disorders (most commonly an eating disorder called anorexia nervosa), gastrointestinal issues, cancer, infections, or side effects of medication. In this definition, we are primarily referring to anorexia as a symptom rather than the specific eating disorder anorexia nervosa.

Anorexia nervosa is a psychological eating disorder characterized by:

1. Restriction of energy intake leading to significantly low body weight (in context of age, sex, developmental trajectory, and physical health)
2. Intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain
3. Disturbed body image, such as overvaluation of self-worth regarding shape or weight, or denial of the seriousness of low body weight

Anorexia nervosa has two subtypes: restricting type and binge eating/purging type. The restricting type involves limiting food intake without engaging in binge eating or purging behaviors (such as self-induced vomiting or misuse of laxatives, diuretics, or enemas). In contrast, the binge eating/purging type includes recurrent episodes of binge eating and compensatory behaviors to prevent weight gain.

It is essential to differentiate between anorexia as a symptom and anorexia nervosa as a distinct psychological disorder when discussing medical definitions.

Appetite stimulants are medications or substances that increase the desire to eat or improve appetite. They work by affecting brain chemicals, hormones, or other systems involved in regulating hunger and fullness. Some commonly used appetite stimulants include:

1. Megestrol acetate: a synthetic progestin hormone that is often prescribed for cancer-related weight loss and anorexia. It works by stimulating appetite and promoting weight gain.
2. Dronabinol: a synthetic form of THC, the active ingredient in marijuana. It is approved for treating AIDS-related anorexia and chemotherapy-induced nausea and vomiting. Dronabinol can increase appetite and promote weight gain.
3. Corticosteroids: medications that mimic the effects of hormones produced by the adrenal gland. They can help improve appetite, but their long-term use is associated with significant side effects.
4. Cyproheptadine: an antihistamine medication that can also stimulate appetite. It is sometimes used off-label to treat appetite loss in various conditions, such as cancer or HIV/AIDS.
5. Ghrelin agonists: these are medications that mimic the effects of ghrelin, a hormone produced by the stomach that increases hunger and appetite. Currently, there are no FDA-approved ghrelin agonists for appetite stimulation, but research is ongoing.

It's important to note that while appetite stimulants can help improve food intake in some individuals, they may not be effective for everyone, and their use should be carefully monitored due to potential side effects and interactions with other medications. Always consult a healthcare professional before starting any new medication or supplement.

Wasting syndrome is a condition characterized by significant weight loss and muscle wasting, often accompanied by weakness and decreased appetite. It can be caused by various underlying medical conditions, including HIV/AIDS, cancer, tuberculosis, and other chronic infections or diseases that cause chronic inflammation. In some cases, wasting syndrome can also result from severe malnutrition or gastrointestinal disorders that affect nutrient absorption.

The diagnostic criteria for wasting syndrome vary depending on the underlying cause, but generally, it is defined as a significant loss of body weight (typically more than 10% of body weight) and muscle mass over a period of several months. In addition to weight loss and muscle wasting, individuals with wasting syndrome may also experience fatigue, weakness, decreased immune function, and impaired physical functioning.

Wasting syndrome can have serious consequences on an individual's health and quality of life, and it is often associated with increased morbidity and mortality. Treatment typically involves addressing the underlying cause of the wasting syndrome, as well as providing nutritional support to help individuals regain weight and muscle mass.

Muscular atrophy is a condition characterized by a decrease in the size and mass of muscles due to lack of use, disease, or injury. This occurs when there is a disruption in the balance between muscle protein synthesis and degradation, leading to a net loss of muscle proteins. There are two main types of muscular atrophy:

1. Disuse atrophy: This type of atrophy occurs when muscles are not used or are immobilized for an extended period, such as after an injury, surgery, or prolonged bed rest. In this case, the nerves that control the muscles may still be functioning properly, but the muscles themselves waste away due to lack of use.
2. Neurogenic atrophy: This type of atrophy is caused by damage to the nerves that supply the muscles, leading to muscle weakness and wasting. Conditions such as amyotrophic lateral sclerosis (ALS), spinal cord injuries, and peripheral neuropathies can cause neurogenic atrophy.

In both cases, the affected muscles may become weak, shrink in size, and lose their tone and mass. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, exercise, and medication to manage symptoms and improve muscle strength and function.

Megestrol acetate is a synthetic progestin, which is a hormone that acts like progesterone in the body. It is used to treat various conditions such as endometrial cancer, breast cancer, and anorexia associated with AIDS. It works by blocking the action of certain hormones in the body, which can slow or stop the growth of some types of cancer cells. In addition, megestrol acetate can help increase appetite and weight gain in people with HIV/AIDS.

The medication is available in various forms, including tablets and oral suspension, and its use should be under the supervision of a healthcare professional who will determine the appropriate dosage based on the patient's medical condition and response to treatment. Common side effects of megestrol acetate include nausea, vomiting, diarrhea, gas, headache, dizziness, and changes in mood or sex drive.

Skeletal muscle, also known as striated or voluntary muscle, is a type of muscle that is attached to bones by tendons or aponeuroses and functions to produce movements and support the posture of the body. It is composed of long, multinucleated fibers that are arranged in parallel bundles and are characterized by alternating light and dark bands, giving them a striped appearance under a microscope. Skeletal muscle is under voluntary control, meaning that it is consciously activated through signals from the nervous system. It is responsible for activities such as walking, running, jumping, and lifting objects.

Weight loss is a reduction in body weight attributed to loss of fluid, fat, muscle, or bone mass. It can be intentional through dieting and exercise or unintentional due to illness or disease. Unintentional weight loss is often a cause for concern and should be evaluated by a healthcare professional to determine the underlying cause and develop an appropriate treatment plan. Rapid or significant weight loss can also have serious health consequences, so it's important to approach any weight loss plan in a healthy and sustainable way.

Body weight is the measure of the force exerted on a scale or balance by an object's mass, most commonly expressed in units such as pounds (lb) or kilograms (kg). In the context of medical definitions, body weight typically refers to an individual's total weight, which includes their skeletal muscle, fat, organs, and bodily fluids.

Healthcare professionals often use body weight as a basic indicator of overall health status, as it can provide insights into various aspects of a person's health, such as nutritional status, metabolic function, and risk factors for certain diseases. For example, being significantly underweight or overweight can increase the risk of developing conditions like malnutrition, diabetes, heart disease, and certain types of cancer.

It is important to note that body weight alone may not provide a complete picture of an individual's health, as it does not account for factors such as muscle mass, bone density, or body composition. Therefore, healthcare professionals often use additional measures, such as body mass index (BMI), waist circumference, and blood tests, to assess overall health status more comprehensively.

Neoplasms are abnormal growths of cells or tissues in the body that serve no physiological function. They can be benign (non-cancerous) or malignant (cancerous). Benign neoplasms are typically slow growing and do not spread to other parts of the body, while malignant neoplasms are aggressive, invasive, and can metastasize to distant sites.

Neoplasms occur when there is a dysregulation in the normal process of cell division and differentiation, leading to uncontrolled growth and accumulation of cells. This can result from genetic mutations or other factors such as viral infections, environmental exposures, or hormonal imbalances.

Neoplasms can develop in any organ or tissue of the body and can cause various symptoms depending on their size, location, and type. Treatment options for neoplasms include surgery, radiation therapy, chemotherapy, immunotherapy, and targeted therapy, among others.

A melanocortin receptor (MCR) is a type of G protein-coupled receptor that binds melanocortin peptides. The melanocortin system plays crucial roles in various biological processes such as pigmentation, energy homeostasis, sexual function, and inflammation.

The melanocortin receptor 4 (MC4R) is one of the five subtypes of MCRs, which is widely expressed in the central nervous system, including the hypothalamus, and some peripheral tissues. MC4R is a key component in the regulation of energy balance, appetite, and body weight. Activation of MC4R by melanocortin peptides, such as α-melanocyte stimulating hormone (α-MSH), leads to decreased food intake and increased energy expenditure, while antagonism or deficiency of MC4R results in obesity.

In summary, the medical definition of 'Receptor, Melanocortin, Type 4' is a G protein-coupled receptor that binds melanocortin peptides and plays a critical role in regulating energy balance, appetite, and body weight.

Ghrelin is a hormone primarily produced and released by the stomach with some production in the small intestine, pancreas, and brain. It is often referred to as the "hunger hormone" because it stimulates appetite, promotes food intake, and contributes to the regulation of energy balance.

Ghrelin levels increase before meals and decrease after eating. In addition to its role in regulating appetite and meal initiation, ghrelin also has other functions, such as modulating glucose metabolism, insulin secretion, gastric motility, and cardiovascular function. Its receptor, the growth hormone secretagogue receptor (GHS-R), is found in various tissues throughout the body, indicating its wide range of physiological roles.

Nutritional support is medical care that focuses on providing nutrition to individuals who are unable to consume or absorb adequate nutrients through their regular diet. This may include patients with chronic illnesses, eating disorders, swallowing difficulties, or those recovering from surgery or injury. Nutritional support can take many forms, including oral supplements, enteral feeding (tube feeding), and parenteral nutrition (intravenous feeding). The goal of nutritional support is to maintain or improve the patient's nutritional status, promote healing and recovery, enhance quality of life, and reduce complications associated with malnutrition.

Interleukin-6 (IL-6) is a cytokine, a type of protein that plays a crucial role in communication between cells, especially in the immune system. It is produced by various cells including T-cells, B-cells, fibroblasts, and endothelial cells in response to infection, injury, or inflammation.

IL-6 has diverse effects on different cell types. In the immune system, it stimulates the growth and differentiation of B-cells into plasma cells that produce antibodies. It also promotes the activation and survival of T-cells. Moreover, IL-6 plays a role in fever induction by acting on the hypothalamus to raise body temperature during an immune response.

In addition to its functions in the immune system, IL-6 has been implicated in various physiological processes such as hematopoiesis (the formation of blood cells), bone metabolism, and neural development. However, abnormal levels of IL-6 have also been associated with several diseases, including autoimmune disorders, chronic inflammation, and cancer.

The medical definition of "eating" refers to the process of consuming and ingesting food or nutrients into the body. This process typically involves several steps, including:

1. Food preparation: This may involve cleaning, chopping, cooking, or combining ingredients to make them ready for consumption.
2. Ingestion: The act of taking food or nutrients into the mouth and swallowing it.
3. Digestion: Once food is ingested, it travels down the esophagus and enters the stomach, where it is broken down by enzymes and acids to facilitate absorption of nutrients.
4. Absorption: Nutrients are absorbed through the walls of the small intestine and transported to cells throughout the body for use as energy or building blocks for growth and repair.
5. Elimination: Undigested food and waste products are eliminated from the body through the large intestine (colon) and rectum.

Eating is an essential function that provides the body with the nutrients it needs to maintain health, grow, and repair itself. Disorders of eating, such as anorexia nervosa or bulimia nervosa, can have serious consequences for physical and mental health.

Melanocortins are a group of peptides that are derived from the post-translational processing of the proopiomelanocortin (POMC) gene. This gene is expressed in various tissues, including the pituitary gland, hypothalamus, and skin. The POMC precursor protein is cleaved into several active peptides, including adrenocorticotropic hormone (ACTH), β-melanocyte stimulating hormone (MSH), γ-MSH, and α-MSH. These melanocortins exert their effects through binding to melanocortin receptors (MCRs), which are G protein-coupled receptors.

The different melanocortins have distinct physiological roles, but they all share some common functions, such as modulating pigmentation, energy homeostasis, and immune responses. For instance, α-MSH and β-MSH bind to MCRs in the skin and increase melanin production, leading to skin tanning. Additionally, α-MSH can act on MCRs in the hypothalamus to regulate appetite and energy expenditure. ACTH, on the other hand, primarily stimulates the release of cortisol from the adrenal gland, but it can also bind to MCRs and influence pigmentation and sexual behavior.

Overall, melanocortins are crucial signaling molecules that play a significant role in various physiological processes, and dysregulation of melanocortin signaling has been implicated in several diseases, including obesity, depression, and skin disorders.

Experimental neoplasms refer to abnormal growths or tumors that are induced and studied in a controlled laboratory setting, typically in animals or cell cultures. These studies are conducted to understand the fundamental mechanisms of cancer development, progression, and potential treatment strategies. By manipulating various factors such as genetic mutations, environmental exposures, and pharmacological interventions, researchers can gain valuable insights into the complex processes underlying neoplasm formation and identify novel targets for cancer therapy. It is important to note that experimental neoplasms may not always accurately represent human cancers, and further research is needed to translate these findings into clinically relevant applications.

Diverticulitis is a medical condition characterized by the inflammation or infection of one or more diverticula, which are small pouches that form in the wall of the colon (large intestine). The condition most commonly affects the sigmoid colon, which is the part of the colon located in the lower left abdomen.

Diverticulitis occurs when these pouches become inflamed or infected, often as a result of a small piece of stool or undigested food getting trapped inside them. This can cause symptoms such as:

* Severe abdominal pain and tenderness, particularly in the lower left side of the abdomen
* Fever and chills
* Nausea and vomiting
* Constipation or diarrhea
* Bloating and gas
* Loss of appetite

Diverticulitis can range from mild to severe, and in some cases, it may require hospitalization and surgery. Treatment typically involves antibiotics to clear the infection, as well as a liquid diet to allow the colon to rest and heal. In more severe cases, surgery may be necessary to remove the affected portion of the colon.

Diverticulitis, Colonic is a medical condition characterized by the inflammation or infection of one or more diverticula in the colon. Diverticula are small, bulging pouches that form in the wall of the colon, usually in older adults. They are caused by increased pressure on weakened areas of the colon wall, resulting in the formation of these sac-like protrusions.

When diverticula become inflamed or infected, it leads to the condition known as diverticulitis. Symptoms of colonic diverticulitis may include abdominal pain, fever, nausea, vomiting, constipation or diarrhea, and a decreased appetite. In severe cases, complications such as perforation, abscess formation, or peritonitis (inflammation of the lining of the abdominal cavity) may occur, requiring hospitalization and surgical intervention.

The exact cause of diverticulitis is not fully understood, but it is believed to be associated with a low-fiber diet, obesity, smoking, and lack of exercise. Treatment typically involves antibiotics to clear the infection, a liquid diet to allow the colon to rest, and over-the-counter or prescription pain medications to manage discomfort. In severe cases or in patients who experience recurrent episodes of diverticulitis, surgery may be necessary to remove the affected portion of the colon.

Hypercalcemia is a medical condition characterized by an excess of calcium ( Ca2+ ) in the blood. While the normal range for serum calcium levels is typically between 8.5 to 10.2 mg/dL (milligrams per deciliter) or 2.14 to 2.55 mmol/L (millimoles per liter), hypercalcemia is generally defined as a serum calcium level greater than 10.5 mg/dL or 2.6 mmol/L.

Hypercalcemia can result from various underlying medical disorders, including primary hyperparathyroidism, malignancy (cancer), certain medications, granulomatous diseases, and excessive vitamin D intake or production. Symptoms of hypercalcemia may include fatigue, weakness, confusion, memory loss, depression, constipation, nausea, vomiting, increased thirst, frequent urination, bone pain, and kidney stones. Severe or prolonged hypercalcemia can lead to serious complications such as kidney failure, cardiac arrhythmias, and calcification of soft tissues. Treatment depends on the underlying cause and severity of the condition.

Glomerulonephritis is a medical condition that involves inflammation of the glomeruli, which are the tiny blood vessel clusters in the kidneys that filter waste and excess fluids from the blood. This inflammation can impair the kidney's ability to filter blood properly, leading to symptoms such as proteinuria (protein in the urine), hematuria (blood in the urine), edema (swelling), hypertension (high blood pressure), and eventually kidney failure.

Glomerulonephritis can be acute or chronic, and it may occur as a primary kidney disease or secondary to other medical conditions such as infections, autoimmune disorders, or vasculitis. The diagnosis of glomerulonephritis typically involves a combination of medical history, physical examination, urinalysis, blood tests, and imaging studies, with confirmation often requiring a kidney biopsy. Treatment depends on the underlying cause and severity of the disease but may include medications to suppress inflammation, control blood pressure, and manage symptoms.

Hypoglycemia is a medical condition characterized by an abnormally low level of glucose (sugar) in the blood. Generally, hypoglycemia is defined as a blood glucose level below 70 mg/dL (3.9 mmol/L), although symptoms may not occur until the blood sugar level falls below 55 mg/dL (3.0 mmol/L).

Hypoglycemia can occur in people with diabetes who are taking insulin or medications that increase insulin production, as well as those with certain medical conditions such as hormone deficiencies, severe liver illnesses, or disorders of the adrenal glands. Symptoms of hypoglycemia include sweating, shaking, confusion, rapid heartbeat, and in severe cases, loss of consciousness or seizures.

Hypoglycemia is typically treated by consuming fast-acting carbohydrates such as fruit juice, candy, or glucose tablets to rapidly raise blood sugar levels. If left untreated, hypoglycemia can lead to serious complications, including brain damage and even death.

"Terminology as a topic" in the context of medical education and practice refers to the study and use of specialized language and terms within the field of medicine. This includes understanding the meaning, origins, and appropriate usage of medical terminology in order to effectively communicate among healthcare professionals and with patients. It may also involve studying the evolution and cultural significance of medical terminology. The importance of "terminology as a topic" lies in promoting clear and accurate communication, which is essential for providing safe and effective patient care.

... and laboratory changes to categorize patients into non-cachexia, pre-cachexia, cachexia, and refractory cachexia. The Cachexia ... Cachexia is also a significant problem in South America and Africa. The most frequent causes of cachexia in the United States ... Cachexia is also distinct from sarcopenia, or age-related muscle loss, although they often co-exist. The management of cachexia ... Diagnosis of cachexia can be difficult due to the lack of well-established diagnostic criteria. Cachexia can improve with ...
The Journal of Cachexia, Sarcopenia and Muscle is a quarterly peer-reviewed medical journal that covers research relevant to ... "Journal of Cachexia, Sarcopenia and Muscle". 2017 Journal Citation Reports. Web of Science (Science ed.). Clarivate Analytics. ... As of January 2015, the journal is published by Wiley-Blackwell in association with the Society on Sarcopenia, Cachexia and ... changes in body composition, especially cachexia and sarcopenia, as consequences of chronic illnesses or of the aging process, ...
"What Is Cardiac Cachexia?". WebMD. Retrieved 2 May 2022. "Cachexia". YouTube. "Cachexia: Symptoms, Treatment, and Outlook". ... "Recent developments in the treatment of cachexia: highlights from the 6th Cachexia Conference". Journal of Cachexia, Sarcopenia ... Cachexia has been coined the "last illness" and is sometimes called "body wasting". The prevalence of cachexia ranges from 5-15 ... Cachexia is a major issue, especially in the elderly. Cachexia can occur in most major diseases including infections, cancer, ...
Cachexia Malnutrition "Emaciation". Medical-Dictionary.TheFreeDictionary.com. Retrieved January 19, 2012. Bose, Bholanoth (1877 ...
ISBN 978-1-4020-6854-6. Hofbauer KG, Anker SD, Inui A, Nicholson JR (22 December 2005). Pharmacotherapy of Cachexia. CRC Press ...
Plauth M, Schütz ET (September 2002). "Cachexia in liver cirrhosis". International Journal of Cardiology. 85 (1): 83-87. doi: ... Cachexia associated with muscle wasting and weakness Cirrhosis has many possible causes, and more than one cause may be present ...
"Journal of Cachexia, Sarcopenia and Muscle". Wiley Online Library. "Journal of Cachexia, Sarcopenia and Muscle". doi:10.1007/ ... "SCWD - Sarcopenia, Cachexia and Wasting Disorders". Sarcopenia, Cachexia and Wasting Disorders. Retrieved 2017-05-17. Search ... "Endpoints for Cachexia Trials & Nutrition for Cachexia and Sarcopenia" (Morley et al., JAMDA 2010) Nutritional recommendations ... Stefan D. Anker is Head of Field "Tissue Homeostasis and Cachexia" at Charité University, Berlin, Germany. Previously, he was ...
Cachexia is a poor prognostic sign in patients with chronic heart failure. ACE inhibitors are under early investigation for the ... J Cachexia Sarcopenia Muscle. 1 (2): 129-133. doi:10.1007/s13539-010-0014-2. PMC 3060646. PMID 21475695. "Angiotensin- ... preliminary findings in cardiac cachexia". European Journal of Heart Failure. 3 (3): 359-63. doi:10.1016/S1388-9842(00)00146-X ... in cardiac function in congestive heart failure The ACE inhibitor enalapril has also been shown to reduce cardiac cachexia in ...
Strasser F, Bruera ED (June 2002). "Update on anorexia and cachexia". Hematology/Oncology Clinics of North America. 16 (3): 589 ... Holmes S (July 2009). "A difficult clinical problem: diagnosis, impact and clinical management of cachexia in palliative care ...
Argilés JM, Anguera A, Stemmler B (June 2013). "A new look at an old drug for the treatment of cancer cachexia: megestrol ... Mantovani G, Macciò A, Lai P, Massa E, Ghiani M, Santona MC (1998). "Cytokine involvement in cancer anorexia/cachexia: role of ... Strang P (1997). "The effect of megestrol acetate on anorexia, weight loss and cachexia in cancer and AIDS patients (review)". ... Taylor JK, Pendleton N (September 2016). "Progesterone therapy for the treatment of non-cancer cachexia: a systematic review". ...
... and cachexia in COVID‐19: facts and numbers". Journal of Cachexia, Sarcopenia and Muscle. 12 (1): 9-13. doi:10.1002/jcsm.12674 ...
Journal of Cachexia, Sarcopenia and Muscle. 12 (6): 2079-2090. doi:10.1002/jcsm.12813. PMC 8718031. PMID 34687171. S2CID ...
Connolly, Martin (2017). "miR-424-5p reduces ribosomal RNA and protein synthesis in muscle wasting". Journal of Cachexia, ...
Journal of Cachexia, Sarcopenia and Muscle. 9 (3): 453-464. doi:10.1002/jcsm.12287. PMC 5989853. PMID 29392922. Krops LA, ...
Journal of Cachexia, Sarcopenia and Muscle. 13 (1): 467-480. doi:10.1002/jcsm.12841. ISSN 2190-6009. PMC 8818613. PMID 34877816 ...
Journal of cachexia, sarcopenia and muscle. 9 (4): 786-787. doi:10.1002/jcsm.12308. PMID 29786955. Kiebzak GM, Leamy LJ, ...
Journal of Cachexia, Sarcopenia and Muscle. 13 (2): 1134-1150. doi:10.1002/jcsm.12843. PMC 8977972. PMID 35233984. Gharahdaghi ... Journal of Cachexia, Sarcopenia and Muscle. 10 (6): 1276-1294. doi:10.1002/jcsm.12472. PMC 6903447. PMID 31568675. Handelsman ...
September 2018). "Cancer cachexia: rationale for the MENAC (Multimodal-Exercise, Nutrition and Anti-inflammatory medication for ... Although there is only limited scientific evidence on the subject, people with cancer cachexia are encouraged to engage in ... Grande AJ, Silva V, Maddocks M (September 2015). "Exercise for cancer cachexia in adults: Executive summary of a Cochrane ... Sadeghi M, Keshavarz-Fathi M, Baracos V, Arends J, Mahmoudi M, Rezaei N (July 2018). "Cancer cachexia: Diagnosis, assessment, ...
Cachexia Ageing Frailty syndrome Geriatrics Dynapenia Peterson SJ, Mozer M (February 2017). "Differentiating Sarcopenia and ... Anker SD, Morley JE, von Haehling S (December 2016). "Welcome to the ICD-10 code for sarcopenia". Journal of Cachexia, ... It is distinct from cachexia, in which muscle is degraded through cytokine-mediated degradation, although both conditions may ... One aspect hindering drug approval for treatments for cachexia and sarcopenia is disagreement in endpoints. Several clinical ...
... and other supplements for the treatment of cachexia in cancer: a European Palliative Care Research Centre cachexia project". ... The efficacy of Juven for the treatment of cancer cachexia was also examined in a phase 3 clinical trial which found a strong ... Further research involving the treatment of cancer cachexia with Juven over a period of several months is required to ... but not rheumatoid cachexia. Clinical trials with Juven for AIDS have also demonstrated improvements in immune status, as ...
Journal of Cachexia, Sarcopenia and Muscle. 8 (1): 48-56. doi:10.1002/jcsm.12122. ISSN 2190-6009. PMC 4863930. PMID 27239418. ...
Although androstanolone itself has not been approved for cachexia in any country, an orally active synthetic derivative of ... 766-. ISBN 978-1-133-00809-5. Mantovani G (6 October 2007). Cachexia and Wasting: A Modern Approach. Springer Science & ... Androstanolone (for hypogonadism and cachexia) - AdisInsight Androstanolone (for hypogonadism and BPH) - AdisInsight ... and cachexia (in cancer patients) and in Australia for the treatment of benign prostatic hyperplasia (BPH). It reached phase II ...
Cancer Associated Cachexia He was married to Professor Marie Fallon and together they had two children, Christopher and Katie ... He was Professor of Surgical Oncology at the University of Edinburgh with a special interest in cachexia. He was born in ... Glasgow Herald obituary 16 September 2016 Skipworth, R. J; Ross, J. A (2017). "Ken Fearon". Journal of Cachexia, Sarcopenia and ...
Journal of Cachexia, Sarcopenia and Muscle. 9 (2): 400-416. doi:10.1002/jcsm.12266. PMC 5879973. PMID 29215200. Online ...
DuBois, F.S. (1949). "Compulsion neurosis with cachexia (Anorexia Nervosa)". American Journal of Psychiatry. 106 (2): 107-115. ...
Increases in myostatin levels during chronic heart failure have been shown to cause cardiac cachexia. Systemic inhibition of ... Journal of Cachexia, Sarcopenia and Muscle. 10 (3): 662-686. doi:10.1002/jcsm.12404. PMC 6596402. PMID 30916493. MYO-029 press ...
Journal of Cachexia, Sarcopenia and Muscle. 2 (3): 153-161. doi:10.1007/s13539-011-0034-6. PMC 3177038. PMID 22031847. " ...
Journal of Cachexia, Sarcopenia and Muscle. 9 (1): 3-19. doi:10.1002/jcsm.12238. ISSN 2190-5991. PMC 5803609. PMID 29151281. ...
DuBOIS FS (August 1949). "Compulsion neurosis with cachexia (anorexia nervosa)". The American Journal of Psychiatry. 106 (2): ...
Rubin, Harry (2003). "Cancer cachexia: Its correlations and causes". Proceedings of the National Academy of Sciences. 100 (9): ...

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