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At least 973 records · Page 54Linked to original sources
PubMed1992

[Actinomycosis of the ovary as a cause of cachexia in a young patient].

The authors describe the case of a 40-year-old female patient treated for prolonged periods unsuccessfully with several antibiotics on account of a febrile condition of obscure aetiology and subsequently repeatedly subjected to laparotomy on account of intra-abdominal abscesses. The cause of the fever, abdominal pain and gradual cachectization was an abdominal form of actinomycosis. After establishment of the diagnosis the patient was successfully treated by long-term penicillin administration and recovered completely. The authors discuss experience reported in the literature and therapeutic possibilities in actinomycosis.

Actinomycosis↗
PubMed2005

[Cachexia].

Explore the source record for details and available documents.

Cachexia↗
PubMed2005

[Pathomechanism of cachexia in chronic obstructive pulmonary disease].

Weight loss is a characteristic for advanced chronic obstructive pulmonary disease (COPD), but its mechanism remains unexplained. The decrease of lean body mass is due to a negative energy balance with a noncatabolic hypermetabolic state. Pulmonary inflammation or tissue hypoxia might contribute to it, the decrease in protein content is accompanied by an increase in reactive oxygen forms. Tumor necrosis factor (TNF) has been implicated, other candidates are cytokines IL-1B and IL-6. Activation of apoptosis may be noticed. Pulmonary inflammation and changes in serum leptin may be interrelated. Other hormonal disturbances involve serum IGF-1 level decrease, increase of insulin resistance, raised catecholamine and cortisol levels and other mechanisms which need further investigations. Up to now the attempts undertaken to counteract the observed hormonal changes failed to success.

Apoptosis↗
PubMed2006

[Cachexia in chronic pulmonary obstructive disease].

Weight loss is a characteristic feature of chronic obstructive pulmonary disease (COPD) and a negative, independent predictor of outcome. It is a consequence of a misbalance between protein synthesis and breakdown resulting from increased energy requirement unbalanced by dietary intake. A depletion of fat-free mass is seen, especially in muscles (up to 60% of their mass) and leads to the loss of their power and endurance. The impairment of quality of life is very distinct. So far, there is no systemic treatment in cachectic patients with COPD, anti-catabolic treatment by polyunsaturated fatty acid may be of significance but needs further investigation.

Cachexia↗
PubMed2006

Effects of ghrelin on anorexia in tumor-bearing mice with eicosanoid-related cachexia.

Ghrelin is a novel brain-gut peptide that stimulates food intake and may secondarily increase body weight via a growth hormone secretagogue receptor (GHS-R). Tumor-bearing mice (MCG101), characterized by anorexia, fat loss and muscle wasting due to increased concentration of PGE2 and proinflammatory cytokines (IL-1beta, IL-6, TNF-alpha), were provided ghrelin i.p. at a low (20 microg/day) and high dose (40 microg/day) to examine the ability of ghrelin to counteract tumor-induced anorexia. Immunohistochemical staining and Western blot analyses were used to identify GHS-R expression in the brain as well as its relationship to NPY expression in hypothalamic neurons. GHS-R mRNA in hypothalamus and ghrelin mRNA in gastric fundus were quantified by RT-PCR. Body composition was determined by carcass extractions. GHS-R expression in hypothalamus and plasma ghrelin levels were significantly increased in freely-fed tumor-bearing mice, while gastric fundus expression of ghrelin was unaltered compared to non-tumor-bearing mice (controls). Ghrelin treatment increased food intake, body weight and whole body fat at both low and high doses of ghrelin in normal controls, while tumor-bearing mice showed improved intake and body composition at the high dose of ghrelin only. Exogenous ghrelin normalized the GHS-R expression in hypothalamus from tumor-bearing mice without alterations in the gastric fundus expression of ghrelin. Tumor growth was not altered by exogenous ghrelin. Our results indicate that MCG 101-bearing mice became ghrelin resistant despite upregulation of hypothalamic GHS-R expression, which confirms similar indirect observations in cancer patients. Thus, other factors downstream of the ghrelin-GHS-R system appear to be more important than ghrelin to explain cancer-induced anorexia.

Animals↗
PubMed1990

[Monitoring and management of the central nervous system in treatment of tumor cachexia].

After palliative surgery artificial nutrition is indicated primarily in patients receiving postoperative chemotherapy or radiotherapy. The techniques of ambulatory enteral or parenteral nutrition have been standardized during the past decade. They can be used with minimal risk even in patients with advanced cancer. An improvement of the nutritional status can be expected in most of the patients. Further clinical trials are needed to determine whether the patients' quality of life improves.

Cachexia↗
PubMed1976

[Cachexia in mice induced by a fraction of Brucella melitensis. Modification by levamisole or by diethyldithiocarbamate of soda].

The PMF fraction of B. melitensis creates a wasting disease in newborn mice (J. infect. Dis., 1973, 127, p. 139). Administered to adult mice, PMF induces a 4 to 8 g loss of weight in 20 g mice and more markedly in males than in females. Treatment with Levamisole (LMS) suppresses this difference in response to PMF and restores normal weight in 24 days. Diethyldithiocarbamate (DDC), another immunostimulant sulfur derivate, abolishes the emaciating effect of PMF. Furthermore, DDC is an anabolizing agent which increases the weight of normal or PMF-treacted mice above the mean level of normal untreated control mice.

Animals↗