cachexia/inflammatie

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Chronic heart failure: an example of a systemic chronic inflammatory disease resulting in cachexia.

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Chronic heart failure is no longer a mere cardiac entity, but involves several, initially adaptive and later detrimental, neurohumoral compensatory mechanisms. Peripheral manifestations of the disease, such as endothelial dysfunction, skeletal muscle changes, and disturbances in ventilatory control,

Counteracting inflammation: a promising therapy in cachexia.

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Disease progression in cancer is dependent on the complex interaction between the tumor and the host inflammatory response. Indeed, both the tumor and the patient produce cytokines that act on multiple target sites such as bone marrow, myocytes, hepatocytes, adipocytes, endothelial cells, and

Leptin and inflammation-associated cachexia in chronic kidney disease.

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Leptin is an adipocyte-derived hormone that acts as a major regulator of food intake and energy homeostasis. It circulates both as a free and as a protein-bound entity. Leptin is released into the blood in proportion to the amount of body fat and exerts sustained inhibitory effects on food intake

Cachexia in rheumatoid arthritis is associated with inflammatory activity, physical disability, and low bioavailable insulin-like growth factor.

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OBJECTIVE To examine the impact of inflammation, insulin-like growth factor (IGF-1) and its regulating binding protein (IGFBP-1) on lean body mass (LBM) in patients with rheumatoid arthritis (RA). METHODS In 60 inpatients (50 women), inflammatory activity was measured by Disease Activity Score 28

Copper chelation with tetrathiomolybdate suppresses adjuvant-induced arthritis and inflammation-associated cachexia in rats.

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Tetrathiomolybdate (TM), a drug developed for Wilson's disease, produces an anti-angiogenic and anti-inflammatory effect by reducing systemic copper levels. TM therapy has proved effective in inhibiting the growth of tumors in animal tumor models and in cancer patients. We have hypothesized that TM

Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 1: eradication of Helicobacter in the cachexia of idiopathic parkinsonism.

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BACKGROUND Neuronal damage in idiopathic parkinsonism may be in response to ubiquitous occult infection. Since peptic ulceration is prodromal, Helicobacter is a prime candidate. OBJECTIVE To consider the candidature of Helicobacter in parkinsonism with cachexia. METHODS We explore the relationship

Adjuvant arthritis as a model of inflammatory cachexia.

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OBJECTIVE To determine whether adjuvant arthritis (AA) leads to changes in body composition and cytokine production similar to those seen in patients with rheumatoid arthritis. METHODS AA was induced in Lewis rats using Freund's complete adjuvant. Body cell mass was measured by determining the

Effects of aging and cytokine blockade on inflammatory cachexia.

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OBJECTIVE To evaluate the role of aging and specific cytokine blockade in the etiology of cachexia caused by adjuvant arthritis (AA), a model of cytokine-associated cachexia. METHODS AA was induced in Lewis rats using CFA. In Experiment 1, severity of AA and inflammatory cachexia was assessed in

Pro-inflammatory cytokines and oxidative stress/antioxidant parameters characterize the bio-humoral profile of early cachexia in lung cancer patients.

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Cancer-related cachexia, that is present in about 50% of cancer patients and accounts for 20% of all cancer deaths, is clinically characterized by progressive weight loss, anorexia, metabolic alterations, asthenia, depletion of lipid stores and severe loss of skeletal muscle proteins. The main

Circulating leptin and inflammatory response in esophageal cancer, esophageal cancer-related cachexia-anorexia syndrome (CAS) and non-malignant CAS of the alimentary tract.

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We investigated the association between esophageal cancer and cachexia-anorexia syndrome (CAS) of the alimentary tract and leptin, an adipocytokine crucial for body weight regulation, a modulator of inflammatory/immune response, implication of which in cancer and CAS development remains debatable.

Sosiho‑tang ameliorates cachexia‑related symptoms in mice bearing colon 26 adenocarcinoma by reducing systemic inflammation and muscle loss.

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Cachexia accompanied by muscle wasting is a key determinant of poor prognosis in cancer patients and cancer‑related death. Previous studies have demonstrated that inflammatory cytokines such as interleukin‑6 (IL‑6), tumor necrosis factor‑α (TNF‑α), IL‑1 and interferon‑γ (IFN‑γ) secreted from host

IL-6-like cytokines and cancer cachexia: consequences of chronic inflammation.

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An estimated 30% of cancer deaths are attributed to cachexia and its consequences. Cachexia (wasting syndrome) is the hypercatabolism of the body's carbon sources, proteins and lipids, for conversion into energy. It is induced by a variety of pathological conditions, including cancer. Among the

Cachexia induced by Yoshida ascites hepatoma in Wistar rats is not associated with inflammatory response in the spleen or brain.

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Recent data indicate that peripheral, as well as hypothalamic pro-inflammatory cytokines play an important role in the development of cancer cachexia. However, there are only a few studies simultaneously investigating the expression of inflammatory molecules in both the periphery and hypothalamic

Pulmonary cachexia, systemic inflammatory profile, and the interleukin 1beta -511 single nucleotide polymorphism.

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BACKGROUND Cachexia is common in chronic obstructive pulmonary disease (COPD) and is thought to be linked to an enhanced systemic inflammatory response. OBJECTIVE We investigated differences in the systemic inflammatory profile and polymorphisms in related inflammatory genes in COPD

Tumor necrosis factor as a mediator of shock, cachexia and inflammation.

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Tumor necrosis factor is a cytokine made by macrophages, monocytes and T cells that has been formed to play an important role in shock, cachexia and inflammation. The importance of this cytokine eliciting shock and cachexia in mammals is reviewed.

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