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PubMed1997

[Overproduction of tumor necrosis factor-alpha in African patients with HIV-1 infection, cachexia and low tri-iodothyronine syndrome].

Sick euthyroid syndrome characterized by low triiodothyronine (T3) levels is observed in advance stages of HIV infection. The purpose of this prospective study was to determine if proinflammatory cytokines play and role in the pathogenesis of this syndrome in HIV-1-infected patients. Serum levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1 beta were measured in 40 African patients presenting HIV-1 infection associated with low T3 levels in 20 cases (group I) and normal or elevated T3 levels in 20 cases (group II). Elevation of serum TNF-alpha levels was more common and mean serum TNF-alpha level was significantly higher in group I than group II (116 +/- 39 versus 3.05 +/- 0.04 pg/ml; p < 0.01). Serum IL-1 beta levels were not significantly different between the two groups. These findings are consistent with previous experimental data and suggest that sick euthyroid syndrome in cachectic HIV-1 infected patients may be due to overproduction of TNF-alpha.

AIDS-Related Opportunistic Infections↗
PubMed1998

Energy expenditure and protein metabolism in human immunodeficiency virus infection and cancer cachexia.

Malnutrition and weight loss are clinically significant complications of both human immunodeficiency virus (HIV) infection and cancer. Over the last two decades, multiple abnormalities in energy and protein metabolism have been documented in patients with cancer and, more recently, in HIV infection. In HIV infection, studies of the components of energy balance have demonstrated that weight loss results primarily from decreased energy intake, coupled with a failure to consistently reduce resting energy expenditure. Although several studies have shown that resting energy expenditure is elevated in many patients with HIV infection, other studies have shown that not all patients with HIV infection are hypermetabolic. Likewise, protein turnover is increased, decreased, or unchanged in patients with HIV infection and varies with the physiologic state of the patient. In cancer patients, studies of resting energy expenditure have produced similarly varying results, depending in part on tumor type and dietary intake. Protein turnover studies in patients with cancer suggest that support of the tumor may occur at the expense of host skeletal muscle. Abnormalities of glucose and lipid metabolism have been noted as well. Thus, pharmacologic intervention may be needed to restore weight and lean tissue in patients with weight loss associated with either HIV infection or cancer.

Cachexia↗
PubMed1990

Energy balance in relation to cancer cachexia.

The aim of the current study was to determine the contribution of increased resting energy expenditure (REE) and/or decreased energy intake (EI) to the development of weight loss in gastric and colorectal (GCR) and lung cancer patients. REE was measured in 22 GCR cancer patients and 17 lung cancer patients and was compared with REE values in 40 apparently healthy controls. REE in lung cancer patients expressed per kg fat free mass (REE/FFM) was significantly increased when compared to healthy controls (33.5 +/- 5.4 and 29.6 +/- 2.9 kcal, respectively; p < 0.01). GCR cancer patients had no elevated REE compared to these healthy controls. No significant differences in EI were established between the three groups. Eight GCR cancer patients reported a decrease in food intake compared to pre-disease intake, in contrast to only one lung cancer patient. Semi-starving GCR cancer patients showed a significant weight loss (8.7 +/- 8.1%), a low respiratory quoteint (RQ) (0.76 +/- 0.04) and a high beta-hydroxybutyrate level (259 +/- 192 mumol/l), but they showed no difference in REE compared to patients with a normal EI. The current study suggests that weight loss in GCR cancer patients is initiated by decreased food intake, whereas weight loss in lung cancer patients represents a combination of an increased REE and a relatively low EI.

Journal Article↗
PubMed1987

Early development of protein metabolic perturbations in the liver and skeletal muscle of tumour-bearing rats. A model system for cancer cachexia.

In rats into which a fast-growing ascites hepatoma (Yoshida AH-130) had been transplanted, tumour growth elicited a marked loss of body weight until the animal's death in about 2 weeks. Overall tissue protein metabolism was simultaneously studied in vivo in the gastrocnemius muscle and liver after labelling with [14C]bicarbonate. Early and progressive atrophy developed in the gastrocnemius muscle, the underlying metabolic imbalance being expressed by an elevation in the apparent protein-degradation rate, with no changes in the apparent synthesis rate. A transient hyperplastic response preceded waste in the liver, both states being associated with alterations in protein-degradation rate: an initial decrease during liver growth, then an acceleration as liver regressed. Protein-synthesis rates, virtually unchanged during liver growth, were elevated in the subsequent phase, although not sufficient to balance the enhanced breakdown. Thus, in the tumour host tissues examined, altered states of protein turnover appeared to result mostly from changes in rates of protein breakdown. In sharp contrast with the negative protein balance in the host, the ascites hepatoma cells had the ability to grow or at least, in advanced stages, to maintain a stationary state.

Animals↗