TY - JOUR
T1 - Tumor necrosis factor and steroid metabolism in chronic heart failure
T2 - Possible relation to muscle wasting
AU - Anker, Stefan D.
AU - Clark, Andrew L.
AU - Kemp, Michael
AU - Salsbury, Colin
AU - Teixeira, Mauro M.
AU - Hellewell, Paul G.
AU - Coats, Andrew J S
PY - 1997/10
Y1 - 1997/10
N2 - Objectives. We sought to assess the possible relations between clinical severity of chronic heart failure and catabolic factors, specifically tumor necrosis factor (TNF), soluble TNF receptors 1 and 2 (sTNFR-1 and sTNFR-2), cortisol, testosterone and dehydroepiandrosterone (DHEA). Background. Chronic heart failure is associated with loss of muscle bulk that may be related to alteration of the balance between catabolism and anabolism. Methods. Sixty- three patients (average age ±SD 60.4 ± 11.3 years) with stable chronic heart failure and 20 control subjects aged 52.8 ± 11.4 years were studied. We measured body mass index (BMI) and obtained maximal incremental exercise testing with metabolic gas exchange measurements and measurements of venous levels of TNF, sTNFR-1 and sTNFR-2, cortisol and DHEA. Results. There was no difference in total TNF-alpha levels between patients and control subjects (9.76 ± 8.59 vs. 6.84 ± 2.7 pg/ml). sTNFR-1 (128.9 ± 84.5 vs. 63.6 ± 23.3 pg/ml, p <0.003) and sTNFR-2 (250.1 ± 109.5 vs. 187.9 ± 92.2 pg/ml, p = 0.03) were higher in patients. DHEA was lower in patients (9.88 ± 6.94 vs. 15.64 ± 8.33 nmol/liter, p = 0.004). The ratio of log cortisol to log DHEA correlated with log TNF level (r = 0.50, p <0.001 for the patients alone; r = 0.48, p <0.001 for the group as a whole). Peak oxygen consumption correlated with both sTNFR-1 and sTNFR-2 (r = -0.51, p <0.001 and r = - 0.39, p <0.001, respectively). There was a negative correlation between BMI and TNF levels (r = -0.43, p <0.001 for the patients) and the cortisol/DHEA ratio (r = -0.32, p = 0.01 for the patients). Conclusions. There is an increase in TNF and its soluble receptors in chronic heart failure. This increase is associated with a rise in the cortisol/DHEA (catabolic/anabolic) ratio. These changes correlate with BMI and clinical severity of heart failure, suggesting a possible etiologic link.
AB - Objectives. We sought to assess the possible relations between clinical severity of chronic heart failure and catabolic factors, specifically tumor necrosis factor (TNF), soluble TNF receptors 1 and 2 (sTNFR-1 and sTNFR-2), cortisol, testosterone and dehydroepiandrosterone (DHEA). Background. Chronic heart failure is associated with loss of muscle bulk that may be related to alteration of the balance between catabolism and anabolism. Methods. Sixty- three patients (average age ±SD 60.4 ± 11.3 years) with stable chronic heart failure and 20 control subjects aged 52.8 ± 11.4 years were studied. We measured body mass index (BMI) and obtained maximal incremental exercise testing with metabolic gas exchange measurements and measurements of venous levels of TNF, sTNFR-1 and sTNFR-2, cortisol and DHEA. Results. There was no difference in total TNF-alpha levels between patients and control subjects (9.76 ± 8.59 vs. 6.84 ± 2.7 pg/ml). sTNFR-1 (128.9 ± 84.5 vs. 63.6 ± 23.3 pg/ml, p <0.003) and sTNFR-2 (250.1 ± 109.5 vs. 187.9 ± 92.2 pg/ml, p = 0.03) were higher in patients. DHEA was lower in patients (9.88 ± 6.94 vs. 15.64 ± 8.33 nmol/liter, p = 0.004). The ratio of log cortisol to log DHEA correlated with log TNF level (r = 0.50, p <0.001 for the patients alone; r = 0.48, p <0.001 for the group as a whole). Peak oxygen consumption correlated with both sTNFR-1 and sTNFR-2 (r = -0.51, p <0.001 and r = - 0.39, p <0.001, respectively). There was a negative correlation between BMI and TNF levels (r = -0.43, p <0.001 for the patients) and the cortisol/DHEA ratio (r = -0.32, p = 0.01 for the patients). Conclusions. There is an increase in TNF and its soluble receptors in chronic heart failure. This increase is associated with a rise in the cortisol/DHEA (catabolic/anabolic) ratio. These changes correlate with BMI and clinical severity of heart failure, suggesting a possible etiologic link.
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U2 - 10.1016/S0735-1097(97)00262-3
DO - 10.1016/S0735-1097(97)00262-3
M3 - Article
C2 - 9316530
AN - SCOPUS:0030752660
VL - 30
SP - 997
EP - 1001
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 4
ER -