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Endocrinological disturbances in chronic obstructive pulmonary disease

¹ Dept of Respiratory Medicine, University Hospital Maastricht, The Netherlands and ² Division of Respiratory and Critical Care Physiology and Medicine, and Rehabilitation Clinical Trials Center, Harbor-University of California, Los Angeles (UCLA) Research and Education Institute, Torrance, California, USA

CORRESPONDENCE: E.C. Creutzberg, Department of Respiratory Medicine, University Hospital Maastricht, P.O. Box 5800, 6202, AZ Maastricht, The Netherlands. Fax: 31 433875051. E-mail: E.Creutzberg@PUL.Unimaas.NL

Keywords: anabolic steroids, chronic obstructive pulmonary disease, growth hormone, insulin-like growth factor-1, testosterone, thyroid hormone

Received: June 30, 2003
Accepted June 30, 2003

In this overview, the available literature on endocrinological disturbances in chronic obstructive pulmonary disease (COPD) is reviewed, with stress on growth hormone/insulin-like growth factor I (IGF-I), thyroid hormone and the anabolic steroids.

In COPD, little is known about circulating growth hormone or IGF-I concentrations. Some authors find a decrease in growth hormone or IGF-I, others an increase. An increase of growth hormone might reflect a nonspecific response of the body to stress (for instance, hypoxaemia). Until now, only one controlled study on growth hormone supplementation has been published, which however did not reveal any functional benefits. Before growth hormone supplementation can be advised as part of the treatment in COPD, further controlled studies must be performed to investigate its functional efficacy. The prevalence of thyroid dysfunction in COPD and its role in pulmonary cachexia has not been extensively studied. So far, there is no evidence that thyroid function is consistently altered in COPD, except perhaps in a subgroup of patients with severe hypoxaemia. Further research is required to more extensively study the underlying mechanisms and consequences of disturbed thyroid function in this subgroup of COPD patients.

A few studies have reported the results of anabolic steroid supplementation in chronic obstructive pulmonary disease. Although some studies have discerned that low circulating levels of testosterone are common in males with chronic obstructive pulmonary disease, little is known about the prevalence, the underlying causes or functional consequences of hypogonadism in these patients. The use of systemic glucocorticosteroids and an influence of the systemic inflammatory response have been suggested as contributing to low testosterone levels. It can be hypothesised that low anabolic hormones will reduce muscle mass and eventually result in a diminished muscle function. Further evidence is required before testosterone replacement can be recommended for males with chronic obstructive pulmonary disease.