and foot was not increased in such patients.3What we should therefore be looking for is a trophic factor that selectively stimulates connective tissue overgrowth and induces a periosteal reaction, not a generalised vaso- dilator such as vasointestinal polypeptide, which increases skin blood flow.As for gynaecomastia, it has long been known that this may occur in patients with hypertro- phic pulmonary osteoarthropathy secondary to infective lung disease.Nearly 100 years ago Bamberger noted swelling of the breast in three men with this disease and likened this to the mammary enlargement that may occur in young men at puberty.4Our observation, however, that oestrogen metabolism may be altered irrespective of the presence of gynae- comastia requires reinvestigation in the light of modern endocrinological techniques.5It would therefore be of interest if Dr Braude and his colleagues included endocrinological assessment, with dynamic testing as required, in their proposed prospective study of cystic fibrosis.This would provide objective infor- mation of chemical changes in hypertrophic pulmonary osteoarthropathy rather than yet another unsubstantiated theory of its pathogenesis.
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Takkunen et al. (1984) studied this question.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: