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AMA Arch Intern Med. 1952;89(1):70-81. doi:10.1001/archinte.1952.00240010080007.
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ALTHOUGH it is only thirteen years since the first clinical diagnosis of a pulmonary arteriovenous fistula was made by Smith and Horton,1 there are now more than 65 proved cases in the medical literature.2 The clinical features of cyanosis and clubbed fingers, associated with polycythemia and a pulmonary murmur, enable the full-blown clinical syndrome to be easily recognized once the physician is aware of the entity. As emphasized by Goldman,3 a large proportion of the cases are associated with cutaneous and mucosal hemangiomata and telangiectases of a hereditary nature which probably represent a variant of Rendu-Weber-Osler disease (hereditary capillary telangiectasia). With the study of more cases it has become apparent that the classical clinical picture associated with a large pulmonary arteriovenous shunt and corresponding changes in the peripheral blood does not always occur. One or all of the prominent clinical manifestations may be absent, and the roentgen


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