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from so called GOPD (bronchial asthma, chronic bronchitis and chronic pulmonary emphysema), brochiectasis or alveolitis, has been noted since 1966 in Japan '. Through clinical, radiologic, physiologic and pathologic analysis based on accumulated data by Homma and Yamanaka1^, a nationwide survey with the cooperation of 30 universities, national and municipal institutions throughout the country was organized in 1980 to investigate the incidence and the morbidity of the disease under the aid of the Ministry of Health and Welfare of Japan6*. The results obtained by this project team during 1980 to 1982 disclosed the features of clinical and pathological findings, the gist of which was already reported7'19. As stated later, DPB is associated with HLA-Bw54 antigen which is found specifically in Japanese and Chinese and not in Caucasians, suggesting that DPBmay be an ethnically specific disease.

Concentrations of plasma 6-keto-prostaglandinFltt (6-kcto-PGFl0!), a stable metabolite of prostacyclin, were measured by radioimmunoassay before and after 3 min of induced ischemia in 45 diabetics and 23 controls matched for age. In the 45 diabetics, 15 had no vascular complications (group I), 10 had a macroangiopathy (group II), 10 had a microangiopathy (group III) and 10 had both macroangiopathy and microangiopathy (group IV). Plasma levels of 6-keto-PGFlQ; before forearm ischemia were significantly lower in group IV diabetics than in non-diabetic controls (188 ± 17 pg/ml and 245 ± 14 pg/ml, respectively). After 3 min of ischemia, plasma 6-keto-PGFia concentrations were increased in control subjects by 34% and by 21% in group I diabetics. In group III diabetics as well as diabetics with atherosclerotic vascular lesions (groups II and IV), no significant change was observed after 3 min of ischemia. These results suggest that impaired vessel wall prostacyclin production may to some extent be responsible for the developmentof diabetic retinopathy and nephropathy as well as atherosclerotic vascular complications.

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