南予医学雑誌　第17巻

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南予医誌　Vol.17　No. １　2016－44－of vasodilators such as CGRP caused acute transient and symmetric goiter after FNA３）. Sumiyoshi et al. also reported that the probable cause of a diffuse enlarged thyroid after FNA involved vasodilator substances or allergic reactions７）. In the present case， the mechanism of transient and acute swell-ing of the thyroid was more likely due to vasodilation and capillary leakage rather than an allergic reaction or a hematoma， as the patient’s serum IgE levels showed no remarkable change between the time of FNA and 1 year later. Furthermore， tingling of the neck developed 2 hours after FNA. Most studies reported secondary pain devel-oping at the puncture site after FNA３，５－６，８）; this pain could be an important indicator of vasodilator release. On the other hand， the literature suggests that ARDS is induced by a complex network of cytokines and other proinflammatory compounds９）. We considered that ARDS in the present case might be induced by some type of bioactive factors released from the thyroid， such as somatostatin， serotonin， catecholamines， histaminase， and/or others. Unfortunately， serum levels of these substances were not examined， and immunohistological staining was only performed for CGRP. Even with the lack of these data， the patient’s symp-toms support our hypothesis of a relation between ATS and ARDS. Additionally， the cervical CT images re-vealed a small hematoma on the right lobe of the thyroid gland. The hematoma was too small to compress the airway; hence， we concluded that dyspnea developed from thy-roid swelling and ARDS. To our knowledge， this is the rst case of ATS associated with ARDS. However， the actual frequency of ATS is still unclear.Glucocorticoid therapy can be indicated for ATS with ARDS. There is no standard thera-py for ATS because， as almost all cases lack major hemorrhage， treatment usually con-sists of observation and palliative therapies such as cold packs and nonsteroidal anti-inflammatory drugs. In the present case， development of ATS and ARDS seemed to initially resemble a rapid allergic response after FNA. However， the enlarged thyroid size and ARDS did not subside for over 24 hours; thus， glucocorticoid therapy was administered. After glucocorticoid therapy， ATS and ARDS improved in 24 hours. The blood data on admission were analyzed ret-rospectively and showed no evidence of an allergic reaction. Therefore， we suspected that glucocorticoids may lead to the restora-tion of conditions prior to FNA by decreas-ing the release of bioactive substances from the thyroid. According to the literature， only a short course of high-dose glucocorti-coid therapies for ARDS can be considered as rescue therapy in patients with ARDS９）. In the present case， glucocorticoids were effective in improving ATS symptoms and reducing substrate release from the thy-roid， and the ARDS also subsided. There-fore， glucocorticoid therapy should be con-sidered if ATS occurs after FNA whether or not any other complications arise.In conclusion， FNA can induce ATS with ARDS， and glucocorticoid therapy is a