Stein R S, Howard C A
South Med J. 1981 Mar;74(3):293-4. doi: 10.1097/00007611-198103000-00010.
After case reports of alleged cimetidine-induced neutropenia, we investigated the possibility that cimetidine might produce occult bone marrow injury by a mechanism other than idiosyncratic hypersensitivity. We performed hydrocortisone challenge tests to assess the bone marrow granulocyte reserves before, during, and after cimetidine administration. No decrease in marrow granulocyte reserves was associated with the administration of cimetidine. When cimetidine and lithium were given to volunteers, the granulocytosis normally associated with lithium was not diminished. Although a general myelosuppressive effect of cimetidine has been postulated by others, we found no evidence of such a phenomenon in this study. Idiosyncratic drug sensitivity is probably the mechanism of cimetidine-induced neutropenia.
在有关于西咪替丁诱发中性粒细胞减少的病例报告后,我们研究了西咪替丁可能通过非特异性过敏机制以外的其他机制导致隐匿性骨髓损伤的可能性。我们进行了氢化可的松激发试验,以评估西咪替丁给药前、给药期间和给药后的骨髓粒细胞储备。西咪替丁给药后未发现骨髓粒细胞储备减少。当给志愿者同时使用西咪替丁和锂时,锂通常引起的粒细胞增多并未减弱。尽管其他人推测西咪替丁有一般的骨髓抑制作用,但我们在本研究中未发现这种现象的证据。特异性药物敏感性可能是西咪替丁诱发中性粒细胞减少的机制。