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草绿色链球菌所致败血症和休克综合征:易感因素的病例对照研究

Septicemia and shock syndrome due to viridans streptococci: a case-control study of predisposing factors.

作者信息

Elting L S, Bodey G P, Keefe B H

机构信息

Department of Medical Specialties, University of Texas M. D. Anderson Cancer Center, Houston 77030.

出版信息

Clin Infect Dis. 1992 Jun;14(6):1201-7. doi: 10.1093/clinids/14.6.1201.

DOI:10.1093/clinids/14.6.1201
PMID:1623076
Abstract

Between 1972 and 1989, the incidence of viridans streptococcal bacteremia at the University of Texas M. D. Anderson Cancer Center in Houston increased from one case per 10,000 admissions to 47 cases per 10,000 admissions (P less than .0001). A shock syndrome characterized by hypotension, rash, palmar desquamation, adult respiratory distress syndrome, and occasionally death developed in 26% of cases of streptococcal septicemia but in only 4% of cases of septicemia involving other gram-positive bacteria (P = .0005). The risk of streptococcal infection increased with the prophylactic administration of trimethoprim-sulfamethoxazole or a fluoroquinolone (P less than .0001) and with profound neutropenia (P less than .0001). Treatment of chemotherapy-induced gastritis with antacids or with histamine type 2 (H2) antagonists was associated with a sevenfold increase in risk (P less than .001), while sucralfate therapy did not increase risk (P = .65). Streptococcal infection may result from gastric overgrowth of organisms resistant to trimethoprim-sulfamethoxazole in an antacid- or H2 antagonist-induced alkaline environment, with the gastrointestinal tract ulceration caused by antineoplastic therapy providing a convenient portal of entry. In patients receiving chemotherapy, replacement of antacids or H2 antagonists by an acid-sparing regimen should be considered to preserve the natural acidic barrier to infection.

摘要

1972年至1989年间,位于休斯敦的得克萨斯大学MD安德森癌症中心的草绿色链球菌菌血症发病率从每10000例入院患者中有1例增至每10000例入院患者中有47例(P<0.0001)。26%的链球菌败血症患者出现了以低血压、皮疹、掌部脱皮、成人呼吸窘迫综合征且偶有死亡为特征的休克综合征,但在涉及其他革兰氏阳性菌的败血症患者中,这一比例仅为4%(P = 0.0005)。预防性使用甲氧苄啶 - 磺胺甲恶唑或氟喹诺酮(P<0.0001)以及严重中性粒细胞减少(P<0.0001)会增加链球菌感染风险。用抗酸剂或组胺2型(H2)拮抗剂治疗化疗引起的胃炎会使风险增加7倍(P<0.001),而硫糖铝治疗不会增加风险(P = 0.65)。在抗酸剂或H2拮抗剂诱导的碱性环境中,对甲氧苄啶 - 磺胺甲恶唑耐药的微生物在胃内过度生长可能导致链球菌感染,而抗肿瘤治疗引起的胃肠道溃疡提供了便利的感染入口。对于接受化疗的患者,应考虑采用减少胃酸分泌的方案替代抗酸剂或H2拮抗剂,以维持对感染的天然酸性屏障。

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