Gaynor E R, Vitek L, Sticklin L, Creekmore S P, Ferraro M E, Thomas J X, Fisher S G, Fisher R I
Loyola University Stritch School of Medicine, Maywood, Illinois.
Ann Intern Med. 1988 Dec 15;109(12):953-8. doi: 10.7326/0003-4819-109-12-953.
To determine the hemodynamic alterations occurring during therapy with the maximally tolerated doses of interleukin-2 and lymphokine-activated killer cells.
Case series.
Referal-based inpatient oncology service at a university medical center.
A sequential sample of 13 patients with metastatic colon carcinoma, malignant melanoma, or hypernephroma who were receiving treatment with interleukin-2 and lymphokine-activated killer cells in the maximally tolerated doses.
Pretreatment variables of mean arterial pressure, systemic vascular resistance, heart rate, pulmonary capillary wedge pressure, and cardiac index were compared with the same variables measured either immediately before the eighth dose of interleukin-2 or immediately before the initiation of pressor support with dopamine hydrochloride. When these values were compared with the pretreatment values, patients showed a significant decrease in mean arterial pressure (92 mm Hg compared with 75 mm Hg; P less than 0.0001), and systemic vascular resistance (15.1 compared with 8.5 mm Hg/L . min; P less than 0.0001), but an increase in heart rate (73 compared with 110 beats/min; P less than 0.0001) and cardiac index (3.1 compared with 4.7 L/min . m2 body surface area; P less than 0.0001). No significant change was noted in pulmonary capillary wedge pressure. Low systemic vascular resistance persisted throughout interleukin-2 therapy. Although blood pressure normalized in 24 hours, the systemic vascular resistance remained below baseline levels 6 days after interluekin therapy had been stopped.
Blood pressure was successfully supported at greater than 90 mm Hg with dopamine hydrochloride or phenylephrine hydrochloride, or both.
Therapy with high doses of interleukin-2 induces hemodynamic changes consistent with a high-output and low-resistance state similar to changes noted during the early phase of septic shock.
确定使用最大耐受剂量的白细胞介素-2和淋巴因子激活的杀伤细胞进行治疗期间发生的血流动力学改变。
病例系列研究。
大学医学中心基于转诊的住院肿瘤服务机构。
连续选取13例转移性结肠癌、恶性黑色素瘤或肾细胞癌患者,这些患者正在接受最大耐受剂量的白细胞介素-2和淋巴因子激活的杀伤细胞治疗。
将平均动脉压、全身血管阻力、心率、肺毛细血管楔压和心脏指数的治疗前变量与在第8剂白细胞介素-2给药前或开始使用盐酸多巴胺进行升压支持前立即测量的相同变量进行比较。当将这些值与治疗前值进行比较时,患者的平均动脉压显著降低(从92 mmHg降至75 mmHg;P<0.0001),全身血管阻力显著降低(从15.1降至8.5 mmHg/L·min;P<0.0001),但心率增加(从73次/分钟增至110次/分钟;P<0.0001),心脏指数增加(从3.1增至4.7 L/min·m²体表面积;P<0.0001)。肺毛细血管楔压未观察到显著变化。在整个白细胞介素-2治疗期间,全身血管阻力持续较低。尽管血压在24小时内恢复正常,但在白细胞介素治疗停止6天后,全身血管阻力仍低于基线水平。
使用盐酸多巴胺或盐酸去氧肾上腺素或两者成功将血压维持在90 mmHg以上。
高剂量白细胞介素-2治疗可诱导血流动力学变化,与高输出和低阻力状态一致,类似于感染性休克早期观察到的变化。