Nwokolo C U, Fitzpatrick J D, Paul R, Dyal R, Smits B J, Loft D E
Department of Gastroenterology, Walsgrave Hospital, Coventry, UK.
Aliment Pharmacol Ther. 1994 Feb;8(1):45-53. doi: 10.1111/j.1365-2036.1994.tb00159.x.
To search for evidence of subclinical neurotoxicity in patients treated with tripotassium dicitrato bismuthate.
Prospective, controlled, triplicate study using urinary bismuth concentration, magnetic resonance imaging (MRI), nerve conduction studies, visual evoked response and a battery of 10 neuropsychological screening tests.
Out-patient clinics, Walsgrave Hospital, Coventry, UK.
Fourteen dyspeptic patients; 8 (treatment group) treated with tripotassium dicitrato bismuthate one tablet q.d.s and 6 (control group) treated with ranitidine 150 mg b.d. for 8 weeks.
Changes in urinary bismuth, MRI, nerve conduction studies, visual evoked response, and neuropsychological tests performed before, immediately after and 8 weeks after the cessation of treatment.
In the treatment group the median (range) urinary bismuth concentration was 1 (1-12) ng/ml before treatment, increased to 560 (140-1300) immediately after treatment (P < 0.01, Wilcoxon Rank Sum test) and was still significantly elevated (23 (7-53) ng/ml) 8 weeks after the cessation of treatment. In the patient who recorded the highest urinary bismuth, a high intensity signal appeared in the globus pallidus immediately after treatment and was still present (though diminished in intensity) 8 weeks after the cessation of treatment. This isolated MRI finding was not associated with evidence of subclinical neurotoxicity. No changes in the MRI, nerve conduction studies, visual evoked response and neuropsychological tests were observed among the other patients studied.
Bismuth accumulation occurs in patients receiving a conventional course of treatment with tripotassium dicitrato bismuthate but this is not associated with significant changes in the nervous system.
探寻接受枸橼酸铋钾治疗的患者出现亚临床神经毒性的证据。
前瞻性、对照、一式三份研究,采用尿铋浓度、磁共振成像(MRI)、神经传导研究、视觉诱发电位以及一套10项神经心理学筛查测试。
英国考文垂沃尔格雷夫医院门诊。
14名消化不良患者;8名(治疗组)接受枸橼酸铋钾治疗,每日4次,每次1片,6名(对照组)接受雷尼替丁治疗,每日2次,每次150毫克,疗程均为8周。
治疗前、治疗结束即刻及治疗结束8周后进行的尿铋、MRI、神经传导研究、视觉诱发电位及神经心理学测试的变化。
治疗组治疗前尿铋浓度中位数(范围)为1(1 - 12)纳克/毫升,治疗结束即刻升至560(140 - 1300)纳克/毫升(P < 0.01,Wilcoxon秩和检验),治疗结束8周后仍显著升高(23(7 - 53)纳克/毫升)。尿铋浓度最高的患者在治疗结束即刻苍白球出现高强度信号,治疗结束8周后该信号仍存在(尽管强度减弱)。这一孤立的MRI表现与亚临床神经毒性证据无关。其他研究患者的MRI、神经传导研究、视觉诱发电位及神经心理学测试均未观察到变化。
接受常规疗程枸橼酸铋钾治疗的患者会出现铋蓄积,但这与神经系统的显著变化无关。