Cu. Nwokolo et al., LACK OF EVIDENCE OF NEUROTOXICITY FOLLOWING 8 WEEKS OF TREATMENT WITHTRIPOTASSIUM DICITRATO BISMUTHATE, Alimentary pharmacology & therapeutics, 8(1), 1994, pp. 45-53
Objective: To search for evidence of subclinical neurotoxicity in pati
ents treated with tripotassium dicitrato bismuthate. Design: Prospecti
ve, controlled, triplicate study using urinary bismuth concentration,
magnetic resonance imaging (MRI), nerve conduction studies, visual evo
ked response and a battery of 10 neuropsychological screening tests. S
etting: Out-patient clinics, Walsgrave Hospital, Coventry, UK. Subject
s: Fourteen dyspeptic patients; 8 (treatment group) treated with tripo
tassium dicitrato bismuthate one tablet q.d.s and 6 (control group) tr
eated with ranitidine 150 mg b.d. for 8 weeks. Main outcome measures:
Changes in urinary bismuth, MRI, nerve conduction studies, visual evok
ed response, and neuropsychological tests performed before, immediatel
y after and 8 weeks after the cessation of treatment. Results: In the
treatment group the median (range) urinary bismuth concentration was 1
(1-12) ng/ml before treatment, increased to 560 (140-1300) immediatel
y after treatment (P < 0.01, Wilcoxon Rank Sum test) and was still sig
nificantly elevated (23 (7-53) ng/ml) 8 weeks after the cessation of t
reatment. In the patient who recorded the highest urinary bismuth, a h
igh intensity signal appeared in the globus pallidus immediately after
treatment and was still present (though diminished in intensity) 8 we
eks after the cessation of treatment. This isolated MRI finding was no
t associated with evidence of subclinical neurotoxicity. No changes in
the MRI, nerve conduction studies, visual evoked response and neurops
ychological tests were observed among the other patients studied. Conc
lusions: Bismuth accumulation occurs in patients receiving a conventio
nal course of treatment with tripotassium dicitrato bismuthate but thi
s is not associated with significant changes in the nervous system.