D‐penicillamine does not increase urinary bismuth excretion in patients treated with tripotassium dicitrato bismuthate.

Abstract

Twenty‐four urinary bismuth excretion was measured in five patients who had been treated with tripotassium dicitrato bismuthate, before and after single 1 g oral dose of D‐penicillamine. Before dosing with D‐ penicillamine, the median 24 h urinary bismuth output was 55 micrograms 24 h‐1 (range 17‐156 micrograms 24 h‐1) and following dosing with D‐ penicillamine the median 24 h urinary bismuth output was 53 micrograms 24 h‐1 (range 12‐156 micrograms 24 h‐1). D‐penicillamine does not facilitate the urinary excretion of bismuth, hence it is unsuitable for use as an oral chelator in patients with bismuth intoxication.

Bismuth

“…At 2 hours after a single dose of 108 mg Bi as colloidal subcitrate, plasma levels in two volunteers were measured as 1.62 and 24.7 mg L À1 (Versieck et al 1992), while steady-state plasma levels after treatment for 4 -8 weeks ranged between 3 and 58 mg L À1 (Serfontein 1979). Urine levels were significantly increased at the end of treatment, from 100 -130 mg L À1 to 530 mg L À1 (Nwokolo et al 1990). Bowen (1979) reported that 160 mg Bi per day was lethal to rats.…”

“…Except for one patient, all values were < 0.24 mmol L À1 . Leonhardt and Klotz (1991) identified blood lower levels in treatments with Bi subgallate/nitrate (plasma level 60 mg L À1 ), Bi subsalicylate (plasma levels < 6 mg L À1 ) (Raedesch et al 1990, Nwokolo et al 1990), or Bi subnitrate (< 30 mg L À1 ) (Conso et al 1975). Bismuth subcitrate, in different forms, is the most extensively studied bismuth compound.…”

“…Bismuth subcitrate, in different forms, is the most extensively studied bismuth compound. "Alarm" levels can be exceeded for a short time after investigation, without toxic consequences (Nwokolo et al 1990, Raedesch et al 1990, Nwokolo et al 1990). At 2 hours after a single dose of 108 mg Bi as colloidal subcitrate, plasma levels in two volunteers were measured as 1.62 and 24.7 mg L À1 (Versieck et al 1992), while steady-state plasma levels after treatment for 4 -8 weeks ranged between 3 and 58 mg L À1 (Serfontein 1979).…”

“…According to Arena (1974), dimercaprol (British Anti-Lewisite; BAL) and D-penicillamine are either questionable (Slikkerveer and de Wolff 1989, Nwokolo and Pounder 1990, Goule et al 1975 or contradictory (Liessens et al 1978) in the treatment of bismuth toxicity. In severe bismuth poisonings, BAL and 2,2-dimercaptolpropane-1-sulfonate (DMPS) seemed to be successful (Molina et al 1979, Playford et al 1990).…”

“…Blood concentrations of Bi in asymptomatic subjects were well below the currently stated upper safe limit of 0.24 mmol L À1 (50 mg L À1 ) (see Table 5.3). Other authors reported blood levels of 1 mg L À1 (Lee 1981), < 3 mg L À1 (Bruce and Vouk 1986), 1 -9 mg L À1 (Dekker et al 1986); and in serum, levels of 4.2 mg L À1 (Iffland 1993),~2 mg L À1 (Nwokolo et al 1990), < 0.5 mg L À1 (Raedesch et al 1990), and < 1 mg L À1 (range 1 -8 mg L À1 ) (Nwokolo et al 1991). The highest mean concentration in healthy human tissue (400 mg kg À1 wet weight) was found in the kidney, followed by bone (< 200 mg kg À1 ).…”