Thallium poisoning is a rare condition that is often misdiagnosed, delaying appropriate treatment. Left untreated, thallium toxicity can permanently damage the nervous and digestive systems or, in severe cases, lead to paralysis and death. It is most often treated by an oral administration of Prussian blue. Thallium has a long physiological half-life, and Prussian blue cannot sequester thallium outside the digestive tract. Therefore, the first priority in treating severe thallium poisoning is to lower blood levels as soon as possible. We report the case of a patient with supralethal blood levels of thallium treated successfully using combined hemoperfusion (HP) and continuous veno-venous hemofiltration (CVVH). Three rounds of HP alone decreased blood thallium levels by 20.2%, 34.8%, and 32.2%, while each of the five subsequent rounds of CVVH reduced thallium blood levels by 63.5%, 64.2%, 42.1%, 18.6%, and 22.6%. The reversal of symptoms and prevention of lasting neurological damage indicates that HP, CVVH, 2,3-dimercaptopropane-1-sulfonate, neuroprotective agents along with supportive therapy were used successfully to treat a case of severe thallium poisoning.

1 The potential for a drug interaction between cyclosporin A and midazolam was investigated since both compounds appear to be metabolized by the same cytochrome P-450 isoenzyme. 4 The pharmacokinetics of a single intravenous dose of midazolam (0.075 mg kg-') was studied in nine patients receiving cyclosporin A to prevent rejection of their transplanted kidneys. The average steady state blood concentrations of cyclosporin A, measured by r.i.a. using a specific monoclonal antibody, varied during a dosing interval between 175 and 600 ng ml-'.5 In these patients the hepatic elimination of midazolam was characterized by a mean t½, (± s.d.) of 2.3 ± 1.2 h and a plasma clearance (CL) of 414 ± 95 ml min-'. These values were not different from those of normal human subjects (t,, = 1.5 to 4 h, CL = 350 to 700 ml min-').6 From the results of the in vitro experiments it is concluded that cyclosporin A may potentially inhibit drug metabolism. However, therapeutic blood concentrations in vivo do not appear to be sufficient to result in an effective impairment of the hepatic elimination of midazolam when given concomitantly.