Effect of glutathione on the cadmium chelation of EDTA in a patient with cadmium intoxication.

In order to evaluate the efficiency and renal protective effects of glutathione during Ca(++)-EDTA chelation therapy for chronic cadmium intoxication, we measured the renal excretion of cadmium, ß(2)-microglobulin, proteinuria, and hematuria during intravenous administration of glutathione with Ca(++)-EDTA in a 54-year-old patient with chronic cadmium intoxication. We administered 500 mg of Ca(++)-EDTA and 50 mg/kg of glutathione alone or in 1 L of normal saline over the next 24 hours and repeated this over 12 consecutive days. During the first 3 days, the basal levels (only saline administration) were determined; during the second 3 days, Ca(++)-EDTA only was administered, for the third sequence of 3 days, Ca(++)-EDTA with glutathione was provided, and for the last 3 days, glutathione alone was given. One month later, the same protocol was repeated. There were six blood and urine samples to analyze in each group. The blood cadmium level was higher when the EDTA was infused together with glutathione (7.44 ± 0.73 µg/L, p < 0.01) compared to the basal level of 4.6 ± 0.44 µg/L. Also, the renal cadmium excretion was significantly higher in the EDTA with glutathione group than in the basal group (23.4 ± 15.81 µg/g creatinine vs 89.23 ± 58.52 µg/g creatinine, p < 0.01). There was no difference in the protein/creatinine and ß(2)-microglobulin/creatinine ratio in the urine (p > 0.05) among the groups. Furthermore, microhematuria and proteinuria did not develop over the observation period of 6 months. These results suggest that glutathione administration with EDTA might be an effective treatment modality for patients with cadmium intoxication.

Factors for determining survival in acute organophosphate poisoning.

BACKGROUND/AIMS: Organophosphate poisoning has a high mortality rate. Recently, differences among organophosphorus insecticides in human self-poisoning were reported. This study investigated the prognostic risk factors and the mortality of different organophosphates following acute organophosphate poisoning. METHODS: This retrospective study included 68 patients with acute organophosphate poisoning. We investigated patient survival according to initial parameters, including the initial Acute Physiology and Chronic Health Evaluation (APACHE) II score, serum cholinesterase level, and hemoperfusion and evaluated the mortality according to organophosphate types. RESULTS: Thirteen of the 68 patients died. The agents responsible for mortality were different. The APACHE II score was a significant predictor of mortality (odds ratio [OR], 1.194; p<0.01; 95% confidence interval [CI], 1.089 to 1.309) and respiratory failure (OR, 1.273; p<0.01; 95% CI, 1.122 to 1.444). The mortality was 0% for dichlorvos, malathion, chlorpyrifos and profenofos. However, other organophosphates showed different mortality (16.7% for O-ethyl-O-4-nitrophenyl phenylphosphonothioate, 25% for phenthoate, 37.5% for phosphamidon, 50% for methidathion). The usefulness of hemoperfusion appears to be limited. CONCLUSIONS: The initial APACHE II score is a useful prognostic indicator, and different organophosphates have different mortality.

Marked recovery from paraquat-induced lung injury during long-term follow-up.

BACKGROUND/AIMS: Paraquat-induced lung injury has been considered a progressive and irreversible disease. The purpose of this study was to report the long-term evolution of lung lesions in eight survivors with significant paraquat-induced lung injuries who could be followed-up for longer than 6 months. METHODS: We retrospectively examined high-resolution computed tomography and pulmonary function test of eight survivors with significant paraquat-induced lung injurys. RESULTS: High-resolution computed tomography revealed a predominant pattern of irregularly shaped consolidation with traction bronchiectasis at 1-2 months after paraquat poisoning, a mixed pattern of irregularly shaped consolidation and ground-glass opacity at 3-12 months, and a mixed pattern of consolidation, ground-glass opacity, and honeycombing at 1-2 years. At 3-12 months after paraquat ingestion, the areas of consolidation had markedly decreased and the decreased lung volume had returned to normal. At 1-2 years after paraquat poisoning, the cystic changes had disappeared. At 2-3 years after paraquat poisoning, the decrease in forced vital capacity had greatly improved to the normal range. CONCLUSIONS: Recovery of nearly normal pulmonary structure and function may occur over several years following paraquat poisoning. Pulmonary function (both forced vital capacity and forced expiratory volume in 1 sec) evolved toward normal in the long-term survivors of paraquat poisoning with initial prominent lung injuries.