Treatment of adult lead poisoning with D-penicillamine.

Background The aim of the current study was to evaluate the efficacy of D-penicillamine in the treatment of lead poisoning mainly in the outpatient setting. Methods In a case series study performed during the recent epidemic of lead poisoning in Iran, lead-poisoned patients referring to our outpatient clinic were treated with 250-mg D-penicillamine capsules administered every 6 h for 5 or 10 days based on availability of the medication. They were recommended to re-check blood lead level (BLL) 4 weeks after cessation of the treatment and refer to our clinic again. Results In 63 patients with lead poisoning but without signs and symptoms of lead encephalopathy, median BLL was 106 [84, 131] µg/dL on presentation, which declined to a mean of 52.6 ± 28.8 µg/dL after a median treatment period of 7 [5, 10] days (p < 0.001). There was no statistically significant difference between the 5- and 10-day treatment protocols regarding complications and recovery. Treatment had resulted in a median decrease of 54 µg/dL [33, 90] (range: -20 to 231 µg/dL) in the patients' BLLs (33.9% declined in BLL measurements; range: -29.69% to 99.06%). Conclusions D-penicillamine may be an acceptable substitute treatment in adult lead poisoning. Although our sample size was limited, we could not detect any serious adverse effects in our cases showing that D-penicillamine resulted in acceptable recovery rates. This may be helpful especially in epidemics with limitations in antidote access.

Inhibition of glucose-6-phosphate dehydrogenase protects hepatocytes from aluminum phosphide-induced toxicity.

Aluminum phosphide (AlP) poisoning is a severe toxicity with 30-70% mortality rate. However, several case reports presented AlP-poisoned patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency and extensive hemolysis who survived the toxicity. This brought to our mind that maybe G6PD deficiency could protect the patients from severe fatal poisoning by this pesticide. In this research, we investigated the protective effect of 6-aminonicotinamide (6-AN)- as a well-established inhibitor of the NADP+- dependent enzyme 6-phosphogluconate dehydrogenase- on isolated rat hepatocytes in AlP poisoning. Hepatocytes were isolated by collagenase perfusion method and incubated into three different flasks: control, AlP, and 6-AN+ALP. Cellar parameters such as cell viability, reactive oxygen species (ROS) formation, mitochondria membrane potential collapse (MMP), lysosomal integrity, content of reduced (GSH) and oxidized glutathione (GSSG) and lipid peroxidation were assayed at intervals. All analyzed cellular parameters significantly decreased in the third group (6-AN+AlP) compared to the second group (AlP), showing the fact that G6PD deficiency induced by 6-AN had a significant protective effect on the hepatocytes. It was concluded that G6PD deficiency significantly reduced the hepatotoxicity of AlP. Future drugs with the power to induce such deficiency may be promising in treatment of AlP poisoning.

Toxic megacolon as a rare complication following atropine therapy due to organophosphate poisoning: A case report.

The main therapeutic basis for a case of organophosphate poisoning is a combination therapy which includes atropine as an anticholinergic drug and pralidoxime. If the poisoning is severe, a high dose of this combination of medicines may be needed, but this may cause serious side effects: paralytic ileus or even megacolon; however, these gastrointestinal events are very rare. Here, we report a case of organophosphate poisoning where atropine therapy was given and led to drug-associated toxic megacolon.

Lithium Toxicity in a Pregnant Woman.

Lithium is recommended in bipolar disorder and can be accompanied by significant toxicity in pregnant women. A 25-year-old single-gestation pregnant woman (28 weeks) was referred with suspicion of lithium toxicity. Serum lithium was 2.1 meq/L. Despite conservative therapy with intravenous fluids, lithium concentration increased to 5.0 meq/L 6 hr after admission mandating an emergent haemodialysis during which foetal heart rate decreased to 90 bpm. The gynaecologist ordered termination of pregnancy while the mother was still on haemodialysis. Caesarean section was carried out, but the born baby had an apgar of 2 and died. Autopsy findings of the foetus revealed a cord blood lithium concentration of 4.8 mEq/L with no physical abnormalities. Although the foetus had the signs/symptoms of distress, continuation of haemodialysis could probably have saved it as it saved its mother's life. In lithium toxicity in a pregnant woman, it is reasonable to continue haemodialysis even with the signs and symptoms of foetal distress. In similar situations, emergency haemodialysis instead of immediate caesarean section should be considered.