[Measurement of sulfhemoglobin (S-Hb) blood levels to determine individual hydrogen sulfide exposure in thermal baths in Italy]. / La concentrazione di solfo-emoglobina presente nel sangue è una misura affidabile dell'esposizione individuale a vapori solfurei: il caso degli stabilimenti idrotermali in Italia.

Significant exposure to hydrogen sulfide may occur in workers at sulphureous thermal baths. Work-related exposure to hydrogen sulfide may be shown by measuring sulfhemoglobin (S-Hb) blood levels. In this study we measured S-Hb blood levels in two groups of workers at two different thermal baths and compared these with hydrogen sulfide concentrations in the air of the two work environments. Our results show that blood S-Hb levels can be considered a reliable measure of individual exposure to hydrogen sulfide.

A Case of Pendipronil(R) Poisoning Treated by Hemoperfusion and Methylene Blue / 대한신장학회잡지

Pendipronil(R) overdose is uncommon in Korea. Pendipronil(R) is a selective herbicide used to control most annual grasses and certain broadleaf weeds in field corn, potatoes, rice, etc. and is the substance including pendimethalin and propanil. Pendimethalin is slightly to practically nontoxic by ingestion but may be mildly to moderately irritating to the linings of the mouth, nose, throat, and lungs. Propanil toxicity is evidenced by varying clinical pictures ranging from deep cyanosis in an otherwise alert normal appearing individual to restlessness, dyspnea, extensive hemolytic anemia, methemoglobinemia, sulfhemoglobinemia and serious central nervous system dysfunction. For the treatment of methemoglobinemia, gastric lavage, activated charcoal, methylene blue and exchange transfusion should be used. We experienced a case of acute massive Pendipronil(R) intoxication in 31 years old woman due to voluntary ingestion of 48g of this drug as a suicide attempt. A moderate methemoglobinemia developed, accompanied by drowsy mental status, nausea, vomiting, headache, intensive cyanosis. The patient recovered completely after intravenous methylene blue injection and cellulose coated hemoperfusion charcoal (Adsorba 300C(R)) and conservative treatment.

An adolescent case of sulfhemoglobinemia associated with high-dose metoclopramide and N-acetylcysteine.

We describe the case of an adolescent girl who received high-dose metoclopramide in combination with oral N-acetylcysteine therapy for acute acetaminophen toxicity. Whole blood-sample analysis for abnormal hemoglobin pigments established the diagnosis of sulfhemoglobinemia. Metoclopramide has been shown to cause sulfhemoglobinemia, particularly when used in repeated high doses. Although N-acetylcysteine alone has not been associated as the cause, we suggest that sulfhemoglobine-mia is a potential complication in patients treated with metoclopramide for the nausea that often accompanies oral N-acetylcysteine therapy for acetaminophen toxicity. Cyanosis without respiratory distress should suggest this diagnosis.

Topical anesthetic-induced methemoglobinemia and sulfhemoglobinemia in macaques: a comparison of benzocaine and lidocaine.

Benzocaine (BNZ) and lidocaine (LC) are commonly used topical (spray) anesthetics approved for use in humans. Benzocaine has structural similarities to methemoglobin (MHb)-forming drugs that are current candidates for cyanide prophylaxis, while LC has been reported to increase MHb in man. In this study, we compared MHb and sulfhemoglobin (SHb) production in three groups of Macaques (Chinese rhesus and Indian rhesus (Macaca mulatta) and pig-tailed macaques (Macaca nemestrina)) after exposure to BNZ and LC. Formation of SHb, unlike MHb, is not thought to be reversible and therefore is considered to be of greater toxic significance. Both MHb and SHb levels were measured periodically on a CO-Oximeter. All rhesus macaques (n = 8) were administered an intratracheal/intranasal) dose of 56 mg (low dose) or 280 mg (high dose) of BNZ or 40 mg of LC in a randomized cross-over design (all animals received all three treatments). Pig-tailed macaques (n = 6) were given an intranasal dose of 56 mg of BNZ and 40 mg of LC. As no differences in the peak MHb or time to peak (mean +/- SD) were observed among the three macaque subspecies, the data were pooled. Lidocaine did not cause MHb or SHb formation above baseline in any monkey. In contrast, all monkeys (n = 14) had a significant elevation in peak MHb formation after 56 mg of BNZ, which ranged from 4.0% to 19.4% with an average of 8.6 +/- 4.0% (mean +/- SD), with peak MHb levels reached at 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)