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PubMed2001

Lead poisoning and chelation in a mother-neonate pair.

We report the case of a pregnant woman with chronic lead toxicity and a blood lead of 57 microg/dL (2.7 micromol/L) who gave birth to a healthy-appearing neonate with a cord blood lead of 126 microg/dL (6.08 micromol/L). The mother was prescribed a single course of oral succimer late in the third trimester of pregnancy, without any appreciable change in her blood lead. The neonate was initially treated with intramuscular dimercaprol and intravenous edetate calcium disodium. After 3 days, the neonate was then switched to oral 2,3-dimercaptosuccinic acid because the blood lead had declined. The child received two 19-day courses of 2,3-dimercaptosuccinic acid and had a blood lead level of 21.5 microg/dL (1.04 micromol/L) at 5 months of age. Despite extensive investigation, the precise source of the mother's lead toxicity remained undetermined.

Adult↗
PubMedDate not supplied

Estimation of the body burden of arsenic in a child fatally poisoned by arsenite weedkiller.

A three-year-old child died after ingestion of a mouthful of an estimated 44% sodium arsenite solution. Litigation was initiated based on the quality of emergency treatment at a rural hospital. An issue raised in litigation was whether the child could have survived if he had received an additional dose of BAL (dimercaprol). BAL had been sent for from a neighboring city and arrived approximately 2.0 h after admission. The first 50-mg dose of BAL could have combined with a maximum of 30 mg arsenic; a second dose could have brought the total of chelated arsenic to 60 mg. To determine the total body burden of arsenic in the child, multiple tissues were analyzed. The total body burden was estimated at 113 mg, with 100 mg of this total attributable to the ingested solution. The actual body burden after two doses of BAL therefore would have been at least 40 mg, a fatal level.

Arsenic↗
PubMed1992

Elevated lead levels in a patient with sickle cell disease and inappropriate secretion of antidiuretic hormone.

A five-year-old girl with known sickle cell disease presented with severe hyponatremia and findings compatible with syndrome of inappropriate secretion of antidiuretic hormone (SIADH). She was found to have lead levels in the Class III category. By exclusion, we postulated that the SIADH was in some way related to the high lead levels, since this was the only abnormality the patient exhibited. The toxic lead levels and the elevated vasopressin levels rapidly responded to dimercaprol and calcium EDTA chelation therapy.

Anemia, Sickle Cell↗
PubMed1980

Arsenic poisoning.

Arsenic poisoning continues to require awareness of its diverse clinical manifestations. Industry is the major source of arsenic exposure. Although epidemiologic studies strongly contend that arsenic is carcinogenic, there are little supportive research data. Arsenic poisoning, both acute and chronic, is often overlooked initially in the evaluation of the patient with multisystem disease, but once it is suspected, many accurate methods are available to quantitate the amount and duration of exposure. Treatment with dimercaprol remains the mainstay of therapy, and early treatment is necessary to prevent irreversible complications.

Acute Disease↗
PubMed1995

The efficacy of chelation therapy and factors influencing mortality in lead intoxicated petrol sniffers.

BACKGROUND: The use of chelating agents to treat patients with petrol sniffing encephalopathy has been controversial, since alkyllead additives in petrol are not chelatable. A high mortality has also been reported in hospitalised petrol sniffers. AIMS: (i) Evaluate the efficacy of chelating agents in mobilising lead for excretion and lowering blood lead; (ii) Review factors contributing to mortality in hospitalised petrol sniffers. METHODS: All males chelated between 1992-1993 were studied (n = 20). Blood and urinary lead were measured daily before and during chelation then twice weekly until discharge. Parenteral calcium disodium edetate (EDTA) and dimercaprol (BAL) were administered together, every six hours for five days, seven patients subsequently received oral D-penicillamine until discharge. Clinical details were reviewed for eight patients with petrol sniffing encephalopathy who died between 1990-1994. RESULTS: Urinary lead excretion substantially increased during parenteral chelation (median excretion = 113 microM/5 days, compared with pre-chelation excretion = 1.1 microM/day). Median blood lead concentration fell from 4.83 microM/L (pre-chelation) to 1.91 microM/L (post-chelation). D-Penicillamine did not appear to increase urinary lead excretion appreciably. All eight deaths followed sepsis; five from complications of aspiration pneumonia. CONCLUSIONS: Airway maintenance and management are crucial for survival in these patients. In the short-term, parenteral chelation was effective in mobilising lead for excretion and reducing blood lead in encephalopathic petrol sniffers and was comparable to cases of inorganic lead intoxication. However, as in the treatment of inorganic lead intoxication, the long-term efficacy of chelation for petrol sniffers remains controversial. Prevention strategies against petrol sniffing at a community level are recommended.

Chelating Agents↗
PubMed1960

The antitubercular properties of a series of thiols and sulphides.

The antitubercular activity of a series of thiols, dithiolans, thiol esters, dimercaptopropyl esters, and episulphides has been examined in vitro and in vivo in mice infected with the H(37)Rv strain of Mycobacterium tuberculosis. Most of the thiol compounds were inactive, although dimercaprol (2,3-dimercaptopropanol; B.A.L.) and a few closely related compounds showed slight activity in vivo, the only exception being 2,3-dimercaptopropyl chloride which was very active. The dithiolans were inactive, but some of the thiol esters were moderately active, in particular 2,3-di(acetylthio)propyl acetate and 1,2,3-tri(acetylthio)propane. The majority of the dimercaptopropyl esters had significant activity, the most active compounds being 2,3 - dimercaptopropyl benzoate, 1, 3 - dimercapto - 2 - propyl benzoate, 2, 3 - dimercaptopropyl o-chlorobenzoate, and 2,3-dimercaptopropyl p-chlorobenzoate. All the S-acyl derivatives of 3-mercaptopropylene sulphide had good antitubercular activity, some being more active than streptomycin. The most active compound of the series was 3-(2-furoylthio)propylene sulphide. The activity of the compounds is believed to be due to their conversion in vivo to 3-mercaptopropylene sulphide and not due to the formation of ethanethiol. Slight deviation from the basic structure abolishes antitubercular activity.

Acetates↗
PubMed1969

Uptake of antimony potassium tartrate by mouse liver slices.

1. The uptake of (124)Sb-antimony potassium tartrate by isolated mouse liver slices has been measured and found to establish high tissue: medium concentration ratios.2. Uptake was not influenced by oxygen lack, potassium, ouabain, dinitrophenol or sodium arsenate. It was inhibited by dimercaprol and reduced at low temperature. No evidence was found of counter-transport. After subcellular fractionation, most of the radioactivity was recovered from particulate fractions.3. Kinetic studies of uptake from media containing different concentrations of antimony suggest that uptake is due partly to diffusion and partly to a saturable binding mechanism, probably involving chelation by non-diffusible thiol groups. Saturation studies suggest that only a small proportion of thiol groups bind antimony, the remainder undergoing catalytic oxidation.

Animals↗
PubMed1997

Enhancement of bismuth antibacterial activity with lipophilic thiol chelators.

The antibacterial properties of bismuth are greatly enhanced when bismuth is combined with certain lipophilic thiol compounds. Antibacterial activity was enhanced from 25- to 300-fold by the following seven different thiols, in order of decreasing synergy: 1,3-propanedithiol, dimercaprol (BAL), dithiothreitol, 3-mercapto-2-butanol, beta-mercaptoethanol, 1-monothioglycerol, and mercaptoethylamine. The dithiols produced the greatest synergy with bismuth at optimum bismuth-thiol molar ratios of from 3:1 to 1:1. The monothiols were generally not as synergistic and required molar ratios of from 1:1 to 1:4 for optimum antibacterial activity. The most-active mono- or dithiols were also the most soluble in butanol. The intensity of the yellow formed by bismuth-thiol complexes reflected the degree of chelation and correlated with antibacterial potency at high molar ratios. The bismuth-BAL compound (BisBAL) was active against most bacteria, as assessed by broth dilution, agar diffusion, and agar dilution analyses. Staphylococci (MIC, 5 to 7 microM Bi3+) and Helicobacter pylori (MIC, 2.2 microM) were among the most sensitive bacteria. Gram-negative bacteria were sensitive (MIC, < 17 microM). Enterococci were relatively resistant (MIC, 63 microM Bi3+). The MIC range for anaerobes was 15 to 100 microM Bi3+, except for Clostridium difficile (MIC, 7.5 microM). Bactericidal activity averaged 29% above the MIC. Bactericidal activity increased with increasing pH and/or increasing temperature. Bismuth-thiol solubility, stability, and antibacterial activity depended on pH and the bismuth-thiol molar ratio. BisBAL was stable but ineffective against Escherichia coli at pH 4. Activity and instability (reactivity) increased with increasing alkalinity. BisBAL was acid soluble at a molar ratio of greater than 3:2 and alkaline soluble at a molar ratio of less than 2:3. In conclusion, certain lipophilic thiol compounds enhanced bismuth antibacterial activity against a broad spectrum of bacteria. The activity, solubility, and stability of BisBAL were strongly dependent on the pH, temperature, and molar ratio. Chelation of bismuth with certain thiol agents enhanced the solubility and lipophilicity of this cationic heavy metal, thereby significantly enhancing its potency and versatility as an antibacterial agent.

Antacids↗
PubMed1984

Haemodialysis and charcoal haemoperfusion in acute inorganic mercury poisoning.

A 29-year-old gardener developed acute renal failure following the ingestion of 'Mersil', a combination of mercurous and mercuric chloride, achieving a plasma mercury concentration of 22,000 nmol/litre (400 micrograms/litre). Haemodialysis and charcoal haemoperfusion were ineffective in removing mercury despite prior treatment with the chelating agent dimercaprol. The acute renal failure resolved after 10 days and there are no residual sequelae.

Adult↗
PubMed2004

Suicidal mercury injection into the upper limb: a case study.

We report a rare case of self-injection of mercury into the subcutaneous tissue of the upper limb. A multi-disciplinary management approach was adopted including cooperation between toxicologists, orthopaedic surgeons, radiologists and environment safety personnel. Surgical removal of mercury under radiological screening and systemic intoxication treated by chelating agents, namely dimercaprol and succimer. Serial serum and urine mercury levels showed an initial rise despite surgical removal and returned to normal after a prolonged period of time. Safety precautions were taken during surgery to avoid inadvertent intoxication of staff. Contamination of the operation theatre was monitored by the amount of mercury vapour released into the air. All personnels involved in the management of the patient did not show any evidence of mercury intoxication.

Adult↗
PubMed1990

Evaluation of the efficacy of dimercapto chelating agents for the treatment of systemic organic arsenic poisoning in rabbits.

1 The standard drug for the treatment of arsenic poisoning is BAL (dimercaprol). BAL possesses marked side-effects and a low safety ratio, drawbacks which new BAL analogues, DMPS and DMSA, do not possess. 2 The efficacy of three chelating agents, BAL, DMPS and DMSA, has been evaluated as a treatment for systemic organic arsenic poisoning, induced by intravenous dichloro(2-chlorovinyl)arsine (lewisite) administration to rabbits. Equimolar dosing schedules were used based upon realistic doses for the most toxic agent, BAL. 3 It was concluded that all three dimercapto chelating agents provided significant protection against the lethal systemic effects of lewisite, and, under the test conditions reported here, there was no significant difference between them in therapeutic efficacy. 4 The cause of mortality following intravenous lewisite in treated and untreated rabbits was pulmonary damage. 5 It is considered that DMPS and DMSA are worthy of further study as replacements for BAL in the treatment of systemic poisoning by lewisite.

Animals↗
PubMed2003

Subcutaneous injection of metallic mercury.

Deliberate self-injection of metallic mercury into subcutaneous tissue is uncommon. A 41-year-old lady with a history of schizophrenia was admitted to our hospital after deliberate injection of metallic mercury into her right wrist and antecubital fossa. Physical examination was unremarkable except for the injection marks over right antecubital fossa and wrist. The presence of subcutaneous mercury deposits in her right elbow and wrist was confirmed by X-rays and ultrasound scan. Three days later, erythema, swelling, induration and tenderness were seen over the injection sites. At the operation on day 9, mercury streaks were seen within the brachialis muscle belly, surrounded by friable necrotic tissues along the tract. A similar picture was noted in her right wrist. The necrotic tissues and mercury streaks were removed. The patient had been unco-operative and she only received incomplete treatment with dimercaprol and 2,3-dimercaptosuccinic acid. Her total blood mercury level (normal < 50 nmol/L) decreased from 101-151 nmol/L in the first two weeks to 42 nmol/L 3 months later. Her 24-hour urinary mercury excretion (normal < 10 nmol) changed from 55.7-209.5 nmol in the first 7 weeks to 125.4 nmol 3 months later. This case illustrates that soft tissue metallic mercury can produce local necrosis and may allow continuous absorption with persistent elevations in blood and urinary mercury levels. Therefore, early surgical removal of subcutaneous mercury deposits is required to prevent local complications and minimize the risk of systemic absorption and toxicity.

Adult↗
PubMed1984

Study of the mechanism behind adjuvant action of diethylethoxymethylene malonate enhancing the rectal absorption of cefmetazole and lysozyme.

Diethylethoxymethylene malonate (DEEMM) and diethyl maleate (DEM) enhanced the rectal absorption of cefmetazole in rats when studies were carried out using in vivo, in situ rectal loop and in vitro rectal everted sac method. Since an increase of cefmetazole transport was found when concentration of nonprotein sulfhydryls in rectal tissue was decreased by the presence of either DEEMM or DEM in the study using in vitro everted sac method and the enhancement of cefmetazole absorption by the coadministration of either DEEMM or DEM was suppressed by the treatment with dimercaprol, membrane permeability of rectal tissue seems to be regulated by the concentration of nonprotein sulfhydryls in rectal tissue. On the other hand, it was also found that there were differences between the action of DEEMM and the action of DEM from the following two results: 1) enhancing action of DEEMM was suppressed by the presence of calcium ion in microenema while action of DEM was not so much influenced, and 2) DEEMM enhanced the rectal absorption of lysozyme in rabbits but DEM did not.

Adjuvants, Pharmaceutic↗
PubMed2004

Combined exchange transfusion and chelation therapy for neonatal lead poisoning.

OBJECTIVE: To describe the results of combined exchange transfusion and chelation therapy in a neonate with an elevated blood lead level (BLL). CASE SUMMARY: A 34-year-old Latina woman with a long history of pica (eating glazed pottery) gave birth to a healthy-appearing girl at 40 weeks of gestation. The mother's preconception BLL was 117 microg/dL and remained elevated throughout pregnancy. At parturition, the mother's BLL was 87 microg/dL and the infant's cord BLL was 100 microg/dL. The infant underwent single-volume exchange transfusion within 12 hours of birth. BLL was 28 microg/dL following the exchange, and a 5-day course of chelation with dimercaprol and CaNa2 ethylenediamine tetraacetic acid was initiated at 36 hours of life. The infant's BLL was 37 microg/dL at the end of inpatient chelation. DISCUSSION: Long-term neurologic disability from in utero lead exposure is well described, but the optimal treatment of elevated neonatal BLLs in healthy-appearing infants at the time of birth is not established. This strategy of combined chelation and exchange transfusion therapy was well tolerated and resulted in decreased lead levels, but the long-term neurologic efficacy of our combination strategy remains to be seen. CONCLUSIONS: Combined exchange transfusion and chelation therapy resulted in rapidly decreased lead levels in a neonate with chronic in utero lead exposure.

Adult↗
PubMed1979

Acute respiratory failure following severe arsenic poisoning.

A 47-year-old man had an episode of severe respiratory failure after acute intoxication with arsenic. Features of the initial clinical presentation included nausea, vomiting, and diarrhea, acute psychosis, diffuse skin rash, and marked pancytopenia. A peripheral neuropathy then developed which resulted in severe weakness of all muscles of the limbs, the shoulder and pelvis girdles, and the trunk. The neuropathy continued to progress despite treatment with dimercaprol (BAL in oil). Five weeks after the initial exposure, the patient was no longer able to maintain adquate ventilation and required mechanical ventilatory support. Improvement in the patient's neuromuscular status permitted successful weaning from the ventilator after one month of mechanical ventilation. Long-term follow-up revealed no further respiratory difficulty and slow improvement in the strength of the peripheral muscles.

Arsenic Poisoning↗
PubMed2000

Cupric sulfate intoxication with rhabdomyolysis, treated with chelating agents and blood purification.

We report a case of cupric sulfate intoxication complicated by hemolytic anemia, hepato-renal damage and acute rhabdomyolysis. The patient was successfully treated with dimercaprol, penicillamine, direct hemoperfusion and hemodiafiltration. We discuss the pathophysiology of cupric intoxication, and propose a treatment combined with chelating agents and blood purification.

Acute Disease↗
PubMed1979

Atempted homicide with arsenic.

An unusual method of introducing arsenic to water with homicidal intentions, where five members of the same family were poisoned, is reported. The obvious initial diagnosis of food poisoning or food allergy was reviewed when the story of noticing an unusual substance in the well was revealed. The patients recovered fully after conventional intramuscular dimercaprol.

Adult↗
PubMed1982

Methoxyethylmercury chloride poisoning: clinical findings and in vitro experiments.

A patient attempting suicide ingested 5682 mg methoxyethylmercury chloride, which corresponds to 4375 mg mercury. The bulk of the dose was eliminated by vomiting and gastric rinsing. About 706 to 977 mg mercury were absorbed in the gastrointestinal tract. Only 11.2 mg mercury could be removed by two activated charcoal hemoperfusions. Chelating agents were given for 12 weeks. The terminal elimination half-life calculated from blood and urine mercury levels was 23 and 25 d, respectively. No toxic effects on the kidneys and central nervous system were seen. The identification of methoxyethylmercury chloride in the gastric rinsing fluid was done by gas chromatography/mass spectrometry. The protein binding of methoxyethylmercury chloride was determined by ultrafiltration (93%). In the presence of dimercaprol sulfonate and penicillamine, protein binding was 83 and 88%, respectively. Activated charcoal and amberlite hemoperfusion revealed equal in vitro clearances for methoxyethylmercury chloride (62 mL/min at a flow rate of 80 mL/min).

Dimercaprol↗