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PubMed1987

Meso-2,3-dimercaptosuccinic acid in the diagnosis and treatment of lead poisoning.

Lead poisoning remains one of the hazards of industrialized civilization. CaNa2 EDTA and dimercaprol, the usual therapeutic measures, have many side effects and can be given by parenteral route alone. The authors present a case of chronic lead poisoning caused by ingestion of contaminated flour ground in a primitive flour mill. The diagnosis was confirmed by the CaNa2 EDTA provocative test. Dimercaptosuccinic acid (DMSA) was given orally as a further provocation and resulted in an 11-fold increase in urinary lead excretion. A 5-day course of treatment with DMSA was instituted, during which symptoms abated, urinary lead excretion increased and the blood lead level decreased. No side effects were noticed. There has been no relapse over several months of follow-up. The authors conclude that the oral use of DMSA is effective, safe and convenient both as a provocative test in establishing the diagnosis of lead poisoning and as a therapeutic tool.

Adult↗
PubMed2000

Lightening the lead load in children.

More than 4 percent of preschool-aged children in the United States have blood lead levels above 10 microg per dL (0.50 pmol per L), and these levels have been associated with a decline in IQ. The Centers for Disease Control and Prevention advocates the use of a screening questionnaire to identify lead exposure or toxicity in all children. Primary prevention through the removal of lead from gasoline and paint has led to a reduction of blood lead levels in children. Secondary prevention through paint hazard remediation is effective in homes that have a high lead burden. Children with lead levels of 45 to 69 microg per dL (2.15 to 3.35 pmol per L) should receive chelation therapy using succimer (DMSA) or edetate calcium disodium (CaNa2EDTA). Use of both CaNa2EDTA and dimercaprol (BAL in oil) is indicated in children with blood lead levels higher than 70 microg per dL (3.40 micromol per L). Current treatment recommendations are based on the reduction of blood lead levels, which may not represent a significant overall reduction of the lead burden. Clinical trials of existing agents are needed to determine patient-oriented outcomes, such as the effect on IQ.

Body Burden↗
PubMed2000

Antidote availability in Quebec hospital pharmacies: impact of N-acetylcysteine and naloxone consumption.

OBJECTIVES: To study the availability of 13 specific antidotes in hospitals and correlate the availability of those antidotes to the number of poisonings seen in hospitals using N-acetylcysteine and naloxone consumption as a surrogate. METHODS: Pharmacy directors of hospitals with an emergency department were surveyed for number of adequately stocked antidotes (N-acetylcysteine, ethanol, cyanide antidote kit or hydroxycobalamine, deferoxamine, digoxin-immune FAB, dimercaprol, flumazenil, glucagon, methylene blue, naloxone, physostigmine, pralidoxime and pyridoxine). RESULTS: Data were obtained from 96 of 112 (86%) of the pharmacies surveyed. Number of adequately stocked antidotes per hospital ranged from zero to nine of 13. There was a correlation between all hospital characteristics evaluated and the number of adequately stocked antidotes (P<0.05). Correlations between the number of adequately stocked antidotes and the amount of N-acetylcysteine and naloxone consumed were significant (rs=0.58, P<0.001; r(s)=0.53, P<0.001). The amount of N-acetylcysteine consumed, the number of annual visits to the emergency department and the number of hours of pharmacy coverage on weekends independently predicted the presence of adequately stocked antidotes. CONCLUSIONS: Larger hospitals are more likely to have adequate stocks of antidotes. Adequate stocking of antidotes is significantly correlated with the amount of N-acetyl- cysteine and naloxone consumed. This suggests that hospitals more likely to see serious acetaminophen and opiate poisonings are more likely to maintain adequate stocks of antidotes.

Acetylcysteine↗
PubMed2002

[Serum and urine total arsenic concentration in a case of acute arsenic intoxication].

The 68-year-old man took arsenic pasta 1 g (arsenic trioxide 0.45 g) to commit suicide and was admitted 16 hours after ingestion. He developed vomiting and coma, followed by pancytopenia. He was treated with activated charcoal, laxative, dimercaprol, sodium thiosulfate and direct hemoperfusion with good recovery. Total arsenic concentrations in serum and urine were 39 ng/ml and 89 ng/ml on admission, respectively. Urine arsenic concentration showed the second peak around 48 hours after admission.

Acute Disease↗
PubMed2003

[Metal poisoning].

Metals are amongst the oldest toxic substances known to man. In today's industrialized world the sources of exposure to metals are ubiquitous both in the field of work and from polluted water, foodstuffs and the environment. Their toxicity is characterized by the metallic element in question, but this is modified by the type of compound, whether organic or inorganic, and its characteristics of hydrosolubility and liposolubility, which determines its toxicokinetics and thus the possibilities of it reaching its targets. The biomolecules most affected by metals are the proteins with enzymatic activity, which is why their pathology is multisystemic. The principal systems affected are the gastrointestinal, central and peripheral neurological, haematic and renal. Some metallic compounds are carcinogenic. Metals's treatment is conditioned by their chemical reactivity. They can be deactivated and eliminated by the administering of chelating agents that produce complex molecules, which are non-toxic and can be excreted. The principal chelating agents are: BAL (British Anti-Lewisite or dimercaprol) DMPS (2,3-Dimercapto-1-propanesulfonic Acid) and DMSA (meso-2,3-Dimercaptosuccinic or Succimer), EDTA, Penicilamine (b,b-dimethylcysteine) and Deferoxamine. Toxicokinetic characteristics, mechanism of action, clinical picture and treatment of some of the most relevant metals and metalloids: lead, mercury and arsenic, are considered.

Acute Disease↗
PubMed1992

Somatostatin depleting potency of cysteamine-related thiols and amines in the rat: structure-activity relation.

Cysteamine, a potent duodenal ulcerogen, stimulates gastric acid and gastrin secretion and decreases immunoreactive somatostatin (IRS) from the gut and hypothalamus of the rat. To elucidate the structural requirements for this effect, we tested a series of cysteamine analogs for their IRS decreasing activity in comparison with their nucleophilic and reducing potencies. Adult female rats were sacrificed 4 hr after p.o. administration of the test chemicals given in molar equivalents to 30 mg/100 g of cysteamine-HCl. IRS decreasing activity in gastric mucosa, expressed as percentage of controls is listed in descending order: cystamine (55%), cysteamine (59%), 2-dimethylaminethanethiol (59%), ethylamine (66%), 1,3-propanedithiol (70%), propylamine (75%) and 3-aminothiophenol (79%). The following thiols and amines had no IRS decreasing effect (80% of controls): L-cysteine, ethanethiol, 1-propanethiol, penicillamine, dimercaprol, 1-4-dithiothreitol, ethanolamine, propionitrile, n-butyronitrile, o-, m- or p-aminophenol. The aryl 2-, 3- or 4-aminothiophenols, unlike most of their aminophenol analogs also decreased immunoreactive prolactin in the pituitary by 38 to 78%. IRS decreasing activity was independent of the reducing potency of cysteamine derivatives but was correlated significantly (r = 0.793, P < .01) with electron affinity of -SH, -NH2, -OH and -CN radicals in terminal alkyl chemicals. The structural requirement for decreasing activity is the presence of either -SH and -NH2 on a 2 to 3 carbon alkyl or aryl molecule. Both radicals when present together increase potency.(ABSTRACT TRUNCATED AT 250 WORDS)

Amines↗
PubMed2003

[Acute poisoning caused by intravenous arsenic].

INTRODUCTION: During acute sodium arsenite intoxication, absorption is usually oral and rarely respiratory. We report the first case of acute intoxication by intravenous administration, with pharmacokinetic modelling. OBSERVATION: A 38 year-old man had attempted suicide by injecting a solution of sodium arsenite. The first symptoms upon admission to an emergency unit were hypotension, electrocardiographical disorders with prolonged QT and aqueous diarrhoea. Dimercaprol therapy was immediately set-up but was stopped on 48 hours later because of acute renal failure. Eleven successive blood and urine samples were drawn. Hairs and nails were sampled at the 130th hour. Results of the confirmed the elevated arsenic concentrations in all the samples. The pharmacokinetic parameters were computed following a two-compartment model with intravenous administration and with elimination from the central compartment. DISCUSSION: During this acute intravenous induced arsenic poisoning, the symptomatology was comparable to that following oral intoxication. The chelating treatment, although rapidly suspended, obviously contributed to survival. The eventual occurrence of other cases should permit the adaptation of therapeutic protocols to these types of intoxication.

Adult↗
PubMed1977

An extrarenal source of "renin-like" activity in anephric man.

To examine extrarenal sources of "renin-like" activity plasma was obtained from 19 anephric males. Plasma renin activity (PRA), concentration (PRC) (obtained after addition of exogenous renin substrate) and total renin concentration (TRC) (obtained after acid-activation of plasma and subsequent incubation with exogenous renin substrate) demonstrated values for several anephric patients comparable or above those seen in plasma from 10 normal subjects. Incubation of untreated plasma (PRA and PRC) and acid-dialyzed plasma (TRC) for angiotensin I generation was performed at pH 7.5, at 37 degrees C with EDTA, dimercaprol, and 8-OH-quinoline as angiotensinase and converting enzyme inhibitors. The pH optimum for acid-activation of TRC in anephric plasma was the same as that in normal plasma (pH 3.3). Molecular weight determinations following Sephadex gel chromatography demonstrated that the renin-like enzyme in normal plasma had a molecular weight of about 42,000 before and after acid-activation, while that in anephric plasma had a molecular weight of approximately 61,000. A saliva sample from one anephric subject with the highest levels of PRA, PRC, and TRC in plasma also demonstrated measurable amounts of PRA, PRC, and TRC. The molecular weight of this salivary "renin-like" activity also was 61,000. These observations suggest a possible extrarenal source of "renin-like" activity in anephric man. The physiological significance of these studies remains to be clarified.

Adolescent↗
PubMed1992

Development of a therapeutic procedure for bismuth intoxication with chelating agents.

Although bismuth poisoning is still a rare phenomenon, the increasing use of bismuth-containing drugs warrants a systematic approach to the treatment of bismuth overdose. An effective method of enhancing the elimination of toxic amounts of bismuth from the body has not been reported. Therefore we performed a study to select the best chelator to treat bismuth poisoning. Dimercaprol (BAL), meso-2,3-dimercaptosuccinic acid (DMSA), D,L-2,3-dimercapto-propane-I-sulfonic acid (DMPS), D-penicillamine (D-PEN), N-acetyl-D,L-penicillamine (Ac-PEN), thiopronine (TP), sodium-calcium edetate (EDTA) and deferoxamine (DFO) were tested with an in vitro model of equilibrium dialysis and an in vivo model of rats poisoned with bismuth. The rats (n = 6 per substance tested) were treated with the chelators in intraperitoneal doses of 250 mumol/kg.day for 3 consecutive days. Afterward, tissue and blood samples were collected. Bismuth concentrations were determined with electrothermal atomic absorption spectrometry in serum, buffer, urine, blood, brain, kidney, liver, spleen, and bone. Using in vitro results, we constructed a ranking of chelating agents; it appeared not to predict the in vivo results. The dithiol compounds (DMPS, DMSA and BAL) were effective in most organs (especially in kidney and liver) resulting in a higher elimination of bismuth in urine by DMPS and BAL. BAL was the only chelator effective in lowering brain bismuth concentrations, whereas treatment with EDTA resulted in increased brain bismuth levels. For D-PEN and DFO, no effects could be demonstrated. For clinical practice, DMSA and DMPS may well be the chelators of choice; the application of BAL should be reserved for very severe cases of poisoning because of its own toxicity.

Animals↗
PubMed2006

Management of metallic mercury injection in the hand.

This case report discusses a patient who injected 20 mL of metallic mercury subcutaneously in his left hand during an attempted suicide. The blood mercury level was 118 microg/L and the urinary mercury level was 43 microg/L, which confirmed the diagnosis of metallic mercury poisoning. A good result was obtained in this patient and the local and systemic toxicity and its management are discussed. A chelation therapy with dimercaprol and early surgical excision of injected material are recommended because this treatment effectively lowers mercury blood levels and controls the local inflammatory reaction. Intraoperative fluoroscopy is useful to confirm the extent of removal.

Aged↗
PubMed1991

Arsenic poisoning in livestock.

Arsenic is an important heavy metal intoxicant to livestock. Arsenical pesticides present significant hazards to animal health. The toxicity of arsenic varies with several factors--its chemical form, oxidation states, solubility. The phenylarsonic compounds are the least toxic and are used as feed additives in swine and poultry rations. However, roxarsone has a higher absolute toxicity than arsanilic acid. The mechanism of action is related to its reaction with sulfhydryl groups values to enzyme function and to its ability to uncouple oxydative phosphorylation. Most animals excrete arsenic quite readily. Toxicoses caused by inorganic and aliphatic organic arsenicals result in a different clinical syndrome than that from the phenylarsonic compounds. Arsenic poisoning may be confused with other types of intoxication. The specific antidote for inorganic arsenical poisoning is dimercaprol (BAL).

Animals↗
PubMed1991

A clinical pathologic study of four adult cases of acute mercury inhalation toxicity.

We report four cases of fatal mercury vapor inhalation, a rare occurrence. The mercury vapor was released at a private home, where one of the occupants was smelting silver from dental amalgam containing an unknown amount of mercury. Within 24 hours of the incident, all occupants began having shortness of breath necessitating hospital admission. The clinical courses are briefly detailed; however, all included rapid deterioration with respiratory failure. Chest roentgenograms in all four cases were consistent with adult respiratory distress syndrome. All patients were treated with dimercaprol, a mercury chelator, but all died, with survival varying from 9 to 23 days postexposure. Autopsies were performed on all four patients. The lungs in all cases were heavy, firm, and airless. Histologic examination revealed severe diffuse alveolar damage, with variable amounts of fibrosis, conforming with acute lung injury in various stages of organization. Additional postmortem findings included acute proximal renal tubular necrosis, vacuolar hepatoxicity, and a spectrum of central nervous system alterations including multifocal ischemic necrosis, gliosis, and vasculitis.

Adult↗
PubMedDate not supplied

The L6 muscle cell line as a tool to evaluate parenteral products for irritation.

A rat skeletal muscle cell line (L6) was evaluated for its utility in assessing cellular damage caused by parenteral administration of eight commercially available pharmaceuticals. The physical forms of the eight pharmaceuticals were diverse, including aqueous and non-aqueous suspensions and solutions. The L6 cells were exposed to therapeutic as well as diluted concentrations of methocarbamol, lorazepam, dimercaprol, phytonadione, menadiol sodium phosphate, penicillin G procaine, penicillin G benzathine, and iron dextran complex. Irritation assessment was based on the depletion of creatine phosphokinase (CK) from treated cultures versus untreated controls. The results obtained correlate well with reports of irritation and side effects noted in clinical use, and demonstrate the versatility of the model for testing suspensions and non-aqueous parenteral solutions. The L6 model is a useful tool to assist in determining the relative local irritancy of parenteral products.

Animals↗
PubMedDate not supplied

N-acetylcysteine in the treatment of human arsenic poisoning.

A 32-year-old man was brought to the emergency department 5 1/2 hours after ingesting a potentially lethal dose (900 mg) of sodium arsenate ant poison in a suicide attempt. The patient deteriorated progressively for 27 hours. After intramuscular dimercaprol and supportive measures failed to improve his condition, he was given N-acetylcysteine intravenously. The patient showed remarkable clinical improvement during the following 24 hours and was discharged from the hospital several days later.

Acetylcysteine↗
PubMed1987

The Nebraska Veterinary Medical Association antidote depot.

The Nebraska Veterinary Medical Association provided financial assistance to establish an antidote depot system statewide at the 3 University of Nebraska veterinary diagnostic laboratories located in Lincoln, North Platte, and Mitchell. The depot system currently stocks atropine sulfate, methylene blue, activated charcoal, dimercaprol, and EDTA. Antidotes are available to all Nebraska veterinarians. Depot withdrawals are used for emergency treatment only and not for a convenient source of supply to replenish individual inventory. The depot system was designed to assist veterinary practitioners in treating toxicoses during catastrophic occurrences in which available inventories have been exhausted. Since time is of essence in most toxicoses, withdrawals from depot sites normally are made by veterinarians or their authorized representatives. There are no fees for using the depot system, but patrons are required to replace drugs at the specific storage site on an item-for-item basis, in like amount, and at current unit cost. Items are issued and replaced only as intact units.

Animals↗
PubMed1976

Theoretical approaches to estimation of plasma renin activity: a review and some original observations.

Performance of accurrate, reproducible, and interpretable assays for plasma renin activity and other components of the renin/angiotensin system in the clinical setting requires a clear understanding of the various reactions in the renin/angiotensin cascade and the nature of their interactions. Plasma renin activity, the rate of angiotensin generations from plasma incubated in vitro, is the most commonly used clinical index of function in the renin/angiotensin system. Renin activity is measured by radioimmunoassay of angiotensin I generated in vitro under carefully controlled conditions. The value obtained for plasma renin activity depends on pH and duration of incubation and on the method used to protect the angiotensin I generated. We recommend incubation at neutral pH in buffered plasma for three hours in the presence of either ethylenediaminetetraacetate + 8-hydroxyquinolone + dimercaprol or ethylenediaminetetraacetate + phenylmethylsulfonylfluoride. Addition of a standard preparation of human renin to the plasma incubation step of the renin activity assay serves the dual purpose of permitting measurement of renin activity and furnishing an internal standard for comparison of assay procedures. The many variables among renin assay methods can be cancelled by referring to a common internal renin standard.

Angiotensin II↗
PubMed1984

Effects of multiple putative anticarcinogens on the carcinogenicity of trans-5-amino-3-[2-(5-nitro-2-furyl)vinyl]-1,2,4-oxadiazole.

In an attempt to dissociate the chemotherapeutic from the carcinogenic properties of the antischistosomal and antitrypanosomal nitrovinylfuran trans-5-amino-3-[2-(5-nitro-2-furyl)vinyl]1,2,4-oxadiazole [(SQ18506) CAS: 28754-68-9; (E)-5-amino-3-(2-(5-nitro-2-furyl)vinyl)-1,2,4-oxadiazole], potential inhibitors of carcinogenesis were administered to female outbred CD-1 mice before and during exposure to SQ18506. The compounds tested were ascorbic acid, etretinate, butylated hydroxyanisole (BHA), cysteamine hydrochloride, cysteine hydrochloride, dimercaprol, disulfiram, 1,4-dithiothreitol, reduced glutathione, and spermidine phosphate. The primary types of tumors observed were squamous cell carcinomas of the stomach and thymic and nonthymic lymphomas. BHA reduced the incidence of malignant tumors to control levels, whereas cysteine hydrochloride, spermidine phosphate, and disulfiram reduced the incidence of chemically induced tumors by 42, 34, and 32%, respectively. Although cysteamine hydrochloride and disulfiram had no or only a modest effect on the overall incidence of tumors, the data suggested possible tissue-specific anticarcinogenic properties for these agents. Of the 8 antioxidants tested, only 1 had marked anticarcinogenic properties against SQ18506. These data indicate that antioxidant properties alone cannot account for the anticarcinogenic activity of the compounds tested. Coadministration of the anticarcinogen BHA with SQ18506 also blocked the chemotherapeutic effects of this agent on female CD-1 mice infected with Schistosoma mansoni.

5-Amino-3-((5-nitro-2-furyl)vinyl)-1,2,4-oxadiazol↗
PubMedDate not supplied

Chelation therapy in nickel poisoning.

For the treatment of acute poisoning from the inhalation of nickel carbonyl, sodium diethyldithiocarbamate (Dithiocarb) has proved to be a specific antidote; tetraethylthiuram (Antabuse) is effective to a lesser degree; d-penicillamine and dimercaprol (BAL) have limited therapeutic value. For the treatment of nickel eczema and dermatitis, favorable response has been obtained by placing patients on a diet of low nickel content together with the oral administration of Dithiocarb or Antabuse. No specific therapy has been advanced for the treatment of nickel cancer in humans. In experimental animals, Dithiocarb has an inhibitory effect on the production of rat rhabdomyosarcomas induced by the intramuscular implantation of nickel subsulfide, and N-methyl formamide inhibits the growth of transplantable nickel fibromas in rats. It is suggested that for the treatment of tumors arising from the implantations of nickel-containing prostheses in humans, chelation therapy be considered.

Animals↗