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PubMed1979

A case of poisoning with mercuric chloride.

A male patient was admitted to hospital 12 h after self-poisoning with mercuric chloride. He suffered multiple complications including acute renal failure, ulcerative colitis, anaemia, disseminated intravascular coagulation, chronic sepsis and severe weight loss. Initially he responded well to resuscitative measures and intensive supportive therapy, which included ventilation of the lungs, haemodialysis, dimercaprol, antibiotics, parenteral feeding and gastrointestinal surgery. Unfortunately the sepsis was never satisfactorily eradicated despite satisfactory serum concentrations of the appropriate antibiotics. On day 43 after poisoning he had a grand mal fit; after this there were focal neurological signs and on lumbar puncture he was found to have a raised protein concentration and raised pressure in his cerebrospinal fluid. The condition of the patient rapidly deteriorated and on day 47 he died. Post-mortem examination revealed a large cerebellar abscess. The literature on mercury poisoning is reviewed.

Acute Kidney Injury↗
PubMed1988

Dithiocarbamate treatment of chronic cadmium intoxication in mice.

The dithiocarbamate analogs, N-benzyl-N-dithiocarboxy-D-glucamine (BDCG) and N-cyclohexyl-N-(2-hydroxy-3-sulfonatopropyl)dithiocarbamate (CAPSO-DTC), were evaluated as cadmium (Cd) antagonists in mice which had received repetitive injections of Cd to effect accumulation of substantial levels of metallothionein-bound Cd in kidneys and livers. BDCG was highly effective in lowering whole body Cd stores and renal Cd concentrations. While the percent of renal Cd mobilized decreased with increasing Cd concentrations, the total amount of Cd mobilized increased. CAPSO-DTC was also effective in reducing whole body Cd levels, but appeared to have less affinity for renal Cd than did BDCG. Treatment of Cd-laden mice with BDCG provoked only a modest elevation of serum creatinine levels, suggesting that the complex of Cd with BDCG may be less nephrotoxic than the complex of Cd with EDTA or dimercaprol. The log of the percent reduction of renal Cd by BDCG was found to be a linear function of the pretreatment renal Cd concentration, and reductions of whole body Cd burdens correlated closely with reductions of liver and kidney Cd concentrations. It was suggested that a Cd complexing agent of the dithiocarbamate class may have ultimate application in a provocative methodology to estimate body or organ Cd stores based upon the amount of Cd excreted following a standard dose of the chelator.

Animals↗
PubMed1995

A report on the composition of mercurials used in traditional medicines in Oman.

A brick red powder, used by a 'native physician' (a practitioner of traditional medicine in Oman) to treat a female patient for vitiligo, has been analysed by X-ray powder diffraction and scanning electron microscopy (S.E.M.). It was found to be a mixture of cinnabar (HgS) and calomel (Hg2Cl2). Symptoms of acute mercury poisoning resulted from the patient repeatedly breathing in elemental mercury vapour after this brick red powder and elemental mercury encased in a lime, were thrown on an open fire in a closed room. The patient also presented with central nervous system toxicity which improved gradually after treatment with Dimercaprol was discontinued. The use of mercurials as traditional medicines in Oman is briefly reviewed; as is the variation in literature values for 'normal'/'abnormal'/toxic levels of mercury in human blood.

Adult↗
PubMed1992

Toxicity of a family from vacuumed mercury.

A family of four developed toxic blood levels of mercury after the mother vacuumed a spilled jar of liquid mercury from a closet in their apartment. The youngest son developed severe thrombocytopenia which was initially diagnosed as idiopathic thrombocytopenic purpura secondary to viral illness. A possible association between acute mercury toxicity and idiopathic thrombocytopenic purpura has not been previously reported. Chelation therapy with penicillamine for the older child was administered soon after toxic blood mercury levels were known by the physician. Because thrombocytopenia has been reported to occur in up to 5% of patients receiving penicillamine therapy, the younger child was treated with dimercaptosuccinic acid. The mother was also treated with dimercaptosuccinic acid. The father received dimercaprol therapy. The toxic effects and rationale for now outdated therapeutic uses of mercury are discussed.

Adult↗
PubMed2004

Molecular recognition based cadmium removal from human plasma.

Molecularly imprinted polymers (MIPs) are easy to prepare, stable, inexpensive and capable of molecular recognition. MIPs can be considered as affinity separation media. Cadmium is a carcinogenic and mutagenic element. There is no specific treatment available for acute or chronic metal poisoning. Besides supportive therapy and hemodialysis, metal poisoning is often treated with commercially available chelating agents including EDTA and dimercaprol. However, there is histopathological evidence for increased toxicity in animals when these agents are utilized. The aim of this study is to prepare ion-imprinted polymers, which can be used for the selective removal of Cd2+ ions from Cd2+-overdosed human plasma. N-Methacryloly-(L)-cysteinemethylester (MAC) was chosen as the complexing monomer. In the first step, Cd2+ was complexed with MAC and the Cd2+ -imprinted p(HEMA-MAC) beads were synthesized by suspension polymerization. After that, the template (i.e., Cd2+ ions) were removed using 0.1 M thiourea solution. The specific surface area of the Cd2+ -imprinted poly(HEMA-MAC) beads was found to be 19.4 m2/g with a size range of 63-140 microm in diameter and the swelling ratio was 78%. According to the elemental analysis results, the beads contained 42.1 micromol MAC/g polymer. The maximum adsorption capacity was 32.5 micromol Cd2+/g beads. The relative selectivity coefficients of imprinted beads for Cd2+/Pb2+ and Cd2+/Zn2+ were 7.8 and 1683 times greater than non-imprinted matrix, respectively. The Cd2+-imprinted poly(HEMA-MAC) beads could be used many times without decreasing their adsorption capacities significantly.

Adsorption↗
PubMed1978

Neutropenia associated with chrysotherapy for juvenile rheumatoid arthritis.

Severe neutropenia, in the absence of generalized bone marrow depression, is a rare complication in adults receiving chrysotherapy for rheumatoid arthritis and has not been described in children. Isolated, severe neutropenia developed in five children with systemic onset JRA while they were receiving gold injections. This potentially fatal complication occurred within eight weeks of beginning therapy in four patients, and after 24 weeks of well-tolerated therapy in the fifth. Leukopenia preceded neutropenia in two children. Localized infection was successfully treated in one child; septicemia was fatal to a second child. Neutropenia resolved within eight to 14 days of its onset in the four survivors; chelation with dimercaprol in one child did not appear to alter the recovery time. It is suggested that a systemic onset of JRA in children less than 6 years of age identifies a higher risk group developing severe neutropenia during chrysotherapy. Cessation of gold therapy upon recognition of a decreasing neutrophil count may prevent or ameliorate a developing neutropenia; careful observation for, and early treatment of, infection may alter its outcome.

Agranulocytosis↗
PubMed1987

Acute arsenic ingestion.

A 21-year-old man presented in shock after ingesting 2 g of arsenic trioxide. He died within 37 hours despite intensive treatment that included intramuscular dimercaprol and hemodialysis. Hemodynamic and laboratory data are presented illustrating the multisystem toxicities of inorganic arsenic. Hemodialysis, previously described as an effective therapeutic adjunct, was shown to be ineffective in this case.

Acute Kidney Injury↗
PubMed2003

2,3-Dimercaptopropane-1-sulfonic acid and meso-2,3-dimercaptosuccinic acid increase mercury- and cadmium-induced inhibition of delta-aminolevulinate dehydratase.

Compounds derived from Dimercaprol, such as meso-2,3-dimercaptosuccinic acid (DMSA) and 2,3-dimercaptopropane-1-sulfonic acid (DMPS), are becoming common agents for treating humans exposed to heavy metals. Heavy metals such as Pb(2+), Hg(2+) and Cd(2+) can inhibit delta-aminolevulinate dehydratase (delta-ALA-D) activity. Delta-ALA-D catalyzes the condensation of two delta-aminolevulinic acid (delta-ALA) molecules with the formation of porphobilinogen, a heme precursor. The effects of DMSA and DMPS alone or in combination with Cd(2+), Hg(2+), or Pb(2+) on hepatic delta-ALA-D were examined. DMPS and DMSA caused a dose-dependent inhibition of hepatic delta-ALA-D. In the presence of Hg(2+) or Cd(2+) the inhibitory potency of DMPS increased. Similarly, the inhibitory effects of Hg(2+) and Cd(2+) were markedly increased in the presence of DMSA. In contrast, the inhibitory effect of DMPS was not changed by inclusion of Pb(2+). As observed with DMSA, Zn(2+) did not modified the inhibitory effect of DMPS. Data of the present report support the idea that the complexes formed (metals-DMSA or DMPS) were more inhibitory than the metal (Hg(2+) and Cd(2+)) or the chelating agent alone to the hepatic delta-ALA-D activity, in vitro. The mechanism of hepatic delta-ALA-D inhibition by Hg(2+)-DMPS/DMSA and Cd(2+)-DMPS/DMSA complexes involve the essential thiol groups of the enzyme.

Animals↗
PubMed2002

Chronic arsenic poisoning.

Symptomatic arsenic poisoning is not often seen in occupational exposure settings. Attempted homicide and deliberate long-term poisoning have resulted in chronic toxicity. Skin pigmentation changes, palmar and plantar hyperkeratoses, gastrointestinal symptoms, anemia, and liver disease are common. Noncirrhotic portal hypertension with bleeding esophageal varices, splenomegaly, and hypersplenism may occur. A metallic taste, gastrointestinal disturbances, and Mee's lines may be seen. Bone marrow depression is common. 'Blackfoot disease' has been associated with arsenic-contaminated drinking water in Taiwan; Raynaud's phenomenon and acrocyanosis also may occur. Large numbers of persons in areas of India, Pakistan, and several other countries have been chronically poisoned from naturally occurring arsenic in ground water. Toxic delirium and encephalopathy can be present. CCA-treated wood (chromated copper arsenate) is not a health risk unless burned in fireplaces or woodstoves. Peripheral neuropathy may also occur. Workplace exposure or chronic ingestion of arsenic-contaminated water or arsenical medications is associated with development of skin, lung, and other cancers. Treatment may incklude the use of chelating agents such as dimercaprol (BAL), dimercaptosuccinic acid (DMSA), and dimercaptopanesulfonic acid (DMPS).

Arsenates↗
PubMed2002

Lead poisoning: case studies.

Early clinical features of lead toxicity are non-specific and an occupational history is particularly valuable. Lead in the body comprises 2% in the blood (t1/2 35 days) and 95% in bone and dentine (t1/2 20-30 years). Blood lead may remain elevated for years after cessation from long exposure, due to redistribution from bone. Blood lead concentration is the most widely used marker for inorganic lead exposure. Zinc protoporphyrin (ZPP) concentration in blood usefully reflects lead exposure over the prior 3 months. Symptomatic patients with blood lead concentration >2.4 micromol l-1 (50 microg dl-1) or in any event >3.8 micromol l-1 (80 microg dl-1) should receive sodium calciumedetate i.v., followed by succimer by mouth for 19 days. Asymptomatic patients with blood lead concentration >2.4 micromol l-1 (50 microg dl-1) may be treated with succimer alone. Sodium calciumedetate should be given with dimercaprol to treat lead encephalopathy.

Acute Disease↗
PubMed2000

Combined evidence-based literature analysis and consensus guidelines for stocking of emergency antidotes in the United States.

STUDY OBJECTIVE: To develop guidelines for the stocking of antidotes at hospitals that accept emergency admissions using combined evidence-based and consensus methods. METHODS: Study participants were 12 medical care providers from disciplines that are affected by insufficient stocking of emergency antidotes (clinical pharmacology, critical care, clinical pharmacy, emergency medicine, hospital pharmacy, internal medicine, managed care pharmacy, clinical toxicology, pediatrics, poison control centers, pulmonary medicine, regulatory medicine). Selection of individuals for the study panel was based on evidence of previous antidote research or perspective regarding the purchase and use of antidotes. The literature regarding each antidote was systematically amassed using pre-1966 literature files, current MEDLINE searches, the reference lists of major medical textbooks, and citations solicited from the consensus panel. Articles relevant to 4 defined core questions were included. These articles formed the basis of an evidence-based analysis performed by the principal investigator. After literature analysis, a literature summary and proposed guidelines for antidote stocking were submitted to the panel. Consensus was formed by electronic iterative presentation of alternatives to each panel member using a modified Delphi method. All panel members participated in 5 rounds of guideline analysis of 20 antidotes. RESULTS: Of the 20 antidotes, 16 antidotes were ultimately recommended for stocking (N -acetylcysteine, atropine, Crotalid snake antivenin, calcium gluconate and chloride, cyanide antidote kit, deferoxamine, digoxin immune Fab, dimercaprol, ethanol, fomepizole, glucagon, methylene blue, naloxone, pralidoxime, physostigmine, sodium bicarbonate), 2 were not recommended for stocking (black widow antivenin, ethylenediamine tetraacetic acid), and consensus could not be reached for 2 antidotes (flumazenil, physostigmine). CONCLUSION: These guidelines provide a tool to be used in revising or creating policies and procedures with regard to the stocking of antidotes in hospitals that accept emergency patients.

Antidotes↗
PubMed1999

Vanadate induction of NF-kappaB involves IkappaB kinase beta and SAPK/ERK kinase 1 in macrophages.

The present studies investigated the signaling pathways of vanadate, a vanadium ion with +5 oxidation state, to activate NF-kappaB transcription factor, a pivotal regulator of inflammatory responses. Treatment of macrophages with vanadate results in the activation of both NF-kappaB and c-Jun N-terminal kinase (JNK). The activity of a recently identified cellular kinase, IkappaB kinase-beta (IKKbeta), was significantly elevated concomitant with the increased degradation of IkappaBalpha and enhanced NF-kappaB activity in cells exposed to vanadate. To determine whether the IKK pathway and JNK pathway are interconnected or bifurcate upon vanadate stimulation, cells were transfected with either a kinase inactive form of IKKbeta or a kinase inactive form of SAPK/ERK kinase 1 (SEK1). Inactive IKKbeta was able to block vanadate-induced degradation of IkappaBalpha, yet it was unable to influence the activation of JNK by vanadate. Conversely, blockage of JNK activation by transfection of a kinase-inactive form of SEK1 resulted in partially inhibition of vanadate-induced IkappaBalpha degradation. Both vanadate-induced degradation of IkappaBalpha and activation of JNK were potently inhibited by pretreatment of cells with N-acetylcysteine or dimercaprol. These results demonstrate that early activation of stress kinases or change of cellular redox states plays a key role in vanadate-induced activation of NF-kappaB and JNK.

Animals↗
PubMed2000

Repetitive endoscopy and continuous alkaline gastric irrigation in a case of arsenic poisoning.

BACKGROUND: The poor prognosis of patients with persistent gastrointestinal radio-opacities after oral arsenic poisoning supports efficient gastrointestinal decontamination as critical for survival. In a case of massive arsenic ingestion, we performed repetitive gastric endoscopy and a continuous alkaline irrigation of the stomach over several days. CASE REPORT: A 41-year-old woman was admitted 4 hours after intentional ingestion of trivalent arsenic powder 5 g. The admission abdominal X-ray confirmed the presence of multiple gastric opacities. Initial treatment was gastric lavage with normal saline, dimercaprol chelation, and supportive therapy. Since gastric opacities persisted on the abdominal X-ray at 34 hours despite repeated gastric lavage, a gastroscopy was performed showing nonremovable agglomerates. In an attempt to achieve further gastric decontamination, we performed a continuous gastric alkaline irrigation. After 3 days of alkaline irrigation, the abdomen was normal on X-ray but the gastroscopy still showed arsenic concretions. Alkaline irrigation was continued for another 3 days until total disappearance of arsenic agglomerates at the gastroscopy. Admission urinary arsenic was 3663 microg/L. A total of 46.2 mg of inorganic arsenic, or less than 1% the ingested dose, was extracted from the stomach by this technique. The patient was discharged from the intensive care unit 20 days after admission without sequelae.

Adult↗
PubMed2003

Acute arsenic poisoning treated by intravenous dimercaptosuccinic acid (DMSA) and combined extrarenal epuration techniques.

Arsenic poisoning was diagnosed in a 26-year-old man who had been criminally intoxicated over the last two weeks preceding admission by the surreptitious oral administration of probably 10 g of arsenic trioxide (As2O3). The patient developed severe manifestations of toxic hepatitis and pancreatitis, and thereafter neurological disorders, respiratory distress, acute renal failure, and cardiovascular disturbances. In addition to supportive therapy, extrarenal elimination techniques and chelating agents were used. Dimercaprol (BAL) and dimercaptosuccinic acid (DMSA or succimer) were used simultaneously as arsenic chelating agents for two days, and thereafter DMSA was used alone. DMSA was administered by intravenous (20 mg/kg/d for five days, then 10 mg/kg/d for six days) and intraperitoneal route. Intravenous DMSA infusion was well tolerated and resulted in an increase in arsenic blood concentration immediately after the infusion. Continuous venovenous hemofiltration combined with hemodialysis, and peritoneal dialysis were proposed to enhance arsenic elimination. It was calculated that over an 11-day period 14.5 mg arsenic were eliminated by the urine, 26.7 mg by hemodialysis, 17.8 mg by peritoneal dialysis, and 7.8 mg by continuous venovenous hemofiltration. These amounts appeared negligible with regard to the probable ingested dose. The patient died on day 26 from the consequences of multiple organ failure, with subarachnoid hemorrhage and generalized infection caused by Aspergillus fumigatus.

Acute Kidney Injury↗
PubMed1996

The use of chelating agents in occupational lead poisoning.

Chelating agents have long been used in the pharmacological treatment of lead poisoning, whose management is still a problem, particularly in developing countries. This article reviews the pharmacological properties of dimercaprole, peniclliamine. CaNa2EDTA and dimercaprosuccinic acid, examines their indications, contraindications and side effects and discusses the possible use of each drug in occupational Pb poisoning. Proposals are also presented for the treatment and follow-up of subjects with signs and symptoms of poisoning and of subjects with low-moderate Pb absorption. CaNa2EDTA seems to be the most reliable and safer chelating agent nowadays available and with a wider spectrum of action. DMSA seems to be promising in the treatment of occupational Pb poisoning. Even though there is no doubt that chelation therapy has significantly contributed to reduce mortality and morbidity from occupational Pb poisoning, the efficacy of this treatment in subjects with subtle neurological or renal damage has not yet been studied properly.

Body Burden↗
PubMed1979

Gold-induced thrombocytopenia responsive to cyclophosphamide.

Thrombocytopenia and nephrotic syndrome developed in a 51-year-old patient receiving gold therapy for rheumatoid arthritis. Marrrow findings and platelet infusion studies were consistent with a pattern of increased platelet destruction, known to occur in gold-induced thrombocytopenia. Improvement in the platelet count after therapy with dimercaprol was transient, and although steroids and splenectomy were not effective, a response was achieved with cyclophosphamide. The use of immunosuppressive drugs can be considered in refractory cases of gold-induced thrombocytopenia in which a significant hemorrhagic risk is present.

Aurothioglucose↗
PubMed2002

Treatment and toxicokinetics of acute pediatric arsenic ingestion: danger of arsenic insecticides in children.

OBJECTIVES: To describe the toxicokinetics and management of acute pediatric arsenic ingestion. DESIGN: Case report and literature review. SETTING: Tertiary pediatric intensive care unit, St. John's Children's Hospital, Springfield, IL. PATIENT: A 22-month-old boy ingested approximately twice the estimated lethal dose of arsenic trioxide (As(2)O(3)) ant bait. Only one household arsenical insecticide is available in the United States and is presumed to be shielded from human exposure. He survived without detectable sequelae. Initially, the patient developed signs of acute hemodynamic compromise with tachycardia, hypertension, gastrointestinal symptoms, and poor urine output. He became lethargic with muscle weakness and was somnolent but never developed encephalopathy, seizures, or late onset peripheral neuropathy. INTERVENTIONS: He was stabilized with fluid resuscitation, placed on a sodium bicarbonate intravenous drip, and treated with intramuscular dimercaprol (British anti-Lewisite), 5 mg/kg every 6 hrs for 3 days. When the British anti-Lewisite and the sodium bicarbonate drip were discontinued, oral meso 2,3-dimercaptosuccinic acid (Succimer) was administered three times a day for 5 days and thereafter twice daily until the urine arsenic concentration decreased below 50 microg/L. MEASUREMENTS AND MAIN RESULTS: Continuous monitoring in the pediatric intensive care unit included continuous electrocardiogram, arterial blood pressure, urine output, vital signs, arterial blood gases, serum and urine arsenic concentrations, electrolytes, electromyography, and determination of arsenic toxicokinetics. The child's serum arsenic concentration was the highest ever reported with survival. CONCLUSIONS: Recovery from arsenic poisoning was attributable to the restoration and maintenance of adequate cardiac output and renal perfusion in early shock, which allowed depot intramuscular British anti-Lewisite to circulate and eliminate the poison. Although an intravenous antiarsenical chelating agent would be advantageous in treating shock from arsenic poisoning, none is currently available. We urge the immediate use of British anti-Lewisite therapy on patient presentation with suspected toxic arsenic ingestion.

Journal Article↗
PubMed1974

Effect of drugs on rat paw oedema induced by mercury.

1 Metallic mercury (0.04 ml) injected into the foot pad of rats induced a consistent inflammatory reaction, which at 4 h showed oedema but no cellular infiltration or vascular changes. The lesions exhibited lymphocytic infiltration, vasodilatation and haemorrhages at 24 and 48 h, and often became cystic after 2-3 weeks, before healing. The oedema volume at 4 h was used to test anti-inflammatory activity of drugs.2 Cortisone, phenylbutazone, indomethacin, acetylsalicylic acid, flufenamic acid and propranolol exhibited potent, dose-related anti-inflammatory activity. Aminopyrine, chloroquine and chlorpromazine were only moderately effective. Dimercaprol, adrenaline, and to some extent, mepyramine also inhibited mercury-induced oedema.3 This simple model of acute inflammation may be useful for preliminary tests of anti-inflammatory activity.

Animals↗