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At least 883 records · Page 49Linked to original sources
PubMed1997

The effect of 2,3 dimercaptosuccinic acid in the treatment of lead poisoning in adults.

Four patients, aged 22-60, belonging to a single family that had been exposed to lead-contaminated food for an unknown period, and nine workers, aged 20-65, who had been exposed to air-borne lead for 6-8 years, were evaluated for lead poisoning in our centres. Blood lead levels were 3.57 +/- 0.39 micromol/L (mean +/- SD) in the family members and 3.46 +/- 0.43 micromol/L (mean +/- SD) in the group of workers. 2,3 dimercaptosuccinic acid (DMSA) therapy was instituted in the four family members while the nine workers were closely monitored after being removed from the contaminated environment without receiving any chelation therapy. DMSA therapy given for the duration of 19 days reduced the blood lead levels to 0.63 +/- 0.44 micromol/L (mean +/- SD), P<0.01, in the four family members. No significant change was observed in the untreated group. The exposure time in the untreated group was probably longer than that in the treated group. Following long-term exposure most of the lead in the body is found in the bones and therefore not easily removed by chelation therapy. No side-effects were reported in the treated group and no rebound elevation of blood lead levels was observed during the therapy period or during the 12-week follow-up period following cessation of therapy. We conclude that 19 days of chelation therapy with DMSA in adults with moderate to severe lead poisoning is effective and safe.

Administration, Oral↗
PubMedDate not supplied

The effect of DMSA loading on the renal handling of technetium-99m in rats.

The renal handling of technetium-99m dimercaptosuccinic acid (99mTc DMSA) was studied in rats treated with high doses of nonradioactive DMSA to inhibit the renal uptake mechanism(s). A static scan was obtained 1 hour after the intravenous (iv) injection of 99mTc DMSA and the radioactivity in kidneys and bladder was calculated as a percentage of the injected amount. Total glomerular filtration rate (GFR) and effective renal plasma flow were also determined. Preloading with DMSA caused a fall in the renal accumulation of 99mTc DMSA together with a small increase in the amount excreted into the urinary bladder. Despite a stable GFR, the total amount of 99mTc DMSA handled by the kidneys (i.e., renal plus bladder activity) was reduced. These findings are compatible with the hypothesis that peritubular uptake and subsequent intracellular fixation are of importance in the renal accumulation of 99mTc DMSA. On the other hand, the radioactivity excreted into the urine probably stems from non-reabsorbed 99mTc DMSA initially filtered by the glomeruli.

Animals↗
PubMed1999

Protection against cis-diamminedichloroplatinum-induced nephrotoxicity by 2,3-dimercaptosuccinic acid in rats.

The present study was designed to examine the usefulness of 2,3-dimercaptosuccinic acid (DMSA) for the purpose of reducing cis-diamminedichloroplatinum (DDP)-induced nephrotoxicity and effective clinical use of DDP and safe. The effectiveness of DMSA on the DDP-excretion in rat kidney was observed by measuring the platinum concentration using Atomic Absorption Instrument. Co-administration of DMSA (1.0 or 2.0 mmol/kg) 1 hour after DDP injection (20 mumol/kg) showed more decrease in the platinum concentration than that immediately after DDP injection. The alleviating effect of DMSA on DDP toxicity was evaluated by lipid peroxidation, enzymatic antioxidants, and glutathione levels. The administration of DDP alone caused a significant increase in lipid peroxidation and significant decreases in enzymatic antioxidants and glutathione levels in the kidney. Co-administration of DMSA (2.0 mmol/kg) 1 hour after DDP injection showed the most effective reduction of these enzymatic damages caused by DDP. These findings suggested that the co-administration of DMSA (2.0 mmol/kg) 1 hour after DDP injection leads DDP to effective excrete from renal tissue and suppresses the lipid peroxide reaction and results in reduction of nephrotoxicity.

Animals↗
PubMed1987

Changes in renal function during physical and mental effort.

Aim of the study was to evaluate the renal responses to physical and mental effort in essential hypertension by means of a non-invasive radioisotopic method. Renal uptake rate of Tc99m-DMSA was evaluated in 10 subjects. Starting from 5 to 15 minutes after dose injection counts over the kidney region were acquired by means of a gamma-camera time-activity curves were obtained for each kidney. In non-stimulated patients DMSA uptake rate increased regularly; in the remaining cases both isometric exercise and mental effort induced an abrupt reduction of the uptake rate which increased again after the end of the test. Although the relation of DMSA uptake rate to renal function is not yet fully understood, we tentatively interpret these results as indicating blood flow reductions during these stressful conditions.

Humans↗
PubMed1996

Hydrogen peroxide in relation to proliferation and apoptosis in BHK-21 hamster fibroblasts.

Addition of H2O2 at 100 microM, or 1 mM, to the culture medium of BHK-21 fibroblasts results in increased intracellular levels of H2O2. Whilst exposure of BHK-21 cells to lower levels of H2O2 (1 microM) actually stimulates proliferation, these higher oxidant concentrations not only depress proliferation rates but also lead to an increase in the appearance of apoptotic-like cells in the cultures. Other agents such as inhibitors of glutathione peroxidase and catalase, or mimics of superoxide dismutase, which also bring about elevated cellular levels of H2O2 in BHK-21 cells, similarly lead to decreased proliferation and an apparent increase in cells with apoptopic features. Thus intracellular conditions which are considered more prooxidant than normal, appear to favour apoptosis over proliferation in BHK-21 fibroblasts. Additionally these abnormal cellular conditions also appear to favour excessive DNA replication, in remaining non-apoptotic cells.

Amitrole↗
PubMed1982

Treatment of mercuric chloride poisoning with dimercaptosuccinic acid and diuretics: preliminary studies.

The distribution and excretion of mercury were studied in mice given a single injection of HgCl2 with or without chelation treatment. DMS (2,3-dimercaptosuccinic acid) given intravenously (0.5 mmol SH/kg) to mice 24 h after the mercury injection reduced the kidney Hg level significantly, while NAPA (N-acetyl-DL-penicillamine) and BAL (2,3-dimercaptopropanol) did not. The effectivity of DMS to remove Hg from kidneys was comparable to that of BAL-sulph (2,3-dimercaptopropane-1-sulfonate), irrespective of whether these chelating agents were given orally or intravenously. Immediate chelation treatment with DMS or mercaptodextran reduced the renal Hg level to about 50% of control levels, as measured 3 d after the treatment. Combination of DMS with immediate intraperitoneal treatment with spironolactone was even more effective in reducing the renal levels, and acted both by increasing the fecal and urinary excretion. The DMS treatment, as well as DMS + spironolactone in combination, could protect against kidney damage following injection of 30 mumol HgCl2/kg. Such treatment was essentially nontoxic.

Animals↗
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↗
PubMed1992

Human studies with the chelating agents, DMPS and DMSA.

Meso-2,3-dimercaptosuccinic acid (DMSA) is bound to plasma albumin in humans and appears to be excreted in the urine as the DMSA-cysteine mixed disulfide. The pharmacokinetics of DMSA have been determined after its administration to humans po. For the blood, the tmax and t1/2 were 3.0 h + 0.45 SE and 3.2 h + 0.56 SE, respectively. The Cmax was 26.2 microM + 4.7 SE. To determine whether dental amalgams influence the human body burden of mercury, we gave volunteers the sodium salt of 2,3-dimercaptopropane-1-sulfonic acid (DMPS). The diameters of dental amalgams of the subjects were determined to obtain the amalgam score. Administration of 300 mg DMPS by mouth increased the mean urinary mercury excretion of subjects over a 9 h period. There was a positive correlation between the amount of mercury excreted and the amalgam score. DMPS might be useful for increasing the urinary excretion of mercury and thus increasing the significance and reliability of this measure of mercury exposure. DMSA analogs have been designed and synthesized in attempts to increase the uptake by cell membranes of the DMSA prototype chelating agents. The i.v. administration of the monomethyl ester of DMSA, the dimethyl ester of DMSA or the zinc chelate of dimethyl DMSA increases the biliary excretion of platinum and cadmium in rats.

Adult↗
PubMed1994

Disappearance of heme metabolites following chelation therapy with meso 2,3-dimercaptosuccinic acid (DMSA).

A lead poisoned adult (blood lead level 384 micrograms/dL) had a specific urinary porphyrin profile of elevated porphyrins including coproporphyrin III and 5-carboxylic acid derivatives. A multilinear gradient elution, modified with an ion-pair and a reversed phase column were employed for the separation of the diagnostically important porphyrin isomers. Fluorescence detection enhanced both sensitivity and selectivity. Both compounds were restored to normal levels following two courses of meso 2,3-dimercaptosuccinic acid: 90 mg/kg/d x 5 d at one month intervals. The decrease of clinical symptoms was associated with increase of delta aminolevulinic acid dehydratase from 53 to 230 U/mL blood and hemoglobin from 8.4 to 12.7 g/dL. Blood lead decreased from 384 to 24 micrograms/dL, urine lead from 1286 to 188 micrograms/L and urine coproporphyrin III from 5712 to 25 micrograms/L.

Administration, Oral↗
PubMed1996

Lead intoxication in children with pervasive developmental disorders.

OBJECTIVE: To investigate the observation that children with pervasive developmental disorders have later and more prolonged lead exposure and are more likely to be reexposed when compared to lead-poisoned children without pervasive developmental disorders. DESIGN: Retrospective chart review. SETTING: A large, urban lead treatment program. RESULTS: Over a six year period 17 children with pervasive developmental disorders (including autism) were treated. Compared to a randomly selected group of 30 children without pervasive developmental disorders who were treated for plumbism over the sam interval, those with pervasive developmental delay were significantly older at diagnosis (46.5 vs 30.3 months, p = .03) and had a longer period of elevated blood lead levels (39.1 vs 14.1 months, p = .013) during management. Despite close monitoring, state-mandated environmental inspection and prompt lead hazard reduction or alternative housing, 75% of children with pervasive developmental disorders were reexposed to lead during medical management compared with 23% of children without pervasive developmental disorders (p = .001). CONCLUSIONS: 1) lead intoxication among children with pervasive developmental disorders may appear de novo beyond the third year of life and is associated with a high rate of reexposure; 2) the provision of deleaded housing (by current techniques) may not be sufficient to protect these children from repeated lead exposure; 3) these data support recommendations by the Centers for Disease Control that children with developmental delays be closely monitored for the appearance of lead intoxication. This monitoring should continue beyond the third year of life.

Chelating Agents↗
PubMed1996

Clinical course of severe poisoning with thiomersal.

CASE REPORT: A 44-year-old man ingested 83 mg/kg Thiomersal. He developed gastritis, renal tubular failure, dermatitis, gingivitis, delirium, coma, polyneuropathy and respiratory failure. Treatment was symptomatic plus gastric lavage and the oral chelating agents dimercaptopropane sulfonate and dimercaptosuccinic acid. The patient recovered completely. Maximum mercury concentrations were blood 14 mg/L, serum 1.7 mg/L, urine 10.7 mg/L, and cerebrospinal fluid 0.025 mg/L. Mercury concentration in blood declined with two velocities: first with half-time 2.2 days, then with half-time 40.5 days. The decline of mercury concentration in blood, urinary mercury excretion, and renal mercury clearance were not substantially influenced by chelation therapy.

Administration, Oral↗
PubMed1998

Randomized placebo-controlled trial of 2,3-dimercaptosuccinic acid in therapy of chronic arsenicosis due to drinking arsenic-contaminated subsoil water.

INTRODUCTION: Chronic arsenic toxicity producing various clinical manifestations is currently epidemic in West Bengal, India, Bangladesh, and other regions of the world. Animal studies have indicated that 2,3-dimercaptosuccinic acid can be used as an oral chelating agent. A prospective, double-blind, randomized controlled trial was carried out to evaluate the efficacy and safety of 2,3-dimercaptosuccinic acid for chronic arsenicosis due to drinking arsenic-contaminated (> or = 50 micrograms/L) subsoil water in West Bengal. METHOD: Twenty-one consecutive patients with chronic arsenicosis were individually randomized (random number; assignment made by individual not evaluating patients) into 2 groups: 11 patients (10 male, age 25.5 +/- 8 years) received 2,3-dimercaptosuccinic acid 1400 mg/d (1000 mg/m2) in the first week and 1050 mg/d (750 mg/m2) during the next 2 weeks with a repeat course 3 weeks later. The other 10 patients (all male, age 32.2 +/- 9.7 years) were given placebo capsules for the same schedule. The clinical features were evaluated by an objective scoring system before and after treatment. Routine investigations including liver function tests, arsenic concentrations in urine, hair, and nails, and skin biopsy evaluations were also completed. RESULTS: Though there was improvement in the clinical score of 2,3-dimercaptosuccinic acid-treated patients, similar improvement was observed in the placebo-treated group. There were no statistical differences in the clinical scores between the 2 groups at the beginning and at the end of treatment. Similarly, no differences were found for the other investigated parameters. CONCLUSION: Under the conditions of this study, 2,3-dimercaptosuccinic acid was not effective in producing any clinical or biochemical benefit or any histopathological improvement of skin lesions in patients with chronic arsenicosis.

Adolescent↗
PubMed1994

Poor renal uptake of technetium-99m-DMSA and technetium-99m-MDP in a patient with Fanconi syndrome and near normal glomerular filtration rate.

We present a patient with Fanconi syndrome who demonstrated poor renal uptake of 99mTc-DMSA and high urinary concentration of the tracer. A 99mTc-DTPA scan was normal and the creatinine clearance only minimally decreased. These findings suggest that 99mTc-DMSA may be accumulated in the kidney by glomerular filtration and subsequent tubular reabsorption, with the nonabsorbed fraction appearing in the urine. In Fanconi Syndrome the tubular reabsorption of DMSA may also be reduced, thus explaining the poor renal uptake in this patient. A 99mTc-MDP bone scan showed faint renal uptake and diffuse high uptake mainly in the spine, demonstrating that the metabolic bone disease associated with Fanconi Syndrome can be another mechanism for poor renal visualization on bone scan.

Fanconi Syndrome↗
PubMed1977

[Study of distribution of 203Hg-chlormerodrin, 203Hg-nitrate and 99mTc-DMSA in kidney by macroautoradiography (author's transl)].

Serial macroautoradiograms were obtained to determine the distribution of 203Hg-chlormerodrin, 203Hg-nigrate and 99mTc-DMSA in kidney. In the study, normal rats were used and these three radiopharmaceuticals were injected intravenously. Initial images of 203Hg-chlormerodrin showed the accumulation in the outer cortex, but no significant radioactivity in the medullary. On the other hand, delayed images revealed radioactivity shifting in concentration from the outer cortex to the inner cortex. Distribution pattern of 203Hg-nitrate was similar to that of 203Hg-chlormerodrin. In contrast to 203Hg-chlormerodrin and 203Hg-nitrate, 99mTc-DMSA was retained in the outer cortex without temporal changes in the distribution.

Animals↗