Idiopathic erythrocytosis in a patient on chronic hemodialysis.

A 78-year-old man on hemodialysis presented to our hospital with erythrocytosis. He had started hemodialysis 4 years previously, with a hemoglobin level of 9.8 g/dL, and was administered erythropoiesis stimulating agents and ferrous sulfate. Two years previously, his hemoglobin level increased to 14.5 g/dL and the treatment for anemia was discontinued. He continued hemodialysis thrice weekly; however, the hemoglobin level had increased to 17.0 g/dL at the time of presenting to our hospital. His serum erythropoietin level was 31.4 mIU/mL (range, 3.7-31.5 mIU/mL), carboxyhemoglobin level was 0.6% (range, 0-1.5%), and oxygen saturation in ambient air was 95.4%. The JAK2 V617F mutation was not observed and other bone marrow abnormalities were not identified. The patient was diagnosed with bladder cancer and a transurethral resection was performed. Eight months after the treatment of bladder cancer, his hemoglobin level was 15.1 g/dL, and he was diagnosed with idiopathic erythrocytosis.

Changes in serum magnesium concentration after use of a proton pump inhibitor in patients undergoing percutaneous coronary intervention.

BACKGROUND: Although cross-sectional studies have suggested a relationship between proton pump inhibitor (PPI) use and hypomagnesemia, no large-scale cohort study has been conducted to date. Here, we examined the changes in serum magnesium levels in response to PPI use. We hypothesized that PPI use might change the serum magnesium concentration. METHODS: Of the 2,892 patients hospitalized for percutaneous coronary intervention between January 2007 and May 2012, 1,076 patients with normal baseline (1.6-2.5 mg/dL) and follow-up serum magnesium concentrations were enrolled. These patients were divided into two groups: the PPI group and the control group. RESULTS: The mean follow-up period was 9.51 ± 2.94 months. The incidence of hypomagnesemia (< 1.6 mg/dL) was 0.4% (3/834) in the PPI group and 0.4% (1/242) in the control group (P = 0.904). The change in magnesium levels did not differ between the two groups, and this result was maintained in the analysis of covariance after adjusting for confounding factors (P = 0.381). Moreover, magnesium levels did not significantly differ between the long-term (duration of use ≥ 12 months, n = 71) and short-term PPI groups (duration of use < 12 months, n = 763), and the control group (n = 242; P = 0.620). The effect of PPI use on change in serum magnesium concentration was affected by the use of multiple diuretics (-0.01 ± 0.25 mg/dL; P = 0.025), although a single diuretic use with PPI did not alter the change in magnesium level (0.12 ± 0.27 mg/dL). CONCLUSION: Changes in magnesium levels might be subtle after PPI use in patients with normal baseline magnesium values.

Urokinase, urokinase receptor, and plasminogen activator inhibitor-1 expression on podocytes in immunoglobulin A glomerulonephritis.

BACKGROUND/AIMS: The purpose of this study was to investigate the expression of urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), and plasminogen activator inhibitor (PAI)-1 on podocytes in immunoglobulin A (IgA) glomerulonephritis (GN). METHODS: Renal biopsy specimens from 52 IgA GN patients were deparaffinized and subjected to immunohistochemical staining for uPA, PAI-1, and uPAR. The biopsies were classified into three groups according to the expression of uPA and uPAR on podocytes: uPA, uPAR, and a negative group. The prevalences of the variables of the Oxford classification for IgA GN were compared among the groups. RESULTS: On podocytes, uPA was positive in 11 cases and uPAR was positive in 38 cases; by contrast, PAI-1 was negative in all cases. Expression of both uPA and uPAR on podocytes was less frequently accompanied by tubulointerstitial fibrosis. CONCLUSIONS: Our results suggest a possible protective effect of podocyte uPA/uPAR expression against interstitial fibrosis.

Incidence, etiology, and outcomes of rhabdomyolysis in a single tertiary referral center.

We have encountered numerous cases of rhabdomyolysis associated with acute pesticide intoxication; however, the cause, incidence, and treatment outcomes of rhabdomyolysis have not been studied. The current study involved 2,125 patients hospitalized with acute chemical poisoning. Based on clinical and laboratory parameters and treatment outcomes, we found that overall incidence of rhabdomyolysis in our hospital was 0.06% (93 of 143,830 patients admitted), but the incidence associated with acute pesticide intoxication was 1.8% (33 of 1,793 cases). The incidence of rhabdomyolysis after pesticide intoxication was significantly higher in men than in women (P = 0.010). The amount of pesticide ingested was significantly higher in rhabdomyolysis patients than that in those who did not develop rhabdomyolysis (mean ± SD, 114.1 ± 79.5 mL vs 74.1 ± 94.2 mL, P = 0.010). Our results show that pesticide intoxication is a frequent cause of rhabdomyolysis and is more common among men than women. The volume of pesticide ingested, and not the degree of human toxicity, is the main factor influencing the incidence of rhabdomyolysis.

A case of scrub typhus requiring maintenance hemodialysis.

Renal failure caused by scrub typhus is known to be reversible. In most cases, renal function is almost fully restored after appropriate antibiotic treatment. A 71-year-old man was diagnosed with scrub typhus complicated by renal failure. A renal biopsy revealed histopathologic findings consistent with acute tubulointerstitial nephritis. Renal function did not improve 18 months after discharge and the patient required continuous hemodialysis. Although severe renal failure requiring dialysis is a rare complication of scrub typhus, we describe a case of scrub typhus requiring maintenance hemodialysis. To the best of our knowledge, this is the first such report.

Acute oral poisoning due to chloracetanilide herbicides.

Chloracetanilide herbicides (alachlor, butachlor, metachlor) are used widely. Although there are much data about chronic low dose exposure to chloracetanilide in humans and animals, there are few data about acute chloracetanilide poisoning in humans. This study investigated the clinical feature of patients following acute oral exposure to chloracetanilide. We retrospectively reviewed the data on the patients who were admitted to two university hospitals from January 2006 to December 2010. Thirty-five patients were enrolled. Among them, 28, 5, and 2 cases of acute alachlor, metachlor, butachlor poisoning were included. The mean age was 49.8 ± 15.4 yr. The poison severity score (PSS) was 17 (48.6%), 10 (28.6%), 5 (14.3%), 2 (5.7%), and 1 (2.9%) patients with a PSS of 0, 1, 2, 3, and 4, respectively. The age was higher for the symptomatic patients (1-4 PSS) than that for the asymptomatic patients (0 PSS) (43.6 ± 15.2 vs 55.7 ± 13.5). The arterial blood HCO3⁻ was lower in the symptomatic patients (1-4 PSS) than that in the asymptomatic patients (0 PSS). Three patients were a comatous. One patient died 24 hr after the exposure. In conclusion, although chloracetanilide poisoning is usually of low toxicity, elder patients with central nervous system symptoms should be closely monitored and cared after oral exposure.

Cellular toxicity of surfactants used as herbicide additives.

The cellular toxicities of surfactants, a solvent, and an antifreeze that are included in herbicide formulations were assessed by measuring their effects on membrane integrity, metabolic activity, mitochondrial activity, and total protein synthesis rate in a cell culture. Polyethylene glycol, propylene glycol, and monoethylene glycol exhibited no cellular toxicity even at a high concentration of 100 mM. Sodium lauryl ether sulfate and polyoxyethylene lauryl ether significantly damaged the membrane, disturbed cellular metabolic activity, and decreased mitochondrial activity and the protein synthesis rate; however, their toxicity was far below those of the severely toxic chemicals at comparable concentrations. The severely toxic category included polyoxypropylene glycol block copolymer, polyoxyethylene tallow amine, and polyoxyethylene lauryl amine ether. These surfactants were cytotoxic between 3.125 µM and 100 µM in a dose-dependent manner. However, the toxicity graph of concentration vs toxicity had a point of inflection at 25 µM. The slope of the toxicity graph was gentle when the concentration was below 25 µM and steep when the concentration was greater than 25 µM. In conclusion, our results suggest that the toxicity of surfactants be taken care of pertinent treatment of acute herbicide intoxication.

Effects of neutral pH and low-glucose degradation product-containing peritoneal dialysis fluid on systemic markers of inflammation and endothelial dysfunction: a randomized controlled 1-year follow-up study.

BACKGROUND: The local peritoneal effects of low-glucose degradation product (GDP)-containing peritoneal dialysis fluid (PDF) have been extensively described. However, the systemic effects of prolonged prescription of these solutions are unknown. This study aimed to evaluate the effects of neutral pH and low-GDP PDF on systemic inflammation and endothelial dysfunction markers in peritoneal dialysis (PD) patients. METHODS: This is a multicenter, open labeled, randomized controlled trial including one hundred fifty-two patients initiating continuous ambulatory peritoneal dialysis for end-stage renal disease from seven centers in Korea. Participants were randomly allocated to conventional PDF (Stay safe®; Fresenius Medical Care, Bad Homburg, Germany) or low-GDP PDF (Balance®; Fresenius Medical Care) and were followed for 1 year. Primary outcome variable was the inflammation and endothelial dysfunction index (IEDI), a composite score derived from serum levels of soluble intercellular adhesion molecule (sICAM)-1, soluble vascular cellular adhesion molecule (sVCAM)-1 and high-sensitivity C-reactive protein (hs-CRP). sICAM-1, sVCAM-1, residual renal function (RRF), peritoneal membrane transport characteristics, ultrafiltration volume and nutritional parameters were measured as secondary outcome variables. RESULTS: Of 152 patients randomized, 146 (low-GDP: conventional PDF, 79:67) patients entered the trial (46% male, 53% with diabetes mellitus). At 12-month follow-up, the low-GDP group had significantly lower levels of IEDI, sICAM-1 and sVCAM-1 compared to the conventional group; hs-CRP was not different between groups. Peritoneal transport characteristics, RRF, nutritional parameters, incidence of peritonitis and death-censored technique survival were not different between groups. CONCLUSION: Neutral pH and low-GDP PDF likely produce fewer changes in markers of endothelial dysfunction compared to conventional PDF in incident PD patients.

Hyperuricemia as a marker for progression of immunoglobulin A nephropathy.

BACKGROUND: The variable clinical and histopathological manifestations of immunoglobulin A nephropathy (IgAN) make it difficult to predict disease progression. A recent study showed that hyperuricemia, a condition common in hypertension and vascular disease, may contribute to renal dysfunction and histological changes including renal arteriosclerosis, tubular atrophy, and interstitial fibrosis. Herein, we investigated the clinical significance of uric acid level at the time of biopsy, as a marker of IgAN progression. METHODS: We included 193 patients with biopsy-proven IgAN. Renal disease progression was defined as serum creatinine elevation above 1.2 mg/dL or over 20% elevation from baseline. Hyperuricemia was defined as a serum uric acid level ≥7.3 mg/dL in men and ≥5.3 mg/dL in women, which were 1 standard deviation above the mean value in the normal subjects. RESULTS: The hyperuricemia group (n=50) had higher blood pressure, body mass index, and serum creatinine, and a greater amount of proteinuria and a lower glomerular filtration rate than the nonhyperuricemia group (n=143). Hyperuricemia increased the risk of IgAN progression (odds ratio, 4.53; 95% confidence interval, 1.31-15.66). The disease progression group (n=26) had a greater frequency of hyperuricemia, hypertension, and nephrotic range proteinuria than the nonprogression group (n=119). The renal survival analysis showed that the hyperuricemia group had a higher rate of IgAN disease progression. CONCLUSION: Hyperuricemia at the time of diagnosis is an important marker for IgAN progression.

Surfactant volume is an essential element in human toxicity in acute glyphosate herbicide intoxication.

BACKGROUND: Glyphosate, one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The purpose of this study was to determine the effect of glyphosate-surfactants ("glyphosate-surfactant toxicity") in patients with acute glyphosate intoxication. METHODS: In all, 107 patients (69 men and 38 women, aged 52.3 ± 15.5 years) with acute glyphosate intoxication were enrolled in this study. From their medical records, we identified the formulation of ingested glyphosate products and derived clinical parameters, which focused on clinical outcome, admission days, duration in the intensive care unit, development of respiratory failure, cardiovascular deterioration, renal failure, altered mental status, and convulsions. The effect of surfactants on clinical complications was also assessed. RESULTS: For surfactant ingestion volumes of 8 mL, the incidence of clinical complications was (in rank order) as follows: hypotension, 47.1%; mental deterioration, 38.6%; respiratory failure, 30.0%; acute kidney injury, 17.1%; and arrhythmia, 10.0%. These complications were influenced by the volume of surfactant and not the type of surfactant-ingredient in the herbicide product. Two patients died of refractory shock, metabolic acidosis, and respiratory failure. However, the final clinical outcomes of the surviving patients were benign, and cardiovascular, respiratory, kidney, and mental functions were fully restored to normal levels. CONCLUSIONS: Our results indicate that treatment of patients with acute glyphosate herbicide intoxication should take into account the volume and not the type of surfactants in herbicide formulations.

Clinical outcome of acute intoxication due to ingestion of auxin-like herbicides.

BACKGROUND: The human toxicity of synthetic auxin analogue herbicides has not been extensively studied. METHODS: Clinical outcome was assessed from medical records of 17 patients who had intentionally ingested auxin pesticides with active ingredients like dicamba, triclopyr, MCPA or mecoprop. The patients were interviewed after discharge to follow outcome (interval 2 to 56 months). RESULT: One patient who had ingested 500 mL of a mecoprop product died of hypotension and respiratory failure 36 hours after hospital admission. The other 16 patients recovered and were discharged by hospital day 28. After discharge, four patients died from causes not related to herbicide intoxication. In the 12 surviving patients, no long-term effects were reported. CONCLUSION: Human toxicity of synthetic auxins appears relatively benign with conservative treatment. However, when the amount ingested is above several hundred milliliters of commercial product, especially in combination of mecoprop with other intoxicants (e.g. alcohol), shock with respiratory failure may develop and lead to death.

Tissue plasminogen activator and plasminogen activator inhibitor-1 levels in patients with acute paraquat intoxication.

To investigate the effects of reactive oxygen species (ROS) on tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) plasma levels, and their possible implications on clinical outcome, we measured tPA and PAI-1 levels in 101 patients with acute paraquat (PQ) intoxication. The control group consisted of patients who ingested non-PQ pesticides during the same period. tPA and PAI-1 levels were higher in the PQ group than in the controls. PQ levels were significantly correlated with ingested amount, timelag to hospital, tPA level, and hospitalization duration. tPA levels were correlated with PAI-1, fibrin degradation product (FDP), and D-dimer. D-dimer levels were lower in the PQ group than in the controls. Univariate analysis indicated the following significant determinants of death: age, ingested amount, PQ level, timelag to hospital, serum creatinine, lipase, pH, pCO(2), HCO(3) (-), WBC, FDP, PAI-1, and tPA. However, multivariate analysis indicated that only PQ level was significant independent factor predicting death. In conclusion, tPA and PAI-1 levels were higher, while D-dimer levels were lower in the PQ group than in the controls, implying that ROS stimulate tPA and PAI-1, but PAI-1 activity overrides tPA activity in this setting. Decreased fibrinolytic activity appears to be one of the clinical characteristics of acute PQ intoxication.

Serum uric acid level as a marker for mortality and acute kidney injury in patients with acute paraquat intoxication.

BACKGROUND: Paraquat (PQ) is a non-selective herbicide that generates reactive oxygen species (ROS) in vivo. Uric acid emerged as a marker of oxidative stress and may enhance ROS-mediated injury in acute PQ intoxication. Therefore, we investigated the association between uric acid levels and mortality and acute kidney injury (AKI) in the present study. METHODS: From January 2007 to December 2008, patients who arrived at our hospital with acute PQ intoxication (n = 513) were included in the study. Patients were divided into two groups (hyperuricaemia vs non-hyperuricaemia) based on uric acid levels. Mortality and AKI were analysed in reference to uric acid level. RESULTS: Patient mortality was higher in the hyperuricaemia group than the non-hyperuricaemia group (68.4% vs 38.3%, P < 0.05). The incidence of AKI and kidney failure was 64% and 43.3%, respectively. Hyperuricaemia increased the risk of mortality and kidney failure to 3.7- and 3.3-fold after adjustments for age, sex and the estimated amounts of PQ ingestion. Mean serum uric acid level was higher in death group than survival group and higher in kidney failure group than non-AKI group and non-failure group. CONCLUSIONS: Baseline serum uric acid level might be a good clinical marker for patients at risk of mortality and AKI after acute PQ intoxication.

Effect of glutathione on the cadmium chelation of EDTA in a patient with cadmium intoxication.

In order to evaluate the efficiency and renal protective effects of glutathione during Ca(++)-EDTA chelation therapy for chronic cadmium intoxication, we measured the renal excretion of cadmium, ß(2)-microglobulin, proteinuria, and hematuria during intravenous administration of glutathione with Ca(++)-EDTA in a 54-year-old patient with chronic cadmium intoxication. We administered 500 mg of Ca(++)-EDTA and 50 mg/kg of glutathione alone or in 1 L of normal saline over the next 24 hours and repeated this over 12 consecutive days. During the first 3 days, the basal levels (only saline administration) were determined; during the second 3 days, Ca(++)-EDTA only was administered, for the third sequence of 3 days, Ca(++)-EDTA with glutathione was provided, and for the last 3 days, glutathione alone was given. One month later, the same protocol was repeated. There were six blood and urine samples to analyze in each group. The blood cadmium level was higher when the EDTA was infused together with glutathione (7.44 ± 0.73 µg/L, p < 0.01) compared to the basal level of 4.6 ± 0.44 µg/L. Also, the renal cadmium excretion was significantly higher in the EDTA with glutathione group than in the basal group (23.4 ± 15.81 µg/g creatinine vs 89.23 ± 58.52 µg/g creatinine, p < 0.01). There was no difference in the protein/creatinine and ß(2)-microglobulin/creatinine ratio in the urine (p > 0.05) among the groups. Furthermore, microhematuria and proteinuria did not develop over the observation period of 6 months. These results suggest that glutathione administration with EDTA might be an effective treatment modality for patients with cadmium intoxication.

Association of the superoxide dismutase (V16A) and catalase (C262T) genetic polymorphisms with the clinical outcome of patients with acute paraquat intoxication.

BACKGROUND/AIMS: Many patients with acute paraquat (PQ) intoxication die even at low PQ concentrations, whereas others with similar concentrations recover. Therefore, it is possible that individual differences in antioxidant capacity are responsible for the variable clinical outcome in patients with acute PQ intoxication. METHODS: We investigated whether there was a relationship between the genetic polymorphisms of SOD (V16A), catalase (C262T), and GPX1 (C593T) in 62 patients with acute PQ intoxication and the clinical outcomes of these patients. RESULTS: The frequency of the Mn-SOD V/V, V/A, and A/A genotypes were 56.3, 43.5, and 0% in survivors and 86.9, 13.1, and 0% in non-survivors (p > 0.05). The GPX1 C/C, C/T, and T/T genotypes were present in 100, 0, and 0% of all subjects. The catalase C/C, C/T, and T/T genotypes were present in 100, 0, and 0% of survivors, and in 82.6, 17.4, and 0% of non-survivors. Neither erythrocyte SOD activity nor catalase activity were significantly different between survivors and non-survivors. CONCLUSIONS: No association was found between clinical outcome of acute PQ intoxication and the genetic polymorphism of GPX1 (C593T) or the genetic polymorphisms or enzyme activity of superoxide dismutase (V16A) or catalase (C262T).

Sequential change of asymmetric dimethylarginine levels after initiation of peritoneal dialysis in patients with end-stage renal disease.

BACKGROUND: We hypothesized that the asymmetric dimethylarginine (ADMA) metabolism in end-stage renal disease may be linked to the rate of protein turnover and to the vast pool of amino acids. In order to determine a correlation between the plasma levels of ADMA and the protein catabolic rate, we measured the ADMA levels as well as nutritional markers such as the normalized protein catabolic rate (nPCR) in patients with newly initiated continuous ambulatory peritoneal dialysis (CAPD). METHODS: Twenty-four patients were recruited for this study. All patients were on the standard CAPD protocol, and followed for at least 1 year. Blood samples were collected at baseline before the initiation of peritoneal dialysis, and every 6 months for 1 year. The blood parameters studied included the serum albumin, total cholesterol, glucose, urea nitrogen, creatinine and ADMA. Peritoneal equilibrium test and measurements of weekly Kt/Vurea and nPCR were performed within 4 weeks of the blood sampling. RESULTS: The change of ADMA levels over 1 year was positively correlated with that of haemoglobin (r = 0.592, P = 0.002) and nPCR during the same period (r = 0.508, P = 0.026). CONCLUSION: The findings of our study suggest that nPCR might influence the change of ADMA levels after initiation of CAPD.

Effect of glutathione administration on serum levels of reactive oxygen metabolites in patients with paraquat intoxication: a pilot study.

BACKGROUND/AIMS: Based on preliminary in vitro data from a previous study, we proposed that 50 mg/kg glutathione (GSH) would be adequate for suppressing reactive oxygen species in patients with acute paraquat (PQ) intoxication. METHODS: Serum levels of reactive oxygen metabolites (ROM) were measured before and after the administration of 50 mg/kg GSH to each of five patients with acute PQ intoxication. RESULTS: In one patient, extremely high pretreatment ROM levels began to decrease prior to GSH administration. However, in the remaining four cases, ROM levels did not change significantly prior to GSH administration. ROM levels decreased significantly after GSH administration in all cases. In two cases, ROM levels decreased below that observed in the general population; one of these patients died after a cardiac arrest at 3 hours after PQ ingestion, while the other represented the sole survivor of PQ intoxication observed in this study. In the survivor, ROM levels decreased during the first 8 hours of GSH treatment, and finally dropped below the mean ROM level observed in the general population. CONCLUSIONS: Treatment with 50 mg/kg GSH significantly suppressed serum ROM levels in PQ-intoxicated patients. However, this dose was not sufficient to suppress ROM levels when the PQ concentration was extremely high.

Clinical outcome of hemoperfusion in poisoned patients.

Extracorporeal removal techniques are effective methods for toxin removal from the body. To define the safety and clinical outcomes of hemoperfusion, we evaluated retrospectively clinical outcomes of hemoperfusion over a 3-year period in our clinical center. From January 2006 to December 2008, we analyzed 803 patients. Mortality, catheter-related bleeding, systemic bleeding, hypocalcemia, and thrombocytopenia were investigated. Medical drugs (n = 54) and pesticide toxins (n = 749) were represented. Pesticides included herbicides (n = 598), insecticides (n = 130), mixed herbicides and insecticides (n = 4), and unknown pesticides (n = 17). Among those with herbicide poisoning, 493 cases were caused by paraquat, and among those affected by insecticides, 67 cases were caused by organophosphate insecticides. After hemoperfusion, systemic bleeding complications were observed in 26 cases (3.0%). Systemic bleeding was a greater mortality risk factor than nonsystemic bleeding (OR 2.779, 95% CI 1.07-7.23). Hypocalcemia was observed in 69.1% and thrombocytopenia in 31.1%. Excess mortality was 44.4%. In hemoperfusion cases, systemic bleeding is a major factor to predict adverse outcome.

Comparison of patients starting hemodialysis with those underwent hemodialysis 15 years ago at the same dialysis center in Korea.

BACKGROUND/AIMS: Maintenance dialysis is made decreased the death rate of patients with end-stage renal disease; however, mortality is still high. The aim of this study was to identify the association between clinical parameters at the start of hemodialysis with survival and compare these findings with data from patients who underwent hemodialysis about 15 years ago at the same dialysis center. METHODS: We reviewed 117 patients who started hemodialysis between 2000 and 2004. We analyzed medical histories, laboratory findings, and clinical outcomes, and compared them with patients who started hemodialysis 15 years ago at the same center. RESULTS: The proportion of elderly patients and those with diabetes increased from 17% and 18% in the previous study to 33% and 49% in this study, respectively. Elderly and patients with diabetes had much higher mortalities than their counterparts. Nevertheless, the overall survival rate (66% vs. 71% at 5 years) and survival of patients with diabetes improved (55% vs. 75% at 1.5 years). Common causes of death were infection and cardiovascular disease in the present study; however, inadequate dialysis accounted for 25% of deaths in the previous study. CONCLUSIONS: The overall survival rate of patients undergoing hemodialysis has improved over the 15-year interval, even with an increased proportion of elderly patients and patients with diabetes. Adequate dialysis and further medical improvements could ameliorate mortality in patients undergoing dialysis.

Plasma level of malondialdehyde in the cases of acute paraquat intoxication.

UNLABELLED: BACKGROUND, MATERIAL, AND METHODS: To assess plasma malondialdehyde (MDA) level as a clinical marker in acute paraquat (PQ) intoxication, we sequentially investigated 74 patients (40 males and 34 females, aged 49.9 +/- 16.2 years), all of whom ingested PQ as a means of suicide from July to December 2008. RESULTS: The baseline level of MDA (10.8 +/- 3.5 microM) had no correlation with plasma PQ levels of 22.1 +/- 48.7 microg/mL (median: 1.9, range <0.01-228.5) or with volume of PQ ingested. However, the following parameters were significantly different between survivors and nonsurvivors: the amount of PQ ingestion, plasma PQ levels, basal MDA levels, WBC, hemoglobin, hematocrit, platelet counts, albumin, BUN, creatinine, potassium, amylase, and arterial blood gas analysis (pH, pCO(2), HCO(-)(3)).The nonsurvivors' baseline MDA (11.4 +/- 3.8 vs. 9.8 +/- 2.8, p = 0.040) was higher than the survivors. However, the baseline level was not a predictor of mortality in the univariate and the multivariate binary logistic analyses. Among the patients whose MDA levels were measured sequentially, 58.3% of the patients (35 out of 60) showed fluctuating MDA levels, 25% (n = 15) showed steady decreases, with only 16.6% (n = 10) showing steady increases in MDA levels during the observation period. These findings imply the presence of active MDA metabolism and/or that the half-life of MDA is very short in the human body. CONCLUSION: Both cross-sectional and sequential measurements of plasma MDA do not provide reliable information on outcome in patients with acute PQ intoxication.