123I-FP-CIT SPECT and MRI Findings in a Patient With Parkinsonism After Fenpyroximate Intoxication.

Fenpyroximate is a widely used acaricide. Its main action is to inhibit the mitochondrial respiratory chain. Chronic exposure to fenpyroximate is associated with dopaminergic cell loss and parkinsonism; however, to date, there has not been a reported case of parkinsonism as a result of acute fenpyroximate intoxication. Here, we report a 58-year-old man who developed parkinsonism after deliberate fenpyroximate intoxication, but with normal presynaptic I-Ioflupane SPECT image.

A case of Fanconi syndrome due to a deferasirox overdose and a trial of plasmapheresis.

WHAT IS KNOWN AND OBJECTIVE: Deferasirox has nephrotoxic effects in the context of chronic therapy. This case report illustrates proximal tubular dysfunction (Fanconi syndrome) due to an acute deferasirox overdose. CASE DESCRIPTION: In response, we trialled plasmapheresis to eliminate the drug. Deferasirox levels were obtained in the context of three rounds of plasmapheresis. Given the half-life model of decay, we concluded that plasmapheresis may not have been successful. The patient ultimately recovered normal tubular function after 2 months. WHAT IS NEW AND CONCLUSION: This report is the first to describe acute deferasirox-induced nephrotoxicity, and the application of plasmapheresis that, ultimately, did not change the typical time to recovery.

A case of near-fatal fenpyroximate intoxication: the role of percutaneous cardiopulmonary support and therapeutic hypothermia.

INTRODUCTION: Fenpyroximate is a potent inhibitor of the mitochondrial proton-translocating NADH-quinone oxidoreductase (complex I). Although it is widely used as an acaricide, data on the acute toxicity of fenpyroximate in humans are very limited. CASE DETAIL: A 44-year-old woman was brought to our hospital with a reduced level of consciousness, hypotension, and severe lactic acidosis after deliberate ingestion of 5% fenpyroximate solution. The acidosis progressively deteriorated despite maximal supportive treatment, and cardiac arrest refractory to standard cardiopulmonary resuscitation developed. The patient was successfully resuscitated with percutaneous cardiopulmonary support, therapeutic hypothermia, and intravenous acetylcysteine. Blood gases of simultaneously obtained arterial and central venous blood revealed decreased arteriovenous oxygen difference. DISCUSSION: The present case, along with previous cases of fatal complex I inhibitor poisoning, indicates that impaired oxygen utilization at the tissue level is the major mechanism underlying the fatality of this condition. Percutaneous cardiopulmonary support may help restore vital organ perfusion by increasing oxygen delivery even in the presence of decreased oxygen consumption, thereby allowing additional time for recovery and drug metabolism. Therapeutic hypothermia also may be beneficial in treating severe complex I inhibitor poisoning, since hypothermia itself attenuates oxidative processes and decreases the metabolic rate.

Acute human self-poisoning with bispyribac-containing herbicide Nominee: a prospective observational study.

INTRODUCTION: Self-poisoning with herbicides is an important reason for hospital admission and death in Asia. Although some herbicides have a well-described toxicity profile in humans, many of the newer compounds rely on extrapolation from animal results as no published literature on clinical outcomes of human self-poisoning has been described. One example of these compounds is bispyribac, a selective herbicide used in rice and wheat cultivation that is marketed in two containers, one containing bispyribac 400 g/L with a solvent and the other the surfactant, polyethylene glycol. We present the first case series of acute human self-poisoning with an herbicide product containing bispyribac. METHODS: Clinical data for all patients who presented with acute poisoning from a bispyribac-containing herbicide (Nominee) to two general hospitals in Sri Lanka from June 2002 to January 2009 were collected prospectively. Admission and serial blood samples were collected from consenting patients to confirm exposure and to study the toxicokinetics of bispyribac, respectively. RESULTS: One hundred ten patients with a history of bispyribac ingestion presented after a median time of 4 h post-ingestion. There were three deaths at 15, 6, and 5 h post-ingestion because of asystolic cardiac arrest. All three patients had reduced Glasgow Coma Score (GCS) (3, 12, and 13, respectively) of whom the former two had co-ingested ethanol and developed tonic-clonic seizures. Admission blood sample was obtained from the former two of these patients but bispyribac was detected in only one of these patients. The other patient presented 2.5 h post-ingestion with a GCS of 12 but bispyribac was not detected. Excluding the patient with undetectable bispyribac, a conservative estimate of the case fatality ratio at 1.81% (95% confidence interval 0.32-5.8) can be made. The majority of the remaining patients had self-limiting upper gastrointestinal symptoms and eight patients had an abnormal GCS on presentation to hospital. The overall median hospital stay was 3 days. Bispyribac was not detectable on admission in 21 patients; in the remaining patients, the median plasma concentration was 50.55 microg/mL (interquartile range 1.28-116.5; n=32). The peak concentration was noted around 3 h post-ingestion and plasma bispyribac concentration did not predict the severity of poisoning. CONCLUSION: The majority of patients developed self-resolving symptoms and were successfully managed in rural general hospitals without transfer to larger tertiary hospitals. Patients who died developed significant poisoning within 6 h and plasma bispyribac concentrations did not appear to predict mortality. The lack of correlation between bispyribac outcomes and the available plasma concentrations may be because of exposure to nonbispyribac components or other undefined factors. Clinical outcomes from acute self-poisoning with bispyribac-containing herbicides appear to be relatively more favorable than other commonly used herbicides.

Pharmacokinetic study of a patient intoxicated with 2,4-dichlorophenoxyacetic acid and 2-methoxy-3,6-dichlorobenzoic acid.

A simultaneous pharmacokinetic study of two chemicals has been conducted on a clinically stabilized human who had intentionally ingested a mixture of 2,4-D and Dicamba. The information developed can be useful to the clinical toxicilogist in the management of similar cases.