Case of levodopa toxicity from ingestion of Mucuna gigantea.

Hawai'i is home to 1000 native species of flowering plants. Mucuna gigantea is one such Hawaiian species which has been studied as affordable sustenance and as a cover crop in developing countries. Mucuna gigantea and other Mucuna species (spp.) in general, are known to contain natural levodopa and its utility in the treatment of Parkinson's Disease has also been evaluated. Levodopa is converted in the periphery into dopamine which can then act on dopamine receptors to cause nausea, vomiting, arrhythmias, and hypotension. We describe a case in which a patient presents with abdominal pain, nausea, and vomiting after legume ingestion. The bean was ultimately identified as Mucuna gigantea and the patient was diagnosed with levodopa-induced gastrointestinal toxicity from consumption of the legume. A literature review was conducted using the database search engines, Biological Abstracts and PubMed, with a broad combination of keywords of which include "mucuna, "gigantean," "levodopa," "l-dopa," "toxicity," and the association between Mucuna gigantea ingestion and levodopa toxicity is discussed. These findings expand the differential diagnosis of abdominal pain associated with nausea and vomiting in the correct clinical context.

Acute overdose with controlled-release levodopa-carbidopa.

INTRODUCTION: Reports of acute levodopa-carbidopa overdose are rare and no case of an acute overdose with a controlled-release formulation has been described. We describe such a case in which serial concentrations of catecholamines were measured. CASE REPORT: A 55-year-old man ingested 89 tablets of Sinemet 50/200 (17.8 g of levodopa, 4.45 g of carbidopa). Clinical effects and plasma concentrations of dopamine, noradrenaline and adrenalin were assessed over 66 hours. On admission 2.5 hours after the ingestion, his physical examination was normal except for mydriasis and urine retention. Five hours post-ingestion he had psychomotor agitation, delirium with logorrhea, joviality, visual hallucinations, regular sinus tachycardia and xerostomia. The clinical course included two episodes hypotension and four of transient tachycardia. Treatment was symptomatic and supportive. Clinical toxicity reappeared 48 hours after the intoxication. The patient was discharged at the end of the fourth day with amnesia for the event. DISCUSSION: Dopamine showed an initial plasma concentration peak 14 hours after the toxic ingestion, followed by a second peak 38 hours after the ingestion. The initial peak of noradrenaline occurred 20 hours post-ingestion with a second lower peak at 38 hours. There were no elevations in adrenalin concentrations. CONCLUSION: There appeared to be no correlation between the intensity of the clinical signs and the blood concentrations of dopamine and noradrenaline, although the resolution of the clinical signs did correspond to these catecholamines return to normal values. Patients who ingest controlled-release formulations need to be observed until after the second catecholamine peak.

Glia protect fetal midbrain dopamine neurons in culture from L-DOPA toxicity through multiple mechanisms.

Mesencephalic glia produce soluble factors that protect dopamine neurons from L-DOPA toxicity. The chemical composition of these soluble factors is unknown. We investigated the protective effect against L-DOPA neurotoxicity in midbrain dopamine neurons of fractions of different molecular size of glia conditioned medium and candidate neuroprotective agents produced by glia including neurotrophic factors and antioxidants. Protective effects were evaluated according to the number of tyrosine hydroxylase immunoreactive cells, high affinity dopamine uptake and levels of quinones. Both fractions of glia conditioned medium, smaller and larger than 10kD, protected against L-DOPA, but the fraction of smaller molecular size, that contains small free radical scanvenger molecules, was more effective than the fraction of larger molecular size, that contains large neurotrophic peptides. Among the neurotrophic factors GDNF and BDNF totally prevented L-DOPA neurotoxicity, while NGF and bFGF were less effective. However, only NGF significantly reduced the elevation of quinones induced by L-DOPA. Ascorbic acid, at the concentration found in glia conditioned medium, provided partial protective effect against L-DOPA toxicity. Glutathione, had neurotrophic effects on untreated midbrain dopamine neurons and prevented the effect of L-DOPA. In conclusion, the protective effect against L-DOPA neurotoxicity by glia conditioned medium is mediated by several compounds including neurotrophic factors and small antioxidants.

Carbidopa-levodopa overdose.

A 57-year-old woman ingested 15 to 17 tablets of carbidopa-levodopa 10/100 tablets (carbidopa 150 mg and levodopa 1,500 mg) along with ibuprofen, carisoprodol, hydrocodone, and acetaminophen. The patient developed choreiform movements that persisted despite obtundation and attempts to extinguish them with naloxone, morphine, and diazepam. When the patient developed a rising level of creatine phosphokinase and myoglobinuria, she was treated with ventilatory support and pancuronium. She required paralysis for 60 hours, when her chorea resolved.

Acute overdose with levodopa. Clinical and biochemical consequences.

A 61-year-old parkinsonian patient ingested up to 100 gm of levodopa during a period of 12 hours. Signs of parkinsonism were completely alleviated. Adverse effects included initial hypertension followed rapidly by hypotension of a few hours' duration, prolonged symptomatic postural hypotension, sinus tachycardia, mental confusion, insomnia, and anorexia. The effects of the overdose gradually subsided over 1 week. Analyses of serum and urine for dopa and its metabolites confirmed the overdose, which biochemically resulted in apparent saturation of two enzymatic pathways that inactivate dopamine: conjugation with sulfuric acid and O-methylation.