Iatrogenic pediatric hydroxocobalamin overdose.

INTRODUCTION: Hydroxocobalamin, a precursor molecule to vitamin B12, has emerged as the preferred empiric treatment for patients rescued from enclosed-space fires with concern for inhalational injury and potential concomitant cyanide toxicity. Limited data exist on the effects of hydroxocobalamin toxicity, particularly in pediatric patients. CASE REPORT: We report a case of a healthy three-year old girl who was rescued from an apartment fire and electively intubated by prehospital providers. Due to concern for potential cyanide toxicity, she received 5 g (373 mg/kg) of intravenous hydroxocobalamin, an amount equivalent to one standard adult dose but over five times the appropriate weight-adjusted dose for this 13.4-kilogram child. On hospital arrival, patient was noted to have chromaturia and diffuse erythroderma without cutaneous burns. She was extubated 4 h after prehospital intubation and discharged home the following morning in good condition with persistent erythroderma. Skin color returned to normal within two days. DISCUSSION: We believe this to be the first reported case of iatrogenic pediatric hydroxocobalamin overdose for the treatment of suspected cyanide toxicity. Erythroderma and chromaturia are expected side effects of hydroxocobalamin, even at therapeutic levels. Along with minor airway burns, the only other finding was a transient and hemodynamically neutral bradycardia, which began shortly after prehospital intubation. As this bradycardia occurred prior to hydroxocobalamin administration, more likely culprits include vagal nerve stimulation from direct laryngoscopy, and sinoatrial muscarinic receptor stimulation caused by repeated doses of succinylcholine. In all, we were unable to appreciate any complications due to excess hydroxocobalamin administration.

Fatal Folic Acid Toxicity in Humans.

Folic acid is B-9 vitamin. Folic acid is prescribed commonly for pregnant women to prevent neural tube defects in the fetus, patients under chemotherapy, pernicious anemia and to reduce the risk of stroke and cardiovascular disease. Acute or chronic ingestion of a large dose of folic acid generally manifests as neurological complications, which are reversible. In this present case, a 23-year-old pregnant woman committed suicide by consuming folic acid tablets and succumbed to death within 36 h. Postmortem toxicological analysis detected folic acid in viscera. Death following acute consumption of folic acid is rare and has been not reported in the literature, to the best of our knowledge.

Pyridoxine-induced sensory ataxic neuronopathy and neuropathy: revisited.

High dose pyridoxine is neurotoxic. Previous case reports were sparse and little is known about the clinical and electrodiagnostic findings. Three patients with pyridoxine-induced sensory ataxic neuropathy were studied and a review of the involved literature was performed. Three patients, aged 80, 83 and 83 years old, presented with sensory ataxia for 3-8 months. Examination showed signs of polyneuropathy and sensory ataxia. Six hundred milligrams of pyridoxine was consumed each day for 3-10 years, in the form of vitamin B1-6-12 combination tablet. Investigations for other causes of neuropathy were unremarkable. Blood levels of vitamin B6 were markedly elevated at 104.6, 81.4 and 66.9 times of upper normal limits. Electrodiagnostic tests showed symmetric axonal sensory polyneuropathy in two patients. Two years after vitamin discontinuation, all patients showed no significant improvement in the neuropathy and gait. In conclusion, consumption of high dose pyridoxine can cause sensory neuronopathy and axonal sensorimotor polyneuropathy, leading to sensory ataxia which may not be reversible.

Severe sensorimotor neuropathy after intake of highest dosages of vitamin B6.

We illustrate a white caucasian patient with a severe sensorimotor neuropathy due to vitamin B6 hypervitaminosis. The patient used the pendulum to calculate his daily metabolic demands and ingested 9.6g pyridoxine/day. To our knowledge, this is the highest dosage of vitamin B6 administered to humans over prolonged periods of time ever reported in the medical literature. The unique aspect of this case is the muscle weakness and motor findings on electrophysiological testing in what is suggested by the literature to be a pure sensory neuronopathy.

Toxicity from the use of niacin to beat urine drug screening.

Niacin (vitamin B3) is promoted for rapidly clearing the body of drugs of abuse, such as cocaine and cannabis, and is alleged to interfere with urine drug screening. We present 4 cases of such novel use associated with significant adverse effects. Two cases had isolated skin manifestations, whereas the other 2 presented with life-threatening manifestations, including nausea, vomiting, dizziness, hepatotoxicity, metabolic acidosis, and hypoglycemia evolving into hyperglycemia. One patient also had profound neutrophilia and QT(C)-interval prolongation. All patients improved after cessation of the drug use and supportive treatment. Health care providers should be aware of these potential adverse effects of niacin and of the misguided use of this vitamin by patients seeking to interfere with urine drug screening.

Critical evaluation of the current studies on pangamic acid--vitamin B15.

The research on pangamic acid (vitamin B15) has been conducted by specialists in many fields of science for along time. This, however, has not put an end to controversies around the problem of its therapeutic effect. The solution to the basic problems, i.e. defining the compound structure, finding an explicit method of its determination and identification as well as the evidence of its biochemical and physiological functions in the human organism appears as distant as ever. It has been found out, however, that either some preparations referred to as pangamic acid (vitamin B15) or their components may be detrimental to man's health.