Niacin toxicity resulting from urine drug test evasion.

BACKGROUND: Niacin, a well-established agent for treating dyslipidemia, has been promoted on the Internet as a method for passing urine drug screening, although there are no data to support its use for this purpose. In a handful of cases, this practice has resulted in serious niacin toxicity. OBJECTIVES: The aim of this article is to describe a unique clinical presentation of niacin toxicity. CASE REPORT: A 23-year-old previously healthy man presented to an Emergency Department with altered mental status, fever, acute renal failure, microangiopathic hemolytic anemia, thrombocytopenia, and coagulopathy. It was revealed that he had taken approximately 22.5 g of sustained-release niacin over the preceding 48 h in an attempt to pass a pre-employment urine drug screen. After a complicated hospital course that included mechanical ventilation for respiratory failure and hemodialysis for acute renal failure, the patient made a full recovery and was discharged 10 days after his initial presentation. CONCLUSION: After a massive niacin overdose, the young man in this case presented with a complex clinical picture that mimicked concurrent thrombotic thrombocytopenic purpura and disseminated intravascular coagulation. Although this patient was fortunate to make a full recovery, the case highlights the potential for multi-system toxicity with niacin overdose, and the potential for harm posed by medical misinformation on the Internet.

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.

Treatment advice on the internet leads to a life-threatening adverse reaction: hypotension associated with Niacin overdose.

We describe a case of massive oral niacin overdose that resulted in severe persistent hypotension without the manifestation of cutaneous flushing. This case is the highest overdose of niacin reported in the literature to date and the first time severe persistent hypotension has been attributed to niacin. A 56-year-old male with a history of schizophrenia presented to the emergency department after orally ingesting 11,000 mg of niacin. The patient cited an Internet resource that recommended high-dose niacin for therapy of schizophrenia as the reason for his ingestion. He stopped his psychiatric medications several weeks prior to his niacin overdose. At presentation, the patient was alert and normothermic. His pulse was 68 beats per minute and his blood pressure was initially 92/41 mmHg. Hypotension with a blood pressure of 58/40 developed over the next few hours and persisted despite intravenous infusion of over 4 liters of normal saline. The physical exam was otherwise unremarkable, specifically without signs of an allergic reaction or cutaneous flushing. He required intravenous dopamine infusion for 12 hours to support a mean arterial blood pressure greater than 60 mmHg. Evaluation for other etiologies of hypotension was unrevealing. Serum niacin levels were 8.2 ug/ mL and 5.6 ug/mL at 48 and 96 hours post ingestion, respectively, giving an apparent T1/2 of 87 hours. Massive overdose of niacin appears to be capable of causing severe, persistent hypotension in the absence of cutaneous flushing. In this case, the ingestion of a dietary supplement based on Internet advice led to a severe adverse reaction.

Acute poisoning with a herbicide containing imazapyr (Arsenal): a report of six cases.

BACKGROUND: Acute pesticide poisoning is a major cause of morbidity and mortality in Taiwan and herbicides are most frequently implicated. Imazapyr [2-(4-isopropyl-4-methyl-5-oxo-2 imidazoline-2-yl)nicotinic acid] is a new herbicide, recently registered in Taiwan under the tradename "Arsenal" (Imazapyr 23.1%, Cyanamid Taiwan Corporation, Taipei). Imazapyr is also marketed as Assault, Chopper, Contain, and Pivot. To the best of our knowledge, there is no information in the literature concerning acute toxicity in humans after ingestion of herbicides containing this compound. METHOD: Six cases of acute poisoning with Arsenal occurred during the period 1993-1997 in a single hospital. Emergency room records and medical charts were reviewed. RESULTS: Of 6 cases, 5 were suicide attempts and 1 was an act of violence inflicted on a child. Three of the 6 patients (50%) presented with severe symptoms, including impairment of consciousness and respiratory distress requiring intubation. Other presentations included metabolic acidosis (2), hypotension (2), leukocytosis (3), fever (2), mild elevation of hepatic transaminase and creatinine (2), unconjugated hyperbilirubinemia (2), oral ulceration (2), pharyngolaryngitis (2), and chemical burns of the cornea (1). All cases had copious vomiting after ingestion of Arsenal. No mortality occurred. CONCLUSION: According to our observations, it appeared the toxic syndrome that results from a large quantity (> 100 mL) of Arsenal herbicide ingestion consists of hypotension, pulmonary dysfunction, oral mucosal and gastrointestinal irritation, and transient liver and renal dysfunction. However, the existence of a dose-response relationship, with increasing amounts of ingestion resulting in more severe symptoms, needs further observation and studies that include a larger series.