Ciguatera Fish Poisoning (CFP) is the most frequently reported seafood-toxin illness in the world. It causes substantial human health, social, and economic impacts. The illness produces a complex array of gastrointestinal, neurological and neuropsychological, and cardiovascular symptoms, which may last days, weeks, or months. This paper is a general review of CFP including the human health effects of exposure to ciguatoxins (CTXs), diagnosis, human pathophysiology of CFP, treatment, detection of CTXs in fish, epidemiology of the illness, global dimensions, prevention, future directions, and recommendations for clinicians and patients. It updates and expands upon the previous review of CFP published by Friedman et al. (2008) and addresses new insights and relevant emerging global themes such as climate and environmental change, international market issues, and socioeconomic impacts of CFP. It also provides a proposed universal case definition for CFP designed to account for the variability in symptom presentation across different geographic regions. Information that is important but unchanged since the previous review has been reiterated. This article is intended for a broad audience, including resource and fishery managers, commercial and recreational fishers, public health officials, medical professionals, and other interested parties.

Nitric oxide 10 ppm and inhaled aerosolized prostacyclin 50 ng/kg/min were compared as selective pulmonary vasodilators in five patients with hypoxaemia secondary to acute respiratory distress syndrome. Neither agent resulted in systemic haemodynamic changes, indicating true pulmonary selectivity. Inhaled aerolized prostacyclin improved oxygenation to a degree comparable to nitric oxide, as measured by the arterial alveolar oxygen partial pressure gradient and shunt fraction.

1 We report a case of venlafaxine overdose and describe pharmacokinetic data on drug disposition. 2 Case report. Serial venlafaxine levels were measured and drug half-life calculated and compared to data at therapeutic concentrations. Metabolite concentrations were also measured and the potential for toxicity described with reference to individual variation in such metabolism 3 Venlafaxine can cause significant cardiac and neurotoxicity. Its potential for causing such toxicity may be dependent on whether an individual has the extensive metaboliser cytochrome CYP2D6 phenotype or the poor metaboliser phenotype

Untreated ciguatera was associated acutely with significant subjective neurotoxicity symptoms and anxiety which were transient, but not with objectively measured cognitive changes. Future investigation with a larger sample size is warranted.