Nephrotic syndrome caused by exposures to skin-lightening cosmetic products containing inorganic mercury.

Introduction: Mercury has long been prohibited for use in skin-lightening agents, but such products are still widely available in many parts of the world.Objective: To evaluate the characteristics of subjects with nephrotic syndrome caused by exposures to skin-lightening products containing mercury and the impact of treatments with chelation agents and/or steroids on the time to achieve remission of proteinuria and normal urine mercury concentrations.Methods: We searched Medline and Embase (1971-31 March 2019), Google Scholar (2001-March 2019) and WanFang Data (1999-March 2019), using mercury, mercury poisoning, cosmetics, skin-lightening and nephrotic syndrome as search terms. Affected subjects must have had nephrotic range proteinuria and a renal biopsy performed. The searches revealed 46 citations, but 32 were excluded because of a doubtful history, incomplete data collection, more than one source of mercury exposures, non-nephrotic proteinuria, treatments by herbal medicines and duplicate articles. The 14 remaining reports describing 30 cases formed the basis of this review.Incidence and geographical origins: There was an obvious increase in the number of reports with more complete information from Asia (n = 13) and Europe (n = 1) during 2002-2006 (n = 3) and 2010-2017 (n = 11), involving 3 subjects in 2002-2006 and 27 subjects in 2010-2017.Characteristics of subjects: All 30 subjects were Asian females, mostly aged 18-52 years (median 34 years). Nephrotic syndrome occurred 1-60 months (median 5 months) after exposures to mercury. The proteinuria was heavy (urinary protein excretion 3.2-20.7 g/day, median 5.7 g/day). Other features of mercury toxicity were generally absent. Blood mercury concentrations were normal in 6 subjects and 1.1-10.9 times (median 3.5 times) the upper limit of normal in 14 subjects. Urine mercury concentrations were much higher in 24 subjects, at 1.2-94.6 times (median 9.8 times) the upper limit of normal. Renal biopsy typically revealed minimal change disease (67%) or membranous nephropathy (23%).Etiological importance of mercury: Several clinical observations strongly support the etiological importance of mercury, including a positive relationship between body mercury burden (24-h urine mercury excretion) and severity of proteinuria, the parallel (often proportional) reductions in body mercury burden and proteinuria after cessation of exposures and initiation of chelation therapy and the risk of persistent proteinuria in subjects not treated with chelating agents.Natural history and impact of specific treatments: Spontaneous recovery (within 1.5 months) of mercury-induced nephrotic syndrome was rare.Twenty-three subjects were treated with chelating agents (n = 7) or chelating agents plus steroids (n = 16). There was relatively clear information on the time to remission of proteinuria (urine protein <150 mg/day) in nine subjects following chelation therapy (n = 5) or chelation therapy plus steroids (n = 4) (median 2 months, range 1-9 months). In comparison, the time to remission was longer in three subjects not treated with chelation therapy (≥12 months). There were fewer reports with relatively clear information on the time to achieve normal urine mercury concentrations (<35 nmol/day, <50 nmol/L or <5.0 nmol/mmol creatinine). In four subjects with treatment by chelating agents (n = 1) or chelating agents plus steroids (n = 3), this took 9-16 months (mean ∼11 months). The adjunctive role of steroids in mercury-induced nephrotic syndrome was unclear.Conclusions: Repeated exposures to inorganic mercury in skin-lightening cosmetic products typically cause minimal change disease or membranous nephropathy, resulting in nephrotic syndrome. Apart from cessation of product use, chelation therapy is clearly indicated, in view of the etiological importance of mercury and the presence of increased body burden with target organ damage. The optimal dosages and treatment strategies for unithiol (2,3-dimercapto-1-propanesulfonic acid) and succimer (dimercaptosuccinic acid) have yet to be determined.

The Impact of Lifestyle Changes on Cardiometabolic Health in Modernizing China: A Tale of Three Gorges in the Yangtze River.

Background: Modernization of Chinese adults is associated with increased atherosclerotic diseases. Over 1 million farmers have been resettled upland since 1996 in the Three Gorges dam project of the Yangtze River, with job and other lifestyle changes. We aimed to evaluate the impact of such rapid lifestyle changes on indices of cardiometabolic health. Methods: Ninety-five ex-farmers in Wu Shan (WS) (aged 49.7 ± 9 years) resettled uphill for 3-5 years and 87 age and gender-matched farmers in Da Chang (DC) (aged 48.8 ± 10 years) studied before resettlement were compared. Carotid intima-media thickness (IMT) was measured by ultrasound. Results: Ninety-nine percent WS residents adopted nonfarming jobs or were retired. WS ex-farmers had higher waist-hip ratio (P < 0.0001), low density lipoprotein-cholesterol (P = 0.001), triglycerides (P = 0.001), and prevalence of metabolic syndrome (MS) (43.2% vs. 17.2%, P = 0.01) compared with DC farmers. Smoking status, body mass index, systolic and diastolic blood pressures, high density lipoprotein-cholesterol, and fasting glucose were similar. Carotid IMT was significantly higher in WS residents (0.71 ± 0.16 mm) than in DC farmers (0.64 ± 0.11 mm) (P < 0.001). MS correlated with job changes to more sedentary nature (ß = 0.453, P < 0.0001), but not to leisure exercise activities, nor any specific dietary habits. On multivariate regression, carotid IMT was associated with WS location (ß = 0.196, P = 0.021) and presence of MS (ß = 0.208, P = 0.021), independent of other traditional vascular risk factors (model R2 value = 0.444, F-value 12.0, P < 0.0001). Conclusion: Rapid lifestyle and job changes in ex-farmers in the Three Gorges region are associated with significantly worse cardiometabolic profiles and subclinical atherosclerosis, with potentially important implications for atherosclerosis prevention in modernizing China.

Methanol as an Unlisted Ingredient in Supposedly Alcohol-Based Hand Rub Can Pose Serious Health Risk.

Alcohol-based hand rub (hand sanitizer) is heavily used in the community and the healthcare setting to maintain hand hygiene. Methanol must never be used in such a product because oral, pulmonary and/or skin exposures can result in severe systemic toxicity and even deaths. However, sporadic cases of acute poisoning indicate that alcohol-based hand rub with undeclared methanol may be found in the market from time to time. The unexpected presence of methanol poses a serious threat to public health. Unintentional ingestion by young children and inadvertent consumption by older subjects as alcohol (ethanol) substitute can occur. Methanol is more lethal and poisoning often requires antidotal therapy, in addition to supporting therapy and critical care. However, specific therapy may be delayed because the exposure to methanol is initially not suspected. When repeatedly used as a hand rub, skin absorption resulting in chronic toxicity (e.g., visual disturbances) occurs, particularly if methanol induced desquamation and dermatitis are present. Nationwide surveillance systems, regional/international toxicovigilance networks and situational awareness among the healthcare professionals should facilitate the early detection, management and prevention of such poisoning incidents of public health significance.

Worldwide Occurrence and Investigations of Contamination of Herbal Medicines by Tropane Alkaloids.

Tropane alkaloids occur mainly in Solanaceae plants. In the present review, the main objective is to describe the worldwide occurrence and investigations of anticholinergic poisoning due to the contamination of herbal teas and herbs by tropane alkaloids. Tropane alkaloid poisoning can occur after consumption of any medicinal plant if Solanaceae plants or plant parts are present as contaminants. Globally, almost all reports in 1978-2014 involve herbal teas and one of the prescribed herbs in composite formulae. Contamination most likely occurs during harvest or processing. As for prescribed herbs, on-site inspection is necessary to exclude cross-contamination and accidental mix-up at the retail level. The diagnosis is confirmed by screening for the presence of Solanaceae species and tropane alkaloids. Herbal teas and herbs contaminated by tropane alkaloids can pose a serious health hazard because these relatively heat-stable alkaloids may exist in large quantities. The WHO repeatedly emphasises the importance of good agricultural and collection practices for medicinal plants. DNA barcoding is increasingly used to exclude the presence of contaminants (particularly toxic species) and product substitution. All suspected cases should be reported to health authorities so that investigations along the supply chain and early intervention measures to protect the public can be initiated.

Regional Variations in the Risk and Severity of Ciguatera Caused by Eating Moray Eels.

Moray eels (Gymnothorax species) from tropical waters have long been known to be high-risk species, and the consumption of particularly the viscera or ungutted eels can result in severe ciguatera (known as Gymnothorax or moray eel poisoning), characterized by prominent neurological features. In this review, the main objective was to describe the risk and severity of ciguatera caused by eating moray eels in different parts of the world. Moray eels can accumulate very high ciguatoxin (CTX) levels in the flesh and particularly the liver. Therefore, even the smaller ones can be toxic and the consumption of an average portion (particularly liver) can result in severe or fatal ciguatera. Moray eels (particularly when ungutted) must never be served in gatherings since they can cause mass poisoning because of their large sizes and high CTX levels. Apart from regulatory measures restricting or excluding access, the public should be repeatedly warned to avoid eating moray eels.

The Emergence and Epidemiology of Haff Disease in China.

Haff disease is a rare syndrome of unexplained myalgia and rhabdomyolysis occurring within 24 h of consumption of certain types of cooked freshwater fish or crustacean. It is caused by a yet unidentified heat-stable toxin. In the present review of published case studies and official press releases, the main objective is to report the emergence and epidemiology of Haff disease in China. Haff disease first occurred in Beijing in 2000 and in Lianzhou and Liannan, Guangdong Province in 2009. Subsequent outbreaks mostly occurred in the Jiangsu Province-Nanjing, Yangzhou, Huai'an, and Yancheng. Isolated outbreaks occurred in other cities since 2010-Shijiazhuang, Yueyang, Shanghai, Wuhu, Baoding, Shenzhen, and Hong Kong (imported cases from Shenzhen). Outbreaks occurred predominately in the summer. Crayfish accounted for almost all the outbreaks. Two large outbreaks occurred in Lianzhou and Liannan in 2009 (n = 54) after eating pomfrets and in Nanjing in 2010 (n = 42) after eating crayfish. Other reports or outbreaks involved only 1-9 subjects (median 2 subjects). Variability in individual susceptibility and attack rates were noted, with many subjects remaining asymptomatic despite sharing the same seafood meal as the index cases. Adults were predominately involved. Symptoms occurred within 3-20 h of seafood ingestion, including myalgia, weakness, and, less frequently, nausea, vomiting, abdominal pain, and diarrhea. Myalgia and muscle weakness should normally subside within 2-3 days. Serum creatine phosphokinase became normal within 5-6 days. Abnormal renal function was uncommon. Serious complications (renal failure, multi-organ failure, and prolonged myopathy) and death were rare. In any subjects with unexplained myalgia and rhabdomyolysis, seafood consumption should be included in the history. All suspected cases of Haff disease, including milder presentations, should be reported to public health authorities.

Telmisartan increases systemic exposure to rosuvastatin after single and multiple doses, and in vitro studies show telmisartan inhibits ABCG2-mediated transport of rosuvastatin.

PURPOSE: The ATP-binding cassette transporter G2 (ABCG2) plays an important role in the disposition of rosuvastatin. Telmisartan, a selective angiotension-II type 1 (AT1) receptor blocker, inhibits the transport capacity of ABCG2, which may result in drug interactions. This study investigated the pharmacokinetic interaction between rosuvastatin and telmisartan and the potential mechanism. METHODS: In this two-phase fixed-order design study, healthy subjects received single doses of 10 mg rosuvastatin at baseline and after telmisartan 40 mg daily for 14 days. Patients with hyperlipidaemia who had been taking rosuvastatin 10 mg daily for at least 4 weeks were given telmisartan 40 mg daily for 14 days together with rosuvastatin. Plasma concentrations of rosuvastatin were measured over 24 h before and after telmisartan administration. In vitro experiments using a bidirectional transport assay were performed to investigate the involvement of ABCG2 in the interaction. RESULTS: Co-administration of telmisartan significantly increased the maximum plasma concentration (C max) and the area under the plasma concentration-time curve (AUC) of rosuvastatin by 71 and 26 %, respectively. The T max values were reduced after administration of telmisartan. There was no significant difference in the interaction of rosuvastatin with telmisartan between healthy volunteers and patients receiving long-term rosuvastatin therapy or among subjects with the different ABCG2 421 C>A genotypes. The in vitro experiment demonstrated that telmisartan inhibited ABCG2-mediated efflux of rosuvastatin. CONCLUSION: This study demonstrated that telmisartan significantly increased the systemic exposure to rosuvastatin after single and multiple doses.

Fatal anaphylactic reactions to lignocaine.

Fatal anaphylactic reactions to lignocaine are very rare. In this review of published reports, the main objective is to determine the characteristics of fatal allergic reactions to lignocaine and describe the forensic investigations of anaphylaxis related deaths. From 1957 to 2012, there were seven reports of single case and one report of 8 cases with sufficient information for review. Fatal anaphylactic reactions to lignocaine were generally characterised by fast onset of symptoms (within seconds to <30min of drug exposure) and rapid progression to cardiopulmonary arrest and death (23min to ∼1h). Features of cardiovascular, respiratory and neurological system involvements were often seen. Autopsy might reveal laryngeal oedema, pulmonary oedema, cerebral oedema, eosinophil infiltrates in many organs and other changes. Elevated blood tryptase level caused by mast cell degranulation was also used to diagnose acute anaphylaxis.

Herbal Medicines Induced Anticholinergic Poisoning in Hong Kong.

In the present review, the main objective was to report the incidence and causes of herbal medicines induced anticholinergic poisoning in Hong Kong during 1989-2012 and to emphasize the importance of pharmacovigilance, investigations and preventive measures. Relevant papers, official figures and unpublished data were obtained from Medline search, the Department of Health and the Drug and Poisons Information Bureau. In the New Territories East (where ~20% of the Hong Kong population lived), the incidence of herbal medicines induced anticholinergic poisoning during 1989-1993 was 0.09 per 100,000 population. There were no confirmed cases during 1994-1996. In the whole of Hong Kong, the incidence during 2000-June 2005 was 0.03 per 100,000 population. Contamination of Rhizoma Atractylodis (50%) and erroneous substitution (42%) were the main causes. The incidence during 2008-2012 was 0.06 per 100,000 population. Contamination of non-toxic herbs (50%) and erroneous substitution (41%) were the main causes. In Hong Kong, contamination of non-toxic herbs by tropane alkaloids and substitution of Flos Campsis by toxic Flos Daturae Metelis were the predominant causes of herbal medicines induced anticholinergic poisoning. Systematic studies along the supply chain are necessary to identify the likely sources of contamination. If erroneous substitution of Flos Campsis by Flos Daturae Metelis could be prevented, 40% of herbal medicines induced anticholinergic poisoning would not have occurred. Regular inspection of the retailer, continuing education for the staff in the herbal trade and repeated publicity measures will also be required. Pharmacovigilance of herbal medicines should help determine the incidence and causes of adverse reactions and monitor the effectiveness of preventive measures.

Characteristic Features and Contributory Factors in Fatal Ciguatera Fish Poisoning--Implications for Prevention and Public Education.

In this review, the main objective was to describe the characteristic features of fatal ciguatera fish poisoning and identify contributory factors, with a view to promote prevention and public education. Ciguatera-related deaths, although rare, have been reported from the Pacific, Caribbean, and Indian Ocean regions. The clinical features were generally dominated by convulsions and coma, with various focal neurological signs. Several contributory factors could be identified, including consumption of ciguatoxin (CTX)-rich fish parts (viscera and head) in larger amounts, the most ciguatoxic fish species (e.g.,Gymnothorax flavimarginatus) and reef fish collected after storms and individuals' susceptibility. Mass ciguatera fish poisoning with mortalities also occurred when G. flavimarginatus and other ciguatoxic fish species were shared in gatherings and parties. The characteristic features of fatal ciguatera fish poisoning must be recognized early. The public should be repeatedly reminded to avoid eating the most ciguatoxic fish species and the CTX-rich parts of reef fish. To prevent mass poisoning in gatherings and parties, the most ciguatoxic fish species and potentially toxic fish species must be avoided. Particularly after hits by disastrous storms, it is important to monitor the toxicity of reef fish and the incidence rates of ciguatera.

Aconitum Alkaloid Poisoning Because of Contamination of Herbs by Aconite Roots.

Aconitum alkaloid poisoning can occur after drinking decoction and soup made from non-toxic herbs contaminated by aconite roots. In the present review, the main objective is to describe the clinical features, investigations and possible sources of contamination. A combination of neurological, gastrointestinal and cardiovascular signs and symptoms was seen. Ventricular tachyarrhythmias could occur in 18% of subjects. Yunaconitine and crassicauline A, mainly found in certain aconite roots from Southwest China, are most commonly involved. Herbal residues and unused herbs should first be inspected for gross contamination. On-site inspection at the retailer should exclude accidental mix-up or cross-contamination when handling aconite roots. Samples of prescribed herbs are examined for gross contamination and analysed for the presence of Aconitum alkaloids. Samples of the implicated herb are also collected from the wholesaler for investigation. If post-import contamination is unlikely, the regulatory authorities of the exporting countries should be notified for follow-up actions. It is a challenging task to work out how non-toxic herbs become contaminated by aconite roots. The source control with good agricultural and collection practices and quality assurance must be enhanced.

Ciguatoxic Potential of Brown-Marbled Grouper in Relation to Fish Size and Geographical Origin.

To determine the ciguatoxic potential of brown-marbled grouper (Epinephelus fuscoguttatus) in relation to fish size and geographical origin, this review systematically analyzed: 1) reports of large ciguatera outbreaks and outbreaks with description of the fish size; 2) Pacific ciguatoxin (P-CTX) profiles and levels and mouse bioassay results in fish samples from ciguatera incidents; 3) P-CTX profiles and levels and risk of toxicity in relation to fish size and origin; 4) regulatory measures restricting fish trade and fish size preference of the consumers. P-CTX levels in flesh and size dependency of toxicity indicate that the risk of ciguatera after eating E. fuscoguttatus varies with its geographical origin. For a large-sized grouper, it is necessary to establish legal size limits and control measures to protect public health and prevent overfishing. More risk assessment studies are required for E. fuscoguttatus to determine the size threshold above which the risk of ciguatera significantly increases.

Ciguatera fish poisoning in East Asia and southeast Asia.

In the coastal countries of East Asia and Southeast Asia, ciguatera should be common because of the extensive tropical and subtropical coral reefs along the coasts and in the neighboring seas with ciguatoxic fishes. An extensive search of journal databases, the Internet and the government websites was performed to identify all reports of ciguatera from the regions. Based on the official data and large published case series, the incidence of ciguatera was higher in the coastal cities (Hong Kong, Foshan, Zhongshan) of southern China than in Japan (Okinawa Prefecture). In Singapore, ciguatera appeared to be almost unknown. In other countries, only isolated cases or small case series were reported, but under-reporting was assumed to be common. Ciguatera may cause severe acute illness and prolonged neurological symptoms. Ciguatera represents an important public health issue for endemic regions, with significant socio-economic impact. Coordinated strategies to improve risk assessment, risk management and risk communication are required. The systematic collection of accurate data on the incidence and epidemiology of ciguatera should enable better assessment and management of its risk. Much more work needs to be done to define the size threshold for important coral reef fish species from different regions, above which the risk of ciguatera significantly increases.

Incidence and Causes of Aconitum Alkaloid Poisoning in Hong Kong from 1989 to 2010.

Aconite roots contain Aconitum alkaloids, which are highly toxic cardiotoxins and neurotoxins. In this review, the main objective was to determine the incidence and causes of Aconitum alkaloid poisoning in Hong Kong between 1989 and 2010, based on six published reports from the territory-wide poison control units. In the New Territories East of Hong Kong, the incidence of aconite poisoning showed a sudden and sustained decrease from 0.60 (1989-1991) to 0.16 (1992-1993) and 0.17 (1996-1998) per 100 000 population, after publicity measures in late 1991 to promote awareness of the toxicity of aconite roots. In the whole of Hong Kong, the incidence of aconite poisoning was even lower in January 2000-June 2004 (0.03 per 100 000 population). However, aconite poisoning became more common again in April 2004-July 2009 and 2008-2010 (0.15 and 0.28 per 100 000 population). Overdoses and use of inadequately processed aconite roots were important causes. As from 2004 to 2009, 'hidden' aconite poisoning (toxicity caused by contaminants in other dispensed herbs) emerged as an important cause. It is important to continue the safety monitoring of potent herbs and the networking of poison control units. Further systematic studies would be required to identify the likely sources of contamination of herbs.

Emergence and epidemiology of ciguatera in the coastal cities of southern China.

In the present review of 23 published case studies, the main objective is to report the emergence and epidemiology of ciguatera in the coastal cities of southern China. There was a sudden surge in ciguatera outbreaks in 2004. Ciguatera mostly occurred in the Guangdong Province. In Shenzhen, the incidence of ciguatera in 2004 was estimated to be over 7.5 per million people. In Foshan and Zhongshan, three large outbreaks each affecting over 100-200 subjects (caused by tiger grouper served at banquets) accounted for the much higher incidence of ciguatera in 2004 (>48.7 and >129.9 per million people). Humphead wrasse and areolated coral grouper were the other important ciguatoxic fish. In some subjects, risk factors for increased likelihood of (severe) ciguatera were present, namely concomitant alcohol consumption and ingestion of large reef fishes and CTX-rich fish parts. To prevent large outbreaks and severe illness, large apex predators from coral reefs should never be served at banquets and the public should realize the increased risk of severe symptoms due to ingestion of CTX-rich fish parts with alcohol. The systematic collection of accurate details, implementation of risk assessment process and continuing education for the public on prevention are of obvious importance.

Epidemiology and clinical features of ciguatera fish poisoning in Hong Kong.

In the present review, the main objective was to describe the epidemiology and clinical features of ciguatera fish poisoning in Hong Kong. From 1989 to 2008, the annual incidence of ciguatera varied between 3.3 and 64.9 (median 10.2) per million people. The groupers have replaced the snappers as the most important cause of ciguatera. Pacific-ciguatoxins (CTX) are most commonly present in reef fish samples implicated in ciguatera outbreaks. In affected subjects, the gastrointestinal symptoms often subside within days, whereas the neurological symptoms can persist for weeks or even months. Bradycardia and hypotension, which can be life-threatening, are common. Treatment of ciguatera is primarily supportive and symptomatic. Intravenous mannitol (1 g/kg) has also been suggested. To prevent ciguatera outbreaks, the public should be educated to avoid eating large coral reef fishes, especially the CTX-rich parts. A Code of Practice on Import and Sale of Live Marine Fish for Human Consumption for Prevention and Control of Ciguatera Fish Poisoning was introduced from 2004 to 2013. The Food Safety Ordinance with a tracing mechanism came into full effect in February 2012. The Government would be able to trace the sources of the fishes more effectively and take prompt action when dealing with ciguatera incidents.

Aconitum alkaloid poisoning related to the culinary uses of aconite roots.

Aconite roots (roots or root tubers of the Aconitum species) are eaten as root vegetables and used to prepare herbal soups and meals, mainly for their purported health benefits. Aconite roots contain aconitine and other Aconitum alkaloids, which are well known cardiotoxins and neurotoxins. To better understand why Aconitum alkaloid poisoning related to the culinary uses of aconite roots can occur and characterize the risks posed by these "food supplements", relevant published reports were reviewed. From 1995 to 2013, there were eight reports of aconite poisoning after consumption of these herbal soups and meals, including two reports of large clusters of cases (n = 19-45) and two reports of cases (n = 15-156) managed by two hospitals over a period of 4.5 to 5 years. The herbal formulae used did not adhere to the suggested guidelines, with regarding to the doses (50-500 g instead of 3-30 g per person) and types (raw instead of processed) of aconite roots used. The quantities of Aconitum alkaloids involved were huge, taking into consideration the doses of aconite roots used to prepare herbal soups/meals and the amounts of aconite roots and herbal soups/meals consumed. In a large cluster of cases, despite simmering raw "caowu" (the root tuber of A. kusnezoffii) in pork broth for 24 h, all 19 family members who consumed this soup and boiled "caowu" developed poisoning. Severe or even fatal aconite poisoning can occur after consumption of herbal soups and foods prepared from aconite roots. Even prolonged boiling may not be protective if raw preparations and large quantities of aconite roots are used. The public should be warned of the risk of severe poisoning related to the culinary and traditional medicinal uses of aconite roots.

Large outbreaks of ciguatera after consumption of brown marbled grouper.

Brown marbled grouper (Epinephelus fuscoguttatus) is an apex predator from coral reefs of the Indo-Pacific region. All five published case series of ciguatera after consumption of brown marbled grouper were reviewed to characterize the types, severity and chronicity of ciguatera symptoms associated with its consumption. Three of these case series were from large outbreaks affecting over 100-200 subjects who had eaten this reef fish served at banquets. Affected subjects generally developed a combination of gastrointestinal, neurological and, less commonly, cardiovascular symptoms. Gastrointestinal symptoms occurred early and generally subsided in 1-2 days. Some neurological symptoms (e.g., paresthesia of four limbs) could last for weeks or months. Sinus bradycardia and hypotension occurred early, but could be severe and prolonged, necessitating the timely use of intravenous fluids, atropine and dopamine. Other cardiovascular and neurological features included atrial ectopics, ventricular ectopics, dyspnea, chest tightness, PR interval >0.2 s, ST segment changes, polymyositis and coma. Concomitant alcohol consumption was associated with a much higher risk of developing bradycardia, hypotension and altered skin sensation. The public should realize that consumption of the high-risk fish (especially the ciguatoxin-rich parts and together with alcohol use) and repeated ciguatoxin exposures will result in more severe and chronic illness.