Tetramine Poisoning Research Articles

Respiratory paralysis in a patient with myasthenia gravis after ingestion of marine carnivorous gastropods: A case report.

The salivary glands of marine carnivorous gastropods contain tetramines, which usually cause mild symptoms of poisoning. However, these symptoms may be fatal in rare cases. A 58-year-old woman with a history of myasthenia gravis complained of dyspnea after consuming marine carnivorous gastropods with intact salivary glands. Upon arrival at the hospital, her blood gas analysis revealed type II respiratory failure with a pCO2 of 154 mmHg. Tracheal intubation was immediately performed. Her respiratory condition improved the following day, and she therefore could be weaned off the ventilator. Tetramine poisoning can be fatal for patients with certain underlying medical conditions.

Tetramine Contents in the Salivary Glands from 16 Species of Marine Carnivorous Gastropods Collected along Japanese Coasts

Tetramine (tetramethyl ammonium ion), a neurotoxin, is present at high levels in the salivary glands of buccinid gastropods and is responsible for human intoxication due to consumption of the gastropods. We used LC-MS/MS to examine the tetramine contents of salivary glands from 16 species of carnivorous gastropods collected along Japanese coasts. Tetramine was detected in all specimens except for Babylonia japonica. High levels of tetramine were detected in whelks, Neptunea lamellosa (1,380-9,410 μg/g of salivary gland) and N. purpurea (1,190-7,400 μg/g of salivary gland). Although consumption of N. lamellosa is well-known cause of foodborne tetramine poisoning, it was newly discovered that N. purpurea has tetramine. In addition, we found 7 other species of gastropods containing tetramine: Siphonalia cassidariaeformis (117-135 μg/g), S. fusoides (204 μg/g), Buccinum inclytum (2.94-3.40 μg/g), and B. aniwanum (0.700 μg/g) of the family Buccinidae, and Fusinus perplexus (397 μg/g), F. ferrugineus (105 μg/g), and F. forceps salisburyi (67.5 μg/g) of the family Fasciolariidae. The present study, together with previous studies, shows that gastropods with salivary glands containing more than 1,000 μg tetramine/g of salivary gland, including the genus Neptunea as well as Fusitriton oregonesis and Hemifusus tuba, carry a high risk of tetramine poisoning, and their salivary glands should be removed before consumption to prevent food poisoning.

Tetramine in the Salivary Glands of Marine Carnivorous Snails: Analysis, Distribution, and Toxicological Aspects

Focusing on tetramine, tetramethylammonium ion, contained in the salivary glands of marine carnivorous snails, this paper gives an overview of analytical methods, distribution in marine snails, and toxicological aspects. Some Neptunea snails have often caused food poisoning in North Atlantic and Northeast Asia regions, especially in Japan. The toxin of both N. arthritica and N. antiqua was first proven to be tetramine in 1960. Subsequent research on marine snail tetramine has progressed with the development of analytical methods. Of the various methods developed, the LC/ESI-MS method is most recommended for tetramine analysis in terms of sensitivity, specificity, and versatility. Accumulated data show that tetramine is ubiquitously contained at high concentrations (usually several mg/g) in the salivary glands of Neptunea snails. Tetramine is also found in the muscle and viscera of Neptunea snails and even in the salivary gland of marine snails other than Neptunea species, although mostly at low levels (below 0.1 mg/g). Interestingly, the major toxin in the salivary glands of Fusitriton oregonensis and Hemifusus tuba is distinguishable from tetramine. In tetramine poisoning, diverse symptoms attributable to the ganglion-blocking action of tetramine, such as visual disturbance, headache, dizziness, abdominal pain, and nausea, develop within 30 min after ingestion of snails because of rapid absorption of tetramine from the gastrointestinal tract. The symptoms are generally mild and subside in a short time (within 24 at most) because of rapid excretion through the kidney. However, it should be kept in mind that tetramine poisoning can be severe in patients with kidney dysfunction, as shown by two recent case reports. Finally, given the diffusion of tetramine from the salivary gland to the muscle during boiling and thawing of snails, removal of salivary glands from live snails is essential to avoid tetramine poisoning.

An investigation on a family tetramine poisoning accident

Objective: To investigate and analyze the clinical data of tetramine poisoning in a family and prevent similar incidents from happening again. Methods: The study was conducted in July 2016 in a fami-ly with thiamine poisoning in shandong province, and the clinical data were analyzed. Results: In this case, there are six cases of poisoning caused by the tetramine poisoning, and the convulsions are the main clinical manifestations, and the blood perfusion can have a good effect on the severe patients. After positive treatment, all 6 patients were cured. Conclusions: The tetramine poisoning can cause severe convulsion, although the country has banned the production and use of it, the tetramine poisoning case still exist and cannot be ignored.

Two Cases of Tetramine Intoxication from Neptunea contricta

Even though Neptunea contricta appears similar to Batilus cornutus and Rapana venosa, they are different in tetramine content which inhibits the neuronal calcium channel. Therefore, mistaking Neptunea contricta for Batilus cornutus or Rapana venosa, can result in the occurrence of toxic symptoms. Three patients developed nausea, epigastric pain, chest pain, dizziness, blurred vision, dyspnea, hypertension and tachycardia after eating Neptunea contricta. Moreover, consumption of one only piece was sufficient to cause symptoms because each Neptunea contricta has 17.3 mg of tetramine. Accordingly, care should be taken when patients are consuming more than 5 pieces because toxic symptoms such as dyspnea can occur. Moreover, correct species identification is important because the quantity of tetramine varies among sea snail species. Finally, it is important to educate people to remove the salivary glands completely before consuming Neptunea contricta.

Tetramine poisoning in China: changes over a decade viewed through the media's eye.

BackgroundTetramine, or tetramethylenedisulfotetramine, is an internationally banned compound that had been used primarily as a rodenticide. Despite its regulatory status, there are widespread reports of its intentional use in human poisonings, primarily in China, and often in mass poisonings. Enhanced governmental regulations were implemented in 2003 to further reduce the availability of tetramine, though the effects of these regulations, and the current use of tetramine, remains unknown.MethodsReports from the website of the China News Agency were collected from 2000 to 2012. Details such as the location, date, and intent of the events were compared before and after the regulations were implemented.ResultsThere were a total of 148 events during the study period (95 from 2000 to 2003, and 53 after 2003). There were a total of 3526 victims, including 225 fatalities. The majority of the events were homicidal/terroristic in nature. The incidence of events fell after 2006. More poisoning events occurred in central China, such as Henan and Jiangsu province, and an increase was noted in April and September.ConclusionTetramine poisoning events, as reported in the national Chinese media, fell after the implementation of strict regulation on tetramine. The causal relationship is not known.

Effects of acetamide at different doses on expression of amino acids in cerebral cortex of rats with acute tetramine poisoning

To investigate the effects of acetamide at different doses on the expression of inhibitory amino acids (gamma-aminobutyric acid, GABA) and excitatory amino acid (glutamate, Glu) in the cerebral cortex of rats with acute tetramine (TET) poisoning. Eighty Sprague-Dawley rats (SPF) were randomly divided into five groups, with 16 rats in each group: saline control group, dimethyl sulfoxide (DMSO) control group, TET exposure group, high-dose (2.8 g/kg/d) acetamide treatment group, and super-high-dose (5.6 g/kg/d) acetamide treatment group. Rats in the exposure group and treatment groups were exposed to TET by intragastric administration after fasting, and were then intramuscularly injected with saline or different doses of acetamide in the following 5 days. The cortex of the temporal lobe was collected at 3 h, 12 h, 48 h, or 7 d after treatment. The expression levels of GABA and Glu in the cortex of the temporal lobe were determined by average optical density (OD) values in immunohistochemistry. 1) Expression of GABA: The OD value of GABA in TET exposure group started to increase at 12 h after treatment, reached the peak at 48 h, and decreased to the normal level at 7 d. In the high-dose acetamide treatment group, the increase in OD at 12 h was not so significant as that in the TET exposure group, OD value decreased to the normal level at 48 h and was lower than that in the exposure group, and the changes were more like those in the control groups. In the super-high-dose acetamide treatment group, OD value began to increase significantly at 3 h and was significantly higher than that in the TET exposure group (P < 0.01), it reached the peak at 12 h, and was restored to the normal value at 48 h. 2) Expression of Glu: The OD value of Glu in TET exposure group at 3 h after treatment was significantly lower than those in the two control groups, it increased gradually from 12 h to 48 h, and recovered to the normal level at the 7th d. The changes in the high-dose acetamide treatment group were similar to those in the TET exposure group, but became more like those in the control groups after 48 h; the OD value in super-high-dose acetamide treatment group was significantly higher than that in the TET exposure group at 3 h after treatment (P < 0.01), while no significant difference was found at 12 h; it was significantly lower than those of all other groups at 48 h and 7 d (P < 0.01). Treatment with high dose of acetamide has some curative effect on TET poisoning-induced central nervous lesion, while the effect of super-high-dose acetamide on expression of neurotransmitters is too complex to evaluate.

Effect of acetamide on histopathology in cerebral cortex of rats with tetramine poisoning

To observe the effect of different doses of acetamide on the histopathology in the cerebral cortex of rats with tetramine (TET) poisoning and to provide a basis for the treatment of fluoroacetamide poisoning with acetamide. Eighty clean Sprague-Dawley rats were randomly divided into five groups: saline control group,dimethylsulfoxide water solution control group,TET poisoning group, acetamide (2.88 g/kg/d) treatment group, and acetamide (5.68 g/kg/d) treatment group, with 16 rats in each group. Rats in the poisoning group and treatment groups were poisoned with TET by intragastric administration after fasting; then, saline was injected intramuscularly into rats of the poisoning group, and different doses of acetamide were injected intramuscularly into rats of treatment groups; the course of treatment was 5 d. At 3 h, 12 h, 48 h, and 7 d after treatment, the cerebral cortex was harvested from rats in each group, and the histopathological changes in the cerebral cortex were evaluated under light and electron microscopes. The light microscopy showed that the TET poisoning group had hypoxia changes in the cerebral cortex, which worsened over time; the treatment groups had reduced hypoxia changes, and the acetamide (2.88 g/kg/d) treatment group had more reduction than the acetamide (5.68 g/kg/d) treatment group. The electron microscopy showed that the apoptosis of neuronal cells were the main pathological changes in the TET poisoning group; the treatment groups had reduced apoptotic changes, and the acetamide (2.88 g/kg/d) treatment group had more reduction than the acetamide (5.68 g/kg/d) treatment group. No pathological changes associated with the synergistic toxic effect of acetamide and TET are found in the cerebral cortex. Acetamide (2.88 g/kg/d) could reduce central nervous lesions, but the efficacy is not improved after increasing the dose. For patients who cannot be identified with TET or fluoroacetamide poisoning, acetamide could be considered for treatment.

Long term effects of tetramine poisoning: An observational study

Context. Tetramine is an illegal rat poison that has resulted in a number of accidental mass poisonings in China. Objective. To investigate the long term outcome of tetramine poisoning. Materials and methods. A survey of epileptic attacks in 370 patients in the Hubei province of P. R. China who had survived tetramine poisoning in the last decade was undertaken by means of telephone calls, letters, and interviews. Data describing the initial acute episode was gathered from medical and public health records. Results. Among the 370 patients surveyed (188 males, 182 females, age range 10 to 71 y), 352 experienced seizures during the initial poisoning. One hundred fifty-eight individuals are currently seizure-free, after an average medication period of 2.93 years. The other patients have recurrent epilepsy, including 156 with tonic–clonic seizures and 39 with partial seizures. Six patients have other neurological problems. Discussion and conclusion. Tetramine, a rat poison sometimes ingested by mistake, blocks GABA receptors and causes seizures. These seizures can persist for years after the initial poisoning, even when no seizures are present initially. Sodium valproate, which has the ability to increase the amount of GABA in the CNS, would be a reasonable choice for the treatment of epilepsy caused by tetramine poisoning.

Tetramine poisoning: A case report and review of the literature

Background Tetramethylene disulfotetramine (TETS), a banned neurotoxic rodenticide, has accounted for numerous intentional and unintentional poisonings in mainland China. Since the first known case of human illness caused by tetramine occurred in NewYork, in May 2002, TETS has caused more than 50 human poisonings in Western countries. Aim To analyze pathological changes of TETS poisoning and to provide evidence for forensic identification. Methods We report the case of a 28-year-old female who suffered from tetramine poisoning and died of multi-organ failure. We also performed a retrospective study of 40 cases of poisoning, from pathological autopsy reports, by analyzing and summarizing the related the literature from 1996 to 2010. Based on pathologic autopsies and the literature, we summarize the pathological changes related to tetramine poisoning. Results Signs of asphyxia were obvious upon pathological examination. Edema and congestion of organs, particularly in the brain, were seen in all cases. Subarachnoid and cerebral hemorrhaging were also common signs of tetramine poisoning. Conclusion In forensic practice, tetramine poisoning should be considered when the patient has signs of abnormal excitation of the central nervous system, convulsions, hyperspasmia, and cerebral hemorrhage.

The therapeutic effects of combination of γ-aminobutyric acid, sodium dimercaptopropane sultanate and vitamin B6 in large doses on liver and heart in rats with acute tetramine intoxication

Objective To observe the therapeutic effects of the co-administration of γ-aminobutyric acid (CABA), sodium dimercaptopropane sulfonate (Na-DMPS) and vitamin B6 in large doses on liver and heart of rats with acute tetramine intoxication, and compare their separate effects of either GABA or Na-DMPS alone with those of the triad combination. Method Thirty rats were randomized into control group (n = 6), tetramine intoxication without treatment group (n = 6), tetramine intoxication treated with GABA group (n = 6), tetramine intoxication treated with Na-DMPS group (n = 6) and tetramine intoxication treated with triad combination (GABA + Na-DMPS + vitamin B6, GNDV n = 6) group. Samples of blood, liver tissue and heart tissue of rats with acute tetramine intoxication were collected immediately two hours after medication with different drugs. Serum alanine aminotrasferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK) and creatine kinase isoenzyme (CK-MB) were measured, and the pathological changes of liver tissue and heart tissue were observed under microscope. Results The symptoms of poisoning were apparently relieved and the latency for convulsion/muscular twitch were obviously delayed in poisoned rats treated with GABA, Na-DMPS and GNDV separately. Furthermore, combination group showed the latent period delayed longer than either GABA or Na-DMPS groups The GABA, Na-DMPS and GNDV significantly lowered the serum levels of ALT, AST, CK and CK-MB in rats with tetramine intoxication, and those serum levels of enzymes were lower in GNDV group than those in either GABA group or Na-DMPS group. However, there were no difference in those serum enzymes between GABA group and Na-DMPS group. Moreover, the intoxicated rats treated with combination treatment had the slightest pathological changes in liver and heart (GNDV < GABA or Na-DMPS). Conclusions The co-administration of γ-aminobutyric acid, sodium demercaptopropane sulfonate and vitamin B6 in large doses for the treatment of tetramine intoxication is a method of choice. Key words: Tetramine; Rats; Therapy; Serum enzyme; γ-aminobutyric acid; Sodium demercaptopropane sulfonate; Vitamin B6

Identification of tetramine, a toxin in whelks, as the cause of a poisoning incident in Korea and the distribution of tetramine in fresh and boiled whelk (Neptunea intersculpta).

An investigation was conducted into the clinical symptoms and causative agent associated with a whelk poisoning incident that occurred in March 2005 in Korea. The whelk consumed in the poisoning incident was identified as Neptunea intersculpta. All of the 17 patients suffered from eyeball pain, headache, dizziness, abdominal pain, and nausea but no diarrhea. The causative agent was identified as tetramine, based on results from liquid chromatography-tandem mass spectrometry. Based on the tetramine concentration in the leftover whelk meat and the amount of meat consumed, the amount of tetramine ingested by the patients was estimated to be > or = 10 mg. This is the first report of the identification of tetramine as the causative agent in whelk poisoning in Korea. The anatomical distribution of tetramine in fresh and boiled N. intersculpta was examined. The toxin concentration in the meat was higher in specimens boiled in the shell than in fresh specimens collected on the same date. In meat boiled separately after removing the shell, the salivary gland, and the midgut gland, the tetramine concentration was much lower than that in fresh specimens or those boiled in the shell. This result suggests that boiling the meat after removing the salivary gland is a suitable way to prevent tetramine poisoning.

Effect of acetamide on cardiac troponin I of rats with tetramine poisoning

目的 观察不同剂量乙酰胺对急性毒鼠强轻度中毒大鼠血清中肌钙蛋白I(cTnI)水平的影响,探讨乙酰胺临床最大量对毒鼠强中毒救治的可行性.方法 实验选用健康成年SD大鼠,设空白对照组、阴性对照组以及毒鼠强轻度中毒生理盐水治疗组、乙酰胺临床最大量用药组和乙酰胺超大量用药组,每组16只,比较中毒大鼠用药后反应以及各组血清中cTnI水甲.结果 各组中毒大鼠未见抽搐发作,但出现纳差,体重下降,活动减少,各时间段体重差异无统计学意义(P>0.05).各组不同处理后3 h血清中cTnI浓度差异均无统计学意义(P>0.05);12、48 h及7 d乙酰胺超人量用药组cTnI浓度分别为(0.45±0.20)、(0.41±0.46)、(0.21±0.06)μg/L,空白对照组、阴性对照及生理盐水治疗组比较,差异均有统计学意义(P<0.01或P<0.05),48 h及7 d超大量用药组cTnI水平与临床最大量用药比较,差异有统计学意义(P<0.05).结论 在毒鼠强轻度中毒时,用乙酰胺临床最大量以及超大量治疗会影响血清中cTnI水平,可能存在心肌损伤。

Nongenetic Cause of Epileptic Seizures in 2 Otherwise Healthy Chinese Families

Tetramine, a banned rodenticide, is repeatedly reported to induce epileptic seizures in healthy people. Because both doctors and patients are often not aware of earlier tetramine contact, the occurrence of seizures is easily misdiagnosed as primary epilepsy. In this study, 8 cases in 2 families with generalized tonic-clonic seizures, most probably induced by tetramine, are presented. The clinical manifestation, electroencephalogram characteristics, and treatment measures of tetramine poisoning are summarized. There is the possibility of tetramine toxicity as a cause of epidemic epileptic seizures.

The antidotal effects of high-dosage γ-aminobutyric acid on acute tetramine poisoning as compared with sodium dimercaptopropane sulfonate

To investigate the therapeutic effect of high-dosage gamma-aminobutyric acid (GABA) on acute tetramine (TET) poisoning, 50 Kunming mice were divided into 5 groups at random and the antidotal effects of GABA or sodium dimercaptopropane sulfonate (Na-DMPS) on poisoned mice in different groups were observed in order to compare the therapeutic effects of high-dosage GABA with those of Na-DMPS. Slices of brain tissue of the poisoned mice were made to examine pathological changes of cells. The survival analysis was employed. Our results showed that both high-dosage GABA and Na-DMPS could obviously prolong the survival time, delay onset of convulsion and muscular twitch, and ameliorate the symptoms after acute tetramine poisoning in the mice. Better effects could be achieved with earlier use of high dosage GABA or Na-DMPS. There was no significant difference in prolonging the survival time between high-dose GABA and Na-DMPS used immediately after poisioning. It is concluded that high-dosage GABA can effectively antagonize acute toxicity of teramine in mice. And it is suggested that high-dosage GABA may be used as an excellent antidote for acute TET poisoning in clinical practice. The indications and correct dosage for clinical use awaits to be further studied.

Sequential Hemoperfusion and Continuous Venovenous Hemofiltration in Treatment of Severe Tetramine Poisoning

Objective: It was the aim of this study to observe the effects of sequential hemoperfusion (HP) and continuous venovenous hemofiltration (CVVH) on patients with severe tetramine poisoning and to evaluate the ability of these modalities to remove tetramine. Methods: Eighteen patients diagnosed as having severe tetramine poisoning were treated by blood purification, additional to routine medical therapy. Blood purification procedures included HP using activated charcoal for 3–5 h and consecutive CVVH for 24–36 h. Patients’ clinical conditions, blood routine tests and serum chemical tests were evaluated every day after admission. Plasma tetramine concentrations were determined before and after HP. During CVVH, tetramine concentrations in plasma before and after passing through the filter and ultrafiltration at 2 and 12 h were also determined. Results: Eight patients received blood purification within 12 h after onset of poisoning, and 10 patients received blood purification more than 12 h later. Early-treated patients showed a higher cure rate (100 vs. 60.0%; p < 0.05, χ² test) and shorter coma time than late-treated patients (26.0 ± 23.2 h, range 5–70, vs. 59.7 ± 27.7 h, range 20–96; p < 0.01, rank test). The mean plasma tetramine concentrations in early- and late-treated patients were comparable (0.095 ± 0.036 vs. 0.134 ± 0.110 mg/l; p > 0.05). Mean plasma tetramine concentration was reduced from 0.124 ± 0.082 to 0.080 ± 0.055 mg/l after HP. At 2 h of CVVH, mean plasma tetramine concentration was 0.078 ± 0.064 mg/l, at 12 h of CVVH, 0.074 ± 0.059 mg/l, and the ultrafiltration sieving coefficient at 2 and 12 h was 0.839 ± 0.409 and 0.686 ± 0.253 mg/l, respectively. Conclusion: Early sequential HP and CVVH therapy may significantly improve the outcome of patients with severe tetramine intoxication. HP can rapidly reduce the plasma concentration of tetramine, and CVVH can attenuate the plasma tetramine concentration rebound after HP by continuously removing tetramine from the plasma.

Change of myocardial enzymes in patients with acute tetramine poisoning

To investigate the clinical significance of myocardial enzymes in patients with acute tetramine (TEM) poisoning. The dynamic changes of the activity of myocardial enzymes and ECG were observed in 67 patients with acute TEM poisoning as well as in 67 healthy people for medical checkup at outpatient department as the control group. Myocardial enzymes of the patients with acute TEM poisoning were increased to different extents on the first day. There was significant difference in the activity of aspartate aminotransferase (AST), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) and CPK isoenzyme MB (CK-MB) between the patients and the healthy people in the control group (P < 0.01). There was significant difference in the myocardial enzymes at different time points among the patients with mild, middle and severe poisoning (P < 0.01). The severer the TEM poisoning was, the higher the activity of myocardial enzymes and the abnormal rate of ECG were. The activity of CPK was the earliest to rise with the highest aptitude of fluctuation and the longest time of elevation. The change of the myocardial enzymes was earlier than that of ECG. The abnormal rate of AST, CPK, CK-MB, LDH, alpha-HBDH was 86.57%, 98.51%, 94.03%, 89.55% and 79.10% respectively. The abnormal rate of ECG was 49.3% on the third day of poisoning. Measurement of myocardial enzymes was better than ECG in sensitivity. Acute tetramine poisoning can damage myocardium, which is reversible. CPK is a typical marker for the damage and can serve as one of the important clinical monitoring indices.

The monocyte dysfunction induced by acute tetramine poisoning and corrected by continuous blood purification

The monocyte function of patients with severe tetramine poisoning and the effects of sequential hemoperfusion (HP) and continuous veno-venous hemofiltration (CVVH) on the immune status of the patients were investigated. Eleven patients with severe acute tetramine poisoning were treated with sequential HP and CVVH. The APACHE II score and Glasgow score were used to evaluate the disease status during the therapy. Blood samples were collected at 0, 2, 6, 12, 24, 48, and 72 h. Peripheral monocytes were isolated and stimulated with lipopolysaccharide (LPS) to detect the ability of monocytes to secrete tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, and IL-10. The number of monocytes was counted at the same time. As expected, three patients died and the clinical manifestations were improved in the other patients. The production of cytokines (TNF-alpha, IL-6, and IL-10) by monocytes of patients with tetramine poisoning was much lower than normal controls (P<0.001), and was significantly increased after HP and CVVH in the survivors (TNF-alpha, IL-6, IL-10, P<0.05, P<0.01, P<0.05, respectively). The blood concentration of tetramine was 0.124+/-0.082 mg/l at prehemoperfusion and 0.080+/-0.055 mg/l at posthemoperfusion (P<0.05). It was concluded that there was severe damage to monocyte function in patients with tetramine poisoning, and that sequential HP and CVVH can effectively ameliorated monocyte function and eliminate tetramine from blood.

Some problems in treatment of tetramine poisoning

山东省为毒鼠强中毒高发省份,迄今为止,我们已成功组织抢救山东省急性毒鼠强中毒事件10余起,并主持制订了 .经我们诊治(包括我院急诊、门诊、住院患者及外院会诊救治)过的患者总数已超过200余人.现结合一起中毒事件中典型病例的临床救治经过,并复习相关的文献,对当前毒鼠强临床救治中的几个问题进行探讨。

Rat poison and food security in the People's Republic of China: focus on tetramethylene disulfotetramine (tetramine).

The last several years have seen a large number of mass poisonings in mainland China, particularly those caused by illicit rodenticides. One rat poison, tetramine (tetramethylene disulfotetramine) is responsible for a great percentage of death and injury in the People’s Republic of China (PRC). Tetramine is an acutely toxic substance with human oral toxicity estimated as low as 0.1 mg/kg, and is widely available in open markets in mainland China—this despite being prohibited for manufacture or sale in the PRC. Being a GABA antagonist, and having an extremely potent effect on the brain stem, many victims can quickly fall into convulsions and die within hours following ingestion. With no known effective antidote at this time, clinical data from the PRC show that acute cases of tetramine poisoning are extremely difficult to treat. The widespread use of tetramine—including its reported sale at a Malaysian outdoor market in September 2002—could exacerbate its hazard to public health, particularly in those areas having large overseas Chinese populations.