Ming-Ling Wu

Publications of Ming-Ling Wu

• Acute human Glufosinate-containing herbicide poisoning.

  Authors: Yan-Chiao Mao, Dong-Zong Hung, Ming-Ling Wu, Wei-Jen Tsai, Lee-Min Wang, Jiin Ger, Jou-Fang Deng, Chen-Chang Yang

  Clinical toxicology (Philadelphia, Pa.). 04/2012;

  Background. Glufosinate-containing herbicides are commonly used worldwide. Data on acute human glufosinate poisoning however remain scarce. Methods. We retrospectively reviewed the medical records ofBackground. Glufosinate-containing herbicides are commonly used worldwide. Data on acute human glufosinate poisoning however remain scarce. Methods. We retrospectively reviewed the medical records of all glufosinate poisoned cases reported to the Taiwan National Poison Control Center and two medical centers in Taiwan from August 1993 through February 2010. Their demographic and clinical data were then analyzed to identify potential predictors of severe effects following acute glufosinate poisoning. Results. One hundred and thirty-one patients, including 115 oral and 16 non-oral exposures, were eligible for final analysis. Among patients with oral exposure, 25 were asymptomatic, while the others developed gastrointestinal, neurological, cardiovascular, and/or respiratory manifestations. Seven patients (6.1%) died following deliberate glufosinate ingestion. The median dose of glufosinate ingestion was 30.4 grams (interquartile range 18.5-45.6 grams) in the severe/fatal group compared to 6.8 grams (interquartile range 3.7-16.2 grams) in the non-severe group (p <0.001). Older age (≥61 years; adjusted OR 4.9, 95% CI 1.3-17.9) and larger amount of glufosinate ingestion (≥13.9 grams; adjusted OR 25.2, 95% CI 4.8-132.5) were positively associated with the development of severe toxicity, whereas ethanol consumption (adjusted OR 0.1, 95% CI <0.1-0.5) was inversely associated with the risk of severe toxicity. Conclusion. Although glufosinate is generally thought to be of low toxicity to humans, severe effects can occur and may be associated with older age, larger amount of ingestion and absence of concomitant ethanol consumption.

• Determination of caprolactam and 6-aminocaproic acid in human urine using hydrophilic interaction liquid chromatography-tandem mass spectrometry.

  Authors: Ya-Hsueh Wu, Ming-Ling Wu, Chun-Chi Lin, Wei-Lan Chu, Chen-Chang Yang, Robert Tate Lin, Jou-Fang Deng

  Journal of chromatography. B, Analytical technologies in the biomedical and life sciences. 02/2012; 885-886:61-5.

  A simple and rapid assay based on hydrophilic interaction liquid chromatography with tandem mass spectrometry has been first developed and validated for simultaneous determination of caprolactam (CA)A simple and rapid assay based on hydrophilic interaction liquid chromatography with tandem mass spectrometry has been first developed and validated for simultaneous determination of caprolactam (CA) and 6-aminocaproic acid (6-ANCA) in human urine using 8-aminocaprylic acid as internal standard. A 20μL aliquot of urine was injected directly into the liquid chromatography tandem mass spectrometry (LC-MS-MS) system. The analytes were separated on a Phenomenex Luna HILIC column with gradient elution. Detection was performed on Triple Quadrupole LC-MS in positive ions multiple reaction monitoring mode using electrospray ionization. The calibration curves were linear (r(2)≥0.995) over the concentration range from 62.5 to 1250ng/mL for CA and 31.25 to 1000ng/mL for 6-ANCA. The detection limits of CA and 6-ANCA were 62.5 and 15.6ng/mL, respectively. The intra-day and inter-day precisions were within 8.7% and 9.9%, respectively. The intra-day and inter-day accuracy were between 5.3% and 3.5%, and between 6.1% and 6.6%, respectively. The method proved to be simple and time efficient, and was successfully applied to evaluate the kinetics of caprolactam in one unusual case of caprolactam poisoning.

• Fatal serotonin toxicity caused by moclobemide and fluoxetine overdose.

  Authors: Ming-Ling Wu, Jou-Fang Deng

  Chang Gung medical journal. 11/2011; 34(6):644-9.

  Both moclobemide and fluoxetine are used in the treatment of depression, and have been shown to produce fewer side effects than conventional tricyclic antidepressants. A combination of moclobemideBoth moclobemide and fluoxetine are used in the treatment of depression, and have been shown to produce fewer side effects than conventional tricyclic antidepressants. A combination of moclobemide and fluoxetine has been used in refractory depression, however there is potential for severe serotonin toxicity. We describe a lethal case of serotonin toxicity in a 36 year-old woman after she ingested multiple drugs, including moclobemide 4500 mg, fluoxetine 200 mg, propranolol 300 mg and several benzodiazepines. The clinical features included coma, mydriasis, hyperthermia, tremor, hyperreflexia, rhabdomyolysis, renal failure and respiratory insufficiency. Eventually, the patient died of disseminated intravascular coagulation and circulatory collapse at 22.5 h postingestion. Toxicological analysis of the patient's blood confirmed high levels of moclobemide 150 μg/mL (therapeutic 1-3 μg/mL), fluoxetine 3750 ng/mL (therapeutic 47-469 ng/mL) and several benzodiazepines. In conclusion, a combination of moclobemide and fluoxetine should be avoided in depressed patients with high suicidal tendencies. Moreover, early recognition and aggressive intervention are the mainstays in the management of potentially life-threatening serotonin toxicity.

• Acute hemolysis following iodine tincture ingestion.

  Authors: Yan-Chiao Mao, Wei-Jen Tsai, Ming-Ling Wu, Jiin Ger, Jou-Fang Deng, Chen-Chang Yang

  Human & experimental toxicology. 02/2011; 30(10):1716-9.

  Iodine tincture poisoning is uncommon regardless of its widespread use as an antiseptic in daily practice. Previously reported effects of iodine-containing antiseptic poisoning included topicalIodine tincture poisoning is uncommon regardless of its widespread use as an antiseptic in daily practice. Previously reported effects of iodine-containing antiseptic poisoning included topical irritation, corrosive effects, allergic response, and hepatic or renal injury, which mainly resulted from complications of topical use during surgical procedures. We herein reported an unusual case of severe hemolysis and acute renal failure following intentional ingestion of iodine tincture containing 60 mg/ml iodine and 40 mg/ml potassium iodide in 70% v/v ethanol. The patient completely recovered 8 weeks later after receiving supportive treatment, plasma exchange, and temporary hemodialysis.

• Survival after hypocalcemia, hypomagnesemia, hypokalemia and cardiac arrest following mild hydrofluoric acid burn.

  Authors: Ming-Ling Wu, Juo-Fang Deng, Ju-Sing Fan

  Clinical toxicology (Philadelphia, Pa.). 11/2010; 48(9):953-5.

  Although hydrofluoric (HF) acid burns may cause extensive tissue damage, severe systemic toxicity is not common after mild dermal exposure. A 36-year-old worker suffered a first-degree burn of 3% ofAlthough hydrofluoric (HF) acid burns may cause extensive tissue damage, severe systemic toxicity is not common after mild dermal exposure. A 36-year-old worker suffered a first-degree burn of 3% of his total body surface area as a result of being splashed on the right thigh with 20% HF acid. Immediate irrigation and topical use of calcium gluconate gel prevented local injury. However, the patient developed hypocalcemia and hypomagnesemia, hypokalemia, bradycardia, and eventually had asystole at 16 h post-exposure, which were unusual findings. He was successfully resuscitated by administration of calcium, magnesium, and potassium. This report highlights a late risk of HF acid dermal exposure.

• Methomyl-alphamethrin poisoning presented with cholinergic crisis, cortical blindness, and delayed peripheral neuropathy.

  Authors: Yu-Hui Hu, Chen-Chang Yang, Juo-Fang Deng, Ming-Ling Wu

  Clinical toxicology (Philadelphia, Pa.). 10/2010; 48(8):859-62.

  Methomyl-alphamethrin is a mixture of carbamate and pyrethroid insecticides. Carbamate insecticides function as reversible cholinesterase inhibitors, which may produce life-threatening cholinergicMethomyl-alphamethrin is a mixture of carbamate and pyrethroid insecticides. Carbamate insecticides function as reversible cholinesterase inhibitors, which may produce life-threatening cholinergic syndrome. Cortical blindness and delayed neuropathy were rarely reported complications of carbamate insecticide exposures. Here we reported a case of intentional methomyl-alphamethrin ingestion. A 41-year-old woman attempted suicide by drinking 200 mL of methomyl-alphamethrin insecticide and soon presented with unconsciousness, hypothermia, and shock. She developed pulseless electrical activity and regained spontaneous circulation after resuscitation. Diagnosis of carbamate poisoning was made by her clinical features, decreased levels of cholinesterases and the presence of methomyl in her urine. She complained of blurred vision and blindness 4 days post-exposure. Visual evoked potential and brain magnetic resonance imaging study confirmed the diagnosis of cortical blindness. On day 21, she had low limbs numbness, progressive weakness, and right foot drop. Electophysiological tests performed on day 27 revealed neuropathy of bilateral peroneal nerves. We reported a patient who manifested severe carbamate insecticide poisoning and developed cortical blindness and delayed neuropathy. Physicians should be aware of these rare toxicities among patients with severe carbamate insecticide poisoning.

• Serotonin toxicity caused by moclobemide too soon after paroxetine-selegiline.

  Authors: Ming-Ling Wu, Jou-Fang Deng

  Journal of the Chinese Medical Association : JCMA. 09/2009; 72(8):446-9.

  Serotonin toxicity is an iatrogenic complication of serotonergic drug therapy. It is due to an overstimulation of central and peripheral serotonin receptors that lead to neuromuscular, mental andSerotonin toxicity is an iatrogenic complication of serotonergic drug therapy. It is due to an overstimulation of central and peripheral serotonin receptors that lead to neuromuscular, mental and autonomic changes. Moclobemide is a reversible inhibitor of monoamine oxidase (MAO)-A, selegiline is an irreversible selective inhibitor of MAO-B, and paroxetine is a selective serotonin reuptake inhibitor. Combined use of these agents is known to cause serotonin toxicity. A 53-year-old woman had been treated with paroxetine and selegiline. After moclobemide was prescribed in place of paroxetine without a washout period, she quickly developed confusion, agitation, ataxia, diaphoresis, tremor, mydriasis, ocular clonus, hyperreflexia, tachycardia, moderately elevated blood pressure and high fever, symptoms that were consistent with serotonin toxicity. Discontinuation of the drugs, hydration and supportive care were followed by remarkable improvement of baseline status within 3 days. This case demonstrates that serotonin toxicity may occur even with small doses of paroxetine, selegiline and moclobemide in combination. Physicians managing patients with depression must be aware of the potential for serotonin toxicity and should be able to recognize and treat or, ideally, anticipate and avoid this pharmacodynamically-mediated interaction that may occur between prescribed drugs.

• The epidemiology of glyphosate-surfactant herbicide poisoning in Taiwan, 1986-2007: a poison center study.

  Authors: Ying-Ju Chen, Ming-Ling Wu, Jou-Fang Deng, Chen-Chang Yang

  Clinical toxicology (Philadelphia, Pa.). 08/2009;

  Background. Glyphosate-surfactant herbicide (GlySH) is widely used in agriculture and has been associated with numerous toxicities following oral ingestion. However, there are many controversies withBackground. Glyphosate-surfactant herbicide (GlySH) is widely used in agriculture and has been associated with numerous toxicities following oral ingestion. However, there are many controversies with regard to the exact causes and determinants of developing severe/death outcome after exposure to GlySH. Methods. We conducted an analysis of all GlySH exposures reported to the Taiwan National Poison Control Center between 1986 and 2007. Patients' baseline characteristics and clinical data were reviewed and analyzed. Results. A total of 2,186 patients were eligible for analysis. Most of the exposures were related to oral ingestion (n = 2,023, 92.5%) and attempted suicide (n = 1,631, 74.6%). The mean age of exposure was 42.8 +/- 18.6 years. One hundred patients developed severe effects and 146 patients died following oral GlySH exposure, resulting in a case fatality rate of 7.2%. Shock (n = 85, 58.2%) and respiratory failure (n = 34, 23.3%) accounted for most fatalities. Four out of eight patients with injection exposure manifested severe (n = 3) or fatal outcome (n = 1). In a multivariate logistic regression analysis, increasing age, larger amount of exposure, longer elapsed time to presentation, attempted suicide, receipt of atropine therapy, and being exposed in certain calendar years were positively associated with the severity of poisoning following oral GlySH exposure. Conclusion. Age, ingested amount, delayed presentation, and reason for exposure were likely to be determinants of the severity of GlySH exposure. Because shock is the major cause of death and usually develops early after GlySH exposure, prompt fluid replacement therapy seems critical in the initial management of such exposures. Patients' airway should also be secured to avoid aspiration and subsequent respiratory failure.

• Acute severe chromium poisoning after dermal exposure to hexavalent chromium.

  Authors: Chun-Chi Lin, Ming-Ling Wu, Chen-Chang Yang, Jiin Ger, Wei-Jen Tsai, Jou-Fang Deng

  Journal of the Chinese Medical Association : JCMA. 05/2009; 72(4):219-21.

  Severe acute chromium poisoning related to dermal involvement has rarely been reported in the literature. We report a case of acute severe chromium poisoning through skin exposure as a result of aSevere acute chromium poisoning related to dermal involvement has rarely been reported in the literature. We report a case of acute severe chromium poisoning through skin exposure as a result of a chemical burn of 15% of the body surface area and multiple organ failure after short-term exposure. Medical interventions, including mechanical ventilation, continuous venovenous hemofiltration, and plasmapheresis were performed. In addition, a chelating agent, dimercaptopropane sulfonic acid, was infused intravenously, combined with intravenous N-acetylcysteine and ascorbic acid as adjuvant therapy. The patient was discharged on day 33 without long-term sequelae. The consequence of transdermal exposure of hexavalent chromium should not be overlooked.

• Acute hemolysis caused by incidental trichlorfon exposure.

  Authors: Ming-Ling Wu, Jou-Fang Deng

  Journal of the Chinese Medical Association : JCMA. 05/2009; 72(4):214-8.

  Trichlorfon (o-o-dimethyl-2,2,2-trichloro-hydroxyethylphosphate), an organophosphate, has a moderately potent anticholinesterase activity. Organophosphate poisoning is well known for itsTrichlorfon (o-o-dimethyl-2,2,2-trichloro-hydroxyethylphosphate), an organophosphate, has a moderately potent anticholinesterase activity. Organophosphate poisoning is well known for its characteristic symptoms and signs, but acute hemolysis caused by trichlorfon is rarely reported. We present a patient who developed acute hemolysis and renal function impairment after percutaneous trichlorfon exposure. A 54-year-old man applied trichlorfon powder to his dog to kill its parasites. Half an hour later, the dog was suspected to die of cholinergic crisis and the patient felt abdominal cramping pain. Later, he developed severe nausea, vomiting, chills, high fever, and cold sweat. Laboratory work-up disclosed a picture of acute hemolysis, jaundice, renal function impairment and leukocytosis. However, there were no clinical features of acute cholinergic syndrome except gastrointestinal symptoms, and blood cholinesterase activities were also normal. He eventually had a full recovery. Trichlorfon should be added to the toxins known to cause acute hemolysis.

• Neonicotinoid insecticides: an emerging cause of acute pesticide poisoning.

  Authors: Dong Haur Phua, Chun-Chi Lin, Ming-Ling Wu, Jou-Fang Deng, Chen-Chang Yang

  Clinical toxicology (Philadelphia, Pa.). 05/2009; 47(4):336-41.

  INTRODUCTION: Neonicotinoids are a relatively new class of insecticides. They exhibit agonistic effects at postsynaptic nicotinic receptors in insects and are believed to have low toxicity in humans.INTRODUCTION: Neonicotinoids are a relatively new class of insecticides. They exhibit agonistic effects at postsynaptic nicotinic receptors in insects and are believed to have low toxicity in humans. METHODS: We conducted a retrospective analysis of all neonicotinoid exposures reported to the Taiwan National Poison Center to better understand the toxicity profile of neonicotinoid insecticides. RESULTS: A total of 70 patients were analyzed. Most exposures involved suicidal ingestions of imidacloprid alone. Clinical manifestations of neonicotinoid insecticide toxicity bear some resemblance to those of acute nicotine poisoning. Although most exposures were of mild-to-moderate severity, eight patients developed major effects and two died. Aspiration pneumonia and respiratory failure were the main cause of severe toxicity. CONCLUSION: Significant toxicity of neonicotinoids can occur following large amount of oral ingestion. Poisoned patients may present with cholinergic syndrome, and judicious use of atropine seems justified. Symptomatic treatment, especially ventilator support, remains most important in clinical management.

• Acute hepatic injury and renal failure after ingestion of snake gallbladder.

  Authors: Ta-Chung Chao, Ming-Ling Wu, Wei-Jen Tsai, Jiin Ger, Jou-Fang Deng

  Clinical toxicology (Philadelphia, Pa.). 02/2006; 44(4):387-90.

  Ingestion of snake gallbladder has been practiced in ancient Chinese civilizations to improve vision and relieve arthritic pain. Although little is known about the composition of snake gallbladder,Ingestion of snake gallbladder has been practiced in ancient Chinese civilizations to improve vision and relieve arthritic pain. Although little is known about the composition of snake gallbladder, ingestion is still practiced in some Chinese cultures. Adverse effects of ingesting snake gallbladder have not yet been reported. Here, we present a case of acute hepatic injury and delayed-onset renal failure after ingestion of snake gallbladders. The patient subsequently recovered after supportive care, combined with plasma exchange and hemodialysis. He was the only survivor of the four victims suffering from intoxication of snake gallbladder in the last three years in our hospital.

• Acute Erycibe henryi Prain ("Ting Kung Teng") poisoning.

  Authors: Hsien-Hao Huang, David Hung-Tsang Yen, Ming-Ling Wu, Jou-Fang Deng, Chun-I Huang, Chen-Hsen Lee

  Clinical toxicology (Philadelphia, Pa.). 02/2006; 44(1):71-5.

  Erycibe henryi Prain ("Ting Kung Teng"), a species of Convolvulaceae, has been used in Chinese medicine to relieve pain involving the musculoskeletal system, such as arthritis, sciatica, andErycibe henryi Prain ("Ting Kung Teng"), a species of Convolvulaceae, has been used in Chinese medicine to relieve pain involving the musculoskeletal system, such as arthritis, sciatica, and traumatic tissue swelling. E. henryi can be mistaken for another herbal plant, Tripterygium wilfordii Hook F, used to treat gouty arthritis. We report here three cases of E. henryi poisoning. All three cases presented with vomiting, diarrhea, salivation, diaphoresis, lacrimation, and rhinorrhea; two patients also had miosis, hypothermia, bradycardia, hypotension, and ventricular tachyarrhythmias. Laboratory abnormalities included leucocytosis, hyperglycemia, hyperamylasemia, hypocalcemia, and transiently elevated liver enzymes, creatinine and creatinine phosphokinase. The active constituents of E. henryi include several tropane alkaloids, which exhibit cholinergic activities. Gastrointestinal disturbances and ventricular tachyarrhythmias may occur with ingestion of either E. henryi or T. wilfordii, but the cholinergic symptoms can help to differentiate them.

• Severe bone marrow depression induced by an anticancer herb Cantharanthus roseus.

  Authors: Ming-Ling Wu, Jou-Fang Deng, Jaw-Ching Wu, Frank S Fan, Ching-Fen Yang

  Journal of toxicology. Clinical toxicology. 02/2004; 42(5):667-71.

  We report a 67-yr-old woman with hepatitis C-related liver cirrhosis and hepatoma who had developed severe bone marrow suppression after taking Cantharanthus roseus as an alternative anticancerWe report a 67-yr-old woman with hepatitis C-related liver cirrhosis and hepatoma who had developed severe bone marrow suppression after taking Cantharanthus roseus as an alternative anticancer treatment. The patient developed severe pancytopenia with initial presentations of vomiting, diarrhea, oral ulcer, and fever about 1 week after taking 5-days' course of Cantharanthus roseus. Bone marrow biopsy showed autolysis, which indicated massive necrosis of the hematopoietic cells. There was no malignant cell infiltration. The patient also had severe gastrointestinal disturbances, bacteremia, urinary tract infection, and impaired renal and liver function. Supportive care with broad-spectrum antibiotics, granulocyte colony-stimulating factor, repeated blood transfusions, and albumin supplement was given. She recovered and was discharged after 48 days hospitalization. Coadministration of Cantharanthus roseus and cisapride was noted, and these two drugs are both substrates of cytochrome P450 3A4 enzymes (CYP 3A4). Because the vinca alkaloids are extensively metabolized by the liver cytochrome P450 enzymes, poor hepatic function and drug-herb interaction might predispose the patient to develop the bone marrow toxicity. This case report demonstrated possible effect of oral dose of vinca alkaloids and also hinted that all the substrates and inhibitors of CYP 3A4 have propensity to interfere with metabolism of vinca alkaloids.

• Acute Cycas seed poisoning in Taiwan.

  Authors: Shy-Shin Chang, Yi-Ling Chan, Ming-Ling Wu, Jou-Fang Deng, Te-Fa Chiu, Jih-Chang Chen, Feng-Lin Wang, Ching-Ping Tseng

  Journal of toxicology. Clinical toxicology. 02/2004; 42(1):49-54.

  OBJECTIVE: The seeds of cycads contain cycasin and neocycasin, which belong to the family of cyanogenic glycosides. These glycosides of cycads are considered pseudocyanogenic with little potential toOBJECTIVE: The seeds of cycads contain cycasin and neocycasin, which belong to the family of cyanogenic glycosides. These glycosides of cycads are considered pseudocyanogenic with little potential to liberate hydrogen cyanide as other cyanogenic glycosides do. This study investigated the clinical spectrum of Cycas seed poisoning and its cyanogenic potential. METHODS: This was a retrospective chart review conducted at the Poison Control Center in Taiwan (PCC-Taiwan) from 1990 to 2001. RESULTS: Twenty-one cases of Cycas seed poisoning were identified. The reasons for seed ingestion were misuse as an edible food (70%), health promotion (10%), cancer prevention (10%), cosmetic use (5%), and gastrointestinal discomfort (5%). All patients had eaten the seeds after washing and cooking them. The time from ingestion to the onset of symptoms ranged from 30 min to 7 h (mean 2.8 h); patients had ingested between 1 to 30 seeds. Respiratory depression did not occur. Severe vomiting was the most striking symptom. All patients except one presented with gastrointestinal disturbance, and 90% sought medical care at the emergency department. Within 24 h, all patients had recovered. Six patients had blood cyanide or thiocyanate levels measured. Although the levels were higher than normal, they did not reach the toxic range. CONCLUSIONS: The cyanogenic potential of Cycas seeds is documented in our cases. The gastrointestinal symptoms were severe enough that most patients sought medical attention but recovery was quick and complete.

• Sea-urchin envenomation.

  Authors: Ming-Ling Wu, Shang-Lin Chou, Tzu-Yu Huang, Jou-Fang Deng

  Veterinary and human toxicology. 01/2004; 45(6):307-9.

  Sea-urchin stings may produce injurious and venomous wounds. Although numerous writers refer to the danger of pedicellarial stings, there is little worth-while clinical data. We report a case ofSea-urchin stings may produce injurious and venomous wounds. Although numerous writers refer to the danger of pedicellarial stings, there is little worth-while clinical data. We report a case of sea-urchin injury with severe local reaction and acute hepatitis. A 47-y-o Taiwanese woman accidentally stepped on a sea urchin while scuba diving on a beach in Palau Islands. The puncture wounds were numerous and she felt faintness, and immediate and intense pain. Initial management included partial spine removal, betadine immersion, intravenous fluid and analgesics. She developed fever, chills, nausea, and persistent serous discharge and tenderness from the sites of stings in the following days. She was admitted due to right foot cellulitis, sea-urchin injuries of both soles and suspected toxic hepatitis on the 7th day after envenomation. Serum alanine transaminase was 810 U/L and aspartate transaminase 320 U/L; she received i.v. antibiotics and wound debridement for removal of residual stings. She recovered gradually and was discharged 2 w later. Travel related marine animal injury has an increasing tendency throughout the world. This case had the unusual presentation of severe local reaction and hepatitis; immediate and more aggressive spine removal might have lessened the degree of injury.

• Bile acid composition in snake bile juice and toxicity of snake bile acids to rats.

  Authors: Yen-Hung Yeh, Dar-Yi Wang, Ming-Yi Liau, Ming-Ling Wu, Jou-Fang Deng, Tamao Noguchi, Deng-Fwu Hwang

  Comparative biochemistry and physiology. Toxicology & pharmacology : CBP. 12/2003; 136(3):277-84.

  We determined the bile acid profiles in bile juice of snake gallbladders by HPLC on a silica gel RP-18 reversed-phase column. Cholic acid and chenodeoxycholic acid were predominant components inWe determined the bile acid profiles in bile juice of snake gallbladders by HPLC on a silica gel RP-18 reversed-phase column. Cholic acid and chenodeoxycholic acid were predominant components in three of four snake species. To elucidate the toxic effect of snake bile acids on rats, a synthetic bile acid mixture was prepared mimicking the bile acid composition of a snake Naja naja atra bile juice. Twenty-four male Wistar rats were divided into four groups and treated orally at 3-day intervals with saline (control group) and different doses (1-3x doses) of the bile acid mixture. After treatment, the following parameters increased: the relative ratios of liver and kidney mass to body mass, the concentrations of red blood cell, hemoglobin and hematocrit in the blood, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, plasma urea nitrogen and creatinine in the plasma, and the levels of urine urea nitrogen and creatinine in the urine. Body mass of rats and the levels of Na+, K+, Ca++ in the urine of rats were significantly decreased, especially for groups treated with 2x and 3x doses of the bile acid mixture. Examination of liver and kidney pathology also showed cell enlargement and lesion in cell integrity in treated groups, especially for groups treated with 2x and 3x bile acid mixture, indicating that short-term toxicity of snake N. naja atra bile acids was significant in rats.

• Clinical experience of acute ferric chloride poisoning.

  Authors: Ming-Ling Wu, Wei-Jen Tsai, Jiin Ger, Jou-Fang Deng

  Veterinary and human toxicology. 11/2003; 45(5):243-6.

  Ferric chloride is both a corrosive acid and iron compound; reports of poisoning in humans are rare. A retrospective study was conducted to evaluate patients with ferric chloride exposure reported toFerric chloride is both a corrosive acid and iron compound; reports of poisoning in humans are rare. A retrospective study was conducted to evaluate patients with ferric chloride exposure reported to Poison Control Center-Taipei Veterans General Hospital during 1990-2001. After exclusion of incomplete records, 16 patients with ferric chloride exposure were analyzed (9 male, 7 female aged 12 to 70 y). The exposures were occupational inhalation (18.7%), suicidal ingestion (56.3%), and accidental ingestion (25.0%). Major symptoms and signs were nausea/vomiting (68.8%), sore throat (68.8%), abdominal pain (37.5%), oral ulcers (37.5%), metabolic acidosis (25.0%), aspiration pneumonia (18.8%), respiratory failure (12.5%), diarrhea (12.5%), and hypotension (12.5%). The severity of poisonings were fatal 6.3%, severe 18.8%, moderate 31.2%, mild 37.5%, and asymptomatic 6.3%. Deferoxamine therapy was given in 9 hospitalized patients with good recovery; however the fatal case did not receive deferoxamine due to rapid deterioration and a late diagnosis. The serum iron level known in 7 cases ranged from 40 to 2440 microg/dL. Ingestion of ferric chloride may result in serious morbidity and mortality. Inappropriate labeling and storage lead to accidental swallowing or misdiagnosis. Early diagnosis is important, especially in seriously poisoned patients.

• Multiple thrombotic occlusions of vessels after Russell's viper envenoming.

  Authors: Dong-Zong Hung, Ming-Ling Wu, Jou-Fang Deng, Dar-Yu Yang, Shoei-Yn Lin-Shiau

  Pharmacology & toxicology. 10/2002; 91(3):106-10.

  Systemic bleeding due to consumption coagulopathy and thrombocytopenia due to activation of procoagulants is the leading manifestation and cause of death in Russell's viper systemic envenoming.Systemic bleeding due to consumption coagulopathy and thrombocytopenia due to activation of procoagulants is the leading manifestation and cause of death in Russell's viper systemic envenoming. Thrombotic occlusion of the blood vessels is rare in cases of snakebite. In this report, two adult patients with Russell's viper systemic envenoming presented multiple cerebral infarctions, digital gangrenes and ischaemic organs in addition to typical clinical manifestations of bleeding diathesis and renal involvement. Our findings in these two special cases suggest that the venom-induced coagulopathy and endothelium damage, predisposed by toxin-induced vasoconstriction, might be the possible mechanism of multiple thrombotic vascular occlusions in systemic envenoming of Formosan Russell's viper.

• Russell's viper snakebite in Taiwan: differences from other Asian countries.

  Authors: Dong-Zong Hung, Ming-Ling Wu, Jou-Fang Deng, Shoei-Yn Lin-Shiau

  Toxicon : official journal of the International Society on Toxinology. 10/2002; 40(9):1291-8.

  Formosan Russell's viper (Daboia russelli siamensis) is the sixth most frequent cause of snakebite in Taiwan. Its venom has been thought to have both neurotoxic and hematoxic properties. This viper'sFormosan Russell's viper (Daboia russelli siamensis) is the sixth most frequent cause of snakebite in Taiwan. Its venom has been thought to have both neurotoxic and hematoxic properties. This viper's snakebite is rare and thus scarcely subjected to systemic studies. In this paper, we retrospectively analyzed and described 18 cases of viper snakebite from 1987 to 1999. Like that of the Russell's viper snakebite in other South East Asian areas, varied degrees of acute renal failure, incoagulable blood with bleeding diathesis and hemolysis were the major symptoms found in the systemic envenoming patients. Systemic thrombosis seems to be the distinguishing feature in Formosan Russell's viper snakebite. Neither symptoms nor signs of neuromuscular junction blocking effects were observed, which is another difference from symptoms observed after bites of some other Russell's viper subspecies, suggesting a significant geographic variation. These findings confirmed the clinical importance of Russell's viper snakebite in Taiwan.