Lead, mercury, and arsenic poisoning due to topical use of traditional Chinese medicines.

BACKGROUND: Metal poisonings through a mucocutaneous route are reported rarely in the literature. METHODS: We report 2 cases of heavy metal intoxication from inappropriate use of Chinese mineral medicines confirmed by toxicologic investigations. RESULTS: A 51-year-old man developed perianal gangrene and a high fever after a 2-week anal use of hong-dan herbal mixtures for anal fistula. He presented gastrointestinal and constitutional symptoms, followed by skin rash, anemia, hair loss, peripheral neuropathy, and muscle atrophy. Elevated urine arsenic and mercury confirmed the heavy metal poisonings. The hong-dan mixture contained lead tetraoxide, arsenic, and mercury. He was treated with 2,3-dimercapto-1-propanesulfonic acid, with partial improvement, but peripheral neuropathy persists 4 years later. A 75-year-old man developed anorexia, weight loss, headache, dizziness, nausea, vomiting, constipation, weakness, and anemia after a 3-month use of an herbal patch for chronic leg ulcer. His blood lead concentration was 226 µg/dL, and the lead content of the herbal patch was 517 mg/g. Chelation with ethylene diamine tetraacetic acid and dimercaptosuccinic acid was followed by clinical recovery. CONCLUSION: These cases documented serious systemic poisoning after the short-term use of traditional Chinese medicines containing heavy metals in damaged or infected tissue.

Essential trace element status and clinical outcomes in long-term dialysis patients: a two-year prospective observational cohort study.

BACKGROUND & AIMS: Essential trace elements are involved in many biological processes for normal cell function including immunological defense against oxidation and infection. Deficiency of these elements generally leads to illness or even death in the general population. Therefore, we investigated the predictive values of trace element status on clinical outcomes in dialysis patients, who are more prone to trace element deficiency. METHODS: We enrolled 111 prevalent patients on maintenance dialysis from a Taipei tertiary-care referral hospital and measured serum levels of selenium, copper, and zinc. Patients were followed for 2 years or until death or withdrawal. RESULTS: Multivariate Cox regression analysis indicated that patients with diabetes mellitus (HR, 2.162 [95% CI, 1.105-4.232], p=0.024), prior stroke (HR, 3.876 [95% CI, 1.136-13.221], p=0.030), and zinc deficiency (HR, 0.979 [95% CI, 0.966-0.992], p=0.002) were more likely to be hospitalized for infectious diseases. Furthermore, beyond traditional risk factors, such as old age and hypoalbuminemia, multivariate Cox regression also indicated that lower serum level of zinc independently predicts overall mortality (HR, 0.973 [95% CI, 0.948-0.999], p=0.046). CONCLUSIONS: In long-term dialysis patients, the serum level of zinc was an independent predictor of future hospitalization due to infectious diseases and of overall mortality.

Aconitine intoxication mimicking acute myocardial infarction.

INTRODUCTION: Cardiotoxicity in acute aconitine intoxication is well known; however, elevation of troponin I level and abnormal scintigraphy findings had not previously been reported. CASE REPORT: A 60-year-old man developed chest tightness, syncope and convulsion after ingesting processed Aconitum carmichaeli (Chuanwu) extract for treatment of headache. Electrocardiogram showed first degree atrioventricular (AV) block. Troponin I level was elevated at 14.8 ng/mL 13 hours post-ingestion. Creatine kinase was also increased to 414 U/L. However, echocardiography did not show any abnormal cardiac wall motion. Tc-99m-PYP scintigraphy revealed diffusely increased uptake in the myocardium, suggesting the presence of myocardial necrosis or myocarditis. DISCUSSION: Aconitine poisoning can mimic acute myocardial infarction with chest tightness and elevated cardiac enzymes. Increased cardiac markers and myocardial insult seen in this patient were likely to be related to the toxicity of aconitine. Care should be taken in making the diagnosis in such instances. Management is primarily supportive.

Acute severe chromium poisoning after dermal exposure to hexavalent chromium.

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 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.

Human Melia azedarach poisoning.

INTRODUCTION: In traditional Chinese medicine, Melia azedarach (Ku-lian) is used orally and topically as an antiparasitic and antifungal agent. Although toxicity of this plant has been widely described in veterinary literature, human poisoning is rarely reported. We describe five patients with M. azedarach poisoning who recovered with supportive care. CASE SERIES: Five patients were identified retrospectively from the database of the Taiwan National Poison Center at the Taipei Veterans General Hospital. Three cases were on-site patients, and two were telephone consultations from outside hospitals. Neurological symptoms were the major manifestation in four cases: weakness, myalgia, numbness, and ptosis. Treatment was symptomatic and supportive; all patients recovered without sequelae. DISCUSSION: It is not known which limonoids are responsible for human toxicity. In the Chinese medical literature, human M. azedarach poisoning is said to occur if six to nine fruits, 30 to 40 seeds, or 400 g of the bark is consumed. Onset of symptoms typically occurs within 4-6 h, but as short as 0.5 h had been documented. In our patients, the onset of M. azedarach poisoning was variable, ranging from a few hours to up to 3 weeks after consumption of the herb. CONCLUSIONS: M. azedarach poisoning may result in gastrointestinal, cardiovascular, respiratory, or neurological effects, and death in severe cases.

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

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, 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.

A simple, safe, and efficient way to treat severe fluoride poisoning--oral calcium or magnesium.

PURPOSE: To examine the efficacy and safety of administration of calcium and magnesium orally and intraperitoneally to treat severe sodium fluoride intoxication. MATERIALS AND METHODS: Mice were initially gavaged a lethal dose of sodium fluoride (NaF) or water. Then, mice were treated with water or varying concentrations of calcium chloride (CaCl2) or magnesium sulfate (MgSO4) via intraperitoneal (IP) route or via oral route. Mice were monitored for 24 h, and the time of death was recorded. RESULTS: IP injections of large amounts of CaCl2 or MgSO4 were dangerous. All mice gavaged with water and then treated with oral CaCl2 or MgSO4 survived and displayed normal activity during the experiment. The survival rate of mice gavaged with a lethal dose of NaF and then treated with a high dose of oral CaCl2 or MgSO4 was significantly higher than those of using low dose. CONCLUSION: Oral administration of a high dose of CaCl2 or MgSO4 is a simple, safe, and effective adjunctive method for treating severe oral fluoride poisoning.

Clinical features and management of herb-induced aconitine poisoning.

STUDY OBJECTIVE: We define the potential sources, clinical manifestations, and treatment of aconitine poisoning. METHODS: The database of the National Poison Center in Taiwan was retrospectively searched for the diagnosis of aconitine poisoning for 1990 to 1999. The reasons for taking the aconite roots, the clinical features, management, and possible predisposing factors were noted. RESULTS: A total of 17 cases occurred and consisted of 9 men and 8 women aged 30 to 70 years. Thirteen patients ingested aconite roots as treatment for rheumatism and wounds. Two patients volunteered to test the effects of aconite roots in a drug study. Two patients accidentally ingested the aconite roots. After a latent period of 10 to 90 minutes, patients developed a combination of neurologic (n=17), cardiovascular (n=14), gastrointestinal (n=9), and other (n=5) features typical of aconitine poisoning. Four patients developed ventricular tachycardia. All patients received supportive treatment. Patients with ventricular tachycardia were also treated with charcoal hemoperfusion. All patients made a complete recovery. CONCLUSION: Life-threatening ventricular tachycardia can occur after the consumption of aconite roots. The risk is higher with inadequately processed aconite roots, large doses, or tincture preparations. With increasing popularity of herbal medicines, herb-induced aconitine poisoning may also be seen in Western countries.

Determination of aristolochic acids in medicinal plant and herbal product by liquid chromatography-electrospray-ion trap mass spectrometry.

This paper describes a liquid chromatography-electrospray-ion trap mass spectrometry (LC-ES-ITMS) method for the determination of aristolochic acid I and II (AA-I and AA-II) in medicinal plants and Chinese herbal remedies. A reversed phase C(18) column with gradient elution was utilized. The effects of mobile phase additives, acetic acid and ammonium acetate, on LC separation and ES ionization were investigated. For both AA-I and AA-II, the [M+NH(4)](+) ion was found to be the precursor ion for target MS/MS analysis. The MS/MS product ion, [M+H-44](+), was used for the quantitative measurement of AA-I and AA-II. The linearity was good from 0.03 to 5 mug ml(-1) and good correlation (r(2)=0.999) over the range examined was determined for both AA. The detection limit based on a signal-to-noise ratio of three was 0.012 and 0.015 mug ml(-1) for AA-I and AA-II, respectively. Various Chinese herbal remedies obtained from renal failure patients and medicinal plants were examined by this newly developed method.

Clinical and laboratory investigations in herbal poisonings.

Herbs have been used world-wide, particularly in Chinese society, for thousands of years. Conceptually, herbs are usually considered to be non-toxic by the general public due to their natural origin. However, the consumption of herbs is well-known to be capable of producing prominent adverse health effects. Due to increased morbidity and mortality, poisonings associated with the use of herbs have raised universal attention in the last few years. In daily practice, herbs are dispensed by health professionals, quacks and other non-medical professionals, such as witch doctors, for either therapeutic or tonic purposes. Upon exposure, the clinical toxicity may vary from mild to severe and may even be life-threatening. In the clinical setting, the difficulties involved in handling the poisonings associated with the use of herbs can be categorized as follows: (1) difficulties in the identification of the proprietary substances and active ingredients; (2) problems with characterizing the kinetic pattern and toxicological effects; and (3) the uncertainty of the treatment. A systematic approach, including both clinical and laboratory investigations, is required in handling cases of herbal poisonings. Critical factors for the clinical investigation are the observation and documentation of clinical symptoms and signs, as well as the collection of information concerning prescription, packaging, herbal residues, herbal samples, amount consumed and the processing methods of the herbs. A geographically and culturally oriented data bank of analytical systems should be created to assist in the future laboratory diagnosis of herbal poisonings.

Hepatotoxicity caused by Breynia officinalis.

Breynia officinalis has the Chinese proprietary name, Chi R Yun, which means dizziness or vertigo for 7 d. In daily practice, it has been used to treat venereal diseases, contusion, heart failure, growth retardation and conjunctivitis in combination with other traditional Chinese medicines. Two hospital-based cases of Breynia officinalis poisoning have been reported to the Poison Control Center. Case 1 was a 43-y-old female who consumed a mixture of 1500 g lower stem and root of Ji Mu Ju in boiled water in a suicide attempt. Her AST reached 264 and ALT reached 2443. Case 2 was a 51-y-old female who consumed 20 pieces of lower stem and root of Ji Mu Ju stewed with meat and 100 ml of wine to treat chronic contact dermatitis. Her AST reached 3815 and ALT reached 6625. In both cases Breynia officinalis was identified as the cause of poisoning. Poisoning in humans involves the neurologic, gastrointestinal, hepatic, urinary and respiratory systems. Hepatotoxic effects have been reported for some Chinese herbal medicines, but not Breynia officinalis: Breynia officinalis poisoning causes hepatocellular liver injury rather than cholestatic liver injury.

High-performance liquid chromatographic determination for aristolochic acid in medicinal plants and slimming products.

A HPLC procedure with a silica gel RP-18 reversed-phase column for the determination of aristolochic acids I, II in medicinal plants and slimming products was developed. The mobile system 0.3% ammonium carbonate solution-acetonitrile (75:25, v/v) with pH 7.5 was the optimal buffer to clearly separate aristolochic acids I, II within 20 min. The recovery of aristolochic acids I, II in medicinal plants and slimming products was better than 90% by extracting with methanol and purifying through a PHP-LH-20 column. The major component was aristolochic acid I in Aristolochia fangchi and the level ranged from 437 to 668 ppm. Aristolochic acid II was the major component for Aristolochia contorta and its range was <1-115 ppm. Twelve out of 16 samples of slimming pills and powders contained aristolochic acids I and/or II. The major component in most slimming products was aristolochic acid II and the level ranged from <1 to 148 ppm. It may indicate that slimming products were not mainly made of A. fangchi.