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Aconite

Scientific Name(s): Aconitum napellus L., Aconitum carmichaelii Debeaux, and Aconitum kusnezoffii Rchb. Family: Ranunculaceae.

Common Name(s): Aconite , aconite tuber , monkshood , friar's cap , helmet flower , soldier's cap , wolfsbane , devil's helmet , blue rocket , leopard's bane , chuanwu , caowu , wutou , futzu , bushi 1 , 2 , 3

Uses

Aconite extracts have been used homeopathically in Europe and Asia (orally and externally), but rarely in the United States. Use is not recommended because of its toxicity.

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Dosing

Extreme caution is required. Fresh aconite is extremely toxic, and safe dosage is dependent on processing. Many species are used medicinally in China only after processing. Traditional Western texts recommended 60 mg of the root per dose.

Contraindications

Contraindications have not been identified.

Pregnancy/Lactation

Documented adverse effects. In addition to oral administration, external application is reported to cause toxic symptoms. Avoid use.

Interactions

None well documented.

Adverse Reactions

No data.

Toxicology

Aconitine is highly toxic. As little as 2 mg of pure aconite or 1 g of plant may cause death from paralysis of the respiratory center or cardiac muscle. 4 Clinically important toxicity may develop following percutaneous absorption; even slight contact with the flowers can cause fingers to become numb. 5

Botany

Aconitine is an alkaloid derived from various species of Aconitum . At least 350 species exist throughout the world; about 170 species exist in China, 6 and more than 100 species are found throughout the temperate zones of the United States and Canada. The plants are also found throughout many parts of Asia, Africa, and Europe. 1 A. napellus is the most common species in Europe, and has been naturalized in the eastern United States; A. carmichaelii and A. kusnezoffii are the most common species used in traditional Chinese medicine. Aconitum species are erect perennial plants growing to a height of 0.6 to 1.5 m (2 to 6 feet). In general, they resemble delphiniums. The characteristic helmet-shaped blue or purple flowers grow in a raceme at the top of the stalk in summer or fall. Occasionally, the flowers may be white, pink, peach, or yellow. The seed pods contain numerous tiny seeds. 1

History

Various species of Aconitum have been used for centuries both as poisons and medicines. Some are still being used in traditional medicines of India, China, and Japan. 7 The root is the most toxic, although all parts of the plant are considered to be toxic. The toxicity of the extracts follow the same order as the alkaloid content: roots, flowers, leaves, and stems. 6

Extracts of the Aconitum species have been used orally in traditional medicine to reduce fever associated with colds, pneumonia, laryngitis, croup, and asthma; and for their analgesic, anti-inflammatory, hypotensive, diuretic, diaphoretic (cause sweating), cardiac depressant (slow heart rate), and sedative properties. 3 , 8 In traditional Asian medicine, root extracts are typically mixed with other ingredients, such as licorice or ginger. Extracts also have been used as arrow poisons.

Historically, aconite was most commonly used in Western cultures as a tincture. It was applied topically as a counter irritant liniment for neuralgia, rheumatism, and sciatica. 6

In homeopathy, aconite is used to treat fear, anxiety, and restlessness; acute sudden fever; symptoms from exposure to dry, cold weather or very hot weather; tingling, coldness, and numbness; influenza or colds with congestion; and heavy, pulsating headaches. 9

Chemistry

Alkaloids account for up to 1.5% of the dry weight of Aconitum plant species. A wide variety of alkaloids have been isolated from the various species of aconite, including the major active alkaloid aconitine, as well as mesaconitine, hypaconitine, jesaconitine, napelline, sinomontanitines, lappaconitine, ranaconitine, and others. 3 , 10 , 11 , 12 , 13 , 14 Other alkaloids may be produced by processing (eg, pyro-type aconitine alkaloids by heat 3 or benzylaconines or aconines by hydrolysis). Aconitine and its congeners are considerably more toxic than aconine and related alkaloids. 2

Uses and Pharmacology

Because aconite is highly toxic, its use is not recommended. Raw aconite products are extremely toxic; their alkaloids have a narrow therapeutic index and the alkaloid type and amount vary with species, place of harvest, and adequacy of processing. Processing may reduce alkaloid content and/or alter alkaloid composition, thus reducing potency; however, poisoning may still occur after the consumption of processed aconite root. 2

The following pharmacological effects of Aconitum alkaloid have been described: analgesic, anti-inflammatory, and anti-rheumatic activity 15 , 16 ; positive inotropic effects 17 ; and regulation of neurological disorders. 15 , 18 However, only limited studies are available, and most were performed in China and Japan.

Animal data

In animal models, aconitine and related compounds have been shown to possess anti-inflammatory and analgesic properties. 3 , 15 , 16 Studies using mechanical and thermal stimuli to cause pain in mice have shown that, at sub-analgesic doses, processed Aconitum root administered orally, both partially and dose-dependently inhibited the development of morphine tolerance in morphine-naive mice and reversed already developed morphine tolerance in morphine-tolerant mice when compared with placebo. 19 , 20 , 21 , 22

Human data

Results of a study using Japanese kampo preparations suggest that Aconiti tuber may increase nitric oxide production in humans, a possible mechanism for its purported effect on improving a peripheral feeling of coldness. Eleven and 13 patients, respectively, received kampo formulas including and excluding Aconiti tuber. The nitrite and nitrate levels were increased at 4 weeks in those taking Aconiti tuber formulas. 23

Clinical data

Research reveals no clinical data regarding the use of aconite for medical purposes.

Guanfu base A, a new alkaloid isolated from the root of A. coreanum Rapaics, has been found to be an effective antiarrhythmic agent in preclinical and clinical studies and is now undergoing phase 3 clinical trials in China. 15

Shenfu injection, a traditional Chinese therapy that contains red ginseng and aconite root, has provided a protective effect against ischemia and reperfusion injury during mitral valve replacement with cardiopulmonary bypass, 24 and has also stimulated the immune system and reduce blood viscosity, improving postoperative recovery after abdominal surgery. 25 However, the effect of the aconite component has not been determined.

Dosage

Extreme caution is required. Fresh aconite is extremely toxic, and safe dosage is dependent on processing. Many species are used medicinally in China after processing. Traditional Western texts recommended 60 mg of the root per dose. Pure aconite 2 mg or aconite plant 1 g may cause death. 4

Pregnancy/Lactation

Documented adverse effects. Even external application is reported to cause toxic symptoms. Avoid use. 26

Interactions

None well documented.

Adverse Reactions

Because aconite is not considered safe for human use, all effects are considered toxic.

Toxicology

Aconite is a fast-acting toxin. The active principles are aconitine and related alkaloids. Pure aconite 2 mg or aconite plant 1 g may cause death. 4

Toxicity and death have resulted when the plant has been consumed accidentally, possibly mistaken for wild parsley, horseradish, or other herbs growing in the wild. 7 , 8 Very few cases of aconite poisoning have been reported in North America. 7 Most reports have been related to the use of traditional Chinese remedies. 2 A retrospective search of the Taiwan National Poison Center database between 1990 and 1999 revealed 17 cases of aconitine poisoning. Thirteen patients ingested aconite root for treatment of rheumatism or wounds. Two patients had volunteered to test the effects of aconite root in a drug study. Only 2 patients had accidentally ingested the root. 2 The Toxicology Reference Laboratory in Hong Kong confirmed 10 cases of aconite poisoning between March 2004 and May 2006. In 4 cases, the aconite herb was not listed in written prescriptions. 27

Most incidents of aconite toxicity result from the wide variability in strength of home preparations in Asian countries. 28 However, more lethal poisonings are being reported in Western countries where the use of herbal remedies is increasing. 6 , 29 A homicide attempt 30 and a suicide 31 with the plant have been reported.

Aconitine's toxicity is characterized by a burning or tingling sensation of the lips, tongue, mouth, and throat almost immediately following ingestion. Numbness of the throat and difficulty with speech may ensue. Salivation, nausea, vomiting, dizziness, and diarrhea may occur, as well as visual blurring or yellow-green color vision distortion, weakness, and incoordination. Paraesthesia may spread over the entire body. Toxicity mainly affects CNS, heart, and muscle tissues, primarily resulting in cardiovascular complications. 2 , 7 , 13 , 29 , 31 Cardiac arrhythmias with unusual electrical characteristics have been observed following aconite poisoning. 32 , 33 Putrescine, a compound used experimentally as a molecular probe, has been shown to attenuate aconitine-induced arrhythmias. 34 Death from aconitine may follow, secondary to cardiac arrhythmia, 1 which can occur unpredictably within minutes or days. 8 Several case reports describe poisonings with aconite or its constituents, resulting in ventricular tachycardia, other arrhythmias, and death. 6 , 7 , 35 , 36 , 37 , 38

A single dose of aconitine 0.6 mg/kg administered intraperitoneally to rabbits caused histopathologic damage to the myelin sheath of the visual pathway, spinal cord, and peripheral nerves. 39 Similarly, aconitine has demonstrated arrhythmogenic and cardiotoxic effects on myocardium in anesthetized cats. 40 Some experiments have used aconitine to artificially induce arrhythmias in laboratory animals to study the antiarrhythmic effects of other drugs. 41 , 42

A review has summarized the toxicological mechanisms of Aconitum alkaloids, which include the following: (1) binding to voltage-dependent sodium channels inducing a hyperpolarized state, resulting in permanent activation of the channel; (2) modulation of neurotransmitter release and receptors, particularly norepinephrine and acetylcholine; (3) promotion of lipid peroxidation of the cardiac system, possibly causing cardiac arrhythmias; and (4) induction of cellular apoptosis in the heart, liver, and other organs. 13 Most of the cardiotoxic and neurotoxic effects can be explained by these mechanisms, including their effect on calcium imbalance.

General supportive measures, including fluids for dehydration, intravenous pressor agents (eg, dobutamine, dopamine) for hypotension, and resuscitative measures when indicated, form the basis of aconite toxicity management. 2 , 29 Gastric lavage or induction of emesis following the injection of atropine has been recommended. 43 Control of cardiac dysrhythmias has been attempted with various antiarrhythmic agents (eg, lidocaine, amiodarone, flecainide, procainamide, mexiletine) 2 ; however, no single antiarrhythmic drug has been uniformly effective. 11 , 29 Amiodarone and flecainide have been reasonable first-line choices. 2 , 11 , 44 Several cases of successful treatment using percutaneous cardiopulmonary support and bypass in the first 24 hours have been reported. 45 , 46 , 47 Charcoal hemoperfusion has also been used in patients with ventricular arrhythmias unresponsive to antiarrhythmic agents and supportive care, and may have played a critical role in patient survival. 2 , 48 Recovery time is dependent on amount of intoxication; mildly intoxicated patients may take 1 to 2 days to recover, whereas patients with cardiovascular complications may take 7 to 9 days to recover. 2

Evidence suggests that aconite may lose potency after undergoing certain manufacturing procedures; therefore, processed aconite may not have a toxicity profile similar to that of crude plant material. 49

Bibliography

1. Lampe KF, McCann MA. AMA Handbook of Poisonous and Injurious Plants . Chicago, IL: American Medical Association; 1985.
2. Lin CC, Chan TY, Deng JF. Clinical features and management of herb-induced aconitine poisoning. Ann Emerg Med . 2004;43(5):574-579.
3. Murayama M, Mori T, Bando H, Amiya T. Studies on the constituents of Aconitum species. IX. The pharmacological properties of pyro-type aconitine alkaloids, components of processed aconite powder “kako-bushi-matsu”: analgesic, anti-inflammatory, and acute toxic activities. J Ethnopharmacol . 1991;35(2):159-164.
4. Singh S, Fradnis P, Sharma BK. Aconite poisoning. J Assoc Physicians India . 1986;34(11):825-826.
. Mack RB. Play it again, Voltaire—aconite (monkshood) poisoning. N C Med J . 1985;46(10):518-519.
6. Fatovich DM. Aconite: a lethal Chinese herb. Ann Emerg Med . 1992;21(3):309-311.
7. Pullela R, Young L, Gallagher B, Avis SP, Randell EW. A case of fatal aconitine poisoning by monkshood ingestion. J Forensic Sci 2008;53(2):491-494.
8. Spoerke DG. Herbal Medications . Santa Barbara, CA: Woodbridge Press; 1980.
9. Boericke W. Aconitum napellus . Homeopathic Materia Medica. http://www.homeoint.org/books/boericmm/a/acon.htm . Accessed January 21, 2009.
10. Leung AY. Encyclopedia of Common Natural Ingredients Used in Food, Drugs, and Cosmetics . New York, NY: Wiley; 1980.
11. Tai YT, But PP, Young K, Lau CP. Cardiotoxicity after accidental herb-induced aconite poisoning. Lancet . 1992;340(8830):1254-1256.
12. Fu M, Zhang C, Mao S. Influence of processing on the content of hypaconitine in the roots of Aconitum coreanum (Levl.) Rapaics [in Chinese]. Zhongguo Zhong Yao Za Zhi . 1997;22(5):280-281, 319.
13. Fu M, Wu M, Qiao Y, Wang Z. Toxicological mechanisms of Aconitum alkaloids. Pharmazie . 2006;61(9):735-741.
14. Wang FP, Peng CS, Jian XX, Chen DL. Five new norditerpenoid alkaloids from Aconitum sinomontanum . J Asian Nat Prod Res . 2001;3(1):15-22.
15. Feng H, Wang R, Meng Z, Kuo CL, Lien LL, Lien EJ. A survey of a recent chemical and pharmacological investigations of traditional Chinese medicine aconite root. Int J Oriental Med . 2003;28(2):80-91.
16. Hikino H, Konno C, Takata H, et al. Antiinflammatory principles of Aconitum roots. J Pharmacobiodyn . 1980;3(10):514-525.
17. Honejäger P, Meissner A. The positive inotropic effect of aconitine. Naunyn Schmiedebergs Arch Pharmacol . 1983;322(1):49-58.
18. Herzog WH, Feibel RM, Bryant SH. The effect of aconitine on the giant axon of the squid. J Gen Physiol . 1964;47:719-733.
19. Shu H, Arita H, Hayashida M, Sekiyama H, Hanaoka K. Effects of processed Aconiti tuber and its ingredient alkaloids on the development of antinociceptive tolerance to morphine. J Ethnopharmacol . 2006;103(3):398-405.
20. Shu H, Arita H, Hayashida M, et al. Inhibition of morphine tolerance by processed Aconiti tuber is mediated by kappa-opioid receptors. J Ethnopharmacol . 2006;106(2):263-271.
21. Shu H, Hayashida M, Chiba S, et al. Inhibitory effect of processed Aconiti tuber on the development of antinociceptive tolerance to morphine: Evaluation with a thermal assay. J Ethnopharmacol . 2007;113(3)560-563.
22. Shu H, Hayashida M, Huang W, et al. The comparison of effects of processed Aconiti tuber , U50488H and, MK-801 on the antinociceptive tolerance to morphine. J Ethnopharmacol . 2008;117(1):158-165.
23. Yamada K, Suzuki E, Nakaki T, Watanabe S, Kanba S. Aconiti tuber increases plasma nitrite and nitrate levels in humans. J Ethnopharmacol . 2005;96(1-2):165-169.
24. Zheng CD, Min S. Cardioprotection of Shenfu injection against myocardial ischemia/reperfusion injury in open heart surgery. Chin J Integr Med . 2008;14(1):10-16.
25. Zhou Q, Liang LJ, Zhang L, Zhen YY, Su CK. Effect of Shenfu injection in postoperative recovery after abdominal surgery [in Chinese]. Zhongguo Zhong Yao Za Zhi . 2007;32(4):335-338.
26. McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook . Boca Raton, FL: CRC Press; 1997.
27. Poon WT, Lai CK, Ching CK, et al. Aconite poisoning in camouflage. Hong Kong Med J . 2006;12(6):456-459.
28. Chan TY. Incidence of herb-induced aconitine poisoning in Hong Kong: impact of publicity measures to promote awareness among the herbalists and the public. Drug Saf . 2002;25(11):823-828.
29. McGregor AC, MacMillan MH, Ferguson J. Potter's potions. Emerg Med J . 2008;25(4):217-218.
30. Dobbelstein H. Background of a toxicological emergency: homicide attempt with monk's hood [in German]. MMW Fortschr Med . 2000;142(42):46-47.
31. Guha S, Dawn B, Dutta G, Chakraborty T, Pain S. Bradycardia, reversible panconduction defect and syncope following self-medication with a homeopathic medicine. Cardiology . 1999;91(4):268-271.
32. Tai YT, Lau CP, But PP, Fong PC, Li JP. Bidirectional tachycardia induced by herbal aconite poisoning. Pacing Clin Electrophysiol . 1992;15(5):831-839.
33. Smith SW, Shah RR, Hunt JL, Herzog CA. Bidirectional ventricular tachycardia resulting from herbal aconite poisoning. Ann Emerg Med . 2005;45(1):100-101.
34. Bazzani C, Genedani S, Tagliavini S, Bertolini A. Putrescine reverses aconitine-induced arrhythmia in rats. J Pharm Pharmacol . 1989;41(9):651-653.
35. Gupta BS, Saigal R, Vottery R, Singhal N, Banerjee S. Sustained ventricular tachycardia in a case of aconite poisoning. J Assoc Physicians India . 1999;47(4):455.
36. Ortuño Andériz F, Salaverría Garzón I, Vázquez Rizaldos S, Blesa Malpica AL. Fatal poisoning caused by aconitine alkaloid [in Spanish]. Rev Clin Esp . 1999;199(12):861.
37. Mak W, Lau CP. A woman with tetraparesis and missed beats. Hosp Med . 2000;61(6):438.
38. Imazio M, Belli R, Pomari F, et al. Malignant ventricular arrhythmias due to Aconitum napellus seeds. Circulation . 2000;102(23):2907-2908.
39. Kim SH, Kim SD, Kim SY, Kwak JS. Myelo-optic neuropathy caused by aconitine in rabbit model. Jpn J Ophthalmol . 1991;35(4):417-427.
40. Sheikh-Zade YR, Cherednik IL, Galenko-Yaroshevskii PA. Peculiarities of cardiotropic effect of aconitine. Bull Exp Biol Med . 2000;129(4):365-366.
41. Zhang HM, Li HQ. Anti-arrhythmic effects of sophoridine and oxysophoridine. Zhongguo Yao Li Xue Bao . 1999;20(6):517-520.
42. Pau A, Asproni B, Boatto G, et al. Synthesis of substituted N-(4-piperidyl)-N-(3-pyridyl)amides with antiarrhythmic activity. Note 1. Pharmazie . 2000;55(12):892-895.
43. Duke JA. Handbook of Medicinal Herbs . Boca Raton, FL: CRC Press; 1985.
44. Yeih DF, Chiang FT, Huang SK. Successful treatment of aconitine induced life threatening ventricular tachyarrhythmia with amiodarone. Heart . 2000;84(4):E8.
45. Ohuchi S, Izumoto H, Kamata J, et al. A case of aconitine poisoning saved with cardiopulmonary bypass [in Japanese]. Kyobu Geka . 2000;53(7):541-544.
46. Fitzpatrick AJ, Crawford M, Allan RM, Wolfenden H. Aconite poisoning managed with a ventricular assist device. Anaesth Intensive Care . 1994;22(6):714-717.
47. Niinuma H, Aoki H, Suzuki T, et al. Two survival cases of severe aconite poisoning by percuraneous cardiopulmonary support system and cardiopulmonary bypass for fatal arrhythmia: a case report. Internet J Emerg Intensive Care Med . 2002;6(2):6.
48. Lin CC, Chou HL, Lin JL. Acute aconitine poisoned patients with ventricular arrhythmias successfully reversed by charcoal hemoperfusion. Am J Emerg Med . 2002:20(1):66-67.
49. Thorat S, Dahanukar S. Can we dispense with Ayurvedic samskaras? J Postgrad Med . 1991;37(3):157-159.

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