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MUSHROOMS-COPRINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Since toxins within mushrooms can vary widely, and accurately identifying a species of mushroom can be very difficult, a classification system based on clinical symptoms is used. Mushrooms that contain coprine are referred to as the 'coprine-containing mushrooms' group. This group of mushrooms is also referred to as the "Antabuse" mushroom due to the disulfiram-like reaction following the ingestion of alcohol within 2 hours and as long as 5 days (indicative of a dose-related effect) after a mushroom meal.

Specific Substances

    1) Coprinus atramentaria - Now Coprinopsis atramentaria - "Alcohol inky"
    2) Coprinus atramentarius - Now Coprinopsis atramentaria - "Alcohol inky"
    3) Coprinus insignis - Now Coprinopsis insignis
    4) Coprinus quadrifidus - Coprinus variegatus
    5) Coprinus variegatus
    6) Clitocybe clavipes (suspected)
    7) Inky Cap (common name for Coprinus atramentarius - Coprinopsis atramentaria)
    8) Coprinopsis atramentaria

Available Forms Sources

    A) FORMS
    1) Mushrooms that contain coprine are referred to as the 'coprine-containing mushrooms' group. This group of mushrooms is also referred to as the "Antabuse" mushroom due to the disulfiram-like reaction if ethanol is ingested within a few hours of ingesting these mushrooms; occasionally the effects have been noted long as 5 days after a mushroom meal, suggesting a dose-related effect. The effect generally lasts 3 to 6 hours but may last up to 2 days (Berger & Guss, 2005; Spoerke & Rumack, 1994).
    2) Coprine-containing mushrooms are generally very palatable and safe to eat in the absence of alcohol (Berger & Guss, 2005).
    3) Coprinus atramentarius ("inky cap"), Coprinus insignis, Coprinus variegatus (also called Coprinus quadrifidus), and possibly other species of Coprinus will produce this reaction (Benjamin, 1995; Budmiger & Kochler, 1982).
    4) The following species may also cause adverse reactions following their concurrent ingestion with alcohol (however these mushrooms are NOT known to contain coprine) : Polyporus sulphureus, Pholiota squarrosa, Tricholoma aurantum, Clitocybe clavipes, Boletus luridus, Coprinus erethistes, and Coprinus fuscescens (Benjamin, 1995; Spoerke & Rumack, 1994).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) SOURCES: A genus of mushrooms that is found throughout the United States, more often in autumn months. These mushrooms are often called inky cap mushrooms, because the gills autodigest into an inky liquid shortly after harvesting.
    B) TOXICOLOGY: Coprine is a heat-stable toxin which inhibits aldehyde dehydrogenase causing a disulfiram-like reaction with the co-ingestion of ethanol; it is not otherwise toxic.
    C) EPIDEMIOLOGY: Uncommon poisoning which usually does not result in significant morbidity.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: When ethanol is ingested within a few hours of ingesting these mushrooms, nausea, vomiting, metallic taste, paresthesias, weakness, vertigo, confusion, and tachycardia may develop; occasionally the effects have been noted as long as 5 days after a mushroom meal, suggesting a dose-related effect.
    2) SEVERE TOXICITY: Chest pain, hypotension, and cardiac dysrhythmias.

Laboratory Monitoring

    A) Obtain a basic metabolic panel if the patient is having severe vomiting.
    B) Ethanol concentration may be helpful in determining the expected duration of effect.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is primarily symptomatic and supportive. Intravenous fluid should be administered to patients with gastrointestinal effects. Antiemetics or antihistamines may also be administered.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Rarely, severe reactions can result in hypotension. Intravenous fluid is often sufficient. A direct-acting vasopressor (eg, norepinephrine, epinephrine) may be needed on rare occasions. Theoretically, fomepizole could be beneficial in blocking conversion of ethanol to acetaldehyde, but it has not been studied for this purpose.
    C) DECONTAMINATION
    1) PREHOSPITAL: Prehospital decontamination is not indicated.
    2) HOSPITAL: Activated charcoal is unlikely to be beneficial as the patient is most likely presenting with symptoms after co-ingestion with ethanol.
    D) AIRWAY MANAGEMENT
    1) Patients who are comatose or with altered mental status may need mechanical respiratory support and orotracheal intubation; however, the occurrence would be rare.
    E) ANTIDOTE
    1) Theoretically, fomepizole could be beneficial in blocking conversion of ethanol to acetaldehyde, but it has not been studied for this purpose. Consider its use in a patient with severe hypotension; however, consultation with the poison center is advisable. The dose used for toxic alcohol poisoning is 15 mg/kg IV followed by 10 mg/kg IV every 12 hours.
    F) ENHANCED ELIMINATION
    1) Hemodialysis will effectively remove ethanol and its metabolites; however, it should only be considered for patients with life-threatening reactions not responding to supportive care. The use of hemodialysis in this setting has not been reported.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with more than mild symptoms should be referred to a health care facility.
    2) OBSERVATION CRITERIA: Observation is not necessary if the patient did not co-ingest ethanol. If patients have vomiting without an ethanol ingestion, a different mushroom may have been ingested. Symptomatic patients should be evaluated and observed for 4 to 8 hours, and may be discharged if improved.
    3) ADMISSION CRITERIA: Patients with severe symptoms should be admitted.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing severe poisonings or if the diagnosis is unclear. A mycologist (available through some poison centers) may assist in mushroom identification.
    H) PITFALLS
    1) Other more toxic mushrooms may have been co-ingested.
    I) TOXICOKINETICS
    1) Inhibition of aldehyde dehydrogenase occurs within 30 minutes of ingestion and will persist for 3 to 5 days.
    J) DIFFERENTIAL DIAGNOSIS
    1) The differential diagnosis is primarily allergic/hypersensitivity reactions and disulfiram-like reactions to another agent (eg, metronidazole).

Range Of Toxicity

    A) TOXICITY: These mushrooms do not cause toxicity when ingested alone, but only when ethanol is coingested or consumed within 48 to 72 hours of mushroom ingestion. Toxicity is self-limited and fatalities have not been reported.

Clinical Effects

Summary Of Exposure

    A) SOURCES: A genus of mushrooms that is found throughout the United States, more often in autumn months. These mushrooms are often called inky cap mushrooms, because the gills autodigest into an inky liquid shortly after harvesting.
    B) TOXICOLOGY: Coprine is a heat-stable toxin which inhibits aldehyde dehydrogenase causing a disulfiram-like reaction with the co-ingestion of ethanol; it is not otherwise toxic.
    C) EPIDEMIOLOGY: Uncommon poisoning which usually does not result in significant morbidity.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: When ethanol is ingested within a few hours of ingesting these mushrooms, nausea, vomiting, metallic taste, paresthesias, weakness, vertigo, confusion, and tachycardia may develop; occasionally the effects have been noted as long as 5 days after a mushroom meal, suggesting a dose-related effect.
    2) SEVERE TOXICITY: Chest pain, hypotension, and cardiac dysrhythmias.

Heent

    3.4.2) HEAD
    A) Flushing of the face and neck with throbbing distension of neck veins can occur. Swelling of the hands and face may be noted (Reynolds & Lowe, 1965).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) Tachycardia may develop, and is probably due to a combination of anxiety and volume depletion (Caley & Clark, 1977).
    B) CHEST PAIN
    1) Patients may develop chest pain. Although myocardial ischemia and infarction have been reported with disulfiram-ethanol reactions, these complications have not been reported with disulfiram-like reactions associated with Coprinus mushroom ingestion.
    C) HYPOTENSIVE EPISODE
    1) Patients are usually normotensive. Mild hypotension and orthostatic hypotension may occur, most likely secondary to hypovolemia from prolonged vomiting. Severe disulfiram-ethanol reactions have been associated with death, but the disulfiram-like reaction from Coprinus mushroom ingestion rarely causes fatalities.
    D) CONDUCTION DISORDER OF THE HEART
    1) Dysrhythmias are rare. Atrial fibrillation has been reported (Caley & Clark, 1977).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Dyspnea may occur (Leikin & Paloucek, 1998).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PARESTHESIA
    1) Patients may report paresthesias and a feeling of swelling in their hands and feet (Reynolds & Lowe, 1965).
    B) FATIGUE
    1) Weakness, vertigo, and confusion may occur (Spoerke & Rumack, 1994).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Nausea, vomiting, and metallic taste may develop (Reynolds & Lowe, 1965; Goldfrank, 2006).
    B) RUPTURE OF ESOPHAGUS
    1) ESOPHAGEAL RUPTURE - There is one reported case of esophageal rupture due to excessive vomiting (Mayer et al, 1971).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Facial erythema and a blotchy, red rash have been described (Caley & Clark, 1977).
    B) EXCESSIVE SWEATING
    1) DIAPHORESIS - Patients may develop diaphoresis (Caley & Clark, 1977).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain a basic metabolic panel if the patient is having severe vomiting.
    B) Ethanol concentration may be helpful in determining the expected duration of effect.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Serum electrolytes should be monitored in cases of severe, prolonged vomiting.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with severe symptoms should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with more than mild symptoms should be referred to a health care facility.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing severe poisonings or if the diagnosis is unclear. A mycologist (available through some poison centers) may assist in mushroom identification.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Observation is not necessary if the patient did not co-ingest ethanol. If patients have vomiting without an ethanol ingestion, a different mushroom may have been ingested. Symptomatic patients should be evaluated and observed for 4 to 8 hours, and may be discharged if improved.

Monitoring

    A) Obtain a basic metabolic panel if the patient is having severe vomiting.
    B) Ethanol concentration may be helpful in determining the expected duration of effect.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Prehospital decontamination is not indicated.
    6.5.2) PREVENTION OF ABSORPTION
    A) Activated charcoal is unlikely to be beneficial as the patient is most likely presenting with symptoms after co-ingestion with ethanol.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Obtain a basic metabolic panel if the patient is having severe vomiting.
    2) Ethanol concentration may be helpful in determining the expected duration of effect.
    B) FOMEPIZOLE
    1) Fomepizole (4-methylpyrazole) is an alcohol dehydrogenase inhibitor, which inhibits the metabolism of ethanol to acetaldehyde. In disulfiram-ethanol reactions, fomepizole has been shown to decrease serum acetaldehyde levels and improve clinical symptoms (Stowell et al, 1980). In view of this mechanism, one may consider the use of fomepizole in severe cases of disulfiram-like reactions related to Coprinus mushroom ingestion.
    2) The dose used for toxic alcohol poisoning is 15 mg/kg IV followed by 10 mg/kg IV every 12 hours.
    C) HYPOTENSIVE EPISODE
    1) Begin with intravenous volume resuscitation using isotonic fluid (e.g., normal saline) boluses of 10 to 20 mL/kg. If hypotension persists, consider vasopressors (e.g., norepinephrine) and titrate to desired effect. Norepinephrine is a more logical choice than dopamine, since dopamine acts partially by releasing endogenous norepinephrine stores, which may be depleted by disulfiram-like agents. Disulfiram blocks dopamine beta-hydroxylase, which becomes rate-limiting in norepinephrine synthesis. Severe hypotension may be resistant to dopamine (Motte et al, 1986).
    2) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    D) CONTRAINDICATED TREATMENT
    1) Avoid alcohol containing products, including elixirs, tinctures and extracts, for 48 to 72 hours after eating Coprinus mushrooms.

Abstracts

Case Reports

    A) OTHER
    1) MUSHROOM POISON CASE REGISTRY
    a) MUSHROOM POISON CASE REGISTRY
    1) Mushroom poisoning cases may be reported to the North American Mycological Association's Mushroom Poisoning Case Registry. Reporting is voluntary and patient confidentiality is maintained.
    2) Forms may be obtained from the website and completed forms or questions may be sent to:
    3) Dr. Michael W. Beug, PO Box 116, Husum, WA 98623; phone: (509) 493-2237
    4) Alternatively, reports may be submitted online at www.sph.umich.edu/~kwcee/mpcr. The website also contains a list of volunteers from different regions of North America willing to assist in the identification of mushrooms.

Range Of Toxicity

Summary

    A) TOXICITY: These mushrooms do not cause toxicity when ingested alone, but only when ethanol is coingested or consumed within 48 to 72 hours of mushroom ingestion. Toxicity is self-limited and fatalities have not been reported.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The toxic effects of coprine-containing mushrooms occur only when alcohol is ingested at the time or within 48 to 72 hours after eating these mushrooms. Coprine metabolites inhibit aldehyde dehydrogenase producing a disulfiram-like reaction. Clinical findings include nausea, vomiting, flushing, and tachycardia; this reaction is rarely life threatening (Goldfrank, 2006).
    2) Coprinus mushrooms do NOT cause toxicity if consumed alone.
    3) Recovery is usually spontaneous and complete.

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) COPRINUS ATRAMENTARIUS EXTRACT
    1) LD50- (ORAL)MOUSE:
    a) 11200 mg/kg ((RTECS, 2000))

Pharmacology Toxicology

Toxicologic Mechanism

    A) Coprinus mushrooms contain the toxin coprine. Evidence suggests that the metabolites of coprine, 1-aminocyclopropanol and cyclopropane hydrate, are responsible for the disulfiram-like reaction that occurs with co-ingestion of ethanol.
    1) Both coprine and its metabolite, cyclopropane hydrate, inhibit aldehyde dehydrogenase in vivo, however, only cyclopropane hydrate displays this same effect in vitro. This suggests that coprine must be metabolized prior to producing the disulfiram-like reaction. Inhibiting aldehyde dehydrogenase during the metabolism of ethanol causes an increase in acetaldehyde concentration, which produces the disulfiram-like reaction (Wiseman & Abeles, 1979).
    B) Fomepizole (4-methylpyrazole) is an alcohol dehydrogenase inhibitor, which inhibits the metabolism of ethanol to acetaldehyde. In disulfiram-ethanol reactions, fomepizole has been shown to decrease serum acetaldehyde levels and improve clinical symptoms. In view of this mechanism, one may consider the use of fomepizole in severe cases of disulfiram-like reactions related to Coprinus mushroom ingestion.
    C) Coprine has been found to cause severe changes in the testes of rats and dogs, probably due to a direct effect on the germ cells (Jonsson et al, 1979).

References

General Bibliography

    1) Benjamin DR: Mushrooms poisons and panaceas: A handbook for naturalists, mycologists and physicians, W. H. Freeman and Company, New York, NY, 1995.
    2) Berger KJ & Guss DA: Mycotoxins revisited: Part II. J Emerg Med 2005; 28(2):175-183.
    3) Budmiger H & Kochler F: Hexenrohrling (Boletus luridus) Mit Alcohol:Ein Kaslitischer Beitrag. Schweiz Med Wsch 1982; 112:1179-1181.
    4) Caley MJ & Clark RA: Cardiac arrhythmia after mushroom ingestion. Br Med J 1977; 2:1633.
    5) Goldfrank LR: Mushrooms. In: Goldfrank LR, Flomenbaum N, Hoffman RS, et al, eds. Goldfrank's Toxicologic Emergencies. 8th ed., 8th ed. McGraw Hill, New York, NY, 2006, pp -.
    6) Jonsson M, Lindquist NG, & Ploen L: Testicular lesions of coprine and benzcoprine. Toxicology 1979; 12:89-100.
    7) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    8) Leikin JB & Paloucek FP: Poisoning & Toxicology Compendium, Lexi-Comp Inc, Hudson, OH, 1998.
    9) Mayer JH, Herlocher JE, & Parisian J: Esophageal rupture after mushroom-alcohol ingestion (letter). N Engl J Med 1971; 285:1323.
    10) Motte S, Vincent J, & Gillet J: Refractory hyperdynamic shock associated with alcohol and disulfiram. Am J Emerg Med 1986; 4:323-325.
    11) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    12) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    13) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    14) Reynolds WA & Lowe FH: Mushrooms and a toxic reaction to alcohol: a report of 4 cases. N Engl J Med 1965; 272:630-631.
    15) Spoerke DG & Rumack BH: Handbook of Mushroom Poisoning - Diagnosis and Treatment, CRC Press, Boca Raton, FL, 1994.
    16) Stowell AR, Lindros KO, & Salaspuro MP: Breath and blood acetaldehyde concentrations and their correlation during normal and calcium carbimide modified ethanol oxidation in man. Biochem Pharm 1980; 29:783-787.
    17) Wiseman JS & Abeles RH: Mechanism of inhibition of aldehyde dehydrogenase by Cyclopropanone hydrate and the mushroom toxin coprine. Biochemistry 1979; 18:427-435.