Original Article
Brief Report
Wild-Mushroom Intoxication as a Cause of Rhabdomyolysis
N Engl J Med 2001; 345:798-802September 13, 2001
- Article
The growing popularity of eating wild mushrooms has led to an increase in the incidence of mushroom poisoning. Most fatalities are due to amatoxin-containing species, which cause fulminant hepatocytolysis, and to cortinarius species, which lead to acute renal damage. A 1996 report described a patient with hepatic failure, encephalopathy, and myopathy related to the ingestion of Amanita phalloides.1 Since 1992, 12 cases of delayed rhabdomyolysis have occurred in France after meals that included large quantities of the edible wild mushroom Tricholoma equestre.2 The circumstances of these 12 cases clearly implicate T. equestre as the cause. The mushroom was positively identified, and no other cause, such as bacterial, viral, fungal, or immune disease or exposure to a toxin, was found. Three of the 12 patients died.
The implicated mushrooms were harvested from beneath pine trees on the sandy coast of southwestern France, between late fall and midwinter. T. equestre is widely disseminated throughout the world and is also known as T. flavovirens and colloquially as “bidaou” or “canari” in France, “riddarmusseron” in Sweden, “shimokoshi” in Japan, and “man on horseback” or “yellow-knight fungus” in the United States (Figure 1Figure 1
Tricholoma equestre.).3,4 We investigated the rhabdomyolysis apparently induced in 12 humans by several consecutive meals of T. equestre by administering equivalent doses of extracts of this mushroom to mice.Case Reports
Seven women (age range, 22 to 60 years) and five men (age range, 24 to 61 years) were hospitalized between 1992 and 2000 with severe rhabdomyolysis approximately one week after eating wild mushrooms. All 12 patients had eaten at least three consecutive meals that included T. equestre, and none had a history of trauma, other known underlying cause, or medication use that could explain the occurrence of rhabdomyolysis. All patients reported fatigue and muscle weakness accompanied by myalgia, mainly in the upper part of the legs, 24 to 72 hours after their last meal containing mushrooms. The weakness worsened over a period of three to four days, leading to stiffness of the legs and the production of dark urine. These signs were accompanied by facial erythema, mild nausea without vomiting, and profuse sweating in eight of the patients. No fever was noted, and five patients had hyperpnea. The findings on physical examination, which included pulmonary auscultation and a neurologic examination, were unremarkable.
Initial screening tests showed evidence of rhabdomyolysis, with a mean maximal serum creatine kinase activity of 226,067 U per liter in the women and 34,786 U per liter in the men (Figure 2Figure 2
Serum Creatine Kinase Levels in the 12 Patients during Hospitalization.). No hepatic injury was evident. γ-Glutamyltransferase values were normal (range, 5 to 24 U per liter), and maximal average levels of aspartate aminotransferase and alanine aminotransferase were 8104 and 1392 U per liter, respectively, in the women and 1173 and 325 U per liter, respectively, in the men. Despite the intensity of the clinical rhabdomyolysis, electrolyte levels, including potassium values, were normal, and no renal failure occurred. Coagulation tests were normal. Additional studies were negative for parasites or other microorganisms (coxsackievirus, toxoplasma, toxocara, trichinella, hepatitis B and C viruses, and human immunodeficiency virus), as well as for systemic diseases (as assessed by complement-fixation tests and tests for circulating nuclear antibodies).Given the absence of evidence of deliberate intoxication, the analyses focused on the hypothesis that mushroom intoxication caused the rhabdomyolysis. Electromyography was performed in four patients and revealed muscle injury without peripheral-nerve involvement. The greatest changes were in the proximal thigh muscles. Complex and generally myotonic activity was present, without fibrillation, even at rest. On stimulation, muscle contractile activity was particularly prominent. All the motor and sensory potentials were normal. Electromyography of the diaphragm was performed in one patient and showed similar findings, suggesting the presence of rhabdomyolysis of the diaphragm without phrenic involvement.
In six patients, samples of quadriceps muscle were obtained for histologic analysis. On light microscopy, the fascicular architecture of the muscles was well preserved, the myofibrils had a “nibbled” appearance, and in some cases the fibers were separated from each other by edema in the absence of vacuoles or the accumulation of glycogen or lipid — signs of a direct muscle injury. In the three patients who died, samples of the psoas and other muscles (from the arms, myocardium, and diaphragm) also showed evidence of acute myopathy.
Over the next 15 days, in all but three of the patients, the serum enzyme values gradually normalized and most symptoms disappeared, although the muscular weakness persisted for several weeks. In the three patients who died, the increasing dyspnea at rest was the first symptom of further deterioration and was followed by increasing rales at both lung bases, leading to admission to the intensive care unit. All three patients had hyperthermia (a temperature of up to 42°C); signs of acute myocarditis, including cardiac arrhythmia, cardiovascular collapse, and widening of the QRS complex without severe acidosis (pH, 7.37, with a serum bicarbonate level of 16 to 20 mmol per liter); and evidence of renal dysfunction, including elevated levels of blood urea nitrogen (30 to 52 mg per deciliter [10.7 to 18.7 mmol per liter]) and serum creatinine (1.4 to 2.5 mg per deciliter [126 to 224 μmol per liter]), with hyperkalemia (potassium, 6.0 to 7.2 mmol per liter) and hypocalcemia (calcium, 5.6 to 8.3 mg per deciliter [1.4 to 2.07 mmol per liter]) and a normal total protein level. The three patients had creatine kinase values of 632,000, 138,900, and 295,700 U per liter, with isoenzyme MB making up 0.5 to 0.7 percent of the total. Despite intensive physiological care, including, in one case, continuous venovenous hemofiltration, all three patients died. Autopsy revealed myocardial lesions identical to the muscular lesions in one patient, renal lesions in one patient, and no hepatic lesions.
Methods
Additional studies were necessary to demonstrate that T. equestre was the cause of the rhabdomyolysis in the 12 patients. Since it would have been unethical to administer T. equestre extracts to human subjects, we chose an established model of myonecrosis in mice.5-7 Extracts of T. equestre were prepared and then administered by gavage (gastric intubation) in a dose equivalent to that ingested by the patients. The animals were then assessed for evidence of rhabdomyolysis. Two protocols were employed: a dose-response study with T. equestre alone and one in which mice received extracts of either T. equestre or the nontoxic mushroom Pleurotus ostreatus.
Mushroom Extracts
Specimens of T. equestre collected in southwestern France were identified by qualified mycologists.2-4 The taxonomic denomination of T. equestre is synonymous with that of T. flavovirens (Fries) Lundell.3 Specimens of P. ostreatus obtained commercially were confirmed as such by qualified mycologists. Then 500 g of T. equestre was frozen, ground, and mixed with 200 ml of ultrapure water. The resulting mixture was lyophilized to yield 60 g of powder. Extracts were then obtained. A concentrate of 1.35 g of cold aqueous extract was obtained from 5 g of powdered T. equestre, and a concentrate of 1.65 g of boiled aqueous extract was obtained from 5 g of powdered T. equestre. A concentrate of 1.3 g was obtained from 10 g of powdered T. equestre after chloroform–methanol (vol/vol) extraction, and a concentrate of 50 mg of chloroform–methanol lipid-free extract was then obtained from 200 mg of the chloroform–methanol extract. We obtained a cold aqueous extract, a boiled aqueous extract, and a chloroform–methanol (vol/vol) extract of P. ostreatus in a similar manner.
Experimental Intoxication
Adult male Swiss mice (mean [±SE] weight, 30±5 g) (Depre), were randomly divided into several groups. In each group, T. equestre powder, T. equestre or P. ostreatus extract, or solvent alone was administered to each animal in a standardized fashion.
Twenty-four or 48 hours after the final dose, the mice were anesthetized with ether, and blood was collected from the retroorbital sinus and centrifuged at 2000×g for 15 minutes at 5°C to recover serum. The serum was frozen and stored at –20°C until analysis. Creatinine levels were determined by the Jaffé reaction (Merck kit 3385). Aspartate aminotransferase and alanine aminotransferase activities were determined with the use of enzyme kits (Merckotest, Merck).8 Creatine kinase was measured with a commercial kit (Enzyline kit, Biomérieux). The mice were then killed, and samples of striated muscle, liver, and tissues were obtained.
In the first protocol, three groups of three mice each were given 1 ml of powdered T. equestre suspension in water once a day by gavage for three days. The highest total dose was 6 g per kilogram of the body weight of the mouse (0.18 g per mouse), corresponding to a hypothetical toxic dose in a 60-kg person of 3 kg of fresh mushrooms eaten over the course of six meals in a period of three days (72 hours). Creatine kinase activity was determined in serum collected 48 hours after the final dose.
In the second protocol, five groups of five mice each were given 0.3 ml of tricholoma or pleurotus extract dissolved in water or dimethylsulfoxide once a day by gavage for three days. This dose corresponded to a total dose of 0.18 g of powdered T. equestre suspension. The positive control consisted of p-phenylenediamine (dose, 70 mg per kilogram per day for three days), which is a potent myotoxic compound in mice.6 Levels of aspartate aminotransferase, alanine aminotransferase, creatine kinase, and creatinine were determined in serum collected 96 hours after the final dose.
Statistical Analysis
Data are presented as means ±SE. The results were analyzed with use of the Wilcoxon rank-sum test, a nonparametric statistical test chosen because of the small number of animals.
Results
Mice treated with T. equestre powder (Table 1Table 1
Serum Creatine Kinase Levels in Mice Given a Suspension of Tricholoma equestre Powder (by Gastric Intubation) Every Day for Three Days.) had a concentration-dependent increase in the serum creatine kinase level (up to a mean of 380±25 U per liter). At a total dose of 4 g and 6 g per kilogram, the increase was significant when compared with the levels in controls (mean, 145±40 U per liter; P=0.01 for both comparisons), although there was variability between mice.Mice treated with boiled T. equestre extracts, chloroform–methanol lipid-free extract, and p-phenylenediamine had a significant increase in serum creatine kinase activity (912±425, 883±500, and 1828±450 U per liter, respectively; P=0.01 for each comparison with base-line levels) (Figure 3Figure 3
Mean (+SE) Serum Creatine Kinase Levels in Mice Treated by Gastric Intubation with Extracts of Tricholoma equestre and Pleurotus ostreatus Every Day for Three Days.). No such increase was observed in mice treated with extracts of P. ostreatus. Serum levels of aspartate aminotransferase, alanine aminotransferase, and creatinine were not increased significantly in mice treated with extracts of T. equestre or P. ostreatus (data not shown).All the treated mice had tachypnea, reduced motor activity, and occasional diarrhea. Light microscopy of muscle fibers showed evident disorganization.
Two mice — one that received boiled aqueous extract and one that received chloroform–methanol lipid-free extract — died 72 hours after the last dose. These animals were not autopsied because by the time the deaths were discovered autolysis had set in.
Discussion
Rhabdomyolysis is a rare but potentially fatal condition. Muscle compression is the most common cause, but neither muscle ischemia nor unconsciousness was noted before the onset of symptoms in our patients. Deliberate intoxication with substances including cocaine, amphetamines, alcohol, theophylline, phenothiazines, p-phenylenediamine,9,10 antihistamines, and antihyperlipidemic drugs was ruled out.11,12 Medications that could cause dermatomyositis or polymyositis (penicillamine, phenytoin, levodopa, and quinidine) were ruled out by screening tests. Finally, immunologic screening as well as muscle biopsies did not indicate the presence of other systemic disorders or McArdle's disease.13
Toxic rhabdomyolysis has been described after the ingestion of small wild birds that had eaten water hemlock (Conium maculatum), a direct muscle toxin.14,15 Our patients had not eaten such birds. Although mushroom poisoning is not known to produce rhabdomyolysis, this series of cases clearly associates rhabdomyolysis with the ingestion of T. equestre.
Since 75 percent of the patients with large increases in creatine kinase survived, a genetic muscular susceptibility may be unmasked by the direct muscle toxicant contained in T. equestre when the amount of mushrooms ingested exceeds a certain threshold. Therefore, physicians should be aware of the possibility of severe rhabdomyolysis after repeated consumption of T. equestre. At this time treatment is supportive, and hospitalization is recommended for patients with dyspnea, signs of acute myocarditis, or even mild renal failure. Our experiments in animals confirmed the involvement of T. equestre in the etiology of rhabdomyolysis. Mice receiving T. equestre extract had increased creatine kinase levels, whereas those receiving P. ostreatus extract did not.
Several metabolites have been isolated from various tricholoma species — triterpenoids,16 sterols,17 indoles,18 and acetylenic compounds19 — but their muscle toxicity is unknown. The yellow pigment of T. equestre, 7,7' bi-physcion, has been identified.20,21 However, since this pigment is minimally soluble in water, we think it is unlikely to be the toxic compound. Since all extracts of T. equestre were toxic to mice, inducing increases in creatine kinase levels, the toxic compound appears to be extracted equally well by water and chloroform–methanol. It remains to be identified.
Supported by grants from the Conseil Général d'Aquitaine and the University Bordeaux 2 Victor Segalen.
We are indebted to Dr. John Fowler (United Kingdom) for his assistance.
Source Information
From the Poison Center (R.B.) and the Department of Infectious Diseases (J.M.R., M.D., D.N.), University Hospital Pellegrin, Bordeaux; the Departments of Toxicology (I.B., E.E.C.) and Mycology (G.D.), Faculty of Pharmacy, University Bordeaux 2, Bordeaux; Histotox, La Rochelle (J.P.P.); the Departments of Intensive Care (C.G.) and Internal Medicine (S.D.), University Hospital St. André, Bordeaux; the Department of Gastroenterology, Hospital of Montbrisson, Montbrisson (J.C.C.); and the Department of Internal Medicine, University Hospital Pitié–Salpetrière, Paris (P.G.) — all in France. Jacques Beylot, M.D., Department of Internal Medicine, University Hospital St. André, Bordeaux, France, was also an author.
Address reprint requests to Dr. Creppy at the Department of Toxicology, University Bordeaux 2, 146 rue Leo-Saignat, 33076 Bordeaux, France, or at edmond.creppy@tox.u-bordeaux2.fr.
- References
References
1
Gonzalez J ,Lacomis D ,Kramer DJ . Mushroom myopathy. Muscle Nerve 1996;19:790-792
CrossRef | Web of Science | Medline2
Bon M. Les tricholomes de France et d'Europe occidentale. Paris: Lechevalier, 1984.
3
Miller OK Jr. Mushrooms of North America. New York: E.P. Dutton, 1972.
4
Galli R. I tricolomi: atlante pratico-monografico per la determinazione del genere Tricholoma (Fr.) Staude. Milan, Italy: Edinatura, 1999.
5
Ponraj D ,Gopalakrishnakone P . Renal lesions in rhabdomyolysis caused by Pseudechis australis snake myotoxin. Kidney Int 1997;51:1956-1969
CrossRef | Web of Science | Medline6
Averbukh Z ,Modai D ,Leonov Y , et al. Rhabdomyolysis and acute renal failure induced by paraphenylenediamine. Hum Toxicol 1989;8:345-348
CrossRef | Medline7
Gutierrez JM ,Chaves F ,Gene JA ,Lomonte B ,Camacho Z ,Schosinsky K . Myonecrosis induced in mice by a basic myotoxin isolated from the venom of the snake Bothrops nummifer (jumping viper) from Costa Rica. Toxicon 1989;27:735-745
CrossRef | Web of Science | Medline8
Empfehlungen der Deutschen Gesellschaft für Klinische Chemie: Standardisierung von Methoden zur Bestimmung von Enzymaktivitäten in biologischen Flüssigkeiten: Experimentelle Begründung der optimierten Standard-Bedingungen. Z Klein Chem U Klin Biochem 1972;10:182-184
9
Bourquia A ,Jabrane AJ ,Ramdani B ,Zaid D . Toxicité systémique de la paraphénylène diamine: quatre observations. Presse Med 1988;17:1798-1800
Web of Science | Medline10
Yagi H ,el Hind AM ,Khalil SI . Acute poisoning from hair dye. East Afr Med J 1991;68:404-411
Web of Science | Medline11
Dromer C ,Verdrenne C ,Billey T ,Pages M ,Fournie B ,Fournie A . Rhabdomyolyse à la simvastatine: à propos d'un cas avec revue de la littérature. Rev Rhum Mal Osteoartic 1992;59:281-283
Medline12
Laaksonen R ,Jokelainen K ,Laakso J , et al. The effect of simvastatin treatment on natural antioxidants in low-density lipoproteins and high-energy phosphates and ubiquinone in skeletal muscle. Am J Cardiol 1996;77:851-854
CrossRef | Web of Science | Medline13
Dupond JL ,de Wazieres B ,Monnier G ,Closs F ,Desmurs H . Myopathies enzymatiques d'effort silencieuses au repos chez l'adulte: une cause de confusion avec fibromyalgie. Presse Med 1992;21:974-978
Web of Science | Medline14
Rizzi D ,Basile C ,Di Maggio A , et al. Clinical spectrum of accidental hemlock poisoning: neurotoxic manifestations, rhabdomyolysis and acute tubular necrosis. Nephrol Dial Transplant 1991;6:939-943
Web of Science | Medline15
King LA ,Lewis MJ ,Parry D ,Twitchett PJ ,Kilner EA . Identification of oenanthotoxin and related compounds in hemlock water dropwort poisoning. Hum Toxicol 1985;4:355-364
CrossRef | Medline16
De Bernardi M ,Garlaschelli L ,Toma L ,Vidari G ,Vita-Finzi P . Fungal metabolites XXVI (°): the structure of saponaceolides B, C, and D, new C-30 terpenoids from Tricholoma saponaceum. Tetrahedron 1991;47:7109-7116
CrossRef | Web of Science17
Ohnuma N ,Amemiya K ,Kakuda R ,Yaoita Y ,Machida K ,Kikuchi M . Sterol constituents from two edible mushrooms, Lentinula edodes and Tricholoma matsutake. Chem Pharm Bull (Tokyo) 2000;48:749-751
Web of Science | Medline18
Garlaschelli L ,Vidari G ,Vita-Finzi P . Tricholomenyns C, D, and E, novel dimeric dienyne geranyl cyclohexenones from the fruiting bodies of Tricholoma acerbum. Tetrahedron Lett 1996;37:6223-6226
CrossRef | Web of Science19
Garlaschelli L ,Pang Z ,Sterner O ,Vidari G . New indole derivatives from the fruit bodies of Tricholoma sciodes and T. virgatum. Tetrahedron 1994;50:3571-3574
CrossRef | Web of Science20
Gluchoff K ,Arpin N ,Dangy-Caye M-P , et al. Recherches chimiotaxinomiques sur les champignons: sur le 7,7' bi-physcion, bianthraquinone obtenue à partir de Tricholoma equestre L. per Fr. (basidiomycète, agaricale). C R Acad Sci [D] (Paris) 1972;274:1739-174221
Steglich W ,Topfer E ,Reininger W ,Gluchoff K ,Arpin N . Isolation of flavomannin-6,6'-dimethyl ether and one of its racemates from higher fungi. Phytochemistry 1972;11:3299-3304
CrossRef | Web of Science
- Citing Articles (30)
Citing Articles
1
Kourosh Rezania, Fernando D. Goldenberg, Steven White. (2012) Neuromuscular Disorders and Acute Respiratory Failure: Diagnosis and Management. Neurologic Clinics 30:1, 161-185
CrossRef2
Zhong-Yu Zhou, Guo-Qing Shi, Robert Fontaine, Kun Wei, Tao Feng, Fang Wang, Gang-Qiang Wang, Yan Qu, Zheng-Hui Li, Ze-Jun Dong, Hua-Jie Zhu, Zhu-Liang Yang, Guang Zeng, Ji-Kai Liu. (2012) Evidence for the Natural Toxins from the Mushroom Trogia venenata as a Cause of Sudden Unexpected Death in Yunnan Province, China. Angewandte Chemie International Editionn/a-n/a
CrossRef3
Zhong-Yu Zhou, Guo-Qing Shi, Robert Fontaine, Kun Wei, Tao Feng, Fang Wang, Gang-Qiang Wang, Yan Qu, Zheng-Hui Li, Ze-Jun Dong, Hua-Jie Zhu, Zhu-Liang Yang, Guang Zeng, Ji-Kai Liu. (2012) Evidence for the Natural Toxins from the Mushroom Trogia venenata as a Cause of Sudden Unexpected Death in Yunnan Province, China. Angewandte Chemien/a-n/a
CrossRef4
Lawrance C. Chandra, Brenda J. Smith, Stephen L. Clarke, Denver Marlow, Jean M. D’Offay, Solo R. Kuvibidila. (2011) Differential effects of shiitake- and white button mushroom-supplemented diets on hepatic steatosis in C57BL/6 mice. Food and Chemical Toxicology 49:12, 3074-3080
CrossRef5
F. L. Mastaglia, M. Needham. (2011) Update on Toxic Myopathies. Current Neurology and Neuroscience Reports
CrossRef6
Kunio Gonmori, Hiroki Fujita, Kazumasa Yokoyama, Kanako Watanabe, Osamu Suzuki. (2011) Mushroom toxins: a forensic toxicological review. Forensic Toxicology 29:2, 85-94
CrossRef7
Bożena Muszyńska, Katarzyna Sułkowska-Ziaja, Halina Ekiert. (2011) Indole compounds in fruiting bodies of some edible Basidiomycota species. Food Chemistry 125:4, 1306-1308
CrossRef8
Gianfranco Cervellin, Ivan Comelli, Giuseppe Lippi. (2010) Rhabdomyolysis: historical background, clinical, diagnostic and therapeutic features. Clinical Chemistry and Laboratory Medicine 48:6, 749-756
CrossRef9
Justine Bacchetta, Laurence Dubourg, Laurent Juillard, Pierre Cochat. (2009) Non-drug-induced nephrotoxicity. Pediatric Nephrology 24:12, 2291-2300
CrossRef10
J.F. Benítez-Macías, D. García-Gil, F.M. Brun-Romero, S. Nogué-Xarau. (2009) Intoxicaciones agudas por setas. Revista Clínica Española 209:11, 542-549
CrossRef11
Ralph W Kuncl. (2009) Agents and mechanisms of toxic myopathy. Current Opinion in Neurology 22:5, 506-515
CrossRef12
M.J. Melgar, J. Alonso, M.A. García. (2009) Mercury in edible mushrooms and underlying soil: Bioconcentration factors and toxicological risk. Science of The Total Environment 407:20, 5328-5334
CrossRef13
Nevcihan Gursoy, Cengiz Sarikurkcu, Mustafa Cengiz, M. Halil Solak. (2009) Antioxidant activities, metal contents, total phenolics and flavonoids of seven Morchella species. Food and Chemical Toxicology 47:9, 2381-2388
CrossRef14
R. Bédry, S. Gromb. (2009) Les intoxications particulières de la région aquitaine. La Revue de Médecine Interne 30:7, 640-645
CrossRef15
Masanori Matsuura, Yoko Saikawa, Kosei Inui, Koichi Nakae, Masayuki Igarashi, Kimiko Hashimoto, Masaya Nakata. (2009) Identification of the toxic trigger in mushroom poisoning. Nature Chemical Biology 5:7, 465-467
CrossRef16
Kimiko HASHIMOTO, Masanori MATSUURA, Yoko SAIKAWA, Masaya NAKATA. (2009) KAGAKU TO SEIBUTSU 47:9, 600-602
CrossRef17
Petteri Nieminen, Vesa Kärjä, Anne-Mari Mustonen. (2009) Myo- and hepatotoxic effects of cultivated mushrooms in mice. Food and Chemical Toxicology 47:1, 70-74
CrossRef18
Peter Spiteller. (2008) Chemical Defence Strategies of Higher Fungi. Chemistry - A European Journal 14:30, 9100-9110
CrossRef19
Lillian Barros, Telma Cruz, Paula Baptista, Letícia M. Estevinho, Isabel C.F.R. Ferreira. (2008) Wild and commercial mushrooms as source of nutrients and nutraceuticals. Food and Chemical Toxicology 46:8, 2742-2747
CrossRef20
C.M. Westermann, L. Dorland, D.M. Votion, M.G.M. de Sain-van der Velden, I.D. Wijnberg, R.J.A. Wanders, W.G.M. Spliet, N. Testerink, R. Berger, J.P.N. Ruiter, J.H. van der Kolk. (2008) Acquired multiple Acyl-CoA dehydrogenase deficiency in 10 horses with atypical myopathy. Neuromuscular Disorders 18:5, 355-364
CrossRef21
P. Nieminen, V. Kärjä, A.-M. Mustonen. (2008) Indications of hepatic and cardiac toxicity caused by subchronic Tricholoma flavovirens consumption. Food and Chemical Toxicology 46:2, 781-786
CrossRef22
Philippe Saviuc, Vincent Danel. (2006) New Syndromes in Mushroom Poisoning. Toxicological Reviews 25:3, 199-209
CrossRef23
Markus Bickel, Tilmann Ditting, Henrik Watz, Alexander Roesler, Stefan Weidauer, Volkmar Jacobi, Saskia Gueller, Christoph Betz, Stephan Fichtlscherer, Juergen Stein. (2005) Severe rhabdomyolysis, acute renal failure and posterior encephalopathy after ???magic mushroom??? abuse. European Journal of Emergency Medicine 12:6, 306-308
CrossRef24
James H. Diaz. (2005) Evolving global epidemiology, syndromic classification, general management, and prevention of unknown mushroom poisonings. Critical Care Medicine 33:2, 419-426
CrossRef25
James H. Diaz. (2005) Syndromic diagnosis and management of confirmed mushroom poisonings. Critical Care Medicine 33:2, 427-436
CrossRef26
Petteri Nieminen, Anne-Mari Mustonen, Markku Kirsi. (2005) Increased plasma creatine kinase activities triggered by edible wild mushrooms. Food and Chemical Toxicology 43:1, 133-138
CrossRef27
Theoharis C. Theoharides, Leonard Bielory. (2004) Mast cells and mast cell mediators as targets of dietary supplements. Annals of Allergy, Asthma & Immunology 93:2, S24-S34
CrossRef28
Christine Karlson-Stiber, Hans Persson. (2003) Cytotoxic fungi—an overview. Toxicon 42:4, 339-349
CrossRef29
Alfredo Vannacci, Roberto Baronti. (2002) Mushroom-induced rhabdomyolisis. Cortinarius or Tricholoma?. Toxicon 40:7, 1063
CrossRef30
Ravinder K. Wali, William L. Henrich. (2002) Recent developments in toxic nephropathy. Current Opinion in Nephrology and Hypertension 11:2, 155-163
CrossRef
