The determination of amanitines in the serum of patients poisoned by amanita phalloides (author's transl)

The serum of patients suffering from Amanita phalloides poisoning was analysed in order to determine whether amanitines, which are the principal toxins of this fungus, were still present in the blood at the time of hospitalisation. In addition, the authors measured the concentrations of amanitines in the blood of dogs at different intervals after the ingestion of a fatal dose of Amanita phalloides. Amanitines were detected in the serum of 9 patients out of 16. This discovery, together with the finding that, in the dog, very low concentrations of amanitines in the blood are associated with fatal cellular lesions, suggests the need for very prompt action in order to eliminate these toxins from the blood as soon as the diagnosis of poisoning is suspected.     

Complex orofacial movements and the disappearance of cerebellar mutism: report of five cases

Intoxications with poisonous mushrooms, in particular toadstools, are still a serious medical problem. The author presents contemporary views on the etiopathogenesis of intoxications with Amanita phalloides, the clinical picture of the phalloid syndrome and its prognosis. He emphasizes the importance of a comprehensive therapeutic approach, incl. the administration of antidotes (penicillin G and silibinin) and extracorporeal haemoelimination treatment. Early sorption haemoperfusion, either alone or combined with haemodialysis or plasmapheresis, prevent the development of hepatic and renal failure and significantly reduce the mortality from mushroom poisoning. The results of amanitine sorption in in vitro experiments and in the treatment of human intoxications justify the use of biocompatible synthetic resin sorbents (Amberlite XAD-2) in the treatment of mushroom poisoning rather than active charcoal.     

Safety of mirtazapine in overdose

Mushroom poisoning constitutes the main part of plant intoxications in Turkey. Not only in rural areas, but also in Istanbul, gathering mushrooms is a habit among villagers who have moved to the city and settled in the vicinity of a forest. Phalloides syndrome, Pantherina syndrome and gastro-intestinal syndrome are the most frequently encountered types of mushroom poisonings. Amanita phalloides which is growing widely in Istanbul forests is responsible for many serious cases every year. Haemoperfusion and penicillin are used for the treatment, because Legalon-SIL is not imported in Turkey.     

Effect of osmotic stress on tissue free amino acids in Pila virens

Tolerated doses of phalloidin, a toxin from the mushroom Amanita phalloides, protect mice against lethal doses of phalloidin. Resistance is conferred by the 1/10 LD95 of phalloidin and sets in at about 8 hours after the pretreatment.     

Amanita preissii "mushroom" poisoning

"Mushroom" poisoning has rarely been reported in Australia. We present six cases of Amanita preissii poisoning successfully treated with atropine sulphate. The symptoms and signs were typical of muscarinic poisoning, which suggests that this alkaloid is the principal toxic component. A short time interval between the ingestion of poisonous fungi and the onset of symptoms, in our cases within one hour, indicates a good prognosis. The dangers of mistaking poisonous for edible varieties of fungi are emphasized, particularly in relation to immigrants not conversant with Australian fungi. Public education and control of marketing are advised.     

Poisoning with spotted and red mushrooms--pathogenesis, symptoms, treatment

Amanita pantherina and Amanita muscaria are commonly occurring mushrooms in Polish forests. They contain ibotenic acid and muscimol: the substances reacting with neurotransmitter receptors in central nervous system. The ingestion of these mushrooms produces a distinctive syndrome consisting of alternating phases of drowsiness and agitation with hallucinations, and sometimes with convulsions. The diagnosis of Amanita pantherina or Amanita muscaria poisoning is established by means of mycologic investigation of gastric lavage. The treatment is only symptomatic, and the prognosis is usually good.     

Serious plant poisonings in Switzerland 1966-1994. Case analysis from the Swiss Toxicology Information Center

AIM: To analyze the types, frequency and severity of plant poisonings in Switzerland over 29 years. METHODS: Retrospective analysis of severe poisonings with toxic plants reported to the Swiss Toxicological Information Center (STIC). Assessment of the causality, severity of symptoms and the types of plants involved. RESULTS: During the period under review the STIC registered 24 950 cases of contact with or ingestion of toxic plant material. In 99.4% of all cases the clinical course was either unknown, asymptomatic or associated with only minor symptoms (no hospitalization). Severe plant poisonings occurred in 152 cases. Detailed analysis was possible in 135 cases (23 children, 112 adults) including 5 lethal cases (all adults). The 24 plants involved produced the following severe symptoms: Atropa belladonna (42 cases): anticholinergic syndrome (42), acute psychosis (33), convulsions (2), coma (2). Heracleum mantegazzianum (18): severe photodermatitis (18). Datura stramonium (17): anticholinergic syndrome (17), psychosis (12), coma (2). Dieffenbachia (11): severe stomatitis (8), corneal lesions (3). Colchicum autumnala (10): diarrhea (10), liver necrosis (9), fatal multiorgan failure (2). Veratrum album (8): bradycardia ( < or = 40/min) (6), shock (5). Aconitum napellus (4): tachyarrhythmia (2), AV-block II/III (2). Aesculus hippocastanum (3): allergy (3), anaphylactic shock (2). Hyoscyamus niger (3): anticholinergic syndrome (3). Ricinus communis (3): diarrhea (3), toxic megacolon (1). Oenanthe crocata (2): convulsions (1), lethal coma (1). Taxus baccata (2): tachyarrhythmia (1), fatal asystole (1). Further single cases with severe poisonings were observed with Arum maculatum, Asarum europaeum, Chrysanthemum vulgare, Cyclamen persicum, Datura suaveolens, Glycyrrhiza glabra, Laburnum anagyroides, Lycopodium, Narcissus pseudonarcissus (lethal aspiration), Nerium oleander, Senecio vulgaris and Vicia faba. CONCLUSIONS: Potential and real intoxications with plant materials occurred in 7.2% of all cases registered at the STIC. However, among all plant cases only 0.6% were severe intoxications requiring hospitalization. Although severe plant intoxications are rare events, a small number of specific plants appear to be mainly responsible for continued serious plant poisoning in Switzerland. The present study has identified the plants with the highest toxicological risks and provides a data base for more rational prevention, diagnosis and treatment of plant poisoning cases in the future.     

Pulmonary tuberculosis: diagnostic delay in Ghanaian adults

Pica (pica = magpie) is an eating disorder that is manifested by a craving for oral ingestion of a given substance that is unusual in kind (nonfood items) or quantity (food items). Pica has been described as a world wide phenomenon, but there are more frequent occurrences of selected substances among selected groups--especially young children and black pregnant and nonpregnant women in the southern part of the USA. In Central Europe and Germany this syndrome has not been described in the moderne literature. For this reason, we report a case of pica for starch associated with severe iron deficiency anemia in Germany. Iron deficiency anemia and--less often-potassium and zinc deficiency are the main complications of an excessive starch or clay ingestion, followed by gastrointestinal obstructions due to gastroliths or impaction. Additionally, naphtalene poisoning (in pica for toilet air-freshener blocks), phosphorus poisoning (in matches pica), mercury poisoning (in paper pica), and lead poisoning (in dried paint pica) have been described.     

Molecular characterization of Borrelia burgdorferi sensu lato from Slovenia revealing significant differences between tick and human isolates

The aim of the study was to evaluate the morphological and functional status of the liver in acute, oral cholinesterase inhibitors poisoning using static scintigraphy, hepatography and measurements of chosen enzymes activity. Considering the different clinical picture of cholinesterase inhibitors poisonings in people, it was necessary to estimate the poisoning severity and its dependence on the frequency and intensification of the liver lesion. Under examination there were 37 cholinesterase inhibitors orally poisoned patients, treated at the Department of Toxicology in the years 1992-1995. The examined group comprised 7 women (19%) and 30 men (81%). Organophosphate compounds poisoning was noted in 14 patients, and carbamates poisonings in 23 patients. The reference group comprised 30 healthy men aged 24 to 59 years not exposed to hepatotoxic agents. More than 90% of patients were classified as severe poisoned. Any fatal case was not noted. A differently intensified pathological changes of the liver dependent on age and poisoning severity were found in 97.2% of patients and their frequency was significantly higher than in the control group. Hepatographic picture revealed in 96.6% of cases the liver lesion. Hepatographic picture of the liver was also dependent on poisoning severity. The higher activity of AST, ALT, AP and higher bilirubin concentration in blood were noted in poisoned men compared to the control group. Control scintigraphic examination revealed a considerable improvement in the intensification of the liver scintigraphic picture in 40% of the patients and a higher intensification in 13% of the subjects. In 46.6% of the patients the intensification of scintigraphic changes remained at the same level. Considering arbitrary criteria for the degree of the liver lesion, the improvement in the intensification of hepatographic changes was noted in 42.8% of the patients; the intensification of the liver lesion was not noted even in one case. Analyzing the percentage of the liver lesion for each individual patient, improvement was noted in 92.8% of the examined patients, and the changes with the same level of intensification in 7.2%. Deterioration was not noted at all. Conclusion: The liver scintigraphy and hepatography combined with biochemical analysis allows to assess the liver condition in acute cholinesterase inhibitors poisoning.     

Extraosseous aneurysmal bone cyst

Methanol is a common ingredient in many household products and intoxication can arise easily from inadvertent exposure through ingestion, inhalation or percutaneous absorption. We analysed ten cases of methanol poisoning who presented with visual, neurological and gastrointestinal symptoms, of whom one died and nine were successfully detoxified with ethanol and bicarbonate infusions. Clinical symptoms were not found to correlate with the severity of poisoning. Serum methanol level was found to correlate significantly with arterial pH (correlation coefficient -0.74, p = 0.014) and serum standard bicarbonate levels (correlation coefficient -0.87, p = 0.001). We found that an arterial pH of < 7.33 or a serum standard bicarbonate of < 20 mmol/L correlated well with a serum methanol level of > 45 mg/dL ie severe poisoning (X2 test with Yate's correction factor, p < 0.02). We conclude that arterial pH or serum standard bicarbonate levels can be used as surrogate indicators of the severity of methanol poisoning. They can be used to guide physicians in the method of detoxification (ie whether intravenous or oral ethanol or dialysis should be used) whilst awaiting serum methanol levels in cases where the index of suspicion for methanol poisoning is high. Some cases of severe poisoning can be successfully treated with oral ethanol if the intravenous form is not available.     

Silybin inhibition of amatoxin uptake in the perfused rat liver

Silybin dihemisuccinate, in a concentration of 0.4 mg/ml, almost completely inhibited the uptake of an amatoxin by the perfused rat liver. Similary, silybin should also interrupt absorption of toxins due to enterohepatic circulation, e.g. in dog and man. This effect may become important in the therapy of human Amanita poisoning.     

Acetaminophen toxicity in an urban county hospital

BACKGROUND: The prevalence and characteristics of acetaminophen-associated liver injury in hospitalized patients are not well defined. METHODS: We identified patients hospitalized for excessive acetaminophen ingestion at an urban county hospital over a 40-month period (1992 to 1995) and reviewed their medical records to determine the incidence and clinical features of the ingestions and their outcomes. RESULTS: Of the 71 patients studied, 50 were classified as having taken acetaminophen during suicide attempts and 21 as having accidentally poisoned themselves while attempting to relieve pain. The suicidal patients had ingested almost twice as much acetaminophen as those in the accidental-overdose group (median, 20 vs. 12 g; P=0.009). Among the patients for whom data were available, 63 percent of those in the accidental-overdose group and 25 percent of those in the suicidal group had chronic alcohol abuse (P=0.009). The patients in the accidental-overdose group more often had severe liver necrosis (aminotransferase levels, >3500 IU per liter; 52 percent vs. 14 percent; P=0.002), and were more likely to have hepatic coma (33 percent vs. 6 percent, P=0.006). There were four deaths (19 percent) in the accidental-overdose group and one (2 percent) in the suicidal group (P=0.04). Five patients -- three in the accidental-overdose group and two in the suicidal group -- had ingested 4 g of acetaminophen or less. Acetaminophen ingestion accounted for 12 percent of all patients hospitalized with overdoses (71 of 589) and 40 percent of patients with acute liver failure (10 of 25) during the study period. CONCLUSIONS: In an urban county hospital, patients hospitalized with acetaminophen toxicity related to accidental misuse had higher rates of morbidity and mortality than those who attempted suicide, even though the latter had taken more acetaminophen. A higher frequency of chronic alcohol abuse among the patients with accidental overdoses may be one explanation.     

Treatment of A2-B2 prostatic cancer: results of a hormonoradiotherapy combination in the PSA era

The effect of the dose of oyster mushroom in the diet (1.0, 2.5, and 5.0%) and of the period of application (8, 16, 28, and 52 wk) on cholesterol accumulation in blood and body organs was studied in weanling male Wistar rats fed a diet containing 0.3% cholesterol. Reduction of cholesterol in serum and body organs was found to be dependent on the amount of dietary oyster mushroom administered. A negative correlation between the mushroom dose and cholesterol level was found after 8 and 28 wk of feeding (r=-0.9821 and -0.9803, respectively; P < 0.02 for both cases). The dose of 1% oyster mushroom did not affect cholesterol levels in serum or body organs. A significant reduction of cholesterol levels was observed in serum (31-46%) and liver (25-30%) at a dose of 5% of oyster mushroom for all periods. Reduced cholesterol content in very low-density lipoproteins (VLDL) was also observed at this level. The highest dose of oyster mushroom induced a decrease in conjugated diene levels in erythrocytes and an increase in the levels of reduced glutathione in the liver and stimulated the activities of catalase and glutathione peroxidase in the liver in the final period of the experiment.     

Acute pesticides poisoning in the Kraków Department of Clinical Toxicology in 1986-1995

The aim of the study was to evaluate the number and the course of acute pesticides poisoning treated in the Department of Clinical Toxicology in 1986-1995. During that period 264 cases (189 men and 75 women) of acute pesticides poisoning were treated. Suicidal oral ingestion followed by inhalation and dermal exposure was the most common cause of acute intoxication. Organophosphates and carbamates were the most common cause of acute intoxication. Poisonings with dipyridyls and sulfonylurea derivatives are relatively rare. The highest number of poisonings was noted in age group 30-39 years. In 37% of the total analysed cases the co-ingestion of ethanol was noted. As organophosphorous compounds were the most common cause of acute pesticides poisoning, the gastric lavage + intensive care treatment + specific and non-specific antidotes were the most common therapeutic management. Duration of hospitalisation was dependent on the kind of pesticide. The longest hospitalisation required the patients poisoned with organophosphates. A full recovery was noted in 57.6% of poisoned patients. 34.1% of patients suffered different organ injury mostly from respiratory and central nervous system. 22 (8.3%) the fatal cases were noted in analysed period.     

Jaw and leg claudication in a patient with temporal arteritis, chronic sialoadenitis and previous hepatitis C virus infection

OBJECTIVES: Poisoning by organophosphate insecticides causes cholinergic toxicity. Organophosphate induced delayed polyneuropathy (OPIDP) is a sensory-motor distal axonopathy which usually occurs after ingestion of large doses of certain organophosphate insecticides and has so far only been reported in patients with preceding cholinergic toxicity. Surprisingly, it was recently reported by other authors that an exclusively sensory neuropathy developed in eight patients after repeated unquantified exposures to chlorpyrifos, which did not cause clear-cut cholinergic toxicity. The objective was to assess whether an exclusively sensory neuropathy develops in patients severely poisoned by various OPs. METHODS: Toxicological studies and electrophysiological measurements were performed in peripheral motor and sensory nerves in 11 patients after acute organophosphate poisoning among which two subjects were poisoned with chlorpyrifos. RESULTS: Three patients developed OPIDP, including one poisoned by chlorpyrifos. Exclusively sensory neuropathy was never seen after either single or repeated acute organophosphate poisoning. A mild sensory component was associated with a severe motor component in two of the three cases of OPIDP, the other was an exclusively motor polyneuropathy. CONCLUSION: A sensory-motor polyneuropathy caused by organophosphate insecticides might occur after a severe poisoning and the sensory component, if present, is milder than the motor one. Bearing in mind the toxicological characteristics of these organophosphate insecticides, other causes should be sought for sensory peripheral neuropathies in patients who did not display severe cholinergic toxicity a few weeks before the onset of symptoms and signs.     

Painful muscle cramps in liver cirrhosis and effects of oral taurine administration

We administered 3 g of taurine orally for four weeks to 35 patients suffering from liver cirrhosis with repeated muscle cramp (MC). Improvement of MC was noted in 22 cases (62.9%). We also determined the plasma taurine concentration in eight cases of liver cirrhosis with MC. The plasma taurine concentration before ingestion was 54.1 +/- 20.7 nmol/ml, whereas that of four weeks after ingestion was 125.1 +/- 59.1 nmol/ml, which was significantly elevated by 2.3 fold. As the concentration increased, the frequency of MC decreased, suggesting the good correlation between ingestion and the decrease in frequency of MC. In liver cirrhosis without MC the plasma taurine concentration was 81.0 +/- 16.7 nmol/ml, which was significantly higher than in liver cirrhosis with MC. In a few cases with taurine ingestion, serial plasma taurine concentrations were detected. Plasma taurine reached the peak value during the first week of ingestion and plasma taurine levels were maintained 2-5 fold higher during ingestion.     

The clinical significance of hyperamylasemia in organophosphate poisoning

OBJECTIVE: Hyperamylasemia with a presumptive diagnosis of acute pancreatitis has been reported following organophosphate poisoning but there are no large-scale studies incorporating more specific diagnostic criteria. METHODS: Retrospective review of the medical records of 159 patients with a diagnosis of organophosphate poisoning over 3 years. Serum amylase, pancreatic amylase, salivary amylase, lipase and cholinesterase levels, and the clinical manifestations were analyzed. RESULTS: Serum amylase data was available for 121 of the 159 study patients. Hyperamylasemia (amylase > or = 360 U/L) was found in 44 patients (36%). Lipase was measured in 28 patients with hyperamylasemia; 9 of 28 had hyperlipasemia (lipase > or = 380 U/L). The finding of hyperamylasemia was closely related to clinical severity and presence of shock. A presumptive diagnosis of painless acute pancreatitis was diagnosed by hyperlipasemia associated with hyperamylasemia, clinical severity, serum LDH, and leukocyte counts. Two patients with presumptive pancreatitis died. Shock, coma, and hypoalbuminemia were the factors predicting fatality. CONCLUSIONS: Hyperamylasemia is frequent in severe organophosphate poisoning. However, hyperamylasemia is not synonymous with acute pancreatitis and pancreatic amylase is not a reliable parameter in the diagnosis of organophosphate-induced pancreatitis due to its low sensitivity and specificity. Lipase assay is indicated in patients with hyperamylasemia for early diagnosis of pancreatitis. Proper image studies and even pathological examination are also needed to confirm the extent of pancreatic injury. With prompt diagnosis and appropriate treatment, a complete recovery can be anticipated unless the patient has otherwise unrelated complications.     

Chronic salicylate poisoning and severe malaria

BACKGROUND Salicylates continue to be marketed and to be used in developing countries as over-the-counter (OTC) antipyretics in children, whereas in developed countries they are no longer used in children because of safety concerns. The presenting signs of salicylate poisoning, especially chronic (repeated administration of therapeutic or excessive doses for longer than 12 h), can include metabolic acidosis, hypoglycaemia, lethargy, and coma and fits. These signs are also common in severe malaria in African children. Admission of two probable cases of chronic salicylate poisoning prompted us to look for other cases among children presenting to our hospital in Kenya, apparently with severe malaria. METHODS All children admitted to Kilifi District Hospital between July and September, 1994, who had a positive blood film for Plasmodium falciparum, and one or more of coma, prostration, or respiratory distress were eligible. As well as routine tests for malaria and routine biochemistry, salicylate concentrations were measured. Management of children (aged 6 months to 10 years) in the community was assessed by a cross-sectional survey of 463 households and by interviews with mothers 2 days after they had bought OTC drugs for a child with fever. FINDINGS Data were available for 143 of 154 children with initial primary diagnoses of severe malaria. 129 (90 percent) had detectable (>l mg/dL) salicylate. Six of these had salicylate concentrations of 20 mg/dL or higher. All six had neurological impairment and metabolic acidosis and four were, or became, hypoglycaemic. OTC drugs were the first-line treatment in 188 (74 percent) of 254 fever episodes during the 2 weeks before the cross-sectional survey. Of 250 mothers who bought drugs for a febrile child, 236 (94 percent) bought a preparation containing salicylates and 50 (21 percent) gave a dose higher than the manufacturer's recommended maximum. INTERPRETATION These cases suggest that in some children salicylate poisoning may cause or contribute to the development of metabolic acidosis and hypoglycaemia, complications of severe malaria associated with high mortality.     

Folate supplementation and neural tube defects: a review of a public health issue

OBJECTIVE: To examine the causes and mortality of poisoning in Tehran. METHODS: The 7000 poisoning cases referred to Loghman-Hakim Hospital in Tehran over six months in 1994 were evaluated retrospectively. RESULTS: The overall female to male ratio was 1.8:1. Most poisonings occurred in the age range 2-6 y for children and 21-40 y for adults. Oral ingestion was the most common route of intoxication. In children, boys had a higher frequency of poisonings than girls. Most cases of children were referred to the hospital between 8 am and 8 pm. In adults referred to the hospital, there was little diurnal variation in poisoning presentations. In adults, drugs were the most common cause of intoxication (60.2%). Of these, benzodiazepines (24.5%) were the most frequent, followed by antidepressants (20.5%) and analgesics (18%). Pesticide and opiate intoxications were also commonly observed. In children, after drugs (32.1%), hydrocarbons were the most frequent cause of poisoning (19.2%). Pesticide poisonings were most often fatal (19.2%), followed by barbiturates (18.6%) and opiates (16.2%). Organophosphate insecticides were responsible for 57% of total pesticide poisoning cases. Of the deaths, 87.5% were attributed to suicide. CONCLUSION: The majority of poisoning cases in adults occur intentionally and in children accidentally.     

Mycotoxins as a cause of disease in human beings

Secondary metabolites, toxic to macro-organisms and micro-organisms, are produced by certain molds and some plant parasitic living fungi. A risk is given for man worldwide by ingestion or apparently also be other routes always undetected. In vivo-effects of the various mycotoxins are different, but mainly the liver is affected, expecially by the intake of smaller amounts of these poisons. Accordingly cirrhosis of the liver or primary liver carcinoma are expected in man as well as in animals and were already proved outside of Europe.