Rebound metabolic acidosis following intentional amygdalin supplement overdose.

Introduction: Amygdalin, marketed misleadingly as supplement "Vitamin B17," is a cyanogenic glycoside. When swallowed, it is hydrolyzed into cyanide in the small intestine, which causes histotoxic hypoxia via inhibition of cytochrome c oxidase. It remains available for purchase online despite a ban from the US Food and Drug Administration. We report a case of massive intentional amygdalin overdose resulting in recurrent cyanide toxicity after initial successful antidotal therapy.Case summary: A 33-year-old woman intentionally ingested 20 g of "apricot POWER B17 Amygdalin" supplements. She presented five hours post-ingestion with vital signs: P 127 bpm, BP 112/65 mmHg, RR 25/min, temperature 98.1 °F, and SpO2 98% RA. She was in agitated delirium, diaphoretic, and mydriatic. Her VBG was notable for a pH of 7.27 (rr 7.32-7.42) and lactate 14.1 mmol/L (rr 0.5-2.2), with ECG demonstrating QTc 538 ms (normal <440 ms). She was empirically treated with hydroxocobalamin and supportive care, but worsened clinically, requiring intubation and additional hydroxocobalamin and sodium thiosulfate, which resolved her toxicity. Twelve hours later, she developed recurrent hypotension, acidemia, and QTc prolongation that resolved with repeat hydroxocobalamin and sodium thiosulfate dosing.Discussion: Our case demonstrates rebound metabolic acidosis after massive amygdalin overdose. Toxicity was associated with prolonged QTc, which warrants further investigation into clinical significance. Redosing of combination antidotal therapy suggested efficacy without adverse effects.

Severe cyanide poisoning from an alternative medicine treatment with amygdalin and apricot kernels in a 4-year-old child.

BACKGROUND: The use of complementary and alternative medicine (CAM) is widespread in children with cancer and is poorly regulated. PATIENTS AND METHODS: Case report. RESULTS: We describe a case of severe cyanide poisoning arising from CAM use. A severely agitated, encephalopathic, unresponsive 4-year-old boy (initial Glasgow Coma Scale of 3) with a history of metastatic ependymoma was brought to our emergency department by ambulance services. Initial blood gas analysis demonstrated severe metabolic/lactic acidosis. On detailed questioning of the parents, the use of CAM including intravenous and oral "vitamin B 17" (amygdalin) and oral apricot kernel was reported. After administering sodium thiosulfate, rapid improvement in his medical condition with complete recovery without need for further intensive care treatment was seen. Serum cyanide level was markedly elevated. CONCLUSIONS: Cyanide poisoning can be the cause of severe encephalopathy in children receiving CAM treatment with substances containing cyanogenic glycosides.

Severe cyanide toxicity from 'vitamin supplements'.

The use of alternative medicines is increasing and poorly regulated. We describe a case of severe cyanide poisoning arising from amygdalin, a putative vitamin supplement. A 32-year-old woman arrived in the emergency department by ambulance unresponsive, shocked and with fixed dilated pupils. She was hypothermic and tachycardic but was breathing spontaneously. Despite her age, she had documented breast cancer with hepatic metastases. Conventional treatment having failed, she only took 'vitamin supplements' bought on the Internet, her father said. Over the next 6 h she required mechanical ventilation and increasing doses of inotropes. Diabetes insipidus developed. As the appropriateness of further treatment was considered, a relative arrived with her medications including 'vitamin B 17' or amygdalin. An Internet search identified this as a debunked cancer remedy and cyanogen. Serum thiocyanate level was markedly elevated. She recovered fully over 8 h. While various antidotes to cyanide exist, in this case supportive therapy alone proved effective.

Accidental choke-cherry poisoning: early symptoms and neurological sequelae of an unusual case of cyanide intoxication.

We report the case of a 56-year-old woman who was accidentally poisoned when she ingested choke cherries whose pulp contained cyanide, and describe the acute clinical picture, the neurological sequelae and the neuroradiological findings. After recovery from coma, the patient showed signs of a parkinsonian syndrome, retrobulbar neuritis and sensory-motor neuropathy. MRI showed abnormal signal intensities involving the basal ganglia. Since no memory deficits were observed, we argue that the parkinsonian syndrome was caused by cyanide intoxication rather than by subcortical damage due to hypoxia.

Unproven methods of cancer management. Laetrile.

"Laetrile" is used interchangeably with "amygdalin" to designate natural substances, derived primarily from apricots and almonds, that can release cyanide, which is lethal to living organisms. In the 1920s, Dr. Ernst T. Krebs, Sr., formulated a theory that amygdalin could kill cancer cells. His theory was inconsistent with biochemical facts and has since been modified at least twice by his son, Ernst T. Krebs, Jr. Extensive work has been done by cancer scientists to test the claim that Laetrile fights cancer. Many animal experiments in the 1970s showed a complete lack of tumor killing by Laetrile. Reviews of the medical records of patients whose cancers were claimed to be reduced or cured after Laetrile treatment found insufficient medical evidence to judge Laetrile's efficacy. Finally, in a clinical trial in cancer patients reported in 1982, Laetrile neither caused shrinkage of tumors, nor increased survival time, nor alleviated cancer symptoms, nor enhanced well-being. Several reports in the medical literature document instances in which Laetrile has caused serious, life-threatening toxicity when taken in large doses in the manner prescribed by Laetrile advocates. In light of the lack of efficacy of Laetrile and its demonstrated ability to cause harm, Laetrile should not be used to treat cancer.

Clinical toxicology of cyanide.

Cyanide poisoning causes a high incidence of severe symptomatology and fatality. There are numerous sources of potential cyanide exposure. Without the history of cyanide exposure, diagnosis is often difficult. Treatment with supportive measures and available specific and efficacious antidotes frequently allows survival. The toxicology of cyanide, including sources, clinical features, diagnosis, and treatment, is reviewed.

Cyanide poisoning from laetrile ingestion: role of nitrite therapy.

A 4-year-old child ingested laetrile and almost died of cyanide poisoning. Treatment with the Lilly cyanide antidote kit resulted in rapid, complete recovery. Extremely high whole blood cyanide levels were documented. The necessity for use of the antidote kit in serious cyanide poisoning has recently been questioned. This case demonstrates benefit from antidotal treatment.

Laetrile intoxication and hepatic necrosis: a possible association.

A 65-year-old woman with cirrhosis and hepatoma lapsed into deep coma, hypotension, and acidosis after ingestion of 3 gm of Laetrile, a cyanogenetic glucoside. After initial treatment, the patient regained consciousness, but massive hepatic damage led to her death. We suggested a possible relationship between Laetrile poisoning and massive hepatic necrosis.

Foods, and food and drug combinations, responsible for head and neck pain.

The literature has been reviewed to uncover the existence of head and neck pain syndromes caused by foods and food and drug combinations. Knowledge of the etiology of such syndromes may help in their treatment. At least twenty-five syndromes have been described. These include those induced by coloring and flavoring agents, alcoholic products, chocolate, coffee and tea, foods containing tyramine, vitamins, minerals, pesticides, and several others. Where possible, the active ingredients and the minimal amounts responsible for the induction of pain have been identified.

Cyanide poisoning.

In recent years, the increasing use of laetrile has been added to the traditional sources of exposure to cyanide in industry, chemistry labs, and fumigation. The events in Jonestown in 1978 were a grim reminder of the lethality of cyanide. Nonetheless, advancement in new modes of treatment has been slow. The traditional method of treatment used in the United States is effective, but not without its own morbidity and mortality. Using two case reports as models, we review here the topic of cyanide poisoning including sources of exposure, pathophysiology, clinical manifestations of both acute and chronic exposure, and modes of treatment. Although there is currently no accepted alternate treatment in this country, review of the literature shows promise in other modalities being investigated in Europe, including hydroxocobalamin, cobalt salts, and particularly aminophenols.

Cyanide antidotes and methods of their administration in dogs: a comparative study.

To test the efficacies of various antidotes to cyanide (CN) poisoning, the lethal dose of cyanide in dogs was estimated during constant infusion of potassium cyanide at a rate of 0.1 mg/kg/min. Additionally, arterial blood pressure, right ventricular pressure, heart rate, electrocardiogram, blood-gas and pH values, and whole blood and tissue CN concentrations were measured. The lethal dose in animals whose lungs were ventilated with room air was 2.4 +/- .2 mg/kg (mean +/- SE), while the whole-blood CN concentration was 438 +/- 40 micrograms/dl and the gracilis muscle concentration was 2.0 +/- .3 micrograms/100 g. A low dose of vitamin B12a (100 mg/kg), an infusion of thiosulfate (12 mg/kg/h), or ventilation with 100 per cent O2 increased the amount of CN needed to cause death. A bolus injection of nitrite (5 mg/kg), thiosulfate (150 mg/kg), or cysteine (450 mg/kg) increased the the protection from lethality even further. Protection against CN administration for the total 150-min period of observation was provided by a bolus injection plus a constant infusion of nitrite (5 mg/kg bolus plus 5 mg/kg/h). thiosulfate (30 mg/kg bolus plus 60 mg/kg/h), or vitamin B12a (50 mg/kg bolus plus 100 mg/kg/h). However, nitrite infusion produced high levels of methemoglobin 7.2 +/- 1.1 g/dl, while vitamin B12a infusion and cysteine injection, at the stated doses, did not prevent cyanide-induced circulatory failure. Therefore, thiosulfate appears to be the most effective and safest prophylactic agent against cyanide toxicity in dogs.