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Phytohaemagglutinin

·Å´ó×ÖÌåËõС×ÖÌå·¢²¼ÈÕÆÚ£º2007-05-28
ºËÐÄÌáʾ£ºGeneral characteristics Also known as Red Kidney Bean Poisoning, Kinkoti Bean Poisoning, and possibly other names, it is caused by a a lectin or hemagglutinin. Lectins are very common chemicals in plants, some cause blood to agglutinate, hence the n

      General characteristics

      Also known as Red Kidney Bean Poisoning, Kinkoti Bean Poisoning, and possibly other names, it is caused by a a lectin or hemagglutinin. Lectins are very common chemicals in plants, some cause blood to agglutinate, hence the name hemagglutinin.

      Phytohaemagglutinin, the presumed toxic agent, is found in many species of beans, but it is in highest concentration in red kidney beans (Phaseolus vulgaris). The unit of toxin measure is the hemagglutinating unit (hau). Raw kidney beans contain from 20,000 to 70,000 hau, while fully cooked beans contain from 200 to 400 hau. White kidney beans, another variety ofPhaseolus vulgaris, contain about one-third the amount of toxin as the red variety; broad beans (Vicia faba) contain 5 to 10% the amount that red kidney beans contain.

      Cases are very rare and (reported) cases are mainly limited to the United Kingdom.

      Disease symptoms

      The onset time from consumption of raw or undercooked kidney beans to symptoms varies from between 1 to 3 hours. Onset is usually marked by extreme nausea, followed by vomiting, which may be very severe. Diarrhoea develops somewhat later (from one to a few hours), and some persons report abdominal pain. Some persons have been hospitalised, but recovery is usually rapid (3 - 4 h after onset of symptoms) and spontaneous.

      The disease course is rapid. All symptoms usually resolve within several hours of onset. Vomiting is usually described as profuse, and the severity of symptoms is directly related to the dose of toxin (number of raw beans ingested). Hospitalisation has occasionally resulted, and intravenous fluids may have to be administered. Although of short duration, the symptoms are extremely debilitating.

      Diagnosis

      Diagnosis is made on the basis of symptoms, food history, and the exclusion of other rapid onset food poisoning agents (e.g.,Bacillus cereus,Staphylococcus aureus, arsenic, mercury, lead, and cyanide).

      The syndrome is probably sporadic, affecting small numbers of persons or individuals, and is easily misdiagnosed or never reported due to the short duration of symptoms.

      Associated foods

      The syndrome is usually caused by the ingestion of raw, soaked kidney beans, either alone or in salads or casseroles. As few as four or five raw beans can trigger symptoms. Several outbreaks have been associated with "slow cookers" or crock pots, or in casseroles which had not reached a high enough internal temperature to destroy the glycoprotein lectin. It has been shown that heating to 80¡ãC may potentiate the toxicity five-fold, so that these beans are more toxic than if eaten raw. In studies of casseroles cooked in slow cookers, internal temperatures often did not exceed 75¡ãC.

      Prevention

      Proper cooking destroys the lectins, but improper cooking, as mentioned, above, may increase toxicity initially.

      Risk populations

      All persons, regardless of age or gender, appear to be equally susceptible; the severity is related only to the dose ingested.

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      ¹Ø¼ü´Ê£º Phytohaemagglutinin
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