Abrus precatorius L.1. NAME

   1.1 Scientific name

   1.2 Family

   1.3 Common name(s)

2. SUMMARY

   2.1 Main risks and target organs

   2.2 Summary of clinical effects

   2.3 Diagnosis

   2.4 First-aid measures and management principles

   2.5 Poisonous parts

   2.6 Main toxins

3. CHARACTERISTICS

   3.1 Description of the plant

      3.1.1 Special identification features

      3.1.2 Habitat

      3.1.3 Distribution

   3.2 Poisonous parts of the plant

   3.3 The toxin(s)

      3.3.1 Name(s)

      3.3.2 Description, chemical structure, stability

      3.3.3 Other physico-chemical characteristics

   3.4 Other chemical contents of the plant

4. USES/CIRCUMSTANCES OF POISONING

   4.1 Uses

   4.2 High risk circumstances

   4.3 High risk geographical areas

5. ROUTES OF ENTRY

   5.1 Oral

   5.2 Inhalation

   5.3 Dermal

   5.4 Eye

   5.5 Parenteral

   5.6 Others

6. KINETICS

   6.1 Absorption by route of exposure

   6.2 Distribution by route of exposure

   6.3 Biological half-life by route of exposure

   6.4 Metabolism

   6.5 Elimination by route of exposure

7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY

   7.1 Mode of action

   7.2 Toxicity

      7.2.1 Human data

         7.2.1.1 Adults

         7.2.1.2 Children

      7.2.2 Animal data

      7.2.3 Relevant in vitro data

   7.3 Carcinogenicity

   7.4 Teratogenicity

   7.5 Mutagenicity

   7.6 Interactions8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS   8.1 Material sampling plan

      8.1.1 Sampling and specimen collection

         8.1.1.1 Toxicological analyses

         8.1.1.2 Biomedical analyses

         8.1.1.3 Arterial blood gas analysis

         8.1.1.4 Haematological analyses

         8.1.1.5 Other (unspecified) analyses

      8.1.2 Storage of laboratory samples and specimens

         8.1.2.1 Toxicological analyses

         8.1.2.2 Biomedical analyses

         8.1.2.3 Arterial blood gas analysis

         8.1.2.4 Haematological analyses

         8.1.2.5 Other (unspecified) analyses

      8.1.3 Transport of laboratory samples and specimens

         8.1.3.1 Toxicological analyses

         8.1.3.2 Biomedical analyses

         8.1.3.3 Arterial blood gas analysis

         8.1.3.4 Haematological analyses

         8.1.3.5 Other (unspecified) analyses

   8.2 Toxicological Analyses and Their Interpretation

      8.2.1 Tests on toxic ingredient(s) of material

         8.2.1.1 Simple Qualitative Test(s)

         8.2.1.2 Advanced Qualitative Confirmation Test(s)

         8.2.1.3 Simple Quantitative Method(s)

         8.2.1.4 Advanced Quantitative Method(s)

      8.2.2 Tests for biological specimens

         8.2.2.1 Simple Qualitative Test(s)

         8.2.2.2 Advanced Qualitative Confirmation Test(s)

         8.2.2.3 Simple Quantitative Method(s)

         8.2.2.4 Advanced Quantitative Method(s)

         8.2.2.5 Other Dedicated Method(s)

      8.2.3 Interpretation of toxicological analyses

   8.3 Biomedical investigations and their interpretation

      8.3.1 Biochemical analysis

         8.3.1.1 Blood, plasma or serum

         8.3.1.2 Urine

         8.3.1.3 Other fluids

      8.3.2 Arterial blood gas analyses

      8.3.3 Haematological analyses

      8.3.4 Interpretation of biomedical investigations

   8.4 Other biomedical (diagnostic) investigations and their interpretation   8.5 Overall Interpretation of all toxicological analyses and toxicological investigations   8.6 References

9. CLINICAL EFFECTS

   9.1 Acute poisoning

      9.1.1 Ingestion

      9.1.2 Inhalation

      9.1.3 Skin exposure

      9.1.4 Eye contact

      9.1.5 Parenteral exposure

      9.1.6 Other

   9.2 Chronic poisoning

      9.2.1 Ingestion

      9.2.2 Inhalation

      9.2.3 Skin exposure

      9.2.4 Eye contact

      9.2.5 Parenteral exposure

      9.2.6 Other

   9.3 Course, prognosis, cause of death

   9.4 Systematic description of clinical effects

      9.4.1 Cardiovascular

      9.4.2 Respiratory

      9.4.3 Neurological

         9.4.3.1 CNS

         9.4.3.2 Peripheral nervous system

         9.4.3.3 Autonomic nervous system

         9.4.3.4 Skeletal and smooth muscle

      9.4.4 Gastrointestinal

      9.4.5 Hepatic

      9.4.6 Urinary

         9.4.6.1 Renal

         9.4.6.2 Others

      9.4.7 Endocrine and reproductive systems

      9.4.8 Dermatological

      9.4.9 Eye, ears, nose, throat: local effects

      9.4.10 Haematological

      9.4.11 Immunological

      9.4.12 Metabolic

         9.4.12.1 Acid base disturbances

         9.4.12.2 Fluid and electrolyte disturbances

         9.4.12.3 Others

      9.4.13 Allergic reactions

      9.4.14 Other clinical effects

      9.4.15 Special risks

   9.5 Others

   9.6 Summary

10. MANAGEMENT

   10.1 General principles

   10.2 Relevant laboratory analyses and other investigations

      10.2.1 Sample collection

      10.2.2 Biomedical analysis

      10.2.3 Toxicological/toxinological analysis

      10.2.4 Other investigations

   10.3 Life supportive procedures and symptomatic treatment

   10.4 Decontamination

   10.5 Elimination

   10.6 Antidote/antitoxin treatment

      10.6.1 Adults

      10.6.2 Children

   10.7 Management discussion

11. ILLUSTRATIVE CASES

   11.1 Case reports from literature

   11.2 Internally extracted data on cases

   11.3 Internal cases

12. ADDITIONAL INFORMATION

   12.1 Availability of antidotes/antitoxins

   12.2 Specific preventive measures

   12.3 Other

13. REFERENCES

   13.1 Clinical and toxicological

   13.2 Botanical14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)

POISONOUS PLANTS 1. NAME 1.1 Scientific name Abrus precatorius L. 1.2 Family Leguminosae 1.3 Common name(s) Abrus seed Aivoeiro Arraccu-mitim Buddhist rosary bead Carolina muida Crabs eye Deadly crab's eye Indian bead Indian liquorice Jequirite Jequirity Bean Jumble beads Juquiriti Lucky bean Prayer beads Precatory bean Rosary beads Rosary Pea Ruti Tentos da America Tentos dos mundos Weather plant Wild liquorice 2. SUMMARY 2.1 Main risks and target organs

The main risk is the severe gastroenteritis leading to dehydration and shock. Ingested seeds can affect the gastrointestinal tract, the liver, spleen, kidney, and the lymphatic system. Infusion of seed extracts can cause eye damage after contact. 2.2 Summary of clinical effects The early features of toxicity are burning of the mouth and oesophagus, and severe gastroenteritis with vomiting, haematemesis, diarrhoea, melaena, and abdominal pain. Later, drowsiness, disorientation, weakness, stupor, convulsions, shock, cyanosis, retinal haemorrhages, haematuria, and oliguria can occur. Contact with the eyes can cause conjunctivitis and even blindness. 2.3 Diagnosis Diagnosis is made by the presence of the typical manifestations following ingestion: gastroenteritis with risk of dehydration, haematemesis and melaena. Drowsiness and convulsions may occur. Toxicological analysis of body fluids for the poison is not helpful. Plant material, seeds or remnants of seeds, vomitus, and

gastric aspirate should be collected in clean bottles for identification. 2.4 First-aid measures and management principles First-aid measures: Remove all seed particles from the mouth. Induce vomiting and save it for identification. Ensure that the patient's airway is clear and that there is adequate ventilation. Do not induce vomiting if the patient is semi-conscious or is at risk of having convulsions. If the eyes are contaminated, wash eyes with running water for ten minutes. Medical attention is essential if the seeds were ingested, or if the eyes were contaminated. Collect remaining seeds or plant material or remnants of seeds for identification. Management principles: induce emesis or perform gastric lavage. Supportive measures include parenteral fluids and electrolytes. Keep the patient in hospital for several days because severe symptoms can develop some time after ingestion. 2.5 Poisonous parts The most poisonous parts of the plant involved in poisoning are the small, scarlet seeds, that have a black eye at the hilum. 2.6 Main toxins The main toxin is abrin, which is concentrated in the seeds. 3. CHARACTERISTICS 3.1 Description of the plant 3.1.1 Special identification features Abrus precatorius is a slender, perennial climber that twines around trees, shrubs, and hedges. It has no special organs of attachment. Leaves are glabrous with long internodes. It has a slender branch and a cylindrical wrinkled stem with a smooth-textured brown bark. Leaves alternate compound paripinnate with stipules. Each leaf has a midrib from 5 to 10 cm long. It bears from 20 to 24 or more leaflets, each of which

is about 1.2 to 1.8 cm long, oblong and obtuse. It is blunt at both ends, glabrous on top and slightly hairy below. Flowers are small and pale violet in colour with a short stalk, arranged in clusters. The ovary has a marginal placentation. The fruit, which is a pod, is flat, oblong and truncate- shaped with a sharp deflexed beak is about 3 to 4.5 cm long, 1.2 cm wide, and silky-textured. The pod curls back when opened to reveal pendulous seeds. Each fruit contains from 3 to 5 oval-shaped seeds, about 0.6 cm. They are usually bright scarlet in colour with a smooth, glossy texture, and a black patch on top. 3.1.2 Habitat Abrus precatorius is a wild plant that grows best in fairly dry regions at low elevations. 3.1.3 Distribution It grows in tropical climates such as India, Sri Lanka, Thailand, the Philippine Islands, South China, tropical Africa and the West Indies. It also grows in all

tropical or subtropical areas. 3.2 Poisonous parts of the plant The most poisonous part of the plant is the seed. It is 0.6 cm long (although length may vary), and oval-shaped. It is usually bright scarlet, and has a jet-black spot surrounding the hilum which is the point of attachment. The seed coat, or testa, is smooth and glossy and becomes hard when the seed matures. 3.3 The toxin(s) 3.3.1 Name(s) Abrin, which consists of abrus agglutinin, and toxic lectins abrins [a] to [d] are the five toxic glycoproteins found in the seeds (Budavari, 1989). 3.3.2 Description, chemical structure, stability Five glycoproteins have been purified from the seeds. They are abrus agglutinin (a haemagglutinin) and the toxic principles abrins [a] to [d]. Abrus agglutinin is a tetramer with a molecular weight of 134,900. It is non-toxic to animal cells and a potent haemagglutinator. Abrins a through d (molecular weight: 63,000 - 67,000) are composed of two disulphide-linked polypeptide chains. The larger sub-unit, which is the neutral B- chain has a molecular weight of approximately 35,000. The other sub-unit an acidic A-chain has a molecular weight of approximately 30,000 (Windholz, 1983; Budavari, 1989). Stability: Pure abrin is a yellowish-white amorphous powder. The toxic portion is heat-stable to incubation at 60°C for 30 minutes. At 80°C most of the toxicity is lost in 30 minutes (Budavari, 1989). 3.3.3 Other physico-chemical characteristics Pure abrin is a yellowish-white amorphous powder. Abrin is soluble in sodium chloride solutions, usually with turbidity (Budavari, 1989). 3.4 Other chemical contents of the plant The seeds also contain an amino acid known as abrine (N-methyl-

L-tryptophan), glycyrrhizin and a lipolytic enzyme. The roots, stems, and leaves also contain glycyrrhizin (Windholz, 1983). 4. USES/CIRCUMSTANCES OF POISONING 4.1 Uses Children are attracted by the brightly-coloured seeds. In some countries theyplay with them and in school use them in their handiwork and to count. Necklaces and other ornaments made from the seeds are worn by both children and adults. The seeds were also used to treat diabetes and chronic nephritis. The plant is also used in some traditional medicine to

treat scratches and sores, and wounds caused by dogs, cats, and mice, and is also used with other ingredients to treat leucoderma. The leaves are used for their anti- suppurative properties. They are ground with lime and applied on acne sores, boils, and abscesses. The plant is also traditionally used to treat tetanus, and to prevent rabies. Various African tribes use powdered seeds as oral contraceptives (Watt & Breyer, 1962). Boiled seeds of Abrus precatorius are eaten in certain parts of India (Rajaram& Janardhanan, 1992). 4.2 High risk circumstances Children are attracted to the brightly-coloured seeds and may chew, suck, or swallow them. Because of the hard and relatively impermeable coat of the mature seeds, they are considerably less toxic if swallowed whole. They are more dangerous when the seeds are chewed or sucked because the toxic elements in the seeds are extracted and mixed with enzymes. Immature seeds are also poisonous if ingested because of their soft and easily broken coat. When the seeds are used as ornaments, such as necklaces, holes are drilled in the seeds, which allows contact between the intestinal secretions and the core of the seed resulting in absorption of the toxic ingredients. Another reported circumstance is the drinking of beverages where seeds from a necklace have been soaked (Jouglard, 1977). If swallowed, these seeds easily cause poisoning. 4.3 High risk geographical areas The high-risk areas are the dry regions and lowland tropical areas although necklaces are sold in many countries. 5. ROUTES OF ENTRY 5.1 Oral Abrus precatorius mature or immature seeds are chewed or ingested. 5.2 Inhalation Unknown. 5.3 Dermal Unknown. 5.4 Eye Cold preparations made from soaking the seeds have been used to treat trachoma and corneal opacities (Hart, 1963). 5.5 Parenteral Subcutaneous injections from dried infusions made from the

seeds have been used to poison livestock and human beings in India (Hart, 1963). 5.6 Others Unknown. 6. KINETICS 6.1 Absorption by route of exposure Abrin is very stable in the gastrointestinal tract, from where it is slowly absorbed. It is considerably less toxic after oral administration than after parenteral injection Gunsolus, 1955). 6.2 Distribution by route of exposure Abrin is widely distributed in tissues.

6.3 Biological half-life by route of exposure Unknown. 6.4 Metabolism Unknown. 6.5 Elimination by route of exposure Unknown. 7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY 7.1 Mode of action Abrin exerts its toxic action by attaching itself to the cell membranes. Abrin's toxic effect is due to its direct action on the parenchymal cells (e.g., liver and kidney cells) and red blood cells (Hart, 1963). Both subunits from which abrins [a] through [d] are made up are required for its toxic effects. The larger subunit, the B chain (haptomere) binds to the galactosyl-terminated receptors on the cell membrane, which is a prerequisite for the entry of the other subunit, the A chain (effectomere). This inactivates the ribosomes, arrests protein synthesis, and causes cell death (Stirpe & Barbieri, 1986). The A-chain attacks the 60S subunit of the ribosomes and by cutting out elongation factor EF2, stops protein synthesis (Frahne & Pfander, 1983). Abrus agglutinin agglutinates the red blood cells by combining with the cell stroma (Hart, 1963). 7.2 Toxicity 7.2.1 Human data 7.2.1.1 Adults One seed well masticated can cause fatal poisoning (Budavari, 1989). 7.2.1.2 Children One seed well masticated can cause fatal poisoning (Budavari, 1989). 7.2.2 Animal data Abrin's toxicity has been tested in different animals with widely divergent results. The lethal dose for animals is about 0.01 mg/kg body weight (Gunsolus, 1955). The intra-peritoneal LD50 value in mice is 0.02 mg/kg body weight (Budavari, 1983). The intravenous minimal lethal dose of abrin in mice is 0.7 micrograms/kg (Ellenhorn, 1988). Simpson et al. report that 2 ounces of seeds are fatal to horses, but that cows, goats and dogs are more resistant. The symptoms reported are anorexia, violent vomiting, lassitude, chills, and incoordination. Severe gastroenteritis is also common in animals (Gosselin, 1984).

7.2.3 Relevant in vitro data No data available. 7.3 Carcinogenicity Unknown. 7.4 Teratogenicity Unknown. 7.5 Mutagenicity Unknown.

7.6 Interactions Unknown. 8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS 8.1 Material sampling plan 8.1.1 Sampling and specimen collection 8.1.1.1 Toxicological analyses 8.1.1.2 Biomedical analyses 8.1.1.3 Arterial blood gas analysis 8.1.1.4 Haematological analyses 8.1.1.5 Other (unspecified) analyses 8.1.2 Storage of laboratory samples and specimens 8.1.2.1 Toxicological analyses 8.1.2.2 Biomedical analyses 8.1.2.3 Arterial blood gas analysis 8.1.2.4 Haematological analyses 8.1.2.5 Other (unspecified) analyses 8.1.3 Transport of laboratory samples and specimens 8.1.3.1 Toxicological analyses 8.1.3.2 Biomedical analyses 8.1.3.3 Arterial blood gas analysis 8.1.3.4 Haematological analyses 8.1.3.5 Other (unspecified) analyses 8.2 Toxicological Analyses and Their Interpretation 8.2.1 Tests on toxic ingredient(s) of material 8.2.1.1 Simple Qualitative Test(s) 8.2.1.2 Advanced Qualitative Confirmation Test(s) 8.2.1.3 Simple Quantitative Method(s) 8.2.1.4 Advanced Quantitative Method(s) 8.2.2 Tests for biological specimens 8.2.2.1 Simple Qualitative Test(s) 8.2.2.2 Advanced Qualitative Confirmation Test(s) 8.2.2.3 Simple Quantitative Method(s) 8.2.2.4 Advanced Quantitative Method(s) 8.2.2.5 Other Dedicated Method(s) 8.2.3 Interpretation of toxicological analyses 8.3 Biomedical investigations and their interpretation 8.3.1 Biochemical analysis 8.3.1.1 Blood, plasma or serum 8.3.1.2 Urine 8.3.1.3 Other fluids 8.3.2 Arterial blood gas analyses 8.3.3 Haematological analyses 8.3.4 Interpretation of biomedical investigations 8.4 Other biomedical (diagnostic) investigations and their interpretation 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations 8.6 References 9. CLINICAL EFFECTS 9.1 Acute poisoning 9.1.1 Ingestion Symptoms and signs can occur after a latent period that

ranges from a few hours to several days. They include a burning sensation in the mouth, dysphagia, nausea, vomiting, bloody diarrhoea, and abdominal cramps. Drowsiness, disorientation, convulsions, cyanosis,

stupor, circulatory failure, retinal haemorrhages, haematuria and oliguria may occur. 9.1.2 Inhalation Unknown. 9.1.3 Skin exposure Unknown. 9.1.4 Eye contact Eye irritation leads to a dose-related reaction ranging from mild conjunctivitis to a severe damage (Hart, 1963). 9.1.5 Parenteral exposure The clinical effects after intravenous and subcutaneous administration are similar to ingestion but gastrointestinal symptoms are lesser. There is severe inflammation at the injection site. 9.1.6 Other Unknown. 9.2 Chronic poisoning 9.2.1 Ingestion Unknown. 9.2.2 Inhalation Unknown. 9.2.3 Skin exposure Unknown. 9.2.4 Eye contact Unknown. 9.2.5 Parenteral exposure Unknown. 9.2.6 Other Unknown. 9.3 Course, prognosis, cause of death The major symptoms of poisoning are acute gastroenteritis with nausea, vomiting and diarrhoea leading to dehydration, convulsions, and shock. Dehydration, as well as direct toxicity on the kidneys, could result in oliguria that might progress to death in uraemia. The fatality rate is approximately 5%. Reported fatalities occurred after a 3 to 4 day course characterized by persistent gastroenteritis (Ellenhorn, 1988). Death may occur up to 14 days after poisoning from uraemia (Dreisbach & Robertson, 1987). 9.4 Systematic description of clinical effects 9.4.1 Cardiovascular There is no direct effect on the heart. Shock, hypotension, and tachycardia may occur after prolonged vomiting and diarrhoea. 9.4.2 Respiratory Cyanosis secondary to hypotension and shock may be seen. 9.4.3 Neurological 9.4.3.1 CNS Drowsiness, convulsions, hallucinations, and trembling of the hands. 9.4.3.2 Peripheral nervous system

Unknown. 9.4.3.3 Autonomic nervous system Unknown. 9.4.3.4 Skeletal and smooth muscle Unknown. 9.4.4 Gastrointestinal Because of abrin's irritant action, severe gastroenteritis with nausea, vomiting, diarrhoea, dysphagia and abdominal cramps may occur. Nausea and vomiting are due to direct irritation of the gastric mucosa. Erosion of the intestinal mucosa can cause haematemesis and melaena. 9.4.5 Hepatic The necrotizing action of the toxin causes liver damage. Serum levels of liver cell enzymes, i.e., aspartate- transferase (AST), alanine-transferase (ALT), and lactic dehydrogenase (LDH) are markedly increased. The serum bilirubin level is elevated indicating progression of the lesions. Hypoglycaemia may occur. 9.4.6 Urinary 9.4.6.1 Renal Oliguria and anuria may result from prolonged hypotension, but may also be due to acute renal failure as a result of focal degeneration of the tubular cells. Blocking of the tubules with haemoglobin from haemolysed red cells may also contribute to renal failure. 9.4.6.2 Others Unknown. 9.4.7 Endocrine and reproductive systems Unknown. 9.4.8 Dermatological Skin contact may cause irritation and dermatitis. 9.4.9 Eye, ears, nose, throat: local effects Eye: Retinal haemorrhages can appear early in the course of intoxication. The patient may complain of impaired vision that is caused by changes in the retina. Eye contact can cause severe swelling and reddening of the ocular conjunctiva. Ear, nose, throat: Irritation of the throat may occur after ingestion. 9.4.10 Haematological Abrus agglutinin causes haemagglutination and haemolysis by its direct effect on red cells. Blood loss may also occur because of haemorrhages in the gastrointestinal tract. 9.4.11 Immunological Unknown. 9.4.12 Metabolic 9.4.12.1 Acid base disturbances Prolonged vomiting may cause alkalosis. Shock is likely to lead to acidosis. Acidosis can also occur from renal failure. 9.4.12.2 Fluid and electrolyte disturbances Vomiting, diarrhoea, and haemorrhages lead to

loss of fluids and electrolytes, thus causing lethargy, muscle weakness, cardiac dysrhythmias, and muscle cramps.

9.4.12.3 Others Liver damage may cause hypoglycaemia. 9.4.13 Allergic reactions Unknown. 9.4.14 Other clinical effects Unknown. 9.4.15 Special risks Unknown. 9.5 Others 9.6 Summary 10. MANAGEMENT 10.1 General principles The management of poisoning cases is mainly symptomatic and supportive. Induced emesis or gastric lavage are usually indicated (if the conditions of the patient allow the procedures) to remove the seeds from the stomach. Fluid and electrolyte imbalances should be carefully monitored and corrected. 10.2 Relevant laboratory analyses and other investigations 10.2.1 Sample collection Collect the seeds or any other plant material for identification, also collect the vomitus or gastric contents in a clean jar. Seeds may be identified if vomitus is put inside a transparent plastic bag. 10.2.2 Biomedical analysis Full blood count, liver profile, serum electrolytes blood gases, blood urea and creatinine are the essential analyses. Urinalysis may reveal the presence of protein, red blood cells, haemoglobin, and casts. 10.2.3 Toxicological/toxinological analysis No simple analyses are available in practice. 10.2.4 Other investigations May be indicated according to the patient's condition. 10.3 Life supportive procedures and symptomatic treatment Make a proper assessment of airway, breathing, circulation and neurological status of the patient. Monitor vital signs. Maintain a clear airway. Administer oxygen if the patient is in shock. Monitor acid base balance, and fluid and electrolyte balance. Give adequate oral fluids by mouth, if possible. If the patient is unable to swallow, administer intravenous fluids and electrolytes, according to the severity of the symptoms and the results of serum electrolyte analysis. Correct metabolic acidosis if present.

Fluid loss may lead to hypovolaemic shock with hypotension. If the intravenous fluid therapy does not raise the blood pressure, insert a central venous pressure line and give plasma or dextran to expand the intravascular volume. If hypotension still persists consider administration of dopamine or dobutamine in a continuous infusion.

No cases of severe haemolysis have been reported. However, if significant haemolysis occurs, and if kidney function is normal, maintain the urine output at over 100 ml/hour with alkaline fluids. If anuria persists after receiving fluid replacement, consider the possibility of dialysis. If convulsions occur, administer anti-convulsant drugs (diazepam, intravenously or intrarectally in paediatric emergencies). Demulcents may relieve oropharyngeal and gastric irritation. 10.4 Decontamination Emesis with syrup of ipecacuanha is the best way to remove the seeds or pieces of plant from the stomach unless contraindications to induced emesis exist or orpharyngeal oedema is present. If emesis induction is not possible, gastric lavage may be performed if the condition of the patient allows it. If the patient is obtunded, convulsing or comatose, insert an oro- or naso-gastric tube and lavage after endotracheal intubation. Cathartics should not be used because they can aggravate diarrhoea and fluid loss. In case of eye exposure, irrigate eyes with copious amounts of water or saline. 10.5 Elimination No method has proved to be beneficial. 10.6 Antidote/antitoxin treatment 10.6.1 Adults There is no specific antidote available. An anti-serum used to be supplied under the name of "anti-abrin" or "jequiritol" (Gunsolus, 1955) but is no longer available. 10.6.2 Children There is no specific antidote available. An anti-serum used to be supplied under the name of "anti-abrin" or "jequiritol" (Gunsolus, 1955) but is no longer available. 10.7 Management discussion Gastric lavage may be difficult to perform and may not be successful if the size of the seeds is large. Induction of emesis may be preferred.

A cathartic can be administered to accelerate intestinal transit in cases where entire seeds have been recently ingested and no clinical features of poisoning are present. Cathartics are contraindicated in the symptomatic patient. Magnesium sulphate should be avoided when gastrointestinal irritation is present because it may be absorbed systemically. 11. ILLUSTRATIVE CASES 11.1 Case reports from literature Adults: Some investigators have reported that abrin is

poorly absorbed from the intestine. However, there have been reports of severe, sublethal toxicity in adults after ingestion of only one-half to two seeds (Hart, 1963). A 37-year-old man was severely poisoned after ingesting half a seed (Gunsolus, 1955). A 19-year-old girl died after she was treated for trachoma with jequirity infusions (Gunsolus, 1955). An adult, who homogenized 20 seeds in a blender and a portion of the mixture died (Davis, 1978). Children: Deaths in children have been reported in Florida, USA, in 1949, 1958 and 1962 after ingestion of one or more seeds. In 1955, two seeds caused severe but non-fatal poisoning (Hart, 1963). In Missouri, USA, a child who ingested exactly one-half seed was immediately made forced to vomit. The remainder of the swallowed half seed, whose coat was broken, was found in the vomitus. He was treated immediately and did not develop any symptoms (Kinamore, 1980). In most of the cases, the quantity of the seed ingested has been described as the potentially lethal dose in children. 11.2 Internally extracted data on cases To be added by the centre. 11.3 Internal cases To be added by the centre. 12. ADDITIONAL INFORMATION 12.1 Availability of antidotes/antitoxins No antidotes are available at present. 12.2 Specific preventive measures Do not allow children to play with seeds of Abrus precatorius. Keep seeds or ornaments made out of seeds away from children. Do not grow Abrus precatorius plants in home gardens. Educate older children and the public of the dangers of ingesting seeds. 12.3 Other No data available. 13. REFERENCES

13.1 Clinical and toxicological Budavari S ed. (1989) The Merck Index: an encyclopedia of chemicals, drugs, and biologicals, 10th ed. Rahway, New Jersey, Merck and Co., Inc. Davis JH (1978) Abrus precatorius (rosary pea). The most common lethal plant poison. Journal of Florida Medical Association, 65: 189-191. Dreisbach RH & Robinson WO eds. (1987) Handbook of Poisoning: Prevention, Diagnosis & Treatment, Los Altos, California, Appleton and Lange. p 497. Ellenhorn MJ & Barceloux DG. eds (1988). Medical Toxicology. New York, Elsevier Science Publishing Company, Inc. 1224-

1225. Gosselin RE, Smith RP, & Hodge HC (1984) ed. Clinical Toxicology of Commercial Products, Baltimore/London, Williams & Wilkins. Gunsolus JM (1955). Toxicity of Jequirity beans. J Amer Med Assoc, 157: 779. Hart M (1963). Jequirity bean Poisoning. N Engl J Med, 268: 885-886. Hoehne FC (1978). Plantaxe substancias vegetais toxicase medicinais. Sao Paulo, Novos Horizontes, 355p Jouglard J (1977). Intoxications d'origine vegetale In: Encycl. Med. Chir.; Intoxication Paris, Editions Techniques, 16065 A-10-A-20. Kinamore PA, Jager RW, De Castro FJ, & Peck KO (1980). Abrus & Ricinus Ingestion: Management of three cases. Clinical Toxicology, 17(3): 401-405. Kunkel DB (1983). Poisonous Plants in: Haddad LM & Winchester JF. ed. Clinical Management of Poisoning & Drug Overdosage, Canada, W.B. Saunders Company. pp 1012. Lampe KF (1976). Changes in therapy in Abrus precatorius & Ricinus communis poisoning suggested by recent studies in their mechanism of Toxicity. Clinical Toxicology, 9(1): 21. Lin JY, Tserng, KY, Chen CC, Lin LT, & Tung TC (1970). Abrin & Ricin: New Anti-tumour Substances. Nature, 227: 292 - 293. Reynolds JEF, ed (1982) Martindale, The Extra Pharmacopoeia, 28th ed. London, Pharmaceutical Press, p 2025 Rajaram N & Janardhanan K (1992) The chemical composition and nutritional potential of the tribal pulse, Abrus precatorius L. Plant Foods Hum Nutr, 42(4): 285-290.

Schvartsman S (1979) Plantas venenosas. Sao Paulo, Sarvier. Stripe F & Barbieri L (1986). Symposium: Molecular Mechanisms of Toxicity, Toxic Lectins from Plants. Human Toxicology, 5(2): 108-109. Windholz M. ed (1983) The Merck Index: an encyclopedia of chemicals, drugs, and biologicals, 10th ed. Rahway, New Jersey, Merck and Co., Inc. 13.2 Botanical Frohne D & Pfander HJ (1983) ed. A Colour Atlas of Poisonous Plants, Germany, Wolfe Publishing Ltd. pp 291. 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) Author: Dr Ravindra Fernando National Poisons Information Centre Faculty of Medicine Kynsey Road

Colombo 8 Sri Lanka Tel: 94-1-94016 Fax: 94-1-599231 Date: September 1988 Reviewer: Dr A. Furtado Rahde Poisons Control Centre Rua Riachuelo 677/201 90100 Porto Alegre Brazil Tel: 55-512-275419 Fax: 55-512-391564 Date: November 1988 Peer Review: London, United Kingdom, March 1990 Update: Dr R. Fernando, London, United Kingdom, June 1993 Review: IPCS, May 1994

See Also: Toxicological Abbreviations

http://www.inchem.org/documents/pims/plant/abruspre.htm

 Abrin murni adalah bubuk amorf putih kekuningan. Bagian beracun adalah panas yang stabil untuk inkubasi pada 60 ° C selama 30 menit. Pada 80 ° C sebagian besar toksisitas hilang dalam 30 menit