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DJENKOL BEAN POISONING

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Djenkol bean poisoning (djenkolism) is a primary cause of hematuria, anuria and resultant acute renal failure. Poisoning may occur with the ingestion of only one bean. Djenkol beans are from the tree Archidendron jiringa or Archidendron lobatum (formerly Pithecolobium lobatum), and the family Mimosaceae or Leguminosae, which have been used as a food source in southeastern Asia.

Specific Substances

    1) S,S'-Methylenebis-L-cysteine (djenkolic acid)
    2) 3,-3'-(methylenedithio)dialanine (djenkolic acid)
    3) Archidendron jiringa
    4) Archidendron lobatum
    5) Cha-niang
    6) Danyin-thee
    7) Djengkol
    8) Djenkol
    9) Djenkolic acid
    10) Djenkolism
    11) Genkol
    12) Jenkol
    13) Jering
    14) Krakos
    15) Kra-niang
    16) Ma-niang
    17) Niang
    18) Niang-yai
    19) Pithecolobium lobatum
    20) Yiniking
    21) Yi-ring
    22) Molecular Formula: C7-H14-N2-O4-S2 (djenkolic acid)
    23) CAS 498-59-9 (djenkolic acid)
    24) 3,-3'-(METHYLENEDITHIO)DIALANINE
    25) CAS 498-59-9
    26) S,S'-METHYLENEBIS-L-CYSTEINE

Available Forms Sources

    A) FORMS
    1) Djenkol beans are flat, circular and a shiny yellow when young, and brown when old. The beans are 3 to 4 cm wide and 1.5 to 2 cm in thickness. When the skin of the bean is opened, the content is pale-yellow with an odor of sulfur (Vachvanichsanong & Lebel, 1997; West et al, 1973; Eiam-ong & Sitprija, 1998; Areekul, 1979).
    B) SOURCES
    1) Djenkol beans come from pods grown on the djenkol tree (Archidendron jiringa or Archidendron lobatum, formerly Pithecellobium in Southeast Asia) (Vachvanichsanong & Lebel, 1997; West et al, 1973).
    C) USES
    1) The djenkol bean is a food source or flavoring, sometimes considered a delicacy, in parts of southeastern Asia. Europeans generally find the bean's strong odor of sulfur objectionable (West et al, 1973).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Djenkolism is the terminology applied to djenkol bean poisoning. Characteristics of severe djenkolism include: low-grade fever, transient hypertension, nausea, vomiting, diarrhea or constipation, dysuria, hematuria, anuria, spasmodic pain, acute urinary retention and acute renal failure.
    1) Urinalysis may show erythrocytes, leukocytes, casts, proteinuria and often needle-shaped crystals in bundles or rosettes, which is a typical sign of djenkolism. A strong odor of sulfur can be detected on the breath and the urine.
    2) Two forms of poisoning are noted: a less severe form results in complaints of flank and groin pain and painful passage of milky or bloody urine; a more severe form results in anuria and, rarely, death.
    3) Patients who have suffered from djenkolism have often ingested the beans previously, with no symptoms, and often will ingest them after a previous poisoning with no clinical signs/symptoms.
    0.2.5) CARDIOVASCULAR
    A) Transient hypertension may occur in severe cases of djenkolism.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, diarrhea, and intense colicky pain are common symptoms of djenkol bean toxicity.
    B) A sulfuric odor is noted on the breath.
    0.2.10) GENITOURINARY
    A) Presenting signs and symptoms of djenkolism include dysuria, hematuria, urinary retention, and crystalluria. This may progress to nephrolithiasis and acute renal failure.
    B) A characteristic odor of sulfur is notable in the urine.
    0.2.13) HEMATOLOGIC
    A) Leukocytosis may be present. Anemia may result following severe cases of hematuria.

Laboratory Monitoring

    A) Obtain serum electrolytes, BUN and creatinine and a urinalysis for all symptomatic patients with a history of ingestion.
    B) Monitor vital signs.
    C) Serum djenkolic acid levels are not readily available and would not be clinically useful.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is no antidote for djenkol bean poisoning. Treatment is SYMPTOMATIC and SUPPORTIVE.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) Maintain adequate hydration. Urinary alkalinization may help prevent crystal formation.
    1) URINE ALKALINIZATION
    a) Administer 1 to 2 mEq/kg sodium bicarbonate bolus. Add 132 milliequivalents (3 ampules) sodium bicarbonate and 20 to 40 milliequivalents potassium chloride (as needed) to one liter of dextrose 5 percent in water and infuse at approximately 1.5 times the maintenance fluid rate. Adjust as needed to achieve a urine pH of at least 7.5 and a urine output of 1 to 3 mL/kg/hr.
    b) Assure adequate hydration and renal function. Monitor fluid balance, serum electrolytes, and blood pH. Obtain hourly intake/output and urine pH.

Range Of Toxicity

    A) Djenkol bean poisoning has been reported following ingestion of just one bean. Djenkolism occurs sporadically and not in all persons who consume the bean. Symptoms occur within 2 to 12 hours of ingestion. Generally, djenkolism occurs following ingestion of 5 beans or more without adequate fluid intake.

Clinical Effects

Summary Of Exposure

    A) Djenkolism is the terminology applied to djenkol bean poisoning. Characteristics of severe djenkolism include: low-grade fever, transient hypertension, nausea, vomiting, diarrhea or constipation, dysuria, hematuria, anuria, spasmodic pain, acute urinary retention and acute renal failure.
    1) Urinalysis may show erythrocytes, leukocytes, casts, proteinuria and often needle-shaped crystals in bundles or rosettes, which is a typical sign of djenkolism. A strong odor of sulfur can be detected on the breath and the urine.
    2) Two forms of poisoning are noted: a less severe form results in complaints of flank and groin pain and painful passage of milky or bloody urine; a more severe form results in anuria and, rarely, death.
    3) Patients who have suffered from djenkolism have often ingested the beans previously, with no symptoms, and often will ingest them after a previous poisoning with no clinical signs/symptoms.

Vital Signs

    3.3.3) TEMPERATURE
    A) Low grade fever may commonly occur as a result of djenkol bean poisoning (West et al, 1973; Areekul, 1979; Reimann & Sukaton, 1956).

Cardiovascular

    3.5.1) SUMMARY
    A) Transient hypertension may occur in severe cases of djenkolism.
    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) Transient hypertension has been reported following toxicity with djenkol beans (Areekul, 1979; Eiam-ong & Sitprija, 1998; Reimann & Sukaton, 1956). In one case, a 35-year-old male presented with blood pressure of 160/100 mmHg following ingestion of djenkol beans (Yong & Cheong, 1995).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) ALTERED MENTAL STATUS
    1) Decreased levels of consciousness may occur in patients with severe toxicity resulting from acute renal failure (Suharjono & Sadatun, 1968).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, diarrhea, and intense colicky pain are common symptoms of djenkol bean toxicity.
    B) A sulfuric odor is noted on the breath.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) Nausea, flatulence, vomiting and diarrhea may occur as a result of djenkol bean poisoning (Wiwanitkit, 2005; West et al, 1973; Areekul, 1979; Reimann & Sukaton, 1956; Eiam-ong & Sitprija, 1998; H'ng et al, 1991; Segasothy et al, 1995). Intense abdominal or flank pain may occur (Areekul, 1979; H'ng et al, 1991; Segasothy et al, 1995).
    B) BREATH SMELLS UNPLEASANT
    1) A characteristic odor of sulfur on the breath and urine is typical following djenkol bean poisoning (Segasothy et al, 1995; Areekul, 1979; West et al, 1973).

Hepatic

    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) FATTY LIVER
    a) Histologic examination of liver cells of rats and mice given daily extracts of djenkolic acid were shown to have mild fatty liver (Areekul et al, 1976).

Genitourinary

    3.10.1) SUMMARY
    A) Presenting signs and symptoms of djenkolism include dysuria, hematuria, urinary retention, and crystalluria. This may progress to nephrolithiasis and acute renal failure.
    B) A characteristic odor of sulfur is notable in the urine.
    3.10.2) CLINICAL EFFECTS
    A) KIDNEY STONE
    1) Djenkolic acid crystals are sometimes, present in the urine of patients with djenkolism. Nephrolithiasis has commonly been reported following djenkol bean poisoning, with symptoms developing within 2 hours of ingestion. The bladder neck and urethra may be blocked by calculus formation. If the crystals obstruct the urethra, a milder form of the disease occurs, and the patient will experience painful bladder distension, with crystals seen at the outlet of the urethra. The patient may develop strictures, abscesses, and fistulae. Obstruction of both upper and lower urinary tracts may occur in the same patient (West et al, 1973; Areekul et al, 1978).
    a) CASE REPORT - A urethral calculus was found in a 10-year-old child within 10 to 12 hours of ingestion of 10 djenkol beans (Areekul et al, 1978). Obstruction and infiltrates around the external genital organs appears more frequently in male children than in female children (Suharjono & Sadatun, 1968).
    b) On analysis of the stones, Areekul et al (1978) found the composition to be approximately 65% djenkolic acid, with the remaining constituents composed of uric acid, protein, sodium and potassium. Solubility of djenkolic acid in the stones increases with increasing urinary pH (when pH of urine was increased from 5 to 7.4, solubility of djenkolic acid increased by 43%, and at a pH of 8.1, solubility increased to 92%). Djenkolic acid crystallizes and forms sharp needle shaped crystals in the urinary tract, which in turn can result in urinary tract obstruction and anuria.
    B) BLOOD IN URINE
    1) A turbid or milky urine is followed by gross hematuria and decreased urinary output, which is typical in djenkol bean poisoning cases (Wong et al, 2007; Segasothy et al, 1995; Areekul, 1979; Reimann & Sukaton, 1956). In one case, microscopy of the urine showed the red blood cells were isomorphic, indicating the bleeding was probably non-glomerular (Segasothy et al, 1995).
    2) CASE SERIES - The association between djenkol bean ingestion and urine abnormalities in children was studied. Of 609 children included in the study, 78% had a history of eating djenkol beans, and 31% of these children ingested the bean within the previous 24 hours. Results of urinalysis in all 609 children showed children with microscopic hematuria were more likely to have eaten djenkol beans than those without hematuria (OR 3.7) (Vachvanichsanong & Lebel, 1997).
    C) RENAL FAILURE SYNDROME
    1) Acute renal failure has been reported as a complication of djenkolism. Presenting symptoms may include dysuria, hematuria, vomiting, abdominal or flank pain, oliguria or anuria, and turbid urine. Onset of symptoms and acute renal failure have ranged from 2 to 36 hours following ingestion (Wong et al, 2007; Suharjono & Sadatun, 1968). Azotemia, hematuria, anuria, and hypertension may occur (Reimann & Sukaton, 1956). Chemical similarities between djenkol bean-associated acute renal failure and acute uric acid nephropathy have been reported (Segasothy et al, 1995).
    2) CASE REPORT - A 45-year-old healthy man developed oliguria and was anuric 3 days after ingesting djenkol beans (amount not specified). Clinical features included dysuria, frank hematuria, and foul smelling urine and breath. Renal ultrasound was normal. Initial creatinine concentration was 176 mcmol/L (normal 88 to 150 mcmol/L), which increased to 848 mcmol/L over 3 days. Urgent bilateral ureteric stenting was performed and thick sludge was removed with adequate post-procedure diuresis. The patient recovered completely with a normal creatinine at discharge (Wong et al, 2007).
    3) CASE REPORT - Two days prior to symptoms, a 21-year-old man consumed 20 djenkol beans. He was admitted to the hospital following 3 days of anuria hematuria, flank pain, fever and nausea. Prior to anuria he had passed sandy particles in his urine. Physical examination revealed elevated blood pressure (160/100 mmHg).
    a) Laboratory tests revealed blood urea of 40.8 mmol/L and creatinine of 1249 mcmol/L. Numerous red blood cells were seen on urinalysis. The patient recovered spontaneously following symptomatic therapy, including urine alkalinization and rehydration with intravenous fluids (H'ng et al, 1991).
    4) CASE REPORTS - After ingesting 15 to 50 djenkol beans, 7 patients (12 to 50 years of age) developed djenkolism and experienced nausea, vomiting, flank pain, and gross hematuria. Oliguria occurred in 2 patients and one patient developed acute renal failure. Following supportive care, all patients recovered (Wiwanitkit, 2005).
    D) ACUTE RENAL CORTICAL NECROSIS
    1) Renal cortical necrosis has been seen on renal biopsy following djenkol bean poisoning in patients with resultant renal failure (Eiam-ong & Sitprija, 1998; Segasothy et al, 1995; Reimann & Sukaton, 1956). In some cases swelling of the tubular epithelium, leukocytes in the glomeruli, and acute hemorrhagic inflammation in the perirenal tissue were also observed.
    E) ABNORMAL URINE ODOR
    1) A characteristic odor of sulfur on the breath and urine is typical following djenkol bean poisoning (Wong et al, 2007; Segasothy et al, 1995; Areekul, 1979; West et al, 1973).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL TUBULAR NECROSIS
    a) Animal studies (monkeys, rats and mice) on the toxicity of djenkol beans showed mild to severe acute tubular necrosis, with some glomerular cell necrosis in the kidneys of the rats and mice, but no stone or crystal formation. Urine from the animals was turbid and contained erythrocytes, leukocytes, epithelial cells, albumin, and amorphous particles (Areekul et al, 1976).

Hematologic

    3.13.1) SUMMARY
    A) Leukocytosis may be present. Anemia may result following severe cases of hematuria.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) Low grade fever with leukocytosis has been reported following toxicity with djenkol beans (Areekul, 1979; Reimann & Sukaton, 1956).
    B) ANEMIA
    1) Severe cases of hematuria may result in anemia. Mild degrees of anemia (Hgb 9) have been reported infrequently in children with djenkolism (Suharjono & Sadatun, 1968).

Endocrine

    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPOGLYCEMIA
    a) CATS - An aqueous extract, from seeds of the legume of the plant, Pithecellobium jiringa, was injected into fasting cats at a dose of 1 mL of extract per kg of body weight. An immediate minimal transient rise in blood glucose was followed by a slow steady decrease, reaching a nadir at 4 hours and lasting as long as 5 hours. Glycosuria was not seen (Thevathasan, 1972).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Obtain serum electrolytes, BUN and creatinine and a urinalysis for all symptomatic patients with a history of ingestion.
    B) Monitor vital signs.
    C) Serum djenkolic acid levels are not readily available and would not be clinically useful.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Obtain serum electrolytes and renal function tests, including BUN and creatinine for all symptomatic patients with a history of ingestion.
    4.1.3) URINE
    A) URINALYSIS
    1) Microscopic analysis of the urine for djenkolic acid crystals may aid in the diagnosis of djenkol bean poisoning. The absence of djenkolic acid crystals in the urine does not rule out the diagnosis of djenkol bean poisoning.
    a) Djenkolic acid forms sharp needle-shaped crystals which are gathered in bunches in the urine, which may lacerate renal tissue and cause bleeding or obstruction (Vachvanichsanong & Lebel, 1997).
    2) Urinalysis may be positive for albumin, erythrocytes, leukocytes, pyuria, and hematuria (West et al, 1973).
    3) Monitor fluid intake and urine output.

Methods

    A) CHROMATOGRAPHY
    1) The quantitative amount of djenkolic acid in an alcoholic extract has been determined by paper chromatography in parallel with a standard solution (Areekul et al, 1976).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Obtain serum electrolytes, BUN and creatinine and a urinalysis for all symptomatic patients with a history of ingestion.
    B) Monitor vital signs.
    C) Serum djenkolic acid levels are not readily available and would not be clinically useful.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Decontamination is generally NOT required. Consider gastric decontamination in symptomatic patients with recent, large ingestions and those with significant coingestants.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Obtain a baseline CBC, electrolytes, and renal function test.
    2) Microscopic analysis of the urine for djenkolic acid crystals may aid in the diagnosis of djenkol bean poisoning. The absence of djenkolic acid crystals in the urine does not rule out the diagnosis of djenkol bean poisoning. Solubility of djenkolic acid crystals correlates with urinary pH, with higher pH's resulting in higher solubility.
    a) Ensure a high fluid intake. Urinary drainage may be achieved by nephrostomy, ureterostomy, or ureteral, urethral, or suprapubic catheterization.
    b) For anuria, dialysis should be considered.
    3) Monitor vital signs. Transient elevated blood pressure is common and usually self-limiting, with no specific therapy necessary in most cases. Fever is common.
    B) ALKALINE DIURESIS
    1) Djenkolic acid is a weak acid (West et al, 1973). In theory its solubility is increased by increasing urine pH to 8. The efficacy of urinary alkalinization in preventing stone formation or renal insufficiency has not been studied.
    2) After ingesting 15 to 50 djenkol beans, 7 patients (12 to 50 years of age) developed djenkolism and experienced nausea, vomiting, flank pain, and gross hematuria. Oliguria occurred in 2 patients and one patient developed acute renal failure. All 7 patients recovered following supportive care, including urine alkalinization with intravenous sodium bicarbonate (Wiwanitkit, 2005).
    3) SODIUM BICARBONATE/INITIAL DOSE
    a) Administer 1 to 2 milliequivalents/kilogram of sodium bicarbonate as an intravenous bolus. Add 132 milliequivalents (3 ampules) sodium bicarbonate and 20 to 40 milliequivalents potassium chloride (as needed) to one liter of dextrose 5 percent in water and infuse at approximately 1.5 times the maintenance fluid rate. In patients with underlying dehydration additional administration of 0.9% saline may be needed to maintain adequate urine output (1 to 2 milliliters/kilogram/hour). Manipulate bicarbonate infusion to maintain a urine pH of at least 7.5.
    4) SODIUM BICARBONATE/REPEAT DOSES
    a) Additional sodium bicarbonate (1 to 2 milliequivalents per kilogram) and potassium chloride (20 to 40 milliequivalents per liter) may be needed to achieve an alkaline urine.
    5) CAUTION
    a) Obtain hourly intake/output and urine pH. Assure adequate hydration and renal function prior to alkalinization. Do not administer potassium to an oliguric or anuric patient. Monitor fluid and electrolyte balance carefully. Monitor blood pH, especially in intubated patients, to avoid severe alkalemia.
    C) HEMODIALYSIS
    1) In the event of complete urinary/renal obstruction and anuria, hemodialysis may be warranted.
    D) SURGICAL PROCEDURE
    1) Surgery may be appropriate for severe urinary/renal obstruction, pain, bleeding, or intractable urinary infection. Consultation with a urologist is advised.

Enhanced Elimination

    A) LACK OF INFORMATION
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Abstracts

Case Reports

    A) ADULT
    1) A 26-year-old male developed onset of symptoms (nausea, vomiting, flank pain, hematuria, and oliguria) approximately 4 hours following the ingestion of 3 djenkol beans. Thirty-six hours later he was admitted to the ED with acute renal failure (BUN, 16.2 mmol/L; serum creatinine, 460 mcmol/L). Urinalysis revealed pyuria, 2+ protein, red blood cells, and hyaline, granular and epithelial cell casts. Acute tubular necrosis was seen on renal biopsy.
    a) Symptomatic therapy included rehydration and alkalinization of the urine, and the acute renal failure resolved. He was discharged 11 days later (Segasothy et al, 1995).

Range Of Toxicity

Summary

    A) Djenkol bean poisoning has been reported following ingestion of just one bean. Djenkolism occurs sporadically and not in all persons who consume the bean. Symptoms occur within 2 to 12 hours of ingestion. Generally, djenkolism occurs following ingestion of 5 beans or more without adequate fluid intake.

Therapeutic Dose

    7.2.1) ADULT
    A) SPECIFIC SUBSTANCE
    1) An antidiabetic preparation of Pithecellobium jiringa is available in Indonesia for treatment of type II diabetes (Yong & Cheong, 1995; (Eiam-ong & Sitprija, 1998). However, it is unknown whether this is a standardized tablet and what dosage recommendations are given. Its efficacy as a hypoglycemic agent has not been established.

Maximum Tolerated Exposure

    A) ACUTE
    1) Ingestion of one bean has been reported to result in severe djenkol bean poisoning (Suharjono & Sadatun, 1968). When more than 5 raw beans are ingested without adequate hydration, signs and symptoms of djenkolism, including hematuria, spasmodic pain, oliguria and anuria, and acute renal failure, have been reported. Generally, signs and symptoms develop within 2 to 12 hours of ingestion (Pochanugool et al, 1996; Reimann & Sukaton, 1956; West et al, 1973). Due to the variability of djenkolic acid content from one bean to another, some individuals may require consumption of a larger number of beans to cause toxicity (Pochanugool et al, 1996).
    2) After ingesting 15 to 50 djenkol beans, 7 patients (12 to 50 years of age) developed djenkolism and experienced nausea, vomiting, flank pain, and gross hematuria. Oliguria occurred in 2 patients and one patient developed acute renal failure. Following supportive care, all patients recovered (Wiwanitkit, 2005).
    3) Acute djenkol bean toxicity has occurred in persons ingesting from 1 to 20 beans, with survival reported. Ingestion of raw beans resulted in more symptoms. Ingestion of more mature beans appeared to result in more toxicity than ingestion of younger beans. Laboratory findings have included renal failure, hematuria, proteinuria and leukocyturia (Eiam-ong & Sitprija, 1998; Reimann & Sukaton, 1956).
    B) CASE REPORTS
    1) PEDIATRIC
    a) An 8-year-old boy ingested 10 boiled djenkol beans in the evening and was admitted to the hospital the following morning with anuria and bladder outlet obstruction. A urethral calculus (2 cm by 0.4 cm) was seen on laparotomy at approximately 10 to 12 hours after the ingestion. Following surgery to remove the calculus, the child recovered and was discharged in 4 days. The boy had previously eaten djenkol beans with no symptomatology (Areekul et al, 1978).
    2) ADULT
    a) A 26-year-old male developed onset of symptoms (nausea, vomiting, flank pain, hematuria, and oliguria) approximately 4 hours following the ingestion of 3 djenkol beans. Thirty-six hours later he was admitted to the ED with acute renal failure, as noted on laboratory examinations, and acute tubular necrosis as seen on renal biopsy. Following symptomatic therapy he recovered and was discharged 11 days later (Segasothy et al, 1995).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) DJENKOLOL
    1) LD50- (ORAL)MOUSE:
    a) >5 g/kg (RTECS, 2002).

Pharmacology Toxicology

Toxicologic Mechanism

    A) Djenkol bean poisoning is thought to be a result of blockage of the renal-urinary system with djenkolic acid. It has been proposed that djenkol acid forms sharp needle-shaped crystals in the urine, particularly at lower pH's, which may lacerate renal tissue resulting in bleeding or obstruction. It has been suggested that djenkol beans have an effect on the urinary tract via stone formation causing nephritis, urinary obstruction and acute renal failure (Areekul, 1979; Areekul et al, 1978; Reimann & Sukaton, 1956; West et al, 1973; Segasothy et al, 1995; H'ng et al, 1991; Eiam-ong & Sitprija, 1998).
    B) Hypersensitivity has been suggested as an etiologic factor in djenkolism due to the variability in the development of nephrotoxicity following exposures (Reimann & Sukaton, 1956; Areekul et al, 1978; Segasothy et al, 1995).

Physicochemical

Molecular Weight

    A) 254.33 (djenkolic acid) (Budavari, 1996)

Physical Characteristics

    A) Djenkolic acid, an amino acid extracted from djenkol beans, is in the form of rosettes or needles of various lengths. It is very sparingly soluble in cold water, and readily soluble in aqueous solutions of alkalis or acids. Approximate solubility in boiling water is 1 in 200 (Budavari, 1996).
    B) Djenkolic acid has been extracted from djenkol beans, and were found to contain 0.3 to 1.3 gram percent djenkolic acid, with about 93 percent of this in the free state. (Areekul et al, 1976)

References

General Bibliography

    1) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    2) Areekul S, Kirdudom P, & Chaovanapricha K: Studies on djenkol bean poisoning (djenkolism) in experimental animals. Southeast Asian J Trop Med Pub Hlth 1976; 7:551-558.
    3) Areekul S, Muangman V, & Bohkerd C: Djenkol bean as a cause of urolithiasis. Southeast Asian J Trop Med Pub Hlth 1978; 9:427-432.
    4) Areekul S: Djenkol bean, djenkolic acid and djenkolism. J Med Assc Thailand 1979; 62:529-531.
    5) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996, pp 573.
    6) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    7) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    8) Eiam-ong S & Sitprija V: Tropical plant-associated nephropathy. Nephrology 1998; 4:313-319.
    9) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    10) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    11) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    12) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    13) Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.
    14) H'ng PK, Nayar SK, & Lau WM: Acute renal failure following jering ingestion. Singapore Med J 1991; 32:148-149.
    15) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    16) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    17) Pochanugool C, Chaiyabutr N, & Sitprija V: Natural toxins in Thailand. J Toxicol - Toxin Reviews 1996; 15:19-36.
    18) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    19) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    20) Reimann HA & Sukaton RU: Djenkol bean poisoning (djenkolism): a cause of hematuria and anuria. Am J Sci 1956; 232:172-174.
    21) Segasothy M, Swaminathan M, & Kong NCT: Djenkol bean poisoning (djenkolism): an unusual cause of acute renal failure. Am J Kid Dis 1995; 25:63-66.
    22) Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.
    23) Suharjono & Sadatun: "Djengkol" intoxication in children. Paediatrica Indonesiana 1968; 8:20-29.
    24) Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.
    25) Thevathasan OI: Hypoglycaemia induced in fasted cats by aqueous extracts of Pithecellobium jiringa. Med J Malaysia 1972; 26:217-219.
    26) Vachvanichsanong P & Lebel L: Djenkol beans as a cause of hematuria in children. Nephron 1997; 76:39-42.
    27) West CE, Perrin DD, & Shaw DC: Djenkol bean poisoning (djenkolism): Proposals for treatment and prevention. Southeast Asian J Trop Med Pub Hlth 1973; 4:564-570.
    28) Wiwanitkit V: Renal failure due to djenkolism: an appraisal of previously reported Thai cases. Clin Exp Nephrol 2005; 9(4):343-.
    29) Wong JS, Ong TA, Chua HH, et al: Acute anuric renal failure following jering bean ingestion. Asian J Surg 2007; 30(1):80-81.