Acute demyelinating encephalitis due to Abrus precatorius poisoning – complete recovery after steroid therapy

Abstract

Introduction. Poisoning from Abrus precatorius is attributed to a toxalbumin (abrin) that acts by inhibiting protein synthesis and rarely can cause immuno-mediated demyelination. We report a case of abrin poisoning with demyelination. Case report. A 19-year-old man presented with a history of ingesting crushed Abrus precatorius seeds following a family quarrel. He developed vomiting, abdominal pain, and bloody diarrhea, followed by a seizure and an altered sensorium. Magnetic resonance imaging (MRI) of the brain showed demyelination in the bilateral-medial temporal lobes. The patient was treated with supportive care, and intravenous methylprednisolone followed by oral prednisone, and recovered fully. Discussion. Abrin is an immuno-modulator that may cause immune-mediated demyelination. We report the clinical course of a patient with demyelination after abrin poisoning, treated with corticosteroids, and document his clinical recovery. Conclusion. Demyelination is a rare complication of Abrus precatorius poisoning. In our case, the demyelination was demonstrated by MRI. Although our patient appeared to recover completely following methylprednisolone therapy, the suggestion that methylprednisolone or other corticosteroids might be useful in treating this demyelination needs experimental verification and clinical validation before concluding that it is a beneficial therapy.

Keywords:

• Abrus precatorius
• Poisoning
• Demyelination
• Methylprednisolone

Introduction

Abrus, Castor, Datura, and Oleander seeds are easily accessible in the villages of India. Abrus precatorius is a perennial vine that produces seeds that are believed to have abortifacient, anodyne, aphrodisiac, antimicrobial, diuretic, emetic, and antirheumatic properties. The seeds are also used to treat diabetes and chronic nephritis. Abrus precatorius seeds contain abrin, a potent lectin, that inactivates ribosomes, inhibiting protein synthesis. Central nervous system effects include raised intracranial pressure, papilledema, convulsions, and coma. We report here an unusual case of abrin poisoning with acute demyelinating encephalitis.

Case report

A 19-year-old man was admitted to hospital with history of ingesting a handful (10–15) of crushed Abrus precatorius seeds following an argument with his father. The left over seeds at the site of ingestion were brought by his parents to the hospital.

His vital signs were stable with pulse rate 96 beats/min and blood pressure 120/70 mmHg. He was treated with gastric lavage and intravenous fluids. Gastric lavage showed crushed remnants of seeds that were identified as Abrus precatorius by their distinctive red outer covering. Toxicological analysis of gastric contents was not done. Within 5 h of consuming the seeds, he developed abdominal pain and vomiting. On day 2, he developed initially watery diarrhea that became bloody, five to six episodes per day, associated with upper abdominal pain, and tenderness. Hydration was adjusted to maintain a normal central venous pressure, and an intravenous proton pump inhibitor was started. Clinical findings improved over the following 4 days. On the day 5, he developed repeated episodes of generalized tonic–clonic seizures followed by an altered sensorium (drowsiness and reduced speech output). There was no fever, headache, or ear discharge. His vital signs were stable and he was maintaining good hydration. He had a Glasgow Coma Scale score of 8. He was moving his limbs in response to pain but deep tendon reflexes were exaggerated with extensor planter response. Empirical treatment included intravenous phenytoin, cefotaxime, and metronidazole. There was no improvement in sensorium, and he was transferred to another hospital on the day 7. In that hospital, computerized tomography of the brain was normal. Because there was no improvement in his clinical condition, the case was referred to our institution on day 10. There was no history of seizures prior to poisoning or any other neurological complaint either in the patient or his family. There was no history of jaundice, hematuria, fever, oliguria, or other significant medical illnesses.

He was afebrile. There was no pallor, icterus, clubbing, cyanosis, or lymphadenopathy. He had a pulse of 90 beats/min and blood pressure of 110/70 mmHg. Neurological examination revealed a Glasgow Coma Scale score of 8 (E3 M4 V1). Both pupils were 3 mm in diameter and reacted to light; there was no papilledema. Detailed cranial nerve, motor, and sensory examinations could not be carried out because of his altered sensorium. However, grossly there was a paucity of movements in both lower limbs. Bilateral deep tendon reflexes were brisk with bilateral extensor plantar response. He had no neck stiffness or involuntary movements. Cardiovascular, respiratory, and abdominal examinations were normal without signs of bowel perforation or peritonitis.

Investigations revealed hemoglobin of 12 g/dL, with normal total and differential counts and peripheral smear. Erythrocyte sedimentation rate was 20 mm/h. Biochemistry test results included serum alanine aminotransferase 40 IU/L, aspartate aminotransferase 49 IU/L, bilirubin 0.6 mg/dL, and alkaline phosphatase 166 U/L; serum electrolytes, glucose, urinanalysis, and coagulation profile were normal. A non-contrast computerized tomography scan of brain, electroencephalogram, electrocardiogram, and chest X-ray were normal. A magnetic resonance imaging (MRI) brain scan showed hyper-intensities in the bilateral medial temporal lobes in fluid attenuation inversion recovery (FLAIR), suggestive of demyelination (Fig. 1). Intravenous methylprednisolone 1 gm daily was started and continued for 3 days, followed by oral prednisolone 40 mg daily for 1 week and then tapered. There was rapid improvement in sensorium and seizure activity from day 2 of methylprednisolone therapy. The patient became fully conscious and started taking fluids and food orally after 1 week of admission. He was discharged from hospital with no sequelae on the 15th day of admission. Follow-up visit 15 days later did not show any abnormalities.

Fig. 1.  MRI brain showing hyper-intensities in bilateral medial temporal lobes in FLAIR, suggestive of demyelination.

Discussion

The toxicity of Abrus seed poisoning is mostly attributed to the toxalbumin abrin that acts by inhibiting protein synthesis (1,2). Our patient exhibited the typical findings of abrin poisoning: vomiting, hematemesis, diarrhea, melena, and abdominal pain as well as convulsions (2–6) and altered sensorium. Evidence of hepatic damage, hemolysis, and renal failure were absent. The MRI brain scan was suggestive of demyelination without any signs of cerebral edema. Demyelinating encephalitis should be suspected in an abrus poisoning case if the patient has early central nervous system depression, seizures, or altered sensorium.

Treatment of abrus poisoning is primarily symptomatic and supportive. Our patient's demyelination appeared to respond to the administration of corticosteroids, but this single observation needs validation because another case did not respond to intravenous methylprednisolone, perhaps because of extensive demyelination or delay in the administration of the drug (5).

Demyelination due to Abrus is immune-mediated, and it is an immuno-modulator and stimulator (5,7). The immunological properties of Abrus precatorius have been widely studied. Lectins are polyclonal activators (7) of lymphocytes and work through the induction of a battery of cytokines. Abrus agglutinin is a potential immuno-modulator; it stimulates splenocytes leading to a TH1 response and natural killer cell activation (7). Abrin potentiates the humoral immune response of the host and Abrus agglutinin acts as an immuno-stimulant in vitro (8,9).

Conclusion

Demyelination is a rare complication of Abrus precatorius poisoning. In our case, the demyelination was demonstrated by MRI. Although our patient appeared to recover completely following methylprednisolone therapy, the suggestion that methylprednisolone or other corticosteroids might be useful in treating this demyelination needs experimental verification and clinical validation before concluding that it is a beneficial therapy.