Oleander poisoning and Oleander Containing Herbs

The oleanders are evergreen ornamental shrubs with various colors of flowers that belong to the Dogbane family and grow in the Southern parts of the USA from Florida to California, Australia, India, Sri Lanka, China, and other parts of the world. All parts of the oleander plant are toxic. Human exposure to oleander includes accidental exposure, ingestion by children, administration in food or drink, medicinal preparations from oleander (herbal products), and criminal poisoning (90-93). Despite toxicity, oleander is used in folk medicines (94). The fatality rate from oleander toxicity is around 10% in Sri Lanka whereas approximately 40% of patients require specialized management in a tertiary care hospital. Deliberate ingestion of oleander seeds is also a popular method of suicide in Sri Lanka (95). The toxic effect of oleander can occur with exposure from a small amount of the plant. Boiling or drying the plant does not inactivate the toxins. Death from drinking a herbal tea containing oleander has been reported (96). Oleander toxicity has been studied in a Tunisian toxicology intensive care unit from 1983 to 1998 in connection with plant poisoning and use of herbal medicines. The authors reported that 7% of all poisoning from the use of herbal medicines was due to oleander (97).

Early reports indicated that cardiac glycosides present in oleander cross-react with digoxin RIA (98). Cheung et al. (99) reported detection of poisoning by plant origin (including oleander) using the digoxin immunoassay on the TDx analyzer. Jortani et al. (100) reported rapid detection of oleandrin and oleandrigenin using FPIA, fluoro-metric enzyme assay on Stratus analyzer, RIA, ACS:180, and On-Line digoxin assays. Osterloh et al. reported an apparent digoxin level of 5.8ng/mL after suicidal ingestion of oleander tea in a patient with no history of taking any cardioactive drug. The person eventually died from oleander toxicity (101). Eddleston et al. reported a mean apparent serum digoxin concentration of 1.49nmol/L (1.16ng/mL) in patients who were poisoned with oleander but eventually discharged from the hospital. Severe toxicity from oleander resulted in a mean apparent serum digoxin concentration of 2.83 nmol/L (2.21 ng/mL) as measured using the FPIA digoxin assay (102). In our experience, the FPIA has the highest cross-reactivity with oleander extract as well as oleandrin, an active component of oleander extract. The Beckman digoxin assay on Synchron LX as well as the turbidimetric assay on the ADVIA 1650 analyzer (Bayer Diagnostics) also showed significant interference with oleander, although the magnitude of interference was approximately 65% less with both the Beckman assay and the turbidimetric assay. The CLIA, marketed by Bayer Diagnostics, is virtually free from interference of oleander (103). Although FPIA digoxin assay can be used for indirect detection of apparent digoxin concentration in a suspected oleander poisoning, for a definite diagnosis, the presence of oleandrin, the toxic glycoside in oleander in blood, should be confirmed by HPLC and mass spectrometry (HPLC/MS), a direct analytical technique for detection of oleandrin in blood (104). However, this technique is complex and cannot be used routinely in a small hospital.

Oleandrin is strongly bound to serum protein and is absent in the protein-free ultrafiltrate. Therefore, monitoring free digoxin in the protein-free ultrafiltrate may eliminate some interference of oleander in serum digoxin assay provided that the oleandrin concentration is low to moderate. For total elimination of interference, a specific analytical technique such as HPLC combined with mass spectrometry should be used for measurement of digoxin concentration.

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