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  1. Sinniah D, Baskaran G
    Lancet, 1981 Feb 28;1(8218):487-9.
    PMID: 6110100
    Vomiting, drowsiness, metabolic acidosis, polymorphonuclear leucocytosis, and encephalopathy developed in thirteen infants within hours of ingestion of margosa oil. Liver biopsy of one infant and necropsy examination of ICR strain mice after experimentally induced margosa-oil poisoning demonstrated pronounced fatty infiltration of the liver and proximal renal tubules as well as cerebral oedema. Electron microscopy demonstrated mitochondrial damage. These findings indicate that margosa oil may be involved in the aetiology of Reye's syndrome among Indians in Malaysia.
    Matched MeSH terms: Reye Syndrome/chemically induced*
  2. Sinniah R, Sinniah D, Chia LS, Baskaran G
    J Pathol, 1989 Nov;159(3):255-64.
    PMID: 2593049
    The aetiology and pathogenesis of Reye's syndrome (RS) are incompletely understood. A number of environmental toxins and biological agents, including viruses, have been postulated to cause RS, either acting alone or synergistically. Most investigations have suggested that the primary insult is in the liver mitochondria, leading to a complex biochemical catastrophe, with death from encephalopathy. Margosa oil (MO), a long-chain fatty acid compound, has been shown to cause a Reye-like syndrome with death from hepatoencephalopathy, in children in Malaysia and India. The present time-course study performed in MO-administered mice showed the development of hepatic lesions with many features of RS. MO acts rapidly, within 30 min, on the nuclei of hepatocytes inducing mitoses and binucleated cells. This is followed by mitochondrial injury, with swelling, rarefaction of matrix, loss of dense bodies, pleomorphism, and loss of ribosomes starting at 60 min. There is loss of liver glycogen, and proliferation and hypertrophy of the endoplasmic reticulum (ER), followed by the presence of lipid droplets in the hyaloplasm, and globules within dilated cisterns of the ER. Additional fatty acids from lipolysis of body adipocytes, and fat globules from intestinal MO ingestion further aggravate the liver fatty change. There is evidence of fat globule ingestion by endocytosis into hepatocytes at the level of the sinusoids. The development of microvesicular liver steatosis and glycogen depletion due to involvement of liver cell organelles occur rapidly as in RS.
    Matched MeSH terms: Reye Syndrome/chemically induced*
  3. Sinniah D, Sinniah R, Baskaran G, Pathmanathan R, Yamashita F, Yoshino M
    Acta Paediatr Jpn, 1990 Aug;32(4):462-8.
    PMID: 2288230
    Glucose and steroids have been used in the treatment of children with Reye's syndrome, while carnitine and coenzyme Q10 have been the subject of some recent studies which suggest that these agents may have a role in the treatment of Reye's syndrome and Reye-like syndrome due to margosa oil poisoning. Because of the paucity of causes of Reye's syndrome seen at any one centre, the clinical variability of the disease, and limited knowledge of definite aetiologic factors, controlled clinical trials are not easy to carry out or to interpret in human cases. These caveats were overcome by evaluation of these four treatment modalities in an established margosa-oil-induced animal model of Reye's syndrome. Effectiveness of the treatment modalities was determined from clinical response and histopathologic parameters (grading of light microscopic fatty changes and ultrastructural changes in the hepatocytes). Results show that carnitine per se produces a small improvement in survival, but statistically, more significant benefit is seen with glucose administration. Carnitine plus 10% dextrose appears to produce better results. Evaluation of coenzyme Q10 and carnitine on histopathologic parameters in the liver after a sublethal dose of margosa oil showed no obvious ameliorating effect on liver pathology. Steroids (dexamethasone/methylprednisolone) had no beneficial effects in reducing mortality, affecting glycogen storage or lipid accumulation. Changes in the mitochondria, ribosomes and endoplasmic reticulum were unaltered from the groups treated with margosa oil alone. While glucose and carnitine supplements appear to be beneficial, the other modes of therapy do not seem to hold much promise in the treatment of Reye-like syndrome in the margosa-oil-induced animal model.
    Matched MeSH terms: Reye Syndrome/chemically induced
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