The article reviews the literature on classical and atypical Reye’s syndrome, explores the circumstances that contribute to its occurrence, provides criteria for diagnosing with an illustration in the form of an authentic case of Reye-like disease in a child of 3 years old. Reye’s syndrome is a disease manifested by acute encephalopathy in combination with fatty degeneration of the internal organs, mainly the liver. This condition was first described in 1963 by an Australian pathologist who identified 21 cases of the disease in children with influenza A who were taking acetylsalicylic acid, 17 children died. In the future, the circle of infections that preceded the development of Reye’s syndrome-acute respiratory infections, chickenpox, entero- and rotavirus infections, in rare cases, hepatitis A and HIV, bacterial infections: mycoplasma, chlamydia, whooping cough, shigella, salmonella. Drugs that can cause the development of this syndrome: tetracycline, zidovudine, diclofenac sodium, mefenamic acid, paracetamol, amiodarone, warfarin, phenothiazine derivatives, histaminolytics (dimedrol), valproic acid. Along with drugs, insecticides, herbicides, hepatotoxic fungi can be used as triggers of the syndrome. There is an age dependence of the development of this syndrome. The pathogenesis of classic Reye’s syndrome is associated with generalized damage to the mitochondria primarily in the brain, as well as in the liver, kidneys, muscles, myocardium and pancreas, with the disturbance of oxidation of fatty acids in them and the formation of fat degeneration of varying degrees. In addition to the classic Reye’s syndrome, atypical Reye’s syndrome or Reye-like disease is isolated, occurs in children under 5 with congenital disturbance of oxidation of fatty acids. We observed in our clinic the case of Reye-like disease in a girl of three years with infection and taking antipyretics. In the discussion section, the features of the given case are noted, the question of the appropriateness (in view of the generality of the clinic and the mechanisms of development) of dividing the syndrome into classical and atypical is discussed. A new name for both conditions is proposed — Reye’s disease in honor of the discoverer, highlighting its two forms with an early and late onset. Given the morphological changes in this syndrome — steatosis of internal organs — authors seem to be appropriate measures aimed at treating secondary mitochondrial insufficiency and fatty dystrophy.
