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Reye’s syndrome is an acute encephalopathy with fatty degeneration of the liver and internal organs.
It occurs worldwide with equal frequency in boys and girls. The age at which the disease occurs is within wide limits – from infancy to adolescence, the highest incidence is recorded in the autumn and winter seasons of the year.
The hypotheses about the causes and development of the syndrome include:
• insufficiently documented role of viral infections in the course of which a genetic metabolic error is revealed; the most frequently isolated viruses causing infections preceding Reye’s syndrome are the following viruses: influenza, parainfluenza, smallpox, rubella, common parotitis (mumps), adenoviruses, reoviruses, rhinoviruses, Epstein-Barr, CMV, Herpes simplex, Herpes zoster,
• defect of lipid and amino acid metabolism,
• exogenous toxins that alter the host’s response to viral infection, the most frequently mentioned of which are: salicylates, pesticides, insecticides, aflatoxins, latex paints, and sometimes paracetamol.
symptoms
The disease has a two-phase course. It begins with catarrh of the respiratory tract and gastrointestinal tract, not always with fever. After a short-term improvement, there is rapid vomiting followed by rapidly increasing neurological symptoms associated with brain edema, such as agitation with characteristic screaming, delirium, disturbed consciousness, convulsions, coma. Muscle tension increases, respiratory and heart dysfunction join. The course of the disease is electrifying, most often fatal, and if the child survives, severe neurological defects remain. Very rarely we observe recovery without neurological damage.
Treatment: in a hospital setting.
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