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Children's geneticist, children's doctor

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Reye's syndrome

Alexey Portnov, medical expert
Last reviewed: 23.04.2024

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In 1963, R. Reeve et al. Described the acute fatty degeneration of the internal organs (primarily the liver), which was combined with toxic encephalopathy, which was later called Reye syndrome.

trusted-source [1], [2], [3], [4], [5], [6], [7], [8]

What causes Reye's syndrome?

The pathogenesis of Reye's syndrome is based on congenital mitochondrial insufficiency. The congenital defect of enzymes involved in the synthesis of urea, the ornithine cycle (ornithine transcarbaminase, carbamine phosphate synthetase, etc.) is also important. The syndrome can provoke drugs (salicylates), hepatotropic poisons and other substances.

Symptoms of Reye's Syndrome

Possible prodromal period, proceeding according to the type of ARVI or OCI. Vomiting is often the main clinical symptom before the development of coma. The peculiarity of coma in patients with Reye syndrome is an early increase in muscle tone up to the degree of decerebral rigidity. Practically all patients have badly docked tonic convulsive seizure. The meningeal symptom complex is not fully expressed, unstable. Hepatomegaly is maximally expressed by the 5th-7th day of coma development. Characteristic signs of cerebral edema.

The severity of neurological disorders in the depth of neurological disorders is divided into 4 degrees: I - somnolentia, II - sopor, III - actually coma, IV - terminal coma. The lesion can be of different degrees of severity: grade I is characterized by an increase in the activity of aminotransferases and ammonia levels, for the second degree - the addition of signs of insufficiency of the protein-synthetics function (decrease in the level of albumin, prothrombin, etc.), for III - the appearance of a hemorrhagic syndrome.

Diagnosis of Reye's syndrome

Laboratory indicators: an increase in the level of aminotransferases (2-5 times), short-term hyperammonemia (precedes coma), hypoglycemia (up to 2.5 mmol / l), hypophybrinogenemia without the presence of fibrin degradation products (no DIC), hypoalbuminemia, etc. Jaundice and hyperbilirubinemia are uncharacteristic.

Elevated levels of enzymes and ammonia remain for 3-4 days. To clarify the diagnosis of Reye's syndrome, puncture liver biopsy is often required. Children suffer mainly from the age of 3 months to 3 years.

trusted-source [9], [10], [11], [12]

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