Reye syndrome

Here’s an example label taken from a pretty common bottle of aspirin, notice that the first warning is “Reye’s syndrome”, and it says that “children or teenagers who are recovering from chicken-pox or flu-like symptoms should not use this product.” Why’s that?
Reye’s syndrome is characterized by encephalopathy, where encephalo refers to the brain and pathy means that the tissue or organ isn’t quite functioning properly, so there’s some change in the way the brain’s functioning.
Reye’s syndrome’s also characterized by liver failure.
This disease is extremely rare, but when it does happen it typically happens in children between the ages of 4 and 12, following an infection like the flu or chicken-pox and is highly associated with the use of aspirin during the infection.
Since this association was found, the incidence of Reye’s syndrome has dropped significantly, and has led to the requirement of the warning seen on the label for aspirin.
Why though, does Reye’s syndrome seem to happen most often when aspirin is taken during an infection in children?
Ultimately the answer to this question is still unknown, what is known is that in patients with Reye’s syndrome the mitochondria inside their liver cells, or hepatocytes, become damaged.
Mitochondria do a few super important things for our cells, right? Including oxidative phosphorylation and fatty-acid beta-oxidation, both of which help provide energy as ATP to the cell.
So mitochondria are the energy producers of the cell, right?
And when the cells can’t generate ATP they can eventually die because they have lose their main source of energy.
Since the liver cells seem to be the main cells targeted in Reye’s disease, the liver becomes one of the main organs affected.
Still, the question of how mitochondria, specifically in hepatocytes, become damaged remains mostly a mystery.
It’s known that salicylates like aspirin are able to uncouple oxidative phosphorylation, which might help to explain their involvement in mitochondrial destruction, however it’s unclear what relationship exists with viral infection, though there certainly seems to be one.
Whatever the case, as the hepatocytes die and the liver becomes dysfunctional, blood doesn’t get filtered, and so it doesn’t get the nitrogen-containing toxins filtered by the liver like it normally would. This leads to increased ammonia in the blood.
Since ammonia is able to diffuse across the blood-brain barrier, it begins to interfere with brain function, causing the characteristic encephalopathy seen as Reye’s disease progresses.
Ammonia appears to mainly target astrocytes, a type of glial cell in the brain, and although the mechanisms aren’t fully understood, ammonia seems to cause astrocyte swelling and oxidative damage.
As ammonia damages brain cells, the brain becomes more inflamed, leading to swelling and edema characteristic of encephalopathy. These patients then progress through a series of general encephalopathy signs and symptoms related to declining brain function, increasing cerebral edema, and increasing intracranial pressures.
First the patient might be quiet, lethargic or sleepy, vomiting may also be present.
Next they enter a state of stupor with the potential for seizures, decorticate response to stimuli, along with intact pupillary reflex, or control of the pupil’s diameter in response to light.
At stage 3, patients might enter into a coma, and now might present with a decerebrate response, and no longer have a pupillary response.
Stage four, the patient moves into coma and they lose their deep tendon reflexes, and a rapid decline to stage five, death.
Blood tests for Reye’s syndrome will be reflective of liver damage and mitochondrial damage.
For example you would expect to see an increase in transaminases, which are liver enzymes used for amino acid metabolism that get into the blood as liver cells die.
Again, serum ammonia will be up since the liver’s not removing it from the bloodstream, and higher levels usually indicate more severity.
Prothrombin time, which is the time it takes blood to clot, is usually also elevated, this is because the liver plays a super important role in the production of coagulation factors, which help coagulate blood, or clot, so when the liver’s dysfunctional, coagulation factor production is decreased and so it takes longer to for blood to clot.
The liver also plays a huge role in regulating the storage of glycogen; when food is ingested, the liver helps convert glucose to glycogen, when food is restricted, the liver helps convert glycogen to glucose for energy.
Therefore when the liver’s dysfunctional, it’s not able to convert glycogen to glucose when food is restricted, leading to low blood sugar or Hypoglycemia, likewise with food ingestion, it can’t convert glucose to glycogen and patients get high blood sugar, or hyperglycemia.
Treatment of Reye’s disease usually involves careful monitoring and supportive measures and intravenous fluids.

[@111incognito]

This is such a great video explaining everything about Reye's in a systematic way! The best I've seen for Reye's! Thank you.

[@everydayhealth3337]

Thank you so much for your support,

[@succesprogress4854]

Muy claro Gracias

[@alphahelix91]

Bei Überdosis kann bei einigen Medikamente ein Leberschaden ausgelöst werden.
Allerdings können doch die meisten Eltern der Kinder
die Dosis auf der Packung lesen. Oder geben sie gleich
die ganze Flasche von dem Fiebersenker ?
Sie fragen doch auch ihren Arzt wieviel sie nehmen sollen
oder bekommen es aufgeschrieben auch auf einem Spickzettel.