hyperammonemia

The hyperammonemia is less severe and the symptoms more subtle.

Mental development is normal if prolonged episode of hyperammonemia can be avoided.

As a result, ammonia accumulates in the blood causing hyperammonemia.

Valproic acid also causes hyperammonemia, which can lead to brain damage.

These patients are under the risk of severe hyperammonemia during infections that can lead to comatose states.

Neutropenia and thrombocytopenia may be present, as can moderate hyperammonemia.

Most of them are associated with hyperammonemia.

Article on causes of hyperammonemia in the newborn.

Her initial presentation with hyperammonemia prompted a genetics consult.

About 50% of neonates with severe hyperammonemia have seizures.

Her neurologic status improved steadily after her hyperammonemia was controlled.

Elevated levels of ammonia in the blood (hyperammonemia).

There have been reports of brain encephalopathy developing without hyperammonemia or elevated valproate levels.

The diagnostic criteria for hyperammonemia is ammonia blood levels higher than 35 mol/L.

Transient hyperammonemia of the newborn, specifically in the preterm.

A disorder is associated with ornithine translocase deficiency, and a form of hyperammonemia.

Valproate levels within the normal range are capable of causing hyperammonemia and ensuing encephalopathy.

Ammonia builds to toxic levels, resulting in hyperammonemia.

It is useful for preventing hyperammonemia caused as a side effect of administration of valproic acid.

Deficiency in the liver isozyme leads to argininemia, which is usually associated with hyperammonemia.

Asymptomatic hyperammonemia in children treated with valproic acid.

Severe Transient Hyperammonemia can also cause respiratory distress syndrome.

The duration of hyperammonemia is directly correlated to morbidity as well as the associated neurological conditions.

Despite late presentations in adulthood, hyperammonemia, encephalopathy, cerebral edema and death can occur.

One study suggested that a transient platelet activation of the infant's portal system is responsible for this hyperammonemia.