<unk>  occurs when the body produces excess ammonia. This ammonia primarily exists as ammonium ion that has a concentration less than or around 35 μmol/L in normal referenced serum levels. Excess ammonia is processed in the liver through the urea cycle to produce urea. Excess ammonia can be produced by bacterial hydrolysis of intestinal compounds, purine nucleotide cycles, the transamination of amino acid in voluntary muscles, and other metabolic events of filtration organs(kidneys and liver). In THAN, symptoms of<unk>  are observed within 24 hours of birth, and the causation of<unk>  must exclude urea cycle disorders. If the amount of ammonia entering the brain is increased, neurological disorders such as urea cycle enzyme deficiencies, Reye syndrome, seizures, and encephalopathies may occur. The most common indicator of THAN is respiratory distress syndrome. In newborns with THAN, the primary cause is thought to be genetic, but it has not been narrowed down to one gene or locus so the exact cause remains unknown. Observable CNS depression, comatose, metabolic acidosis, feeding difficulties, cyanosis, abnormal EEG, increased intraventricular hemorrhage, hypotonia, and irratibility are common symptoms of THAN. Individuals that develop<unk>  after birth are more likely to have<unk>  as a result in urea cycle enzyme deficiency (UCED).
Transient hyperammonemia of the newborn
Permanent neonatal diabetes
Neonatal hepatitis
Hemolytic disease of the newborn
Hemolytic disease of the newborn 
Transient neonatal diabetes
Neonatal diabetes
Neonatal hypoglycemia