"As its name suggests, the condition is due to deficiency of ornithine transcarbamylase, which is a core component of the urea cycle. The clinical features are driven by by the accumulation of precursors of urea, principally ammonia and glutamine."
"Clinical features depend on the severity of the condition. In affected neonates/infants, typically with severe disease, there is psychomotor slowing, malaise, vomiting, hypothermia, and apnoea, ultimately progressing to coma 1,3. In adults, typically with milder late-onset "partial" disease, there is evidence of encephalopathy 1. Acute symptoms may be triggered, such as by physiological stress, high protein intake, or medications (e.g. sodium valproate) 6."
"medications to increase waste nitrogen excretion (e.g. sodium phenylbutyrate, sodium benzoate)"
"avoiding medications which may precipitate hyperammonaemia (e.g. sodium valproate)"