Medical screening can confirm occurrences of VLCAD most often in neonatal and infancy stages. Approximately half of all patients show signs of VLCAD<unk>  during the neonatal period, one-fourth present later in the first year of infancy, and the final quarter is split between manifestations in childhood and adulthood. Comorbidity of cardiomyopathy, arrhythmias and rhabdomyolysis are extremely common in patients under 1 year old which can lead to complications later in life. Loss of awareness or seizure can occur from hypoketotic hypoglycemia, which is often fatal if not caught in screening. However, prompt treatment shows high promise for improvement. Late-onset myopathic sufferers may only experience muscle-related, vague, sporadic symptoms, and may never be diagnosed. There is an extremely high genotype-phenotype correlation in a presentation. Mitigation of VLCAD symptoms can be achieved through dietary management.
Very long-chain acyl-coenzyme A dehydrogenase deficiency
Short-chain acyl-coenzyme A dehydrogenase deficiency
2-Methylbutyryl-CoA dehydrogenase deficiency
3-hydroxyacyl-coenzyme A dehydrogenase deficiency
3-Methylcrotonyl-CoA carboxylase deficiency
Succinyl-CoA:3-oxoacid CoA transferase deficiency
Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency
Medium-chain acyl-coenzyme A dehydrogenase deficiency