الفهرس 
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Abstract
Our study group included 150 suspected cases, their age range between 1-36 months. The majority of them had acute metabolic episodes (like recurrent encephalopathy& cardio- respiratory distress), and the rest had chronic manifestations (like cardiomyopathy, hepatic dysfunction, movement disorders). They all tested for their blood glucose level, ketone bodies in urine, ammonia level, lactate level, transaminases, CK level, ACP, and organic acid profile.
from the study group, there were 37 diagnosed patients with FAODs.
These results can be summarized as following:
1. Five patients had MCADD. Hepatic dysfunction was the common manifestation in these patients. Their ACP revealed elevated C6, C8, C10, C10:1, & C8/C10. Their urine contained high amounts of medium chain length DCs.
2. One patient had LCHADD. He had abnormally CK level due to repeated attacks of rhabdomyolysis. He suffered from retinopathy neuropathy, and hepatic dysfunction. His ACP showed elevated levels of 3-hydroxy long chain ACs. His urine showed large quantities of 3-hydroxy long chain dicarboxylic acids.
3. One patient had GA II (MADD). He had non ketotic hypoglycemia, and all the other parameters were elevated. He had a history of unexplained infant death. He presented with acute neurologic manifestations. His ACP was very characteristic; it showed an elevation in almost all the ACs (C4-C16), and his organic acid profile showed enormous amounts of organic acids of the same chain length range.
4. The SCD was found in 28 patients. from these patients, 3 of them known to have chronic RI and they undergo hemodialysis therapy caused depletion of C0. They were suspected to have one of the
FAODs. Their ACP before and after hemodialysis was compared where it showed a very high concentrations of C0 and C2 before hemodialysis, then this elevation is completely inverted to sever depletion in C0. The other 25 patients were on Depakine® antiepileptic drug for long periods of time, and SCD here is resulted from the consumption of C0 in estrification of VPA instead of FFAs. They presented with hepatotoxicity and recurrent encephalopathy. These patients had increased C3 and C5.
5. One case of GA I; she had low blood glucose level, but he had also ketone bodies in her urine. She presented with macrochephaly, acute encephalopathy, and movements disorders. Her ACP included increased C5 and decreased C0. Her urine organic acid profile showed elevated glutaric acid, and 3-hydroxyglutaric acid.
6. One patient had MMA. He had borderline blood glucose level and ketone bodies in his urine. He presented with cardiomyopathy, mental retardation, and movement disorders. The ACP showed increased C4 and decreased C0. His urine analysis revealed abnormal high amounts of methylmalonic acid.