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Secondary disorders of glycosylation in inborn errors of fructose metabolism
E Quintana1, L Sturiale, R Montero
1Institut de Bioquímica Clínica, Servei de Bioquímica i Genètica Molecular, Hospital Clínic, Edificio Helios III, c/ Mejia Lequerica s/n, 08028, Barcelona, Spain.
Insights
Hereditary fructose intolerance (HFI) can mimic CDG, leading to misdiagnosis. Early HFI detection and a fructose-free diet are crucial for patient improvement, even after liver transplantation.
Area of Science:
- Biochemistry
- Genetics
- Pediatrics
Background:
- Atypical hereditary fructose intolerance (HFI) is often misdiagnosed as CDG type 1.
- Early diagnosis and dietary management are critical for HFI patients.
Observation:
- A neonate presented with hypertonia, neurological impairment, and liver abnormalities, initially misdiagnosed as CDG type 1.
- Transferrin isoelectric focusing (Tf IEF) and MALDI-TOF MS showed abnormalities mimicking CDG.
- Clinical suspicion of HFI, confirmed by ALDOB mutations, led to dietary intervention.
Findings:
- The patient improved on a fructose-free diet, with reversal of neurological symptoms and normalization of transferrin glycosylation.
- Fructose-1,6-bisphosphatase (FBP1) deficiency also presented with altered transferrin patterns, suggesting it as a potential secondary cause of CDG.
- Maternal high fructose intake during pregnancy may contribute to neonatal HFI manifestations.
Implications:
- This case highlights the importance of considering HFI in neonates with unexplained neurological and hepatic dysfunction.
- Abnormal Tf IEF patterns can be indicative of metabolic disorders beyond primary CDG.
- FBP1 deficiency should be considered in the differential diagnosis of secondary CDG with altered transferrin profiles.
Abstract:
Adamowicz and colleagues raised the alert in 2007 about patients with atypical hereditary fructose intolerance (HFI) primarily misdiagnosed as CDG Ix. We describe a girl with neonatal hypertonia, facial trismus, absent swallowing and coughing reflexes, gastro-oesophageal reflux and sporadically elevated Krebs cycle metabolites and lactate. At 14 months microcephaly and hepatomegaly were noted, with hypertransaminasaemia but normal blood coagulation, glucose, phosphate, and absent urinary reducing substances. Neurological impairment persisted. Because of hepatic and neurological abnormalities with developmental delay, Tf IEF was performed and showed a severe type 1 pattern, resulting in a wrong diagnosis of CDG. Subsequently, an aversion to fruits suggested HFI, confirmed by the finding of ALDOB mutations (p.A150P/p.N335K). The girl improved with fructose-free diet, but liver cirrhosis led to hepatic transplantation. She is now 7 years old with good evolution; facial trismus and hypertonia reversed, but microcephaly persists. Transferrin MALDI-TOF MS characterization revealed underoccupation of glycosylation sites and glycan abnormalities, which reversed with dietary treatment. High maternal fructose concentrations might have caused neonatal abnormalities. Although in our patient's mother there is no fructose accumulation at present, it is possible that increased ingestion of fruits and vegetables during pregnancy, together with her heterozygosity, caused an accumulation of fructose that finally affected the fetus. We also describe slightly abnormal transferrin isoelectric focusing and MALDI-TOF MS patterns of intact transferrin and N-glycans in a fructose-1,6-bisphosphatase (FBP1)-deficient patient. While HFI is a well-known cause of secondary CDG, we found no reports of abnormal transferrin isoelectric focusing patterns in FBP1 deficiency and we introduce this condition as a possible secondary cause for altered transferrin isoelectric focusing.
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