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Table 1: Demographic, genetic, and clinical features of patients with MNGIE
Case No. Age at MRI (yr)/Sex TYMP Mutation^{^a} Mutation Type TP Activity Age at Neurologic Onset Age at Gastroenterologic^{^b} Onset
1 23/F c.1249 dupC Frame shift Undetectable 20 yr (ptosis/CPEO) Childhood
2 29/F c.1160–2A>G and c.1382_1383insC Splice defect Frame shift Undetectable Childhood (CPEO) Childhood
3 28/M c.215–1G>A and c.328C>T Splice defect p. Q110X Undetectable 24 yr (ptosis/CPEO) 20 yr
4 27/F c.1160–1G>A Splice defect Very low 20 yr (ptosis/CPEO) Childhood
5 38/M c.522T>A Splice defect Undetectable 37 yr (ptosis/CPEO) 30 yr
6 25/M c.1160–1G>A Splice defect Very low 25 yr (peripheral neuropathy) 19 yr
7 36/M c.457G>A p. G153S Undetectable Childhood (ptosis) 25 yr
Note:—CPEO indicates chronic progressive external ophthalmoplegia; TP, thymidine phosphorylase.
↵a All homozygote.
↵b Main gastroenterologic symptoms included irritable bowel and/or functional dyspepsia-like symptoms.