Carbohydrate-deficient Glycoprotein Syndrome (CDGS) Type Ia, Congenital Disorder of Glycosylation (CDG) Type Ia,Phosphomannomutase Deficiency[1],Jaeken Syndrome, PMM2-CDG
, CDG1a
PMM2 protein
PMM2 deficiency or PMM2-CDG, previously CDG-Ia, is a very rare genetic disorder caused by mutations in PMM2. It is an autosomal recessive disease that is the most common type of congenital disorder of glycosylation or CDG.[2] PMM2-CDG is the most common of a growing family of more than 130 extremely rare inherited metabolic disorders.[3] Only about 800 children and adults have been reported worldwide.[4]
Hypotonia - Weak muscle tone, commonly known as floppy baby syndrome.[16]
Diagnosis
PMM2 deficiency is diagnosed through genetic sequencing. More than 115 mutations in the PMM2 gene have been found to cause this disease.[16]
Treatment
Treatment with mannose powder 1 to 2 g / kg per day results in significant improvement in protein glycosylation after 1 year.[17] Other treatments involve management of the symptoms that are apparent in each individual, including physical therapy to improve core strength and mobility, occupational therapy for coordination, speech therapy for talking and eating.[13]
References
^Matthijs G, Schollen E, Pardon E, Veiga-Da-Cunha M, Jaeken J, Cassiman JJ, Van Schaftingen E (May 1997). "Mutations in PMM2, a phosphomannomutase gene on chromosome 16p13, in carbohydrate-deficient glycoprotein type I syndrome (Jaeken syndrome)". Nature Genetics. 16 (1): 88–92. doi:10.1038/ng0597-88. PMID9140401. S2CID22959423.
^"PMM2-CDG". Rare Diseases. National Organization for Rare Disorders (NORD). 6 August 2015 [Originally published 1996]. Retrieved 1 December 2023.
^Al-Maawali AA, Miller E, Schulze A, Yoon G, Blaser SI (February 2014). "Subcutaneous fat pads on body MRI--an early sign of congenital disorder of glycosylation PMM2-CDG (CDG1a)". Pediatric Radiology. 44 (2): 222–5. doi:10.1007/s00247-013-2782-2. PMID24037084. S2CID36990231.
^Barone R, Fiumara A, Jaeken J (July 2014). "Congenital disorders of glycosylation with emphasis on cerebellar involvement". Seminars in Neurology. 34 (3): 357–66. doi:10.1055/s-0034-1387197. PMID25192513. S2CID23836020.
^Marques-da-Silva D, Dos Reis Ferreira V, Monticelli M, Janeiro P, Videira PA, Witters P, Jaeken J, Cassiman D (March 2017). "Liver involvement in congenital disorders of glycosylation (CDG). A systematic review of the literature". Journal of Inherited Metabolic Disease. 40 (2): 195–207. doi:10.1007/s10545-016-0012-4. PMID28108845. S2CID28342989.
^Footitt EJ, Karimova A, Burch M, Yayeh T, Dupré T, Vuillaumier-Barrot S, Chantret I, Moore SE, Seta N, Grunewald S (December 2009). "Cardiomyopathy in the congenital disorders of glycosylation (CDG): a case of late presentation and literature review". Journal of Inherited Metabolic Disease. 32 (Suppl 1): S313-9. doi:10.1007/s10545-009-1262-1. PMID19757145. S2CID40744073.
^ abSparks SE, Krasnewich DM (1993). "PMM2-CDG (CDG-Ia)". In Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). GeneReviews®. Seattle (WA): University of Washington, Seattle. PMID20301289.