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Figueroa Syndrome

Hereditary syndrome associated with Lymphedema Meige or Lymphedema Praecox. First reported by AA Figueroa in 1983 in a study of a family with lymphedema praecox and cleft palate. 

Cause: Mutation of FOXC2 gene - autosomal dominant


Family history and physical examination would be the central diagnostic tools.  Lymphatic dysplasia could be verified through the use of a lymphoscintigraphy test. 



Treatment would include surgery for the cleft palate and the establishment of a lymphedema mangement program. The lymphedema treatment program would include:

Manual lymphatic drainage; compression wraps or compression bandages (using short stretch bandages), compression garments, compression sleeves.

Pat O'Connor

June 8, 2008


Meige disease (familial lymphedema praecox) and cleft palate: report of a family and review of the literature.

Figueroa AA, Pruzansky S, Rollnick BR.

This is a report of a family with lymphedema praecox and cleft palate. The mother had only lymphedema of the lower extremities; she gave birth to five sons, 3 of whom had both lymphedema of the lower extremities and cleft palate. Others have reported similar associations in the literature without calling attention to their relationship. In familial cases, an autosomal dominant mode of transmission with variable expression has been suggested. A common pathogenetic mechanism that might account for the localized lymphedema and associated cleft palate can only be speculated at this stage of our understanding of the condition.


Figueroa Syndrome: Cleft palate; lymphoedema starts during childhood or adolescence. [Autosomal dominant]


Lymphoedema Association of Australia[/b]


FOXC2 truncating mutation in distichiasis, lymphedema, and cleft palate.

Bahuau M, Houdayer C, Tredano M, Soupre V, Couderc R, Vazquez MP.

Service de Biochimie et Biologie Moleculaire, Hopital d'Enfants Armand-Trousseau, AP-HP Paris, France.

We report a family showing autosomal-dominant segregation of upper- and lower-eyelid distichiasis (double row of eyelashes) in seven affected relatives over three generations, in addition to below-knee lymphedema of pubertal onset (lymphoedema proecox) in three. Two children had cleft palate in addition to distichiasis, but without the previously reported association with the Pierre-Robin sequence. Other ophthalmologic anomalies included divergent strabismus and early-onset myopia. This family was found to be completely linked to markers mapped to 16q24.3 and thereby proposed to be allelic to the distichiasis-lymphedema syndrome (DL, MIM 153400), although pterygium colli, congenital heart disease, or facial dysmorphism were not features found here. As FOXC2/FKLH14 mutations were found to underlie DL and diverse hereditary lymphedema conditions, this gene was examined by sequence analysis. An out-of-frame deletion (914-921del) was identified and found to segregate with the disease, further highlighting the phenotypic heterogeneity of lymphedema conditions linked to FOXC2 truncating mutations. Whether such heterogeneity is related to genotype-phenotype correlation, a hypothesis not primarily supported by the apparent loss-of-function mechanism of the mutations, or governed by modifying genes, remains to be determined.

PMID: 12485195 [PubMed - indexed for MEDLINE]


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Page Updated: Dec. 15, 2011