[Essential progressive telangiectasia].

by well-established clinical criteria.5 The abnormality is located on chromosome 17 and exhibits autosomal dominant inheritance. Most cases of Sturge-Weber syndrome are sporadic, but a familial distribution has been reported. As a result, the syndrome is believed to follow paradominant inheritance, such that the individual is heterozygotic for this inherited characteristic and phenotypically normal, and will only suffer from the disease should further mutation occur during the early phases of embryonic development.6 In neurofibromatosis type 1 the underlying alteration encodes a protein, neurofibromin, that is responsible for the pathogenesis of the condition. Sturge-Weber syndrome is explained by increased expression of fibronectin, which regulates angiogenesis and constitutes the cerebral response to chronic ischemic damage. Therefore, there does not appear to be a relationship between the 2 neurocutaneous syndromes in either pathogenesis, transmission, or the underlying genetic defect. We raise the question of whether this case could be the result of the simultaneous occurrence of both process—an extraordinarily rare occurrence. Another explanation could lie in the pathogenesis of neurofibromatosis itself, since numerous articles link this condition with angioma and other vascular abnormalities.7 Thirdly, it is possible that this could correspond to the most common neurocutaneous syndrome of all, Pascual Castroviejo type II syndrome, which encompasses neurologic abnormalities and various vascular abnormalities, including angioma. Reports of Pascual Castroviejo II syndrome include a description of a patient with neurofibromatosis type 1 and cutaneous and hepatic hemangioma.8