12/21/2023 0 Comments Lattice degeneration preventionThe variants are often geographically specific and are occasionally traceable to single founder mutations. They are now considered to be subtypes of the same disease, in which type I is the classic and most common presentation. Specific phenotypic patterns are traceable to specific mutations in the TGFBI gene, which resulted in their being initially described as separate diseases. These are variations of the same disease process that causes type I LCD, with minor changes in their phenotypic features. The variants were formerly described as types IA, III, IIIA, IIIB, IV, V, VI, VII, and polymorphic corneal amyloidosis. The LCD variants are subtypes of LCD caused by a variety of mutations on the TGFBI gene. It usually presents in the first or second decade of life. Although TGFBI and its protein transcript are found throughout the body, there are no known systemic effects outside of the ocular pathology for which it is named. It is autosomal dominant and results from mutations in the transforming human growth factor beta-induced ( TGFBI) gene. Type I LCD (LCD1), also known as classic lattice corneal dystrophy or Biber-Haab-Dimmer dystrophy, is the primary form of LCD. LCD belongs to a broader family of corneal dystrophies and has several subtypes, as described below. The erosions may appear before any noticeable stromal deposits. Recurrent epithelial erosions are often present, causing ocular irritation and additional vision loss. They are radially oriented and are accompanied by gradual, superficial opacification of the cornea. These deposits create linear, “lattice-like” opacities arising primarily in the central cornea, while the peripheral cornea is often spared. Lattice corneal dystrophy (LCD) is an inherited disorder of the eye characterized by the deposition of amyloid resulting in steadily progressive loss of vision.
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