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Biomedical subjects

A Homberg

Publications and source records attributed to A Homberg.

3 recordsLinked to original sources

[Pathology of the corneal endothelium in bullous keratopathy following iris clip lens implants].

12 patients developed pseudophakic bullous keratopathy 2 to 7 years following i.c. cataract-extraction with implantation of 4-loop iris clip lenses necessitating perforating keratoplasty. To study the pathogenesis of pseudophakic bullous keratopathy the corneal endothelium of the excised button was investigated light-microscopically after vital staining of the endothelium. Additionally the surface of the explanted intraocular lenses were examined by the method of Wolter. The result is a central cell density of the excised corneal buttons between 179 and 867 cells/mm2. Large cell-free areas were always found indicating that a disturbance of the endothelial barrier function is the major reason for corneal decompensation. A relation between inflammatory cell deposits on the IOL-surfaces and the endothelial decompensation was not apparent. As the main reason for endothelial decompensation a chronical mechanically induced endothelial cell loss is supposed leading to disturbances of the endothelial barrier function. To prevent a repeated corneal decompensation it is recommended to remove iris-clip-lenses during the procedure of perforating keratoplasty.

Aged↗

[Cytology of the corneal endothelium in endothelial dystrophy].

The corneal endothelium of 17 corneal buttons with endothelial dystrophy was investigated by means of vital staining and light microscopy. Each type of dystrophy was characterized by typical morphological changes in the endothelium: in Fuch's endothelial dystrophy (n = 13), subendothelial guttata formation is characteristic; in congenital hereditary endothelial dystrophy (n = 2), a high amount of multinucleated endothelial cells was found; in posterior polymorphous dystrophy (n = 2), a multilayered endothelium was the striking feature. There is a coherent endothelial cell layer in endothelial dystrophy that may indicate a disturbance in the endothelial pump function rather than a barrier defect caused by gaps between the endothelial cells.

Child↗