Cases reported "Corneal Opacity"

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1/6. Familial band-shaped keratopathy.

    A brother and sister out of a consanguinous family of four siblings are presented as prototypes of primary band-shaped keratopathy. The disease manifested sever progressive changes of secondary nature over two years of follow-up. histology and treatment are described.
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2/6. The histopathology of Peters' anomaly.

    Corneal, iris, and trabecular meshwork tissue in a 23-month-old boy with Peters' anomaly were studied with light and electron microscopy. In the cornea, both Descemet's membrane and endothelium were present beneath the area of the corneal opacity except at the point of iris adhesion. However, Descemet's membrane was thin and embryonal in nature, and the endothelium markedly attenuated. The trabecular meshwork demonstrated changes characteristic of old age such as wide-banded collagen and the presence of phagocytosed pigment granules in the endothelium. The iris appeared normal except for anterior synechiae to the corneal opacity. Developmentally, the primary fault appeared to be a failure in the normal differentiation of endothelial cells of the cornea and trabecular meshwork.
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3/6. Herpesvirus infection of cornea allografts.

    This report describes three patients who have in common an occurrence of ocular epithelial herpes infection following a penetrating keratoplasty for a corneal opacity unrelated to herpesvirus infection. It may be that patients undergoing episodes of graft rejection are at increased risk for the reactivation of herpesvirus latent in the trigeminal ganglia, and corticosteroids should be used with this in mind. Because virtually all adults have been exposed to herpes and therefore harbor latent virus, a viral etiology should be considered for lesions in post-penetrating keratoplasty patients. Although the occurrence of this possibly rejection-related reactivation of herpes simplex virus is undoubtedly rare, management of potential cases of this nature should take this possibility into account.
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4/6. Asymmetric anterior segment changes induced by chlorpromazine.

    A 54-year-old man ingested chlorpromazine, 800 mg/day, for ten years and showed conjunctival, corneal, and lenticular changes. Because of a congenital Marcus-Gunn jaw-wink phenomenon in the right eye with subsequent ptosis, he presented an opportunity to compare the anterior segment changes induced by this drug in an eye exposed to sunlight with an eye relatively protected. The changes in the anterior segment were much more marked in the exposed left eye--supporting the hypothesis that chlorpromazine-induced ocular toxicity is a result of drug interaction with sunlight on anterior segment proteins, causing them to denature, opacify, and accumulate in conjunctiva, cornea, and lens.
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5/6. Clinical pathologic correlation of superficial corneal opacities in X-linked ichthyosis.

    X-linked ichthyosis is a relatively common oculodermal disorder. Characteristic corneal opacities are small punctate or filiform lesions and are located in the deep corneal stroma. In an unusual case, a 73-year-old man with X-linked ichthyosis and steroid sulfatase deficiency had superficial corneal opacities. The corneal opacities were granular in nature, involving the subepithelial and anterior stromal layers. The opacities resulted in irregular overlying corneal epithelium and were white-gray in color in direct illumination. Histopathologic and electron microscopic studies demonstrated abnormalities of the corneal epithelial basement membrane. The epithelial basement membrane was thickened with irregular extensions into Bowman's layers. Abnormal depositions of basement membrane protein were seen in the anterior stroma. These abnormalities may have resulted from increased production of basement membrane proteins by the corneal epithelium, resulting from hyperactive turnover of the basal layer.
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6/6. Central cloudy corneal dystrophy of Francois. A clinicopathologic study.

    Central cloudy corneal dystrophy of Francois was first described in 1955 by J. Francois; its pathophysiology remains unknown. An 80-year-old woman with bilateral central cloudy corneal dystrophy of Francois was examined after having undergone a combined penetrating keratoplasty and cataract extraction. The corneal button was obtained. Light microscopy revealed stromal staining for acid mucopolysaccharide. Transmission electron microscopy revealed extracellular vacuoles, some of which had fibrillogranular material and electron-dense deposits. Fibrillogranular material was present in and around some keratocytes. Numerous endothelial vacuoles contained light-staining fibrillogranular material and round electron-dense granules. Our findings suggest that the opacities in patients with central cloudy corneal dystrophy of Francois are due to the extracellular accumulation of mucopolysaccharide and lipidlike material. Further studies are needed to elucidate the nature of these deposits.
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