Ophthalmic Physiol Opt
January 2005
The cause of keratoconus is unknown. However, an earlier report demonstrated magnesium deficiency in keratoconus patients, and suggested that magnesium deficiency could pathologically affect the mechanisms of the cornea. Experimental and clinical papers concerning a possible relationship between keratoconus and magnesium deficiency were reviewed.
View Article and Find Full Text PDFRecurrent keratoconus is a corneal dystrophy that degrades the optical function of the corneal graft. Recurrence of keratoconus after keratoplasty has been reported previously in some scattered case reports, but the aetiology is still unclear. This report describes the case of a 74-year-old white woman, who presented recurrent keratoconus 40 years after keratoplasty.
View Article and Find Full Text PDFBackground: Previous theories of the pathogenesis of keratoconus have only described partial aspects of the disease.
Methods: Studies are reviewed that have demonstrated a statistical and physiological relation between keratoconus, magnesium deficiency, type A behavior, and allergy, which constitute the Thalasselis Syndrome.
Results: The Thalasselis syndrome integrates old and new theories on keratoconus, mitral valve prolapse, and tetany/menopause.
This report describes the unusual case of 46-year-old white European woman who presented spontaneous keratoconus. This case suggests a new association: keratoconus-tetany-menopause. This can be explained by Thalasselis' syndrome, a syndrome showing a relation between keratoconus, magnesium (Mg) deficiency, type A behavior, and allergy.
View Article and Find Full Text PDFThe etiology of keratoconus is still unclear. This study presents a new clinical sign, Thalasselis' syndrome, defined as: an association between keratoconus, magnesium deficiency, type-A behavior and allergy. Also, it introduces the hypothesis that magnesium deficiency could affect pathologically the osmotic mechanism of the cornea, specifically the Na-K and/or Ca-ATPase pumps; the collagen structure by alteration of the adenylate cyclase activity; and other mechanisms as well.
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