Vorinostat (rINN) also known as Suberoylanilide hydroxamic acid  (suberoyl+anilide+hydroxamic acid abbreviated as SAHA) is a member of a larger class of compounds that inhibit histone deacetylases (HDAC). Histone deacetylase inhibitors (HDI) have a broad spectrum of epigenetic activities. Vorinostat is marketed under the name Zolinza ( zoh-LIN-zə) by Merck for the treatment of cutaneous manifestations in patients with cutaneous T cell lymphoma (CTCL) when the disease persists, gets worse, or comes back during or after two systemic therapies. The compound was developed by Columbia University chemist Ronald Breslow and Memorial Sloan-Kettering researcher Paul Marks

Medical uses
Vorinostat was the first histone deacetylase inhibitor approved by the U.S. Food and Drug Administration (FDA) for the treatment of CTCL on October 6, 2006. It also failed to demonstrate efficacy in treating acute myeloid leukemia in a phase II study. Mechanism of action
Vorinostat has been shown to bind to the active site of histone deacetylases and act as a chelator for zinc ions also found in the active site of histone deacetylases. Vorinostats inhibition of histone deacetylases results in the accumulation of acetylated histones and acetylated proteins, including transcription factors crucial for the expression of genes needed to induce cell differentiation. It acts on class I, II and IV of histone deacetylase. Clinical trials
Vorinostat has also been used to treat Sézary syndrome, another type of lymphoma closely related to CTCL.A recent study suggested that vorinostat also possesses some activity against recurrent glioblastoma multiforme, resulting in a median overall survival of 5.7 months (compared to 4–4.4 months in earlier studies).
Band keratopathy is a corneal disease derived from the appearance of calcium on the central cornea. This is an example of metastatic calcification, which by definition, occurs in the presence of hypercalcemia. Signs and symptoms
Signs and symptoms of band keratopathy include eye pain and decreased visual acuity. Causes
Band keratopathy has several causes. These causes include uveitis, interstitial keratitis, superficial keratitis, phthisis, sarcoidosis, trauma, intraocular silicone oil, systemic diseases (high levels of calcium in the blood, vitamin D intoxication, Fanconis Syndrome, low levels of phosphorus in the blood, gout, milk-alkali syndrome, myotonic dystrophy, and chronic mercury exposure). Pathology
Band keratopathy is seen when there is calcification of the epithelial basement membrane, Bowmans membrane, and the anterior stroma with destruction of Bowmans membrane. The calcium salts are intracellular when the process is due to alteration of systemic calcium metabolism, whereas they are extracellular when due to local disease. Diagnosis
Band keratopathy is diagnosed by slit lamp examination of the eye. Treatment
Treatment is indicated if vision is threatened or if the eye is uncomfortable. It is important to recognize and treat any underlying condition. Improvement of vision may be obtained by scraping off the opacity. Topical disodium EDTA can be used as a chelating agent. It can also be removed with the excimer laser (phototherapeutic keratectomy). Other modalities include diamond burr and lamellar keratoplasty. References


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