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Accutane (Isotretinoin) and MGD

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  • Accutane (Isotretinoin) and MGD

    Isotretinoin is well know to cause MGD (which is a common dry eye factor). In fact, it's used in lab and animal testing to model how MGD works.

    TFOS DEWS II Pathophysiology Report

    (from 7.3) A second model is induced by treatment with isotretinoin [642], a known and significant risk factor for the development of human MGD [643–652]. Treatment of rats for 3 months with isotretinoin led to keratinization and thickening of the meibomian gland ductal epithelium, a decrease in the quantity and size of acini, and many degenerated acini and acinar cell casts in the meibomian gland ducts. These isotretinoin-elicited effects could be inhibited by treatment with dehydroepiadrosterone, presumably, according to the investigators, through conversion to androgens [642]. Topical androgens, in turn, have been reported to be effective in the therapy of human MGD [653] (see TFOS DEWS II Sex, Gender, and Hormones report [1222]).
    (from 7.5) A fourth DED model uses immortalized human meibomian gland epithelial cells [50]. This model involves exposure of these cells in vitro to isotretinoin [45], a well-known risk factor for the development of human MGD in vivo [643–652]. Exposure of human meibomian gland epithelial cells to isotretinoin: [a] alters the expression of thousands of genes, including an upregulation of genes for some inflammatory mediators (e.g. IL-8 and IL-1β), proteases (e.g. MMP-9), MAPK signaling, lytic vesicles, apoptosis and cell death, and suppresses genes linked to DNA replication, cell cycle, RNA transport and mitochondria; [b] increases the levels of pro-IL-1β, IL-1β and MMP-9 proteins; [c] decreases the signaling of the cell growth and survival mediator, phosphoinositide 3-kinase-protein kinase B; and [d] inhibits cell proliferation and induces cellular atrophy and death (e.g. by apoptosis, necrosis and/or autophagy) [45]. It is possible that these effects may be responsible for the acinar epithelial cell degeneration and atrophy, and reduced and abnormal secretions, that occur following isotretinoin induction of human MGD in vivo [643–652].
    References in the pathophysiology report to isotretinoin

    [643] Perry MD, McEvoy GK. Isotretinoin: new therapy for severe acne. Clin Pharm 1983;2:12–19.
    [644] Fraunfelder FT, LaBraico JM, Meyer SM. Adverse ocular reactions possibly associated with isotretinoin. Am J Ophthalmol 1985;100:534–537.
    [645] Fraunfelder FT, Fraunfelder FW, Edwards R. Ocular side effects possibly associated with isotretinoin usage. Am J Ophthalmol 2001;132:299–305.
    [646] Caffery BE, Josephson JE. Ocular side effects of isotretinoin therapy. J Am Optom Assoc 1988;59:221–224.
    [647] Denis P, Nordmann JP, Saiag P, Liotet S, Laroche L, Saraux H. Chronic blepharoconjunctivitis during a treatment with acitretin (Soriatane). J Fr Ophtalmol 1993;16:191–194.
    [648] Mathers WD, Shields WJ, Sachdev MS, Petroll WM, Jester JV. Meibomian gland morphology and tear osmolarity: changes with Accutane therapy. Cornea 1991;10:286–290.
    [649] Bozkurt B, Irke M, Atakan N, Orhan M, Geyik P. Lacrimal function and ocular complications in patients treated with systemic isotretinoin. Eur J Ophthalmol 2002;12:173–176.
    [650] Gross EG, Helfgott MA. Retinoids and the eye. Dermatol Clin 1992;10:521–531.
    [651] Jaanus SD. Ocular side effects of selected systemic drugs. Optom Clin 1992;2:73–96.
    Rebecca Petris
    The Dry Eye Foundation
    dryeyefoundation.org
    800-484-0244
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