May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Ligneous Conjunctivitis in an Adult Patient: A Study of Molecular Pathophysiology and Treatment Options
Author Affiliations & Notes
  • J. Pruzon
    Ophthalmology, Univ Med & Dentistry NJ, Newark, NJ
  • M. Gonzalez–Gronow
    Hematology, Duke University, Durham, NC
  • H. Mohtaseb
    Hematology, Hematology Oncology Associates of North Jersey, Wayne, NJ
  • D.S. Chu
    Ophthalmology, Univ Med & Dentistry NJ, Newark, NJ
  • Footnotes
    Commercial Relationships  J. Pruzon, None; M. Gonzalez–Gronow, None; H. Mohtaseb, None; D.S. Chu, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 2678. doi:
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      J. Pruzon, M. Gonzalez–Gronow, H. Mohtaseb, D.S. Chu; Ligneous Conjunctivitis in an Adult Patient: A Study of Molecular Pathophysiology and Treatment Options . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2678.

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Abstract

Abstract: : Purpose: To present a case of adult onset ligneous conjunctivitis, probable pathophysiology, and treatment options. Methods: A case study of a patient who presented with chronic membraneous conjunctivitis. The patient's serum was analyzed for plasminogen levels and plasminogen activity when activated by urokinase (u–PA) and tissue plasminogen activator (t–PA). In addition, an analysis for anti plasminogen antibodies was conducted using an Elisa technique. The patient was treated with topical plasminogen. Results: A 45 year old caucasion woman presented with chronic membraneous conjunctivitis of the left superior and inferior palpebral conjunctiva. The patient had a history of gingival hyperplasia since childhood and vaginal mucosal lesions. The patient's conjunctival membrane originally responded to topical and systemic steroid treatment but later plateaued and continued to be symptomatic. Lab work revealed a low plasminogen level, low plasminogen function, and high plasminogen activity inhibition. In addition, a conjunctival biopsy showed an exudative membrane with a combination of acute and chronic conjunctivitis. A diagnosis of ligneous conjunctivitis was suggested and the patient was started on topical plasminogen treatment. The patient improved clinically and additional lab work was obtained to investigate the pathophysiology. Serum IgG and IgA anti plasminogen antibodies were identified at a greater level in our patient than in the control. These antibodies inhibit activation at the plasminogen cleavage site. The patient's plasminogen activity showed only one tenth of normal activity when activated by u–PA and less than 0.5% activity when activated by t–PA. Conclusions: Adult onset ligneous conjunctivitis may occur as a result of an autoimmune mechanism in addition to previously suggested molecular mutations. Topical plasminogen may be an effective treatment for ligneous conjunctivitis associated with decreased plasminogen activity.

Keywords: conjunctivitis • autoimmune disease • inflammation 
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