LIGNEOUS CONJUNCTIVITIS

LIGNEOUS CONJUNCTIVITIS
R. MEHTA* and A. D. SHAPIRO

*Department of Clinical Medicine, Section of Hematology/Oncology, Indiana University School of Medicine, Indianapolis, IN; and Indiana Hemophilia and Thrombosis Center, Indianapolis, IN, and Department of Pediatrics, Michigan State
University, East Lansing, MI, USA

LIGNEOUS CONJUNCTIVITIS......................................
Descriptions of ligneous conjunctivitis have appeared in the literature since the 1850s [1,16]. However, the link of this clinical entity to plasminogen deficiency was not established until the 1990s [5]. An excellent review by Schuster and Seregard [1] integrated the numerous reports of ligneous conjunctivitis and better defined the distinct qualities of these lesions. The pseudomembranes typically are preceded by
erythema of the conjunctiva and chronic tearing,
followed by the development of white, yellow-white,
or red masses that form on the conjunctiva and have
the characteristic wood-like texture (Figs 2a,b).
Corneal involvement from these lesions occurs in
20–30% of cases and may result in loss of sight.
Pseudomembranes occur more frequently on the
upper compared with the lower eyelid; approximately
50% of patients have bilateral ocular involvement.
Often the pseudomembranes result from some
stimulus or irritation, such as infection, trauma, and
surgery. Classically, ligneous conjunctivitis was described in infants and children, yet it is now apparent that older individuals may manifest this symptom as well [10,16]. In fact, a case report documented two sisters with ligneous conjunctivitis who were older than 55 years [28]. There appears to be a higher incidence in females compared with males, with a ratio of 1.27:1–1.39:1 [1,10]. Lesions, once they develop, may be present for a variable period, ranging from a few months up to 44 years [1].
Of note is a case ligneous conjunctivitis induced by
tranexamic acid, an inhibitor of fibrinolysis [29].
A 25-year-old woman was treated with tranexamic
acid for control of menorrhagia. She developed
pseudomembranes of the conjunctiva, gingiva, and
the peritoneum shortly after she started taking the
tranexamic acid. After 9 months, she sought care for
these lesions. Three months later, after lack of
response to local therapies, use of all medications
was discontinued; subsequently, after 3 weeks the
lesions began to resolve. The tranexamic acid therapy was restarted, and after 2 days, the lesions began to re-accumulate but again promptly resolved after cessation of the medication. Although it appears that the anti-fibrinolytic contributed to the formation of these lesions, the triggering event was unclear and
her plasminogen level did not appear to have been
measured.