Reply

We thank Dr Chaluvadi for her interest in our editorial. We appreciate hearing about her hypothesis about the pathogenesis of superior limbic keratoconjunctivitis (SLK), and her letter offers us an opportunity to reinforce critical points in our editorial about myths and hypotheses in contrast to data-driven mechanisms of disease. We also have a hypothesis about the pathogenesis of SLK, but with only circumstantial data to support it. We hypothesize that SLK is an autoimmune disease for the following reasons. First, SLK occurs in the context of two other autoimmune diseases of the conjunctiva and episclera: graft-versus-host disease and thyroid eye disease; second, SLK is well-controlled with local immunosuppression; and third, SLK is well-controlled after excision of the conjunctiva and the episclera, the tissues that we hypothesize are under autoimmune attack. Our hypothesis does not require a tight lid, poor lubrication, or an uneven surface of the palpebral conjunctiva for the disease to occur. However, we recognize that our hypothesis is simply a hypothesis, and should not be taught as the cause of SLK to impressionable residents and fellows, lest it quickly achieve myth status.

The data to support either the tight lid hypothesis or the autoimmune hypothesis simply do not exist at this time. Better that we teach our trainees that, although several hypotheses exist, the pathogenesis of SLK remains unknown. Teaching our trainees the difference between myth, hypothesis, and data-driven mechanisms of disease is one of the key points of our editorial. To do this, we need to engage our trainees in critical thinking. In the absence of this, we are concerned that our specialty will become the realm of supertechs, capable of efficiently carrying out amazing surgical procedures and quoting chapter and verse of established texts, but with little capacity to acknowledge or differentiate hypothesis from data-driven science.