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Cell subpopulations in failed human corneal grafts
  1. Moorfields Eye Hospital
  1. f.larkin{at}

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    Editor,—In the well illustrated paper by Kuffová and co-authors,1 conclusions are presented on the roles of different inflammatory cell phenotypes based on immunohistochemical findings in excised corneal transplants. The detailed pathological findings should be interpreted with caution as insufficient information is presented to support the clinical diagnosis of rejection in some of those patients with graft inflammation.

    In several patients in Table 2, and all in Table 3, surface wound healing problems, graft melting, and spontaneous perforation are listed as postoperative complications. However, none of these are clinical features of graft rejection, even in experimental models of unmodified rejection. They are signs typical of HSV epithelial or necrotising stromal keratitis, which can complicate transplantation in patients taking postoperative steroid treatment, particularly in whom HSV keratitis is the primary corneal diagnosis. This possibility would be less likely if the indication for transplantation was a corneal disorder other than HSV or if viral infection was excluded by pathological study of the corneal specimens. It is also possible that in these specimens the immunohistochemical findings represent HSV recurrence accompanied by allograft rejection. However, I question the validity of the conclusions relating to rejection in specimens from those patients with signs indicating possible viral keratitis. This may explain in part, for example, the counterintuitive finding that the number of CD1a/MHC class II double positive cells was not significantly higher in a group with severe inflammation at the time surgery than in the group with no inflammation.



    Editor,—Larkin's letter questions the primary diagnosis in the patients listed in Tables 2 and 3 and suggests possible herpes virus origin of the disease. The question arises from our description of postoperative complications in some of our patients which include graft melting and perforation. We agree that graft melting is not a typical feature of corneal graft rejection.

    We would wish to clarify the clinical status of our patients. Only in two patients was the primary condition related to HSV infection. In all other grafts, in which there were surface wound healing problems, the diagnoses included lime burns, keratoconjunctivitis sicca, and Stevens–Johnson syndrome without signs of herpes simplex virus keratitis. In these patients graft epithelial healing problems are related rather to the limbal stem cells and tear film deficiency than to infectious causes. In fact, it is recognised that there are sometimes difficulties in distinguishing graft rejection from infiltration due to chronic epithelial defect. In our patients we made a diagnosis of rejection in association with epithelial healing problems. We cannot exclude the possibility of HSV infection of the transplanted grafts but clinical signs indicated that limbal stem cell deficiency was the cause of the epithelial healing problem and subsequent graft melting.

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