Dr Folberg provided me with one of my most rewarding professional collaborations when we joined forces in the late 1980s to write a pair of papers on benign conjunctival melanocytic lesions and premalignant and malignant lesions. I do not know who mentored whom, but I can relate that his monumental and enduring papers as a fellow on the precursors of conjunctival melanoma, written in collaboration with the staff at the Armed Forces Institute of Pathology (AFIP), impacted my own thinking profoundly.
This AFIP work was published over 30 years ago. I am still solidly in agreement with its main findings and am guided by them. However, as I explain in my Perspectives article, I have changed my mind (not necessarily an intellectual defect) regarding how well the term “primary acquired melanosis” (PAM) communicates the nature of this frequent precursor of melanoma and effectively facilitates the education of non–ophthalmic pathologists and practicing ophthalmologists. It is correct to say that I offer no new study-derived data or findings—rather, my intention is to improve the transmission of the best available published data, notably those of Folberg and associates, so that ophthalmic clinicians and other colleagues are more aware of what the disease does or does not consist of. Equally important is developing a full awareness of what the best histopathologic parameters are for predicting behavior.
There are 3 specific points that I would like to make. First, I recommend not that all biopsies of PAM be subjected to immunohistochemical evaluation, but the latter should be performed only for those lesions wherein there is ambiguity about atypia or the degree of proliferation in the pathologist’s mind. A statement asserting this premise constitutes the first sentence in the Conclusion section of the Abstract. Fortunately, most lesions can be accurately judged in hematoxylin-eosin-stained sections. Second, not all ophthalmic pathologists and general pathologists are comfortable or adept in assessing atypia in conjunctival melanocytic lesions, which I have discovered from my own pathology consultation practice. Hence, they should be aware that immunohistochemistry can be helpful in difficult diagnostic situations. And third, most clinicians are not fluent in explaining what PAM actually means—some say it is due to pigmentation, others that it is essentially due to “melanocytes.” The concept of intraepithelial proliferation of melanocytes seems to be elusive.
Before preparing this response I quizzed 10 faculty members and trainees in our department on how they would define PAM. Only 2 had reasonably accurate responses. Obviously, educational efforts to date attempting to explain PAM have not been nearly successful enough. My article was therefore aimed at improving overall comprehension of the disease process by introducing a more explicit terminology that better distinguishes for the non-expert the different biologic elements that comprise each diagnostic category. Other investigators have also recognized this lingering problem, namely Damato and Coupland, whose excellent classification scheme closely parallels and approximates my own, with only minor differences, and addresses the same issues. I recently learned that their terminology has supplanted primary acquired melanosis in Australia, where their article was published, and is increasingly used in Great Britain. Any improvement, however modest, in understanding what is actually going on at various points along the spectrum of PAM would be a sufficient justification for promoting a new diagnostic system. The more a clinician knows, the sounder his therapeutic judgment will be.