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Excerpt
In his comments about vasculitis in the section of this journal captioned “On the Cover” the editor, in characterizing the thought processes of Leonardo da Vinci, sought to capture the distinctive turn of mind of that polymath by the word sfumato, which he defined as “smokiness, the ability to hold conflicting thoughts in one's head, to “embrace ambiguity, paradox and uncertainty” (1). In the spirit of sfumato, I seek now to draw attention to the notion set forth first by O'Brien and ratified by Al-Hoqail et al. in the same issue of the journal as appeared the essay about sfumato, to the effect that “AG [actinic granuloma] should be considered a separate, independent condition and should be distinguished from GA [granuloma annulare] even on sun-exposed areas of skin” (2).
Before engaging the idea of sfumato, however, I want to express publicly my high regard for John O'Brien, both as a professional and as a person, and address three matters about “actinic granuloma” that are smoky to me. Al-Hoqail et al. acknowledged, at the outset of their piece, that the “clinical features of AG are often indistinguishable from those of classic GA.” In short, so-called actinic granuloma is not distinguishable from granuloma annulare clinically. In regard to histopathologic findings, even a cursory glance at their Table 1, which is devoted to “A comparison of histologic features of actinic granuloma and granuloma annulare,” reveals striking overlap in each of the parameters assessed by them, to wit, multinucleated giant cells, mucin, type of granuloma, and location of granuloma. The differences between the “two” conditions in terms of histopathologic attributes are negligible. In brief, “actinic granuloma” has not been shown compellingly to be readily distinguishable from granuloma annulare histopathologically. In sum, in regard to “actinic granuloma” on morphologic grounds, that is, clinically and histopathologically, “If it looks like a duck, walks like a duck . . .” The duck in this case is granuloma annulare.
The authors quote O'Brien in regard to pathogenesis of actinic granuloma thus: “. . . it represents an inflammatory reaction in response to actinically degenerate elastotic tissue” and they aver that their own study by conventional microscopy “provides insight into pathogenetic mechanisms” of actinic granuloma and this is how: “. . . the sarcoidal granulomata and multinucleated giant cells of AG suggest an inflammatory response directed toward smaller materials, such as individual elastic fibers, that are more readily destroyed to the point where they are no longer visible by light microscopy. The confinement of the inflammatory reaction to the superficial dermis, corresponding to the zone of solar elastosis, supports the original hypothesis that elastotic material altered by chronic sun exposure is the specific target in this disorder.” In the last sentence, a reader should take note carefully of the word “hypothesis”; everything in the last two sentences quoted is mere supposition, devoid of even a jot of evidence in support of it.
Before coming to the thought that I hope will satisfy the criteria of the Editor for sfumato, I want to alert modern dermatologists, general pathologists, and dermatopathologists to what I was taught in 1966 by Drs. Herman Beerman and Margaret Wood, the two dermatopathologists at the University of Pennsylvania during the year of residency I spent in the Department of Dermatology there, in regard to the “palisading granulomas.” They said repeatedly that there were four of them, namely, granuloma annulare, necrobiosis lipoidica, rheumatoid nodule, and pseudorheumatoid nodule—and, again and again, that granuloma annulare and necrobiosis lipoidica could not be told apart histopathologically from one another with confidence. Nearly 40 years later, that idea seems antiquated.
