In 1975, O’Brien, an Australian general pathologist, described what he considered to be a specific disease induced by longstanding exposure to rays of the sun characterized clinically by annular lesions and typified histopathologically by granulomatous inflammation associated with elastophagocytosis, i.e., ingestion of elastotic fibers by macrophages. O’Brien, and some students of the subject subsequent, remarked that the lesions clinical resembled those of granuloma annulare. Because of elastophagocytosis, and that finding alone, O’Brien averred that the granulomatous dermatitis was unique, and he named it “actinic granuloma.” In our estimation, all of the attributes noted by O’Brien were those of granuloma annulare, including the elastophagocytosis. Ingestion of elastic and elastotic fibers by macrophages is a phenomenon devoid of specificity, one that may occur in circumstances as disparate as granuloma annulare, an inflammatory disease, and granulomatous slack skin, a lymphoma, to wit, mycosis fungoides.
For elastophagocytosis to come into being, damage first must be done to elastic or elastotic fibers, that injury making them appetizing to macrophages. Alteration of those fibers probably is a consequence of the effects of elastases manufactured by inflammatory cells, such as by neutrophils in cutis laxa and neoplastic lymphocytes in mycosis fungoides. Only after elastic and/or elastotic fibers have been changed chemically is the stage set for them to be ingested by macrophages. It is not surprising, therefore, that elastophagocytosis is seen commonly in lesions of granuloma annulare situated in skin damaged badly by sunlight, given the fact that lymphocytes are present around venules and histiocytes are disposed in palisaded and interstitial array.
Granuloma annulare varies greatly in appearance clinical and in distribution regional. Lesions may be papular and missing any hint of an annulus or they may assume the striking configuration of rings. Some lesions may be eroded and crusted (perforating granuloma annulare), whereas others may be seated beneath the skin (subcutaneous granuloma annulare). Although lesions of granuloma annulare tend to favor sites covered by clothing, one expression of it is confined to sites exposed to rays of the sun. Histopathologically, cutaneous granuloma annulare, irrespective of manifestation clinical, displays superficial and deep perivascular infiltrates of lymphocytes in conjunction with histiocytes distributed either in palisaded or interstitial arrangement, or both of them together. When elastic or elastotic fibers devoured by macrophages are observed in lesions characteristic of granuloma annulare, the diagnosis should be granuloma annulare, not actinic granuloma, which to most dermatologists denotes something other than granuloma annulare.
In the analysis ultimate, the diagnosis morphologic of skin diseases must take into account both attributes gross and microscopic. One of those sets is not more important than the other. If clinically a lesion is granuloma annulare and histopathologically it shows all of the findings of granuloma annulare, then the diagnosis is granuloma annulare, irrespective of the presence or absence of elastophagocytosis, “perforation” of degenerated collagen, fibrin, and mucin through the epidermis, or nuclear “dust” of neutrophils in the center of palisades of epithelioid histiocytes. Reasoning specious about findings histopathologic has led to debates about whether lesions were truly those of necrobiosis lipoidica diabeticorum, on one hand, or of granuloma disciformis, on the other; of granuloma annulare on the face or of Miescher’s granuloma of the face; of erythema elevatum diutinum or of extracellular cholesterolosis; of erythema nodosum or of subacute nodular migratory panniculitis; and of long-standing suppurative infundibulitis complicated by imposition of prurigo nodularis or of hyperkeratosis follicularis et parafollicularis in cutem penetrans. “Diseases” that are not authentic do not stand the test of time, and, for that reason, diagnoses of granuloma disciformis, Miescher’s granuloma of the face, extracellular cholesterolosis, subcutaneous nodular migratory panniculitis, and hyperkeratosis follicularis et parafolliculars in cutem penetrans hardly ever are made nowadays by knowledgeable dermatologists or general pathologists. Neither do students of skin diseases hear anymore of Weber-Christian syndrome and Rothman-Makai disease, and neither should they hear of toxic epidermal necrolysis and Spiegler-Fendt sarcoid. The same fate is inevitable for “actinic granuloma” because what is called actinic granuloma is granuloma annulare.
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