Selected pseudoneoplastic lesions of the skin.
Other cutaneous abnormalities that some may consider as pseudotumors are, in our opinion, either true neoplasms or preneoplastic in nature. The latter include proliferations related to the human papillomaviruses, (1) as well as Langerhans cell histiocytosis, (2) "large plaque parapsoriasis," (3) selected cutaneous lymphoid "hyperplasias," (4) lymphomatoid papulosis, (5,6) the spectrum of fibromatoses and melanocytic nevi, (7,8) and spindle cell hemangioendothelioma-hemangioma. (9) They will not be considered here.
PSEUDONEOPLASTIC EPITHELIAL PROLIFERATIONS Hair Follicle "Bulges" (der Wulst)
Der Wulst--also designated central facial folliculocentric basaloid proliferation--is problematic in the interpretation of frozen sections or specimens from Mohs micrographic surgical procedures. In those settings, the normal basaloid expansions of paranasal hair follicles might be confused with basal cell carcinomas (BCCs). Both of those proliferations contain cytologically similar cell populations, both may involve the follicular epithelium, and both are variable in size and shape. However, Leshin and White (10) have documented several points of difference between der Wulst and BCC. Follicular bulge structures are usually vertically oriented (Figure 1, A and B), whereas cell nests in BCC are horizontal. Moreover, der Wulst is surrounded by normal dermis, as opposed to the fibromyxoid stroma and stromal-epithelial clefts of BCC. (11,12) Also, prominent basement membranes are seen only around the basaloid cellular aggregates of der Wulst.
Basal cell carcinoma tends to undermine the overlying epidermis and to form an acute angle beneath it; in contrast, der Wulst has a more rounded profile with its widest point at attachments to the follicle. It also lacks the mitotic activity, apoptosis, melanin, and keratotic microcysts commonly seen in BCC.
Pseudoepitheliomatous (Pseudocarcinomatous) Epidermal Hyperplasia
It has long been recognized that reactive epidermal cells could proliferate with patterns simulating those of squamous cell carcinoma or basal cell carcinoma. This process, termed pseudoepitheliomatous hyperplasia (PEH; or pseudocarcinomatous hyperplasia), is potentially associated with organoid nevi, nonhealing ulcers, chronic dermatitides, reactions to underlying neoplasms, and selected infections of the skin. (13-16) Pseudoepitheliomatous hyperplasia may particularly be misdiagnosed as a carcinoma in very superficial biopsies because only the epidermal reaction to an underlying lesion is sampled.
PEH in Chronic Dermatitides.--Pseudoepitheliomatous hyperplasia is a potentially prominent finding in a variety of chronic dermatitides. Inflammation in scarring disorders, burns, ischemia, reactions to cryosurgery, and other mechanical injuries, (14,17,18) halogenodermas, (19) reactions to arthropod bites, (20) and nutritional diseases of the skin (13) can cause this pseudoneoplastic condition.
PEH Associated With Underlying Neoplasms.--When it represents a reaction to subjacent neoplasms, epidermal PEH is principally seen in conjunction with granular cell tumor, dermatofibroma, xanthogranuloma, dermatofibrosarcoma protuberans, or melanocytic proliferations, such as Spitz nevus and spindle cell nevus of Reed (21-26) (Figure 2, A and B). However, more rapidly evolving proliferations, such as malignant lymphoma, may also incite PEH in selected cases. (27) Hence, 2 diagnostic traps are encountered in this specific setting: first, one may overinterpret PEH as squamous carcinoma (Figure 2, C and D), and second, the presence of an underlying nonsquamous neoplasm may be missed because of overly superficial sampling.
[FIGURE 1 OMITTED]
[FIGURE 2 OMITTED]
[FIGURE 3 OMITTED]
PEH in Cutaneous Infections.--Bacterial, fungal, or parasitic infections of the skin are potentially associated with PEH. These include mycobacteriosis, blastomycosis, sporotrichosis, syphilis, and actinomycosis. (28-33) Typically, the causative organisms in those conditions are not visible in conventional sections stained with hematoxylin-eosin. However, a useful clue to an infectious etiology for PEH is the presence of intraepithelial neutrophilic microabscesses, particularly if they are admixed with microgranulomas. Those findings are more often part of PEH than of squamous carcinoma, although that statement is not an exclusive one.
[FIGURE 4 OMITTED]
Potential Mechanisms for Cutaneous PEH.--Freeman (14) reviewed the potential pathogenetic evolution of PEH, concluding that the epidermal hyperplasia could be a reflection of continued growth of entrapped surface epithelium or, alternatively, a manifestation of appendageal acanthosis. In all likelihood, both mechanisms are operative in individual cases.
Pathologic Findings in PEH.--The basic hallmark of PEH is that of irregular proliferation of the epidermis, centered on rete ridges, acrosyringia, or pilosebaceous units. The resulting process forms broad tongues of invaginating epithelium, often showing a jaggedly irregular interface with the subjacent dermis. (13) However, unlike the case with squamous carcinomas, the surface invaginations have a relative regularity with respect to their depth. Also, some physiologic squamous maturation is retained in the proliferating epithelium, without the individual or grouped cellular dyskeratosis seen in most carcinomas. There is no associated tissue eosinophilia, true desmoplasia, angiolymphatic involvement, or perineural permeation in PEH, as expected in sections of surface carcinomas of the skin. The cells in PEH demonstrate one of 2 morphotypes: either they are keratinized polygonal cells with eosinophilic cytoplasm and distinct intercellular bridges, (14) or they are basaloid cells with compact hyperchromatic nuclei and scanty amphophilic cytoplasm (34) (Figure 3). Nucleoli and mitoses are variably seen in both PEH and carcinomas and, therefore, cannot be used in differential diagnosis. Keratinizing PEH, as seen in chronic infections and halogenodermas, often exhibits keratolytic microabscess formation in the proliferating squamous epithelium and adjacent dermis. (15,19,31,33) That finding is not common in carcinomas. Similarly, basaloid PEH (eg, in association with dermatofibroma or nevus sebaceous) can be distinguished from BCC by attention to the supporting stroma. The former condition is associated with mature collagenous stroma, but BCC instead contains fibromyxoid tissue. Localized expansion of the epidermis is also evident in the prurigo nodularis form of PEH, sometimes with associated dermal neural hyperplasia. (11,12,34)
[FIGURE 5 OMITTED]
[FIGURE 6 OMITTED]
[FIGURE 7 OMITTED]
Verruciform or papillomatous PEH is difficult to separate diagnostically from verrucous squamous carcinoma. The latter lesion is still confused with nonneoplastic conditions because of the persistent use of such antiquated terms as giant condyloma of Buschke and Loewenstein (35) or pseudoepitheliomatous keratotic micaceous balanitis (36) to describe this unusual form of carcinoma. Verrucous carcinoma is characterized by its irregularly invasive interface with the dermis, featuring broad and interanastomosing tongues of mature keratinocytes that involve the dermis to variable depths (Figure 4, A). In contrast, PEH typically shows a relatively uniform, horizontal inferior border and discrete, elongated, acanthotic rete ridges (Figure 4, B). Attention to the macroscopic features of verrucous carcinoma is also critical diagnostically. (37)
Some authors have attempted to address difficult diagnostic cases in this general category by employing the term atypical pseudoepitheliomatous hyperplasia. (38) That designation is intended to convey an inability to decide whether or not a particular epidermal proliferation is benign or malignant. However, we believe that such a practice is inadvisable. As indicated by Johnston et al, (39) most examples of "atypical" PEHs behave aggressively and likely represent well-differentiated carcinomas.
PSEUDONEOPLASTIC MESENCHYMAL LESIONS
Pseudosarcomatous Fibroepithelial Polyps (Acrochordons)
Occasional, acquired cutaneous polyps, with the typical gross features of acrochordons, may demonstrate a marked degree of cytologic atypia. (40,41) One sees a core of fatty or hyalinized tissue admixed with pleomorphic stellate or fusiform cells, like those of pleomorphic lipoma, pleomorphic fibroma, vaginal pseudosarcomatous polyps, and some true sarcomas of deep soft tissue (Figure 5, A and B). The behavior of these lesions has been uniformly benign, and it is felt that the cellular atypia is probably degenerative in nature.
Proliferative Noninfectious Granulomatous Lesions Selected cutaneous granulomatous lesions feature an exuberant histiocytic proliferation that is mistaken for a neoplasm. In particular, isolated rheumatoid nodules or necrobiotic granulomas (deep granuloma annulare) have a decided potential for this mimicry, vis-a-vis the alternative diagnosis of epithelioid sarcoma. (42-48) All of these disorders favor the distal extremities in patient groups with similar demographic attributes. (49) They become manifest as painless or slightly tender nodules but are otherwise relatively nondescript clinically.
Histologically, epithelioid sarcoma and isolated necrobiotic granulomas may also be similar. In fact, the title of the seminal article on epithelioid sarcoma, by Enzinger, (50) emphasized that point. Each of these lesions shows a circumscribed aggregation of polygonal cells that demonstrate only modestly elevated nucleocytoplasmic ratios, vesicular chromatin, small nucleoli, variable mitotic activity, and amphophilic cytoplasm. A central lesional area of collagenolysis is potentially common to both (Figure 6, A and B), and palisading of the lesional cells may be evident. (47,48,50,51) The most effective means of separating epithelioid sarcoma and isolated necrobiotic granuloma is that of immunohistology. The tumor cells of epithelioid sarcoma are reactive to keratin, with or without epithelial membrane antigen and CD34 (Figure 6, C and D), whereas histiocytic elements in isolated necrobiotic granulomas instead are labeled by CD45, factor XIIIa, and CD163. (52,53)
Pseudoneoplastic Vascular Proliferations of the Skin
Interest in Kaposi sarcoma (KS) and other endothelial lesions of the skin has grown during the past 2 decades because of the impact of the human immunodeficiency virus epidemic. This focus has resulted in the recognition of pseudoneoplastic vascular proliferations.
Acroangiodermatitis.--The condition, which is known as acroangiodermatitis ofMali, dermatitis hemostatica, Bluefarb-Stewart syndrome,orpseudo-Kaposi sarcoma is a proliferative vascular reaction associated with stasis dermatitis. (54-58) Thus, this disorder is most common on the legs of older individuals, taking the form of red-blue macules and plaques; the latter description could also be applied to "classical" (Mediterranean) KS.
[FIGURE 8 OMITTED]
Microscopically, both acroangiodermatitis and KS may demonstrate proliferating spindle cells and extravasated erythrocytes. Nevertheless, acroangiodermatitis is not a disorganized vascular proliferation, as seen in KS. Likewise, it fails to show the formation of new blood vessels around preexisting ones (the "promontory" sign) or the intralesional hyaline globules, peritumoral lymphatic dilatation, or plasmacytosis commonly observed in KS. (57,58) Acroangiodermatitis lesions contain more hemosiderin pigment than those of KS, and the former condition exhibits a more fibromyxoid stroma (58) (Figure 7). Additionally, acroangiodermatitis is not immunoreactive for the herpesvirus 8 latent nuclear antigen 1, as seen in most KS cases. (59,60)
Reactive Angioendotheliomatosis and Intravascular Histiocytopathy.--In the past, the term angioendotheliomatosis was used to describe a condition that has now been renamed intravascular lymphomatosis (IVL). Therefore, if one chooses to continue using the diagnosis of angioendotheliomatosis, it must be carefully and fully explained in pathologic reports. Reactive angioendotheliomatosis (RAE) (67-71) shows the proliferation of only modestly atypical, endothelial cells in dermal blood vessels (Figure 8, A and B), accompanied by a perivascular pericytic proliferation71;in IVL, intravascular cells are anaplastic (Figure 8, C). (66) Both RAE and IVL may show the presence of intravascular microthrombi; however, these are thought to represent an etiologic factor in many cases of RAE, (72) possibly associated with cryoglobulinemia or vasculitis, whereas thrombi are a secondary feature of IVL. Reactive angioendotheliomatosis is a topographically and chronologically limited process; IVL has the characteristics of a progressive systemic malignancy. (66,71)
Although we believe that the cytologic features of IVL and RAE allow for a confident diagnostic separation, one can also confirm the lineages of these lesions with adjunctive studies. The proliferating cells of IVL are [CD45.sup.+] immunohistochemically, (64,65) whereas those of RAE are not. Conversely, immunostains for endothelial markers (CD31, CD34, FLI1, and others) confirm the endothelial identity of intravascular cells in RAE (.73,74)
[FIGURE 9 OMITTED]
A somewhat more difficult problem concerns the distinction between IVL and intravascular histiocytopathy, as potentially seen in patients with rheumatoid arthritis. (75,76) The luminal cells in both conditions are seen in venules or lymphatics (Figure 8, D); those in intravascular histiocytopathy are of monocyte-macrophage derivation, reflected by their variable immunoreactivity for CD45 and positivity for CD68 and CD163. (76,77)
Bacillary Angiomatosis.--Bacillary angiomatosis (BA) is a generic term used to describe pseudoneoplastic endothelial proliferations caused by infections with rickettsial and bacterial organisms. The most well-known of these are Bartonella species (henselae, quintana, bacilliformis), although some Afipia species (eg, A. felis) have also been implicated. (78-83)
The clinical disorders associated with such agents are represented by immunosuppression-related bacillary angiomatosis and peliosis, verruga peruana of Carrion disease (bartonellosis), and cat-scratch disease. (78,82-85) All of these conditions manifest the presence of lesions that can be confused with those of true vascular neoplasms, notably epithelioid hemangiomas and patch-stage KS with epithelioid tumor cells. There is a propensity for the specified organisms to infect endothelial cells in BA and to stimulate proliferation with epithelioid transformation.
Thus, on histologic grounds, the shared attribute of BA, epithelioid hemangiomas, and KS is that of cellular intravascular aggregates of plump endothelia. (78-80,85,86) However, as outlined by Adal et al, (78) there are more microscopic differences than similarities between these lesions. Cutaneous BA--including immunosuppression-related forms and verruga peruana--is demarcated from the surrounding dermis with a lobulated architectural pattern; the endothelial cells are polygonal (Figure 9, A and B), accounting for the alternative designation of epithelioid angiomatosis, (80) and may contain visible clumps of purplish granular microorganisms. These can be labeled with silver impregnation stains, such as the Steiner method (Figure 9, C). In BA, there are no hyaline globular inclusions, which are common in KS (Figure 9, D), and, on the other hand, intralesional neutrophilia is frequently seen in BA. That constellation of findings is also not typical of epithelioid hemangiomas (Figures 9, E).
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Mark R. Wick, MD; James W. Patterson, MD
Accepted for publication January 8, 2009.
From the Division of Surgical Pathology & Cytopathology, University of Virginia Medical Center, Charlottesville.
The authors have no relevant financial interest in the products or companies described in this article.
Reprints: Mark R. Wick, MD, University Hospital, University of Virginia Health System, 1215 Lee St, Room 3020, Charlottesville, VA 22908-0214 (e-mail: email@example.com).
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|Author:||Wick, Mark R.; Patterson, James W.|
|Publication:||Archives of Pathology & Laboratory Medicine|
|Date:||Mar 1, 2010|
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