Hyperplasia of hair follicles and other adnexal structures in cutaneous lymphoproliferative disorders: a study of 53 cases, including so-called pseudolymphomatous folliculitis and overt lymphomas.
ABSTRACT We studied 53 cutaneous lymphoproliferative disorders, all of which manifested hair follicle hyperplasia. There were 42 cases conforming to the description of pseudolymphomatous folliculitis (PLF) and 11 cases of authentic lymphomas including mycosis fungoides, CD30+ anaplastic large cell lymphoma, diffuse large B-cell lymphoma, B-cell small cell lymphoma/leukemia, and peripheral T-cell lymphoma, not otherwise specified. All patients with PLF clinically presented with a solitary nodule preferentially involving the face. Beside hair follicle hyperplasia, the typical features were a dense infiltrate of small well-differentiated lymphocytes, lymphoplasmacytoid cells, plasma cells, and epithelioid histiocytes forming tiny granulomas. Some unusual or worrisome features recognized included eccrine/apocrine duct hyperplasia, subcutis/muscle infiltration, lymphocyte "smudging," single file infiltration, and large atypical cells. Immunohistochemically, T-cell predominant cases dominated in the series. All 34 tested cases revealed a polyclonal pattern of kappa and lambda immunoglobulin (Ig) light chain expression. In 4 cases, scattered CD30+ cells were identified. Monoclonal rearrangements of T-cell receptor (TCR) and IgH genes were detected in 19 and 3 cases respectively, including 1 case with dual T-cell receptor/IgH rearrangement. Three of 30 tested cases proved positive for herpes simplex virus-1, whereas herpes simplex virus-2 always tested negative. Of 31 cases tested for Borrelia burgdorferi, 30 specimens were negative. In 9 cases, fluorescent in situ hybridization for t(11;18) and t(14;18) revealed none of the above translocations. The most common treatment modality was surgical removal. Forty patients with a mean follow-up of 3.7 years included 39 patients with no evidence of disease and 1 individual with local recurrence. The comparison of "clonal cases of PLF" and those with polyclonal population or in which clonality remained undetermined revealed no differences between the 2 groups in the clinical presentation, pathologic, and immunohistochemical features. We conclude that hyperplasia of hair follicles and other adnexa can be seen not only in the condition currently known as PLF, but also in genuine cutaneous lymphomas and may be just a happenstance secondary to a basic pathologic process.
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ABSTRACT: : Primary cutaneous T-cell lymphomas (CTCL) represent the majority of cutaneous lymphomas (CLs) and are a spectrum of diseases with a wide variety of clinical, histological, and phenotypic features and diverse biologic behavior. This review focuses on the observations on new variants of CTCL and recent developments in deciphering the pathogenetic mechanisms, which have implication for the nosologic concepts and future classification of CLs. Variants of mycosis fungoides (MF) such as the unilesional and the papular form have been characterized in more detail. Studies analyzed the expression of CD30 and PD-1 in MF and other forms of CTCL. New variants in the group of cutaneous CD30 lymphoproliferative disorders include the epidermotropic CD8 variant of lymphomatoid papulosis (type D) and angiocentric lymphomatoid papulosis (type E), which histologically mimic aggressive lymphomas, and therefore may be diagnostically challenging. Cutaneous proliferations of T cell-expressing markers of follicular helper T cells (PD-1, CXCL-13, and bcl-6) display a prognostically heterogeneous group. There is an increasing spectrum of CTCL with the expression of CD8 by tumor cells, including CD8 MF, CD8 forms of cutaneous CD30 lymphoproliferative disorders, and CD8 small/medium-sized lymphoproliferations, which are not included as distinct entities in the World Health Organization-European Organization for Research and Treatment of Cancer for CLs and the World Health Organization classification. Unusual presentations and incomplete phenotypes of blastic neoplasm of plasmacytoid dendritic cells are discussed. Clinicopathologic correlation is mandatory for the diagnosis of primary CLs. Analysis of genetic and epigenetic alterations in CLs revealed new diagnostic markers and putative targets for therapy of aggressive forms of CLs.The American Journal of dermatopathology 02/2014; 36(2):105-23. DOI:10.1097/DAD.0b013e318289b1db · 1.43 Impact Factor
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ABSTRACT: Background Pseudolymphomatous folliculitis is a lymphoid proliferation that clinically and histopathologically mimics primary cutaneous extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma). In this study we assessed the diagnostic value of three immunohistochemical markers, PD-1, CD1a, and S100.Methods We evaluated 25 cases of cutaneous lymphoid proliferations with established diagnoses, including 9 patients with pseudolymphomatous folliculitis, 11 with MALT lymphoma, and 5 with cutaneous lymphoid hyperplasia (CLH). The clinical, histopathologic, and immunohistochemical characteristics were reviewed and three major characteristics assessed: 1) proportion of T cells expressing PD-1, 2) pattern of expression of CD1a by dendritic cells, and 3) pattern of expression of S100 by dendritic cells.ResultsWe found pseudolymphomatous folliculitis to have a significant increase in PD-1+ T cells compared to MALT lymphoma (p < 0.0001). The pattern of CD1a staining is also informative: MALT lymphoma is significantly more likely to demonstrate a peripheral concentration of CD1a+ dendritic cells around lymphoid nodules than pseudolymphomatous folliculitis (p < 0.0003) or CLH (p < 0.05). Pseudolymphomatous folliculitis demonstrates an interstitial distribution of CD1a+ cells more often than MALT lymphoma (p < 0.04). S100 staining was not a helpful discriminator.Conclusions Histopathologic factors including PD-1 and CD1a staining patterns may allow for more certainty in distinguishing lymphoid hyperplasia, including pseudolymphomatous folliculitis, from MALT lymphoma.Journal of Cutaneous Pathology 11/2014; 42(1). DOI:10.1111/cup.12440 · 1.56 Impact Factor
Actas Dermo-Sifiliográficas 09/2012; 103(7):635–636. DOI:10.1016/j.ad.2011.11.009