EXTRAORDINARY CASE REPORT
Early Morphea Simulating Patch-Stage Mycosis Fungoides Masakazu Fujimoto, MD,*† Juliana L. Basko-Plluska, MD,* Vesna Petronic-Rosic, MD, MSc,* and Christopher R. Shea, MD*
Abstract: Morphea is a rare fibrosing condition of the skin and underlying tissues characterized histopathologically by thickened collagen bundles throughout the dermis, loss of adnexal structures, and “fat trapping.” In the early stages of morphea, the absence of the fully developed characteristic findings may cause diagnostic confusion for the practicing pathologist. The authors report an unusual case of early morphea misdiagnosed as patch-stage poikilodermatous mycosis fungoides (MF) based on the initial clinical, histopathologic, and molecular findings. However, as time elapsed, welldeveloped lesions revealed clinical and histopathologic features diagnostic of morphea. The authors report this case to illustrate that lesions of early morphea may simulate MF. Given the similarities in clinicopathologic presentation, dermatologists and dermatopathologists should be cautious not to inadvertently misinterpret early morphea as MF. Key Words: morphea, localized scleroderma, mycosis fungoides (Am J Dermatopathol 2015;37:409–412)
INTRODUCTION Morphea, or localized cutaneous scleroderma, is a rare fibrosing disorder of the skin and underlying tissues that affects children and adults equally.1 Early lesions of morphea present as erythematous to dusky violaceous patches and plaques. Over time, the lesions become indurated and eventually sclerotic with postinflammatory hyperpigmentation. The underlying etiology of morphea is unknown, although environmental factors and autoimmunity may play a role. Histopathologically, well-developed lesions are characterized by deposition of thickened and sclerotic collagen bundles throughout the dermis and extending into the subcutaneous fat. Loss of eccrine glands and blood vessels and “fat trapping” are common findings in late-stage morphea. In the early stages, however, the most frequent finding is the presence of a prominent lymphoplasmacytic infiltrate around the dermal blood vessels. The collagen bundles may appear swollen; however, there is no obvious fibrosis. These histopathologic findings are nonspecific and may cause diagnostic difficulty, raising the possibility of other dermatologic conditions, From the *Section of Dermatology, Department of Medicine, The University of Chicago Medicine, Chicago, IL; and †Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan. The authors declare no conflicts of interest. Reprints: Christopher R. Shea, MD, Section of Dermatology, Department of Medicine, The University of Chicago Medicine, 5841 South Maryland Avenue, MC 5067, L500, Chicago, IL 60637 (e-mail: cshea@medicine. bsd.uchicago.edu). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Am J Dermatopathol Volume 37, Number 5, May 2015
including cutaneous lymphoma.2 Here, we report an unusual case of early morphea mimicking patch-stage poikilodermatous mycosis fungoides (MF), both clinically and histopathologically.
CASE REPORT A 40-year-old African American woman presented to the dermatology clinic at the University of Chicago with an asymptomatic skin eruption of 2 months duration. Review of systems was negative. Physical examination revealed multiple annular erythematous plaques with fine scale and central poikiloderma (characterized by hypopigmentation and hyperpigmentation, with atrophy and telangiectases) measuring up to 5 · 5 cm in size on the lumbar region, bilateral breasts, and left shin (Fig. 1). There were no mucosal lesions or palpable lymphadenopathy. The clinical differential diagnosis included poikilodermatous MF, subacute cutaneous lupus erythematosus, and dermatomyositis. Skin biopsies were performed from 2 lesions on the breasts. Histopathologic examination demonstrated a superficial lichenoid and deep perivascular lymphoid infiltrate admixed with rare eosinophils and plasma cells. Slight papillary dermal fibrosis was present (Figs. 2A, B). Focally, lymphocytes with perinuclear haloes were arrayed as single units and in small collections resembling Pautrier microabscesses at the dermal–epidermal junction and higher levels of the epidermis (Fig. 2C). Lymphocyte nuclei were hyperchromatic and displayed notably convoluted outlines. Spongiosis was absent. A lymphoid immunohistochemical panel was performed. The epidermotropic lymphocytes strongly expressed CD3 and CD8 (Figs. 3A–C). The dermal lymphoid infiltrate comprised a mixed population of CD4-positive and CD8-positive cells. There was no
FIGURE 1. Patient at initial presentation with annular erythematous plaques with fine scale and central poikiloderma on bilateral breasts. www.amjdermatopathology.com |
409
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Fujimoto et al
Am J Dermatopathol Volume 37, Number 5, May 2015
FIGURE 2. Initial skin biopsy from a lesion on the breast revealed a superficial lichenoid and deep perivascular lymphocytic infiltrate (A and B) with several intraepidermal lymphocytes with perinuclear haloes and irregularity of the nuclear contour (C).
FIGURE 3. Immunohistochemical studies demonstrate the epidermotropic T cells to be positive for CD3 (A) and CD8 (C) and negative for CD4 (B).
significant deletion of CD5 and CD7 antigens. Only small clusters of dermal B lymphocytes were highlighted by anti-CD20 antibody. Even in the absence of deletion of pan–T-cell antigens, the diagnosis of patch-stage MF was suspected from the clinical and histopathologic findings,3 and molecular studies were performed. T-cell receptor (TCR) g and b gene rearrangements were analyzed by polymerase chain reaction (PCR) using the Invivoscribe BioMed 2 primers (www.InVivoScribe.com). The study demonstrated a monoclonal amplification pattern for TCR g on 1 specimen and a monoclonal amplification on a polyclonal background for TCR b on both specimens with the same-sized amplicon, consistent with a modest but readily detected monoclonal T-cell population. A diagnosis of MF, patch-stage (stage IA), was rendered. The patient was initially treated with triamcinolone 0.1% ointment without improvement. Subsequently, narrow-band UVB phototherapy was added; however, this had to be discontinued when the patient developed urticaria. Although left untreated for 6 months, the affected areas developed into hyperpigmented shiny indurated plaques (Fig. 4). An additional biopsy was performed at that time. Histopathologic examination demonstrated dense dermal sclerosis with entrapment of the eccrine glands and loss of the hair follicles (Fig. 5A). A perivascular infiltrate composed predominantly of lymphocytes and plasma cells was present at the dermal–subcutaneous junction. Notably, there was no epidermotropism, and the lymphocytes lacked significant nuclear atypia (Fig. 5B). The lymphoid infiltrate represented a mixed population composed predominantly of T lymphocytes, with 60% of the cells positive for CD4 and 30% positive for CD8. Fewer than 10% of the
infiltrate was composed of B lymphocytes expressing CD20. The PCR study on this specimen demonstrated polyclonal amplification patterns for both TCR g and b. Given these new findings, the diagnosis of a sclerosing dermatitis consistent with morphea was
410
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| www.amjdermatopathology.com
FIGURE 4. Patient at follow-up after 6 months with numerous shiny, hyperpigmented, and indurated plaques on bilateral breasts.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol Volume 37, Number 5, May 2015
Morphea Simulating Patch-Stage Mycosis Fungoides
FIGURE 5. A repeat skin biopsy demonstrates dense dermal sclerosis with loss of hair follicles and entrapment of the eccrine glands. There is a deep perivascular lymphoplasmacellular infiltrate involving the dermal–subcutaneous interface (A). Epidermotropism of lymphocytes is not identified (B).
made. Subsequently, the patient was started on a topical regimen of clobetasol 0.05% ointment and calcipotriene 0.005% cream, which led to partial resolution. Unfortunately, she was lost to follow-up and returned to clinic 3 years later. At that time, the lesions had increased in size. Within a few months of initiating UVA-1 phototherapy, the lesions resolved, leaving only postinflammatory hyperpigmentation.
DISCUSSION
Morphea is an inflammatory fibrosing skin disorder leading to sclerosis of the dermis and subcutis. Histopathologically, well-developed morphea shows deposition of thickened collagen bundles with loss of the adnexal structures. Diagnostic difficulties may arise in certain cases of early morphea where the findings are nonspecific and mimic other skin conditions. Cases of early morphea with histopathologic changes similar to those of MF have apparently not been previously reported in the literature. However, the converse situation of interstitial MF mimicking inflammatory morphea has been described.4 Interstitial plasma cells are more common in morphea than in MF, and this finding can be a helpful feature in this determination. Interface changes can be seen in both, but slight vacuolar interface changes, squamatization of the basal layer, and effacement of the rete ridges also favor morphea. However, these features are not always present, as illustrated by our case. In rendering a final diagnosis for our patient, a few additional diagnoses were considered. First, we considered the possibility that these findings represented MF simulating morphea, especially given the presence of a monoclonal Tcell population in addition to the initial histopathologic findings suggestive of MF. However, this seemed very unlikely given the patient’s benign clinical course and the findings on the repeat skin biopsy. Furthermore, although the presence of clonality is more likely to occur in the setting of an underlying malignancy, it is not synonymous with malignancy. Monoclonal populations of T lymphocytes have been observed in various inflammatory skin diseases, including lichen planus, contact dermatitis, pityriasis lichenoides et varioliformis acuta, and lichen sclerosus, among others, thus reducing the utility of this method in differentiating MF from inflammatory conditions.5,6 The presence of a small number of lymphocytes may cause pseudoclonality Copyright 2015 Wolters Kluwer Health, Inc. All rights reserved.
because of preferential amplification.7 In addition, it is well documented that immune response-related clonal lymphocyte expansion can occur in the setting of infection or autoimmunity.7 In our case, clonality may signify an exaggerated immune response to specific antigens, which may be implicated in the pathogenesis of morphea. Second, we considered the possibility of MF and morphea coexisting in the same patient, as there are a few case reports documenting the coexistence of MF with inflammatory dermatoses. Thus, the coexistence of patch-stage MF and interstitial granuloma annulare in the same patient was described8; cases of sclerodactyly and systemic sclerosis in association with MF have also been described.9,10 However, given the patient’s clinical course and the histopathologic findings from the repeat biopsy, this seemed less likely. Finally, lichen sclerosus is another inflammatory skin condition that can demonstrate T-cell clonality and mimic MF in its early stage.5,6 Epidermotropic T lymphocytes in lichen sclerosus are predominantly CD8 positive.11 Frequently, neoplastic T lymphocytes of the poikilodermatous variant of MF are CD8 positive.12 Such similarities between the two entities may cause early diagnostic confusion; however, the clinical course is very different. Although the possibility of lichen sclerosus was considered in our patient, this seemed less likely given the evolution of the lesions and the findings on the second biopsy, including the presence of deep dermal sclerosis. In summary, we report an unusual case of early morphea simulating patch-stage poikilodermatous MF clinically, histopathologically, and on a molecular basis. Skin biopsy specimens showing features of MF must be carefully interpreted to consider the possibility of an inflammatory condition. Especially in cases revealing a monoclonal population of T lymphocytes by PCR, the correct diagnosis may be overlooked without the proper clinical information. We believe that early morphea should be added to the list of cutaneous T-cell pseudolymphomas. REFERENCES 1. Fett N, Werth VP. Update on morphea: part I. Epidemiology, clinical presentation, and pathogenesis. J Am Acad Dermatol. 2011;64:217–228. 2. Ghatalia P, Porter J, Wroblewski D, et al. Primary cutaneous marginal zone lymphoma associated with juxta-articular fibrotic nodules in a teenager. J Cutan Pathol. 2013;40:477–484.
www.amjdermatopathology.com |
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Fujimoto et al
3. Pimpinelli N, Olsen EA, Santucci M, et al. Defining early mycosis fungoides. J Am Acad Dermatol. 2005;53:1053–1063. 4. Su LD, Kim YH, LeBoit PE, et al. Interstitial mycosis fungoides, a variant of mycosis fungoides resembling granuloma annulare and inflammatory morphea. J Cutan Pathol. 2002;29:135–141. 5. Citarella L, Masone C, Kerl H, et al. Lichen sclerosus with histopathologic features simulating mycosis fungoides. Am J Dermatopathol. 2005; 25:463–465. 6. Lukowsky A, Muche JM, Sterry W, et al. Detection of expanded T cell clones in skin biopsy samples of patients with lichen sclerosus et atrophicus by T cell receptor-gamma polymerase chain reaction assays. J Invest Dermatol. 2000;115:254–259. 7. Langerak AW, Groenen PJ, Brüggemann M, et al. Euro Clonality/ BIOMED-2 guidelines for interpretation and reporting of Ig/TCR clonality testing in suspected lymphoproliferations. Leukemia. 2012;26: 2159–2171.
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| www.amjdermatopathology.com
Am J Dermatopathol Volume 37, Number 5, May 2015
8. Koochek A, Fink-Puches R, Cerroni L. Coexistence of patch stage mycosis fungoides and interstitial granuloma annulare in the same patient: a pitfall in the clinicopathologic diagnosis of mycosis fungoides. Am J Dermatopathol. 2012;34:198–202. 9. Wei N, Foon KA. Sclerodactyly in a patient with mycosis fungoides. Arch Intern Med. 1985;145:139–140. 10. Yasuda M, Amano H, Yamanaka M, et al. Coincidental association of mycosis fungoides and occupational systemic sclerosis? J Dermatol. 2008;35:21–24. 11. Carlson JA, Grabowski R, Chichester P, et al. Comparative immunophenotypic study of lichen sclerosus: epidermotropic CD57+ lymphocytes are numerous—implications for pathogenesis. Am J Dermatopathol. 2000;22:7–16. 12. Abbott RA, Sahni D, Robson A, et al. Poikilodermatous mycosis fungoides: a study of its clinicopathological, immunophenotypic, and prognostic features. J Am Acad Dermatol. 2011;65:313–319.
Copyright 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Early Morphea Simulating Patch-Stage Mycosis Fungoides Masakazu Fujimoto, MD,*† Juliana L. Basko-Plluska, MD,* Vesna Petronic-Rosic, MD, MSc,* and Christopher R. Shea, MD*
Abstract: Morphea is a rare fibrosing condition of the skin and underlying tissues characterized histopathologically by thickened collagen bundles throughout the dermis, loss of adnexal structures, and “fat trapping.” In the early stages of morphea, the absence of the fully developed characteristic findings may cause diagnostic confusion for the practicing pathologist. The authors report an unusual case of early morphea misdiagnosed as patch-stage poikilodermatous mycosis fungoides (MF) based on the initial clinical, histopathologic, and molecular findings. However, as time elapsed, welldeveloped lesions revealed clinical and histopathologic features diagnostic of morphea. The authors report this case to illustrate that lesions of early morphea may simulate MF. Given the similarities in clinicopathologic presentation, dermatologists and dermatopathologists should be cautious not to inadvertently misinterpret early morphea as MF. Key Words: morphea, localized scleroderma, mycosis fungoides (Am J Dermatopathol 2015;37:409–412)
INTRODUCTION Morphea, or localized cutaneous scleroderma, is a rare fibrosing disorder of the skin and underlying tissues that affects children and adults equally.1 Early lesions of morphea present as erythematous to dusky violaceous patches and plaques. Over time, the lesions become indurated and eventually sclerotic with postinflammatory hyperpigmentation. The underlying etiology of morphea is unknown, although environmental factors and autoimmunity may play a role. Histopathologically, well-developed lesions are characterized by deposition of thickened and sclerotic collagen bundles throughout the dermis and extending into the subcutaneous fat. Loss of eccrine glands and blood vessels and “fat trapping” are common findings in late-stage morphea. In the early stages, however, the most frequent finding is the presence of a prominent lymphoplasmacytic infiltrate around the dermal blood vessels. The collagen bundles may appear swollen; however, there is no obvious fibrosis. These histopathologic findings are nonspecific and may cause diagnostic difficulty, raising the possibility of other dermatologic conditions, From the *Section of Dermatology, Department of Medicine, The University of Chicago Medicine, Chicago, IL; and †Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan. The authors declare no conflicts of interest. Reprints: Christopher R. Shea, MD, Section of Dermatology, Department of Medicine, The University of Chicago Medicine, 5841 South Maryland Avenue, MC 5067, L500, Chicago, IL 60637 (e-mail: cshea@medicine. bsd.uchicago.edu). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Am J Dermatopathol Volume 37, Number 5, May 2015
including cutaneous lymphoma.2 Here, we report an unusual case of early morphea mimicking patch-stage poikilodermatous mycosis fungoides (MF), both clinically and histopathologically.
CASE REPORT A 40-year-old African American woman presented to the dermatology clinic at the University of Chicago with an asymptomatic skin eruption of 2 months duration. Review of systems was negative. Physical examination revealed multiple annular erythematous plaques with fine scale and central poikiloderma (characterized by hypopigmentation and hyperpigmentation, with atrophy and telangiectases) measuring up to 5 · 5 cm in size on the lumbar region, bilateral breasts, and left shin (Fig. 1). There were no mucosal lesions or palpable lymphadenopathy. The clinical differential diagnosis included poikilodermatous MF, subacute cutaneous lupus erythematosus, and dermatomyositis. Skin biopsies were performed from 2 lesions on the breasts. Histopathologic examination demonstrated a superficial lichenoid and deep perivascular lymphoid infiltrate admixed with rare eosinophils and plasma cells. Slight papillary dermal fibrosis was present (Figs. 2A, B). Focally, lymphocytes with perinuclear haloes were arrayed as single units and in small collections resembling Pautrier microabscesses at the dermal–epidermal junction and higher levels of the epidermis (Fig. 2C). Lymphocyte nuclei were hyperchromatic and displayed notably convoluted outlines. Spongiosis was absent. A lymphoid immunohistochemical panel was performed. The epidermotropic lymphocytes strongly expressed CD3 and CD8 (Figs. 3A–C). The dermal lymphoid infiltrate comprised a mixed population of CD4-positive and CD8-positive cells. There was no
FIGURE 1. Patient at initial presentation with annular erythematous plaques with fine scale and central poikiloderma on bilateral breasts. www.amjdermatopathology.com |
409
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Fujimoto et al
Am J Dermatopathol Volume 37, Number 5, May 2015
FIGURE 2. Initial skin biopsy from a lesion on the breast revealed a superficial lichenoid and deep perivascular lymphocytic infiltrate (A and B) with several intraepidermal lymphocytes with perinuclear haloes and irregularity of the nuclear contour (C).
FIGURE 3. Immunohistochemical studies demonstrate the epidermotropic T cells to be positive for CD3 (A) and CD8 (C) and negative for CD4 (B).
significant deletion of CD5 and CD7 antigens. Only small clusters of dermal B lymphocytes were highlighted by anti-CD20 antibody. Even in the absence of deletion of pan–T-cell antigens, the diagnosis of patch-stage MF was suspected from the clinical and histopathologic findings,3 and molecular studies were performed. T-cell receptor (TCR) g and b gene rearrangements were analyzed by polymerase chain reaction (PCR) using the Invivoscribe BioMed 2 primers (www.InVivoScribe.com). The study demonstrated a monoclonal amplification pattern for TCR g on 1 specimen and a monoclonal amplification on a polyclonal background for TCR b on both specimens with the same-sized amplicon, consistent with a modest but readily detected monoclonal T-cell population. A diagnosis of MF, patch-stage (stage IA), was rendered. The patient was initially treated with triamcinolone 0.1% ointment without improvement. Subsequently, narrow-band UVB phototherapy was added; however, this had to be discontinued when the patient developed urticaria. Although left untreated for 6 months, the affected areas developed into hyperpigmented shiny indurated plaques (Fig. 4). An additional biopsy was performed at that time. Histopathologic examination demonstrated dense dermal sclerosis with entrapment of the eccrine glands and loss of the hair follicles (Fig. 5A). A perivascular infiltrate composed predominantly of lymphocytes and plasma cells was present at the dermal–subcutaneous junction. Notably, there was no epidermotropism, and the lymphocytes lacked significant nuclear atypia (Fig. 5B). The lymphoid infiltrate represented a mixed population composed predominantly of T lymphocytes, with 60% of the cells positive for CD4 and 30% positive for CD8. Fewer than 10% of the
infiltrate was composed of B lymphocytes expressing CD20. The PCR study on this specimen demonstrated polyclonal amplification patterns for both TCR g and b. Given these new findings, the diagnosis of a sclerosing dermatitis consistent with morphea was
410
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| www.amjdermatopathology.com
FIGURE 4. Patient at follow-up after 6 months with numerous shiny, hyperpigmented, and indurated plaques on bilateral breasts.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol Volume 37, Number 5, May 2015
Morphea Simulating Patch-Stage Mycosis Fungoides
FIGURE 5. A repeat skin biopsy demonstrates dense dermal sclerosis with loss of hair follicles and entrapment of the eccrine glands. There is a deep perivascular lymphoplasmacellular infiltrate involving the dermal–subcutaneous interface (A). Epidermotropism of lymphocytes is not identified (B).
made. Subsequently, the patient was started on a topical regimen of clobetasol 0.05% ointment and calcipotriene 0.005% cream, which led to partial resolution. Unfortunately, she was lost to follow-up and returned to clinic 3 years later. At that time, the lesions had increased in size. Within a few months of initiating UVA-1 phototherapy, the lesions resolved, leaving only postinflammatory hyperpigmentation.
DISCUSSION
Morphea is an inflammatory fibrosing skin disorder leading to sclerosis of the dermis and subcutis. Histopathologically, well-developed morphea shows deposition of thickened collagen bundles with loss of the adnexal structures. Diagnostic difficulties may arise in certain cases of early morphea where the findings are nonspecific and mimic other skin conditions. Cases of early morphea with histopathologic changes similar to those of MF have apparently not been previously reported in the literature. However, the converse situation of interstitial MF mimicking inflammatory morphea has been described.4 Interstitial plasma cells are more common in morphea than in MF, and this finding can be a helpful feature in this determination. Interface changes can be seen in both, but slight vacuolar interface changes, squamatization of the basal layer, and effacement of the rete ridges also favor morphea. However, these features are not always present, as illustrated by our case. In rendering a final diagnosis for our patient, a few additional diagnoses were considered. First, we considered the possibility that these findings represented MF simulating morphea, especially given the presence of a monoclonal Tcell population in addition to the initial histopathologic findings suggestive of MF. However, this seemed very unlikely given the patient’s benign clinical course and the findings on the repeat skin biopsy. Furthermore, although the presence of clonality is more likely to occur in the setting of an underlying malignancy, it is not synonymous with malignancy. Monoclonal populations of T lymphocytes have been observed in various inflammatory skin diseases, including lichen planus, contact dermatitis, pityriasis lichenoides et varioliformis acuta, and lichen sclerosus, among others, thus reducing the utility of this method in differentiating MF from inflammatory conditions.5,6 The presence of a small number of lymphocytes may cause pseudoclonality Copyright 2015 Wolters Kluwer Health, Inc. All rights reserved.
because of preferential amplification.7 In addition, it is well documented that immune response-related clonal lymphocyte expansion can occur in the setting of infection or autoimmunity.7 In our case, clonality may signify an exaggerated immune response to specific antigens, which may be implicated in the pathogenesis of morphea. Second, we considered the possibility of MF and morphea coexisting in the same patient, as there are a few case reports documenting the coexistence of MF with inflammatory dermatoses. Thus, the coexistence of patch-stage MF and interstitial granuloma annulare in the same patient was described8; cases of sclerodactyly and systemic sclerosis in association with MF have also been described.9,10 However, given the patient’s clinical course and the histopathologic findings from the repeat biopsy, this seemed less likely. Finally, lichen sclerosus is another inflammatory skin condition that can demonstrate T-cell clonality and mimic MF in its early stage.5,6 Epidermotropic T lymphocytes in lichen sclerosus are predominantly CD8 positive.11 Frequently, neoplastic T lymphocytes of the poikilodermatous variant of MF are CD8 positive.12 Such similarities between the two entities may cause early diagnostic confusion; however, the clinical course is very different. Although the possibility of lichen sclerosus was considered in our patient, this seemed less likely given the evolution of the lesions and the findings on the second biopsy, including the presence of deep dermal sclerosis. In summary, we report an unusual case of early morphea simulating patch-stage poikilodermatous MF clinically, histopathologically, and on a molecular basis. Skin biopsy specimens showing features of MF must be carefully interpreted to consider the possibility of an inflammatory condition. Especially in cases revealing a monoclonal population of T lymphocytes by PCR, the correct diagnosis may be overlooked without the proper clinical information. We believe that early morphea should be added to the list of cutaneous T-cell pseudolymphomas. REFERENCES 1. Fett N, Werth VP. Update on morphea: part I. Epidemiology, clinical presentation, and pathogenesis. J Am Acad Dermatol. 2011;64:217–228. 2. Ghatalia P, Porter J, Wroblewski D, et al. Primary cutaneous marginal zone lymphoma associated with juxta-articular fibrotic nodules in a teenager. J Cutan Pathol. 2013;40:477–484.
www.amjdermatopathology.com |
411
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Fujimoto et al
3. Pimpinelli N, Olsen EA, Santucci M, et al. Defining early mycosis fungoides. J Am Acad Dermatol. 2005;53:1053–1063. 4. Su LD, Kim YH, LeBoit PE, et al. Interstitial mycosis fungoides, a variant of mycosis fungoides resembling granuloma annulare and inflammatory morphea. J Cutan Pathol. 2002;29:135–141. 5. Citarella L, Masone C, Kerl H, et al. Lichen sclerosus with histopathologic features simulating mycosis fungoides. Am J Dermatopathol. 2005; 25:463–465. 6. Lukowsky A, Muche JM, Sterry W, et al. Detection of expanded T cell clones in skin biopsy samples of patients with lichen sclerosus et atrophicus by T cell receptor-gamma polymerase chain reaction assays. J Invest Dermatol. 2000;115:254–259. 7. Langerak AW, Groenen PJ, Brüggemann M, et al. Euro Clonality/ BIOMED-2 guidelines for interpretation and reporting of Ig/TCR clonality testing in suspected lymphoproliferations. Leukemia. 2012;26: 2159–2171.
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| www.amjdermatopathology.com
Am J Dermatopathol Volume 37, Number 5, May 2015
8. Koochek A, Fink-Puches R, Cerroni L. Coexistence of patch stage mycosis fungoides and interstitial granuloma annulare in the same patient: a pitfall in the clinicopathologic diagnosis of mycosis fungoides. Am J Dermatopathol. 2012;34:198–202. 9. Wei N, Foon KA. Sclerodactyly in a patient with mycosis fungoides. Arch Intern Med. 1985;145:139–140. 10. Yasuda M, Amano H, Yamanaka M, et al. Coincidental association of mycosis fungoides and occupational systemic sclerosis? J Dermatol. 2008;35:21–24. 11. Carlson JA, Grabowski R, Chichester P, et al. Comparative immunophenotypic study of lichen sclerosus: epidermotropic CD57+ lymphocytes are numerous—implications for pathogenesis. Am J Dermatopathol. 2000;22:7–16. 12. Abbott RA, Sahni D, Robson A, et al. Poikilodermatous mycosis fungoides: a study of its clinicopathological, immunophenotypic, and prognostic features. J Am Acad Dermatol. 2011;65:313–319.
Copyright 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
