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Cutaneous T cell pseudolymphomas

Cutaneous T cell pseudolymphomas
Author:
Rein Willemze, MD
Section Editor:
John A Zic, MD
Deputy Editor:
Rosamaria Corona, MD, DSc
Literature review current through: May 2024.
This topic last updated: Jul 19, 2023.

INTRODUCTION — The term "cutaneous pseudolymphoma" refers to a heterogeneous group of benign skin disorders that simulate cutaneous lymphomas histologically and sometimes clinically. Cutaneous pseudolymphomas can be separated into two major subtypes, pseudolymphomas mimicking a cutaneous B cell lymphoma and pseudolymphomas mimicking a cutaneous T cell lymphoma (table 1) [1-3].

This topic will focus on distinct clinicopathologic entities commonly included in the spectrum of cutaneous T cell pseudolymphomas. Other mimickers of early-stage mycosis fungoides (MF) or primary cutaneous CD30+ lymphoproliferative disorders, as well as human immunodeficiency virus (HIV)- and other immunodeficiency-related CD8+ cutaneous pseudolymphomas, will be briefly discussed. Cutaneous T cell lymphomas, lymphomatoid papulosis, and cutaneous B cell pseudolymphomas are discussed separately.

(See "Classification of primary cutaneous lymphomas".)

(See "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides".)

(See "Clinical presentation, pathologic features, and diagnosis of Sézary syndrome".)

(See "Primary cutaneous T cell lymphomas, rare subtypes".)

(See "Clinical manifestations, pathologic features, and diagnosis of systemic anaplastic large cell lymphoma (sALCL)".)

(See "Lymphomatoid papulosis".)

(See "Cutaneous B cell pseudolymphoma".)

OVERVIEW — Histologically, cutaneous T cell pseudolymphomas may show a superficial, band-like pattern simulating early patch/plaque-stage mycosis fungoides (MF) or a nodular or diffuse pattern simulating peripheral T cell lymphoma, not otherwise specified (PTCL, NOS) or tumor-stage MF. Examples of the first category include lymphomatoid contact dermatitis, lymphomatoid drug eruptions, and actinic reticuloid. Examples of the second category include persistent arthropod reactions and nodular scabies.

However, the cause is unknown in most cases. Such idiopathic cutaneous T cell pseudolymphomas may have a band-like, superficial pattern or a nodular or diffuse pattern.

ACTINIC RETICULOID — Actinic reticuloid, also called chronic actinic dermatitis, is a severe photosensitivity reaction to ultraviolet B (UVB) light, ultraviolet A (UVA) light, and (in some cases) visible light, with histologic features suggesting mycosis fungoides (MF) [4,5]. Actinic reticuloid is an extremely rare disorder and almost exclusively affects older adult men [6-8].

Clinical features — Patients with actinic reticuloid present with a pruritic, persistent, eczematous dermatitis with prominent lichenification and/or infiltrated papules and plaques involving sun-exposed skin areas (eg, face, neck, back of the hands, forearms, upper chest) (picture 1A-B). (See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Chronic actinic dermatitis'.)

Pathology — Histologic examination of a skin biopsy shows eczematous features including acanthosis, spongiosis, and variably dense dermal infiltrates of lymphocytes, histiocytes, eosinophils, plasma cells, and multinucleated dendritic cells [6,7]. These infiltrates contain atypical T cells with medium-sized to large cerebriform and hyperchromatic nuclei similar to those observed in MF and Sézary syndrome (picture 2). Exocytosis of atypical lymphocytes in the epidermis can be found.

In contrast to Sézary syndrome, most cases of actinic reticuloid show a CD8+ T cell phenotype (picture 3) [6]. Although there are reports of rare cases of erythrodermic cutaneous T cell lymphoma with severe photosensitivity and a CD8+ immunophenotype mimicking actinic reticuloid, progression of actinic reticuloid to cutaneous T cell lymphoma is unlikely [7,9].

Diagnosis — The diagnosis of actinic reticuloid is suspected in an older patient presenting with a persistent eczematous eruption affecting primarily the sun-exposed skin. The definitive diagnosis requires a skin biopsy for routine histology and immunophenotyping and the documentation of increased sensitivity (decreased minimum erythema dose [MED]) to UVB, often to UVB and UVA, and occasionally to visible light by phototesting [5,6,8]. Patch testing and photopatch testing may reveal positive reactions to one or more allergens, in particular fragrances and sesquiterpene lactone mix, in a significant number of patients [2,6]. (See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Chronic actinic dermatitis'.)

Differential diagnosis — Immunophenotyping and T cell receptor (TCR) gene rearrangement analysis are useful adjuncts to histopathologic examination to differentiate erythrodermic actinic reticuloid from Sézary syndrome. The latter is defined by the presence of clonally related CD4+ malignant T cells in the skin and peripheral blood, with a CD4:CD8 ratio greater than 10 in most cases [10]. In contrast, the skin infiltrates of actinic reticuloid show a predominant CD8+ T cell phenotype, and the peripheral blood often shows a low or even inverse CD4:CD8 ratio [6]. Clonal T cells are not detected in skin or blood of patients with actinic reticuloid [7,11]. (See "Clinical presentation, pathologic features, and diagnosis of Sézary syndrome".)

LYMPHOMATOID CONTACT DERMATITIS — In rare cases, allergic contact dermatitis may show histologic features simulating early-stage mycosis fungoides (MF). Since the term was first coined in 1976, only 23 cases have been reported [12-14].

Lymphomatoid contact dermatitis has been associated with various allergens, including metals (nickel sulphate, gold, cobalt), rubber chemicals, dyes, and preservatives. Patients present with pruritic erythematous patches or plaques that preferentially involve the abdomen, upper legs, and buttocks, as in early-stage MF [13]. A generalized eruption is rare.

Histologic examination of a skin biopsy shows a superficial, band-like infiltrate. The epidermis shows variable acanthosis and spongiosis and usually contains only few atypical T cells. Intraepidermal collections of Langerhans cells (CD1a+) and small T cells may be present but should not be misinterpreted as true Pautrier's microabscesses as observed in MF. In rare cases, clonal T cell receptor (TCR) gene rearrangements have been detected, but a polyclonal T cell population is present in most cases [13,14].

A positive patch test to a relevant allergen and the resolution of the skin lesion with avoidance of the offending allergen confirms the diagnosis of lymphomatoid contact dermatitis.

LYMPHOMATOID DRUG REACTION — Lymphomatoid drug eruptions are the most common mimickers of cutaneous T cell lymphomas. Based upon the clinical and histologic presentation, different types of lymphomatoid drug eruption can be distinguished:

Drug-induced pseudolymphoma syndrome (drug reaction with eosinophilia and systemic symptoms [DRESS] mimicking a cutaneous T cell lymphoma)

Drug reaction without systemic symptoms mimicking early-stage mycosis fungoides (MF) [15,16]

CD30+ lymphomatoid drug reaction [17-20]

Drug reaction with the histologic features of a B cell pseudolymphoma (uncommon) [21,22]

Lymphomatoid drug eruptions, including most cases of DRESS, usually resolve after withdrawal of the offending drug. Progression of lymphomatoid drug eruptions to true malignant lymphoma has been reported but is exceptional.

Drug-induced pseudolymphoma syndrome (DRESS mimicking cutaneous T cell lymphoma) — Several terms, including "drug-induced pseudolymphoma syndrome," "anticonvulsant hypersensitivity syndrome," or "drug-induced hypersensitivity syndrome," have been used to indicate severe drug reactions characterized by the combination of a generalized rash, fever, lymphadenopathy, hematologic abnormalities (eosinophilia; presence of atypical lymphocytes), visceral involvement, and histologic features mimicking a cutaneous malignant lymphoma in some cases.

The term "drug reaction with eosinophilia and systemic symptoms" (DRESS) is now widely used for these severe drug reactions, whether or not they present with histologic features suspicious for cutaneous lymphoma. DRESS is most commonly caused by anticonvulsants, allopurinol, sulfonamides, and antibiotics (table 2) [23]. (See "Drug reaction with eosinophilia and systemic symptoms (DRESS)".)

Some patients with DRESS may have clinical, histologic, and hematologic findings that raise suspicion of MF/Sézary syndrome, such as erythroderma, high numbers of circulating Sézary cells, and highly increased CD4:CD8 ratios. However, clonal T cell receptor (TCR) gene rearrangements are detected only in a small minority of these cases [24-27]:

In a study of 50 skin biopsies from 36 patients with DRESS, a lichenoid interphase dermatitis with atypical lymphocytes, sometimes resembling Sézary cells, was found in 14 [26]. In most cases these cells had the phenotype of CD8+, granzyme B+-activated T cells. T cell clonality was found in only one biopsy from a patient who also had a T cell clone in the blood.

In a prospective study of 117 patients with DRESS, 67 percent had circulating atypical T cells [23].

Drug-induced pseudo-Sézary syndrome with Sézary cell counts higher than 1000/mm3, CD4:CD8 ratio more than 10, and identical clonal TCR gene rearrangements in skin and peripheral blood has been reported in a patient treated with a combination of metoprolol and hydrochlorothiazide [25].

Drug eruptions without systemic symptoms simulating cutaneous T cell lymphoma — Many different drugs have been reported to cause MF-like or CD30+ lymphomatoid drug reactions with minimal or no systemic involvement. They include anticonvulsants, antidepressants, antihypertensives, beta blockers, calcium channel blockers, diuretics, antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), antihistamines, and biologics [2,17,28-31].

Clinical features — Patients with lymphomatoid drug eruption without systemic involvement may develop a solitary or multiple erythematous nodules or plaques several months after the initiation of the offending drug (picture 4) [16,27]. Lesions usually resolve after withdrawal of the offending drug. Progression of lymphomatoid drug eruptions to true malignant lymphoma has been reported but is exceptional [32].

Pathology — Histology of drug reactions without systemic symptoms mimicking cutaneous T cell lymphoma shows dense band-like infiltrates of small lymphocytes, histiocytes, and usually eosinophils, admixed with variable numbers of medium-sized atypical T cells with pleomorphic or cerebriform nuclei and/or variable numbers of CD30+ blast cells. In most cases these atypical cells have a CD4+ T cell phenotype [33]. Exocytosis of T cells is variable, and in some cases, pseudo-Pautrier's microabscesses containing small T cells, CD1a+ Langerhans cells, and (sometimes) eosinophils may be observed.

Genetics — Clonal TCR gene rearrangements have been found in a small number of lymphomatoid drug reactions [27,33]. In most cases, a polyclonal pattern is present.

IDIOPATHIC (SOLITARY) T CELL PSEUDOLYMPHOMA

Clinical features — Idiopathic T cell pseudolymphomas usually present as a solitary nodule or plaque most commonly located on the trunk or head (picture 5). Occasionally, two or more lesions may be present.

Pathology — Idiopathic T cell pseudolymphomas may show two distinct histologic patterns [34,35]:

Superficial, band-like pattern simulating plaque-stage mycosis fungoides (MF) – These lesions show a dense, superficial infiltrate characteristically showing sharply demarcated lateral and lower borders, and no or only focal infiltration of the epidermis (picture 6A-B). (See "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides".)

Nodular/diffuse pattern simulating tumor-stage MF or a peripheral T cell lymphoma, not otherwise specified (PTCL, NOS) – These lesions show dense, diffuse or nodular infiltrates within the dermis with a tendency to infiltrate the subcutis (picture 7). Epidermotropism is generally mild or absent. (See "Clinical manifestations, pathologic features, and diagnosis of peripheral T cell lymphoma, not otherwise specified".)

Both types of lesions show a predominance of small to medium-sized CD3+, CD4+, CD8-, and CD30- pleomorphic T cells. A small proportion of medium-sized to large pleomorphic cells may be present [34]. Characteristically, scattered medium-sized to large atypical T cells typically express programmed death-1 (PD-1), Bcl-6, and CXCL13, suggesting a common follicular helper T cell phenotype (picture 8) [36,37]. Scattered large B cells may be surrounded by PD-1+ T cells forming rosettes [37]. The proliferative rate is generally low. A considerable admixture of reactive CD8+ T cells, CD20+ B cells, plasma cells, and histiocytes, including multinucleated giant cells, can also be observed.

Genetics — Clonal T cell receptor (TCR) gene rearrangements are commonly found in idiopathic T cell pseudolymphomas [34,38]. In one study using the BIOMED-2 protocol [39], clonal TCR gene rearrangements were detected in 6 of 9 cases with a superficial, band-like pattern and 9 of 12 cases with a nodular to diffuse pattern [37].

Differential diagnosis

Other types of T cell pseudolymphoma — Dense atypical band-like infiltrates can also be found in other types of cutaneous T cell pseudolymphomas, such as lymphomatoid drug reactions without systemic symptoms [34,37]. A history of exposure to a high-risk medication (eg, antiseizure medications) and the resolution of the skin lesions after withdrawal of the offending drug help differentiate lymphomatoid drug reaction from idiopathic T cell pseudolymphoma.

Mycosis fungoides — Differentiation between idiopathic T cell pseudolymphomas and patch/plaque mycosis fungoides (MF) is generally not difficult but requires a careful clinicopathologic correlation [1]. Idiopathic T cell pseudolymphomas usually present with a solitary lesion mainly on the trunk (picture 5), whereas early-stage MF usually presents with patches and plaques preferentially on non-sun-exposed skin areas, such as the trunk and buttocks (picture 9).

Histologic differences between early-stage MF and idiopathic T cell pseudolymphomas include a nearly complete absence of epidermotropism, presence of scattered PD-1+ medium-sized to large atypical T cells, and a considerable admixture of reactive CD8+ T cells, CD20+ B cells, plasma cells, and histiocytes. The same cellular composition is observed in nodular T cell pseudolymphomas and facilitates the differentiation from tumor-stage MF and PTCL, NOS.

Moreover, the presence of more than 30 percent large T cells, the demonstration of loss of pan-T cell markers, a high proportion of proliferating cells (MIB-1+), and the clinical finding of concurrent patches and plaques strongly suggest a diagnosis of malignant lymphoma.

Primary cutaneous CD4+ small/medium T cell lymphoproliferative disorder — The clinical, histologic, and immunophenotypical characteristics of nodular idiopathic T cell pseudolymphomas are very similar, if not identical, to tumors previously classified as primary cutaneous CD4+ small/medium pleomorphic T cell lymphoma (PCSM-TCL) presenting with a solitary lesion. Histologic similarities include the presence of scattered medium-sized to large CD4+ T cells expressing PD-1, many admixed B cells, CD8+ T cells, and histiocytes, including multinucleated giant cells [37,40,41]. Clonal T cells are found in both conditions and are no longer considered a useful differential diagnostic criterion [37].

In the fifth edition of the World Health Organization (WHO) classification for tumors of hematopoietic and lymphoid tissues and in the International Consensus Classification of mature lymphoid neoplasms, these lesions are collectively termed "primary cutaneous CD4+ small/medium T cell lymphoproliferative disorder" [42,43]. (See "Classification of primary cutaneous lymphomas".)

Rare cases of PCSM-TCL that present with generalized skin lesions or rapidly growing bulky tumors, or show a high proliferative fraction, or a very low percentage of admixed CD8+ T cells, may have a more aggressive clinical course and are better considered as primary cutaneous PTCL, NOS [44]. (See "Clinical manifestations, pathologic features, and diagnosis of peripheral T cell lymphoma, not otherwise specified".)

Treatment and prognosis — Idiopathic T cell pseudolymphomas may resolve spontaneously after skin biopsy [34]. Persistent lesions can be treated with intralesional steroids or surgical excision, or in rare instances with radiotherapy [34,38].

Recurrence of idiopathic T cell pseudolymphoma is uncommon. Patients have an excellent long-term prognosis and do not require further examinations or staging [34,38].

LYMPHOMATOID KERATOSIS — Lymphomatoid keratosis is clinically and histologically very similar to the superficial mycosis fungoides (MF)-like type of idiopathic T cell pseudolymphoma [45]. It presents in older adults as a solitary scaly plaque that resembles seborrheic keratosis or actinic keratosis.

Histologic examination shows a dense band-like infiltrate, often with prominent epidermotropism mimicking MF. As in idiopathic T cell pseudolymphoma, there is a considerable admixture of small to medium-sized pleomorphic T cells with CD20+ B cells. Clonal T cells have been found in about half of the cases [45].

HIV- AND OTHER IMMUNODEFICIENCY-RELATED CD8+ CUTANEOUS PSEUDOLYMPHOMA — HIV-related CD8+ cutaneous pseudolymphoma is an inflammatory process resulting from a massive infiltration of the skin by activated, oligoclonal, HIV-specific CD8+ lymphocytes [46]. It has been reported in severely immunocompromised patients and was more common before the introduction of potent antiretroviral therapy (ART).

Patients present with pruritic erythematous plaques and nodules located in sun-exposed skin areas that may progress to generalized erythroderma [46,47]. Histologic examination shows a dense infiltrate of cytotoxic CD8+ T cells in the superficial dermis with variable degrees of epidermotropism and folliculotropism. Cellular atypia is usually mild and T cell clonality is generally not detected.

Regression of the skin lesion after the initiation of ART has been reported [48]. One patient with persistent lesions despite ART was successfully treated with low-dose methotrexate [49].

Similar atypical CD8+ T cell infiltrates, often associated with considerable numbers of histiocytes and/or granulomas, have been reported in patients with various types of immunodeficiency presenting with generalized papulonodular skin lesions [50-52]. In most cases, clonal T cells can be detected. In patients, particularly children, presenting with skin lesions showing clonal CD8+ T cell infiltrates, thorough investigations to detect a possible immunodeficiency should be performed.

OTHER MIMICKERS OF EARLY-STAGE MYCOSIS FUNGOIDES — Several benign, inflammatory dermatoses may show histologic features simulating early-stage mycosis fungoides (MF) in rare instances. These include, among others, lichen sclerosus, lichen aureus/pigmented purpuric dermatosis, and early (inflammatory) stage of vitiligo [53-56].

Common histopathologic findings include a superficial, band-like lymphoid infiltrate and variable infiltration of the lower layers of the epidermis. The infiltrates are predominantly composed of small, sometimes slightly atypical T cells, and clonal T cell receptor (TCR) gene rearrangements can be detected in some cases. A careful clinicopathologic correlation is essential and sufficient to make a correct diagnosis in most cases.

In a study of 121 cases of lichen sclerosus et atrophicus, histopathologic features mimicking MF were found in 88 of 94 cases (94 percent) of genital lichen sclerosus et atrophicus but not in any of 27 cases of extragenital lichen sclerosus et atrophicus [57]. Clonal TCR gene rearrangements were found in 16 of 33 tested cases.

The relationship between pigmented purpuric dermatosis and MF is discussed elsewhere. (See "Pigmented purpuric dermatoses (capillaritis)", section on 'Relationship to mycosis fungoides'.)

MIMICKERS OF PRIMARY CUTANEOUS CD30+ LYMPHOPROLIFERATIVE DISORDERS — CD30 is typically expressed by the neoplastic T cells of primary cutaneous CD30+ lymphoproliferative diseases such as lymphomatoid papulosis and cutaneous anaplastic large cell lymphoma. However, a wide variety of inflammatory and infectious skin diseases may contain CD30+ cells [28]. These include viral infections (eg, orf, milker's nodule, herpes virus infections, HIV infections), reactions to arthropod bites, nodular scabies, drug eruptions, and atopic dermatitis. (See "Lymphomatoid papulosis", section on 'Differential diagnosis'.)

SUMMARY AND RECOMMENDATIONS

Definition – The term "cutaneous pseudolymphoma" refers to a heterogeneous group of benign skin disorders that simulate cutaneous B and T cell lymphomas histologically and sometimes clinically (table 1). Histologically, cutaneous T cell pseudolymphomas may show a superficial, band-like pattern simulating early patch/plaque-stage mycosis fungoides (MF) or a nodular or diffuse pattern simulating peripheral T cell lymphoma, not otherwise specified (PTCL, NOS) or tumor-stage MF. (See 'Overview' above.)

Actinic reticuloid – Actinic reticuloid is a severe photosensitivity reaction with histologic features suggesting MF or Sézary syndrome. The predominance of CD8+ T cell phenotype and a normal or even reversed CD4:CD8 ratio in the peripheral blood help distinguish actinic reticuloid from a true lymphoma. (See 'Actinic reticuloid' above.)

Lymphomatoid allergic contact dermatitis – Rare cases of allergic contact dermatitis may show clinical and histologic features simulating early-stage MF. A positive patch test to a relevant allergen and the resolution of the skin lesion with avoidance of the offending allergen support the diagnosis of allergic contact dermatitis. (See 'Lymphomatoid contact dermatitis' above.)

Lymphomatoid drug eruptions – Some patients with drug reaction with eosinophilia and systemic symptoms (DRESS), a severe drug reaction predominantly caused by antiepileptics, allopurinol, sulfonamides, and antibiotics, may have clinical, histologic, and hematologic findings mimicking MF/Sézary syndrome. The resolution of symptoms after withdrawal of the offending drug supports the diagnosis. (See 'Lymphomatoid drug reaction' above.)

Idiopathic T cell pseudolymphoma – Idiopathic T cell pseudolymphomas usually present as a solitary nodule or plaque most commonly located on the trunk or head. They may have a band-like, superficial pattern or a nodular or diffuse pattern. The absence of epidermotropism, presence of scattered PD-1+ atypical T cells, and a considerable admixture of reactive CD8+ T cells, CD20+ B cells, plasma cells, and histiocytes in both superficial, band-like and nodular T cell pseudolymphomas facilitates the differentiation of idiopathic T cell pseudolymphomas from MF and PTCL, NOS. (See 'Idiopathic (solitary) T cell pseudolymphoma' above.)

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Topic 15723 Version 9.0

References

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