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Parapsoriasis (small plaque and large plaque parapsoriasis)

Parapsoriasis (small plaque and large plaque parapsoriasis)
Literature review current through: May 2024.
This topic last updated: Aug 08, 2023.

INTRODUCTION — The term "parapsoriasis" refers to a heterogeneous group of uncommon dermatoses occurring mainly in older adults and characterized by erythematous and scaly patches of variable size, chronic course, and resistance to treatment [1,2]. It is broadly divided in two main types: small plaque parapsoriasis (SPP) and large plaque parapsoriasis (LPP). In both types, lesions are typically asymptomatic or accompanied by mild pruritus and are predominantly located on the trunk. While SPP is generally considered a chronic benign condition, LPP is regarded as a premalignant dermatosis with a substantial risk of progression to mycosis fungoides, the most common type of cutaneous T cell lymphoma. (See "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides", section on 'Premycotic period'.)

SPP and LPP will be discussed in this topic. Other cutaneous lymphoproliferative disorders and mycosis fungoides are discussed separately.

(See "Pityriasis lichenoides chronica".)

(See "Pityriasis lichenoides et varioliformis acuta (PLEVA)".)

(See "Lymphomatoid papulosis".)

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

EPIDEMIOLOGY — Small plaque parapsoriasis (SPP) and large plaque parapsoriasis (LPP) are rare disorders. Their exact incidence and prevalence are not known. Both SPP and LPP occur most commonly in middle-aged or older individuals; approximately two-thirds of patients are male [3].

ETIOLOGY AND PATHOGENESIS — The etiology and pathogenesis of small plaque parapsoriasis (SPP) and large plaque parapsoriasis (LPP) are unknown. Both are thought to be cutaneous T cell lymphoproliferative disorders. However, whether they are precursors of mycosis fungoides (MF) or early MF from the outset (the so-called premycotic stage) is still controversial. The superficial dermal infiltrate is composed primarily of CD4+ T cells. Dominant T cell clonality has been demonstrated in many cases of LPP and in a few cases of SPP, although the presence of a dominant T cell clone does not appear to increase the malignant potential of these dermatoses [4-10].

The hypothesis of a viral etiology for parapsoriasis has not been confirmed. Evidence of infection with lymphotropic viruses (eg, Epstein-Barr virus, cytomegalovirus, and human herpesviruses [HHV] 6 and HHV8) has not been found consistently in patients with parapsoriasis [11-16].

SMALL PLAQUE PARAPSORIASIS — Small plaque parapsoriasis (SPP) is a chronic, asymptomatic dermatosis characterized by the presence of small, persistent, scaly patches predominantly located on the trunk. Several terms have been used to describe this condition, including chronic superficial dermatitis, persistent superficial dermatitis, chronic superficial scaly dermatitis, and digitate dermatosis.

Clinical manifestations — SPP typically presents with pink or yellowish-brown macules or patches 2 to 5 cm in diameter (picture 1A-B). Macules and patches are often round or oval and variably scaly. The trunk, flanks, and proximal extremities are most commonly involved [2].

A distinctive variant of SPP called "digitate dermatosis" presents with elongated (digitate, finger-shaped) patches with an atrophic, cigarette-paper-like surface. Lesions are typically located on the flanks, along the skin cleavage lines (picture 2A-B).

SPP lesions are most often asymptomatic or mildly pruritic. They may fade or disappear after sun exposure during the summer, but typically recur during the winter months.

Histopathology — The histologic features of SPP are nonspecific and resemble those of a mild eczema. The epidermis manifests mild spongiosis (intercellular edema) with focal areas of parakeratosis, scale, and exocytosis of small lymphocytes with normal mature morphology (picture 3). In chronic lesions, the spongiosis is often absent and the epidermis develops a psoriasiform acanthosis [17]. The dermis shows edema, a sparse perivascular lymphocytic infiltrate, and dilation of the papillary vessels [17-19].

Immunostaining reveals a normal mature T cell phenotype, predominantly CD4+. In some cases, polymerase chain reaction studies demonstrate a dominant clonal pattern of T cells [5,7]. However, it is unclear if this finding is associated with an increased risk of progression to MF.

Diagnosis — The diagnosis of SPP is based upon the combination of clinical and histologic findings and clinical course:

Presence of asymptomatic, erythematous macules <5 cm in diameter mainly located on the trunk (picture 1A), especially if presenting as digitate lesions parallel to skin lines (picture 2A-B)

Histopathologic finding of nonspecific, superficial dermatitis (see 'Histopathology' above)

Persistence of the lesions over time and history of resistance to treatment

Multiple skin biopsies may be required if lesions of diverse morphology (eg, erythematous, atrophic, poikilodermatous) are present. Repeated biopsies over time also may be needed in difficult cases.

Differential diagnosis — The differential diagnosis of SPP includes:

Mycosis fungoides – The main differential diagnosis of SPP is with early mycosis fungoides (MF). In MF, lesions are usually larger (>5 cm in diameter) and less uniform in size, color, and shape than SPP lesions. Histology of early MF shows haloed atypical lymphocytes within the epidermis (epidermotropism), sometimes forming intraepidermal aggregates (Pautrier microabscesses), single lymphocytes arranged linearly along the dermoepidermal junction, vacuolar interface dermatitis, and dermal fibrosis [9]. (See "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides".)

Pityriasis lichenoides chronica – Pityriasis lichenoides chronica typically presents with recurrent crops of erythematous scaly papules that spontaneously regress over several weeks to months (picture 4). Histology shows a band-like lymphohistiocytic infiltrate. There is exocytosis, extravasation of erythrocytes, and focal parakeratosis. (See "Pityriasis lichenoides chronica".)

Guttate psoriasis – Guttate psoriasis presents with small, erythematous plaques with fine scale (picture 5A-B). Histology of early lesions demonstrates mild acanthosis, papillary dermal edema, capillary dilatation, and a sparse lymphocytic infiltrate. Older lesions show hyperkeratosis, parakeratosis, acanthosis, and collections of neutrophils in the epidermis (Munro microabscesses). (See "Guttate psoriasis".)

Pityriasis rosea – Pityriasis rosea typically presents in children and young adults with round or oval, sharply delimited, pink or salmon-colored lesions on the chest, neck, or back (picture 6A-D). The presence of a herald patch (picture 7A-B)and resolution within a few weeks to months differentiates pityriasis rosea from SPP. (See "Pityriasis rosea".)

Nummular dermatitis – Nummular dermatitis is characterized by intensely pruritic, coin-shaped lesions of eczematous dermatitis, with crusting and serous oozing on close inspection (picture 8A-B). (See "Overview of dermatitis (eczematous dermatoses)", section on 'Nummular eczema'.)

Management — Patients with SPP are usually asymptomatic and require minimal or no treatment. Scaling and mild pruritus may be controlled with emollients [20]. However, treatment is required for patients whose pruritus is not controlled with emollients or who have cosmetic concerns.

Initial therapy — For patients with SPP who require treatment, we suggest topical corticosteroids rather than simple emollients. We generally use moderate to high-potency corticosteroids (group two to four (table 1)) once or twice a day for 8 to 12 weeks. Emollients can be used liberally in conjunction with topical corticosteroids. The clearance of all skin lesions indicates a good response to treatment. Recurrence is common and may occur weeks to months after stopping the treatment. Recurrent lesions can be treated with another course of topical corticosteroids.

The use of topical corticosteroids for the treatment of SPP has not been evaluated in randomized trials. Their use is based upon clinical experience and indirect evidence of efficacy in inducing lesion regression in early MF [21,22]. (See "Treatment of early stage (IA to IIA) mycosis fungoides", section on 'Topical corticosteroids'.)

The long-term use of topical corticosteroids, particularly those belonging to the high- and super high-potency groups, may result in skin atrophy, telangiectasia, and striae. In addition, if applied to large skin surfaces, topical corticosteroids may result in systemic absorption and adrenal suppression. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

Poor response to initial therapy — For patients with unsatisfactory response to topical corticosteroids (eg, clearance of less than 50 percent of lesions), we suggest phototherapy with broadband or narrowband ultraviolet B (UVB) or, less frequently, psoralen plus ultraviolet A (PUVA). Phototherapy is generally administered two to three times per week for several months until clearance of lesions is achieved. The frequency of treatments is gradually tapered to once per week or less and then discontinued. (See "UVB phototherapy (broadband and narrowband)".)

There is limited evidence of efficacy of phototherapy in the treatment of SPP from small case series or single case reports [23-28]. The optimal length of treatment and the tapering schedule have not been determined. In one study including 14 patients with SPP, treatment duration of less than four months was associated with relapse in all patients after an average time of six months [26].

Monitoring — Given the chronic, benign course of SPP, patients with SPP can be monitored with yearly total body skin examination. Changing or progressing lesions should be biopsied because there are scattered reports of patients with an initial diagnosis of SPP who subsequently developed overt MF [3,5].

Prognosis — SPP may persist for years or decades and then resolves spontaneously. Most experts consider SPP to be a benign disorder without malignant potential. However, there are rare reports of patients with an initial diagnosis of SPP who subsequently developed MF [3,5].

LARGE PLAQUE PARAPSORIASIS — Large plaque parapsoriasis (LPP) is a chronic dermatosis characterized by the presence of fixed, large, atrophic, erythematous patches, usually located on the trunk. Other terms that have been used to describe LPP include poikiloderma vasculare atrophicans and parakeratosis variegata.  

Clinical manifestations — LPP presents with large (>5 cm in diameter), irregularly shaped, erythematous, dusky red or brown patches with fine scaling (picture 9A-D). Lesions frequently show epidermal atrophy ("cigarette paper" wrinkling) or poikiloderma (ie, the combination of mottled pigmentation, telangiectasia, and epidermal atrophy) (picture 10A-B). LPP typically involves areas not exposed to the sun (eg, buttocks, thighs, lower trunk, flexural surfaces, as well as breasts and inframammary areas).

Histopathology — The histopathology of LPP reveals (picture 11) [17]:

Variable psoriasiform epidermal hyperplasia (or atrophy in poikilodermatous areas [ie, areas with a combination of mottled pigmentation, telangiectasia, and epidermal atrophy])

Vacuolization in the basal keratinocyte layer

Capillary dilation

Brisk lymphocytic infiltrate with a band-like distribution that can obscure the dermoepidermal junction

The infiltrate is composed of small lymphocytes, some of which may have cerebriform, convoluted nuclei. There is focal lymphocytic epidermotropism, but Pautrier microabscesses (ie, clusters of atypical lymphocytes in the epidermis), a classic histologic characteristic of mycosis fungoides (MF), are usually absent in LPP [17,18].

Immunophenotyping demonstrates normal CD4/CD8 ratio and maintenance of the pan-T cell antigen CD7, a marker of mature T cells [29]. However, some studies have demonstrated that benign T cell infiltrates, including parapsoriasis, may lose CD7 expression [30,31]. Both small plaque parapsoriasis (SPP) and LPP have increased expression of the dendritic/Langerhans cell marker CD1a [32,33].

Most cases of LPP appear to express the thymocyte selection-associated high-mobility group box protein gene (TOX), a potential marker of MF [34]. However, whether TOX expression is a predictor of progression of LPP to MF or a marker to discriminate those LPP cases that are MF from the outset has not been determined. Cell adhesion molecule 1 (CADM1) has also been found to have upregulated expression in MF as compared with parapsoriasis and may be helpful for identifying a transformation into malignancy [35].

Clonal T cell receptor gene rearrangements have been identified by polymerase chain reaction analysis in up to 50 percent of LPP cases [4,8]. However, the presence of a predominant T cell clone is not diagnostic of LPP nor is an indication of increased risk of progression to MF.

Diagnosis — A careful clinicopathologic correlation is required for the diagnosis of LPP. Multiple skin biopsies may be required if lesions of diverse morphology (eg, erythematous, atrophic, poikilodermatous) are present. (See 'Clinical manifestations' above.)

A diagnosis of LPP is usually made in a patient presenting with multiple, asymptomatic erythematous, scaly, and slightly atrophic patches, mainly located on the trunk (picture 9A-D), showing on histopathologic examination features that are suspicious for MF (eg, dense band-like lymphocytic infiltrate at the dermoepidermal junction, focal epidermotropism) but do not fulfill the morphologic criteria for early MF [9,36]. The diagnosis may be especially difficult in those cases of LPP that show immunophenotypic and molecular features similar to early MF. (See 'Histopathology' above and "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides", section on 'Morphology'.)

Repeated biopsies over time are needed to monitor for possible progression to MF. (See 'Differential diagnosis' below.)

Differential diagnosis — The differential diagnosis of LPP includes:

Mycosis fungoides – The clinical differentiation of early (patch stage) MF and LPP may be difficult or impossible in some cases. Clinical monitoring and repeated skin biopsies often are required for definitive diagnosis. The primary patches of LPP are more likely to fade in the summer than the more persistent patches of early MF.

Histologically, MF is characterized by a papillary dermal infiltrate of small- to medium-sized atypical mononuclear cells with cerebriform nuclei, single-cell epidermotropism of atypical lymphocytes, or atypical lymphocytes forming intraepidermal aggregates (Pautrier microabscesses) (picture 12). Spongiosis (intercellular edema in the epidermis) is not a feature of MF.

However, some of these findings may be missing in early MF. Although there are no universally accepted minimal criteria for the diagnosis of MF, the International Society for Cutaneous Lymphoma and the European Organization of Research and Treatment of Cancer has devised an algorithm for the diagnosis of early MF based upon the integration of clinical, histopathologic, molecular, and immunophenotypic criteria (table 2) [9]. Cases that fail to meet any specific set of criteria for the diagnosis of early MF may be diagnosed as LPP. (See "Clinical manifestations, pathologic features, and diagnosis of mycosis fungoides", section on 'Diagnostic algorithm'.)

Contact dermatitis – Subacute or chronic allergic contact dermatitis (ACD) may be difficult to differentiate from LPP (picture 13). On histology, both diseases show minimal or absent spongiosis and lymphocytic exocytosis. However, history of allergen exposure, positive patch test results to suspected allergens, and response to treatment and avoidance measures support the diagnosis of ACD. (See "Clinical features and diagnosis of allergic contact dermatitis".)

Plaque psoriasis – In contrast with the flat lesions of LPP, the psoriasis plaques are erythematous with sharply defined margins raised above the surrounding normal skin (picture 14A-C). There is frequent involvement of elbows and knees, and nail pitting may be seen at close inspection (picture 15). Histology shows prominent epidermal hyperplasia, parakeratosis, neutrophilic exocytosis, and dilated vessels in dermal papillae, which are typically less prominent or absent in LPP. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Chronic plaque psoriasis'.)

Management — Patients with LPP require treatment to control pruritus if present and suppress the skin lesions. They also require close clinical monitoring because of the substantial risk of developing MF.

Patients for whom a clear-cut distinction between LPP and early MF cannot be made either clinically or histologically may be treated with skin-directed therapies as indicated for stage IA MF. (See "Treatment of early stage (IA to IIA) mycosis fungoides", section on 'Our approach'.)

Initial therapy — We suggest topical corticosteroids as initial treatment for patients with LPP. We typically use high- to super high-potency topical corticosteroids (groups one and two (table 1)) twice daily for 12 weeks and continue once daily or taper off if improvement is noted. Emollients can be used liberally in conjunction with topical corticosteroids.

The clearance of all or most skin lesions indicates a good response to treatment. If no response is observed after 12 weeks of treatment, topical corticosteroids should be stopped. Patients who do not respond to topical corticosteroids may be treated with phototherapy.

In patients who respond to topical corticosteroids, recurrence is common and may occur weeks to months after stopping the treatment. Recurrent lesions can be treated with another course of topical corticosteroids.

The use of topical corticosteroids for the treatment of LPP has not been evaluated in randomized trials. Indirect evidence of efficacy in inducing lesion regression is derived from observational studies of patients with patch stage MF [21,22]. (See "Treatment of early stage (IA to IIA) mycosis fungoides", section on 'Topical corticosteroids'.)

The long-term use of topical corticosteroids, particularly those belonging to the high- and super high-potency groups, may result in skin atrophy, telangiectasia, and striae. In addition, if applied to large skin surfaces, topical corticosteroids may result in systemic absorption and adrenal suppression. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

Extensive or recalcitrant disease — We suggest phototherapy with broadband or narrowband ultraviolet B (UVB) or, less frequently, psoralen plus ultraviolet A (PUVA) for the treatment of LPP in the following situations:

Patients with LPP who have extensive skin involvement, marked skin atrophy, or poikiloderma

Patients who fail to respond to topical corticosteroids (ie, clearance of less than 50 percent of lesions)

Patients who have disease progression

Phototherapy is generally administered two to three times per week for several months, until clearance of lesions is achieved. The frequency of treatments is gradually tapered to once per week or less and then discontinued. The benefits of a long-term maintenance treatment have not been evaluated. Recurrences may be treated by resuming the initial phototherapy schedule. (See "UVB phototherapy (broadband and narrowband)" and "Psoralen plus ultraviolet A (PUVA) photochemotherapy".)

There are no randomized trials or large observational studies of phototherapy for the treatment of LPP. Its use is based upon limited evidence of efficacy from small case series and indirect evidence of efficacy in early MF [37-39]. (See "Treatment of early stage (IA to IIA) mycosis fungoides", section on 'Phototherapy'.)

The short-term and long-term adverse effects of phototherapy are discussed in detail separately. (See "UVB phototherapy (broadband and narrowband)", section on 'Short- and long-term adverse effects' and "Psoralen plus ultraviolet A (PUVA) photochemotherapy", section on 'Adverse effects'.)

The use of topical nitrogen mustard (mechlorethamine) or topical carmustine has been described in patients with LPP, particularly those in whom LPP cannot clearly be distinguished from MF [40,41]. These agents and their adverse effects are discussed separately. (See "Treatment of early stage (IA to IIA) mycosis fungoides", section on 'Topical mechlorethamine' and "Treatment of early stage (IA to IIA) mycosis fungoides", section on 'Topical carmustine'.)

Monitoring — Patients with LPP require a close clinical monitoring because of the substantial risk of evolution to MF [3,42]. A total body skin examination ideally should be performed every six months. Patients should be counseled about the risk of developing MF and advised to seek medical attention if thicker plaques or nodules develop. There are no guidelines suggesting how often patients with LPP should be rebiopsied to detect a possible progression to MF. However, significant clinical change (eg, thicker plaques, increased atrophy, nodules, ulceration, an "ugly duckling" lesion) is an indication for biopsy. Additionally, presence of a cutaneous T cell clone in LPP may increase the risk of progression to MF [10].

Prognosis — LPP may persist for years or decades. In retrospective observational studies, approximately 10 to 30 percent of cases of LPP evolved to overt MF [2,3,42-44]. Patients with LPP may also have an increased risk of non-Hodgkin lymphomas other than MF and nonhematologic cancers [43]. Additionally, patients with parapsoriasis have been found to have an increased risk of venous thromboembolism [45].

SUMMARY AND RECOMMENDATIONS

Definition – Parapsoriasis, including small plaque parapsoriasis (SPP) and large plaque parapsoriasis (LPP) is a group of uncommon dermatoses occurring in adults and characterized by erythematous and scaly patches of variable size, chronic course, and poor response to treatment. (See 'Introduction' above and 'Epidemiology' above.)

Small plaque parapsoriasis:

Terminology – Several terms have been used to describe SPP, including chronic superficial dermatitis, persistent superficial dermatitis, chronic superficial scaly dermatitis, and digitate dermatosis.

Clinical presentation and diagnosis – SPP presents with round or oval erythematous patches <5 cm or elongated "digitate" lesions on the trunk and proximal extremities (picture 1A-B, 2A). The clinical diagnosis is supported by the histologic finding of a nonspecific dermatitis with spongiosis and a sparse perivascular lymphocytic infiltrate. (See 'Clinical manifestations' above and 'Diagnosis' above.)

Treatment – For most patients with SPP, treatment is not necessary. However, for patients who are symptomatic with pruritus or have cosmetic concerns, we suggest topical corticosteroids (Grade 2C). We generally use moderate to high-potency corticosteroids (groups two to four (table 1)) once or twice a day for 8 to 12 weeks. We suggest phototherapy with broadband or narrowband ultraviolet B (UVB) or psoralen plus ultraviolet A (PUVA) if topical corticosteroids are ineffective (Grade 2C). (See 'Management' above.)

Large plaque parapsoriasis:

Clinical presentation and diagnosis – LPP typically presents with erythematous lesions >5 cm, irregularly shaped, frequently atrophic or poikilodermatous, and typically localized in areas not exposed to the sun (eg, lower trunk, buttocks, and thighs) (picture 9A-D). The diagnosis is based upon the clinical presentation and the histologic finding of a dense dermal infiltrate of small lymphocytes, some of which have cerebriform nuclei, and focal single-cell epidermotropism. Differentiating LPP from early mycosis fungoides (MF) may be difficult. (See 'Clinical manifestations' above and 'Diagnosis' above and 'Differential diagnosis' above.)

Treatment – Patients with LPP require treatment to control pruritus and suppress the skin lesions. They also require close clinical monitoring since they have a substantial risk of developing MF:

-For patients with LPP who have limited areas of involvement and mild skin atrophy, we suggest topical corticosteroids rather than phototherapy as initial treatment (Grade 2C). We use high- to super high-potency topical corticosteroids (groups one and two (table 1)) twice daily for 12 weeks. (See 'Initial therapy' above.)

-For patients with LPP who have extensive skin involvement or skin atrophy or poikiloderma, we suggest phototherapy with broadband or narrowband UVB or PUVA rather than topical corticosteroids (Grade 2C). Phototherapy is also appropriate when there is a lack of response to initial treatment with topical corticosteroids or disease progression despite treatment with topical corticosteroids. Phototherapy is generally administered two to three times per week for several months, until clearance of lesions is achieved. (See 'Extensive or recalcitrant disease' above.)

Monitoring – Patients with LPP require a close clinical monitoring, ideally with a total body skin examination every six months, because of the substantial risk of evolution to MF. Significant clinical change (eg, thicker plaques, increased atrophy, nodules, atypical lesions) is an indication for biopsy. (See 'Monitoring' above.)

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Topic 15284 Version 13.0

References

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