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Background
Lymphomatoid papulosis (LyP) is characterised clinically by recurrent papulonecrotic or papulonodular lesions with histological features of a malignant lymphoma. There are also CD 30+ cutaneous T cell lymphomas presenting clinically with solitary or few tumours or ulcers but with histologic features of lymphomatoid papulosis. It is likely the CD 30+ lymphoproliferative disorders represent a clinical and histologic spectrum with lymphomatoid papulosis at one end and T cell lymphoma on the other, with borderline cases in between.
There is a wide age range but the disease is most common in the 5th decade. The typical presentation is an asymptomatic red papule or nodule which may ulcerate or crust to leave a scar. The primary lesions often occur in crops and may take 3 weeks to months to resolve. These crops may number in the hundreds. Diffuse involvement with a predilection for the trunk, proximal extremities, palms, soles, face, and scalp may occur. If the lesions begin to ulcerate or enlarge to >1 cm in diameter, there should be a strong clinical suspicion of evolution to a malignant lymphoma.
OUTLINE
EPIDEMIOLOGY CHARACTERIZATION SYNONYMS LyP INCIDENCE/PREVALENCE Uncommon AGE 5th decade PEDIATRIC
Lymphomatoid Papulosis in Children: A Retrospective Cohort Study of 35 Cases.
Nijsten T, Curiel-Lewandrowski C, Kadin ME.
Department of Dermatology, the Division of Hematology/Oncology, Cutaneous Oncology Program, and the Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass. Drs Curiel-Lewandrowski and Nijsten equally contributed to this article. Dr Nijsten is now with the Department of Dermatology, University Hospital Antwerp, Edegem, Belgium.
Arch Dermatol. 2004 Mar;140(3):306-312. Abstract quote
BACKGROUND: Lymphomatoid papulosis (LyP) is a rare entity, considered to be part of the spectrum of the CD30(+) cutaneous lymphoproliferative disorders. About 10% to 20% of the adult LyP patients will develop an associated lymphoid malignancy. Only a few cases of LyP have been described in children, and the risk of associated lymphoid malignancies in these patients is not known.Objectives To study the association between childhood onset of LyP and other malignancies and to determine the clinical characteristics in this subgroup of patients.
DESIGN: Retrospective cohort study.
SETTING: Referral center at a university hospital. Retrospective registry for patients with LyP of childhood onset (</=18 years).Patients Thirty-five patients with childhood-onset LyP (19 boys and 16 girls) were interviewed by telephone using a standardized questionnaire. The median duration of follow-up was 9.0 years. All included patients were confirmed by histologic examination.
RESULTS: The age distribution was significantly different, with boys having an earlier onset of LyP (P =.03). Of the 35 LyP patients, 3 (9%) developed a malignant lymphoma; all were diagnosed as having non-Hodgkin lymphoma. Compared with the general population, patients with childhood-onset LyP have a significantly increased risk of developing non-Hodgkin lymphoma (relative risk, 226.2; 95% confidence interval, 73.4-697.0). More than two thirds of the patients reported being atopic, which is significantly more than the expected prevalence of atopy (relative risk, 3.1; 95% confidence interval, 2.2-4.3).
CONCLUSIONS: Lymphomatoid papulosis presents similarly in children and adults, including the risk of lymphoid malignancies. Therefore, all LyP patients should be closely monitored throughout their lives.
DISEASE ASSOCIATIONS CHARACTERIZATION HODGKIN'S DISEASE
Hodgkin's disease, lymphomatoid papulosis, and cutaneous T-cell lymphoma derived from a common T-cell clone.Davis TH, Morton CC, Miller-Cassman R, Balk SP, Kadin ME.
Department of Medicine, Beth Israel Hospital, Boston, MA 02215.
N Engl J Med 1992 Apr 23;326(17):1115-22 Abstract quote BACKGROUND. Lymphomatoid papulosis is a benign cutaneous eruption that in 10 to 20 percent of patients is associated with the development of lymphoma. The atypical cells of lymphomatoid papulosis histologically resemble the malignant cells of cutaneous T-cell lymphoma or the Reed-Sternberg cells of Hodgkin's disease. We studied a patient in whom lymphomatoid papulosis developed in 1971, Hodgkin's disease in 1975, and cutaneous T-cell lymphoma in 1985, to determine whether these diseases are clonally related.
METHODS. The T-cell-receptor alpha-chain gene was cloned and sequenced from a cell line derived from the advanced-stage cutaneous T-cell lymphoma, and the polymerase chain reaction was used to search for this rearrangement of the alpha-chain gene in tissues obtained earlier that were affected by Hodgkin's disease or lymphomatoid papulosis.
RESULTS. The tumor-specific rearrangement of the alpha-chain gene was detected in the patient's earlier tissues affected by lymphomatoid papulosis and Hodgkin's disease, but not in control tissue, including uninvolved tissues from the staging laparotomy for Hodgkin's disease. Cytogenetic studies revealed a translocation, t(8;9)(p22;p24), in cutaneous T-cell lymphoma lines and in a dermatopathic lymph node removed two years before the clinical onset of the cutaneous T-cell lymphoma. Immunohistochemical findings were consistent with an activated T-cell phenotype for the atypical cells of lymphomatoid papulosis, the Reed-Sternberg cells of Hodgkin's disease, and the malignant cells of the T-cell lymphoma.
CONCLUSIONS. Lymphomatoid papulosis, Hodgkin's disease, and cutaneous T-cell lymphoma can be derived from a single T-cell clone. A t(8;9) genetic translocation may be involved in the pathogenesis of lymphomatoid papulosis or its progression to malignant disease.
Lymphomatoid papulosis and Hodgkin's disease: are they related?Willemze R, Scheffer E, Van Vloten WA, Meijer CJ.
Arch Dermatol Res 1983;275(3):159-67 Abstract quote Two different characteristic types of lymphomatoid papulosis (type A and type B) can be histologically distinguished, that represent the ends of a spectrum. In the present report, two patients are described.
One patient with both lymphomatoid papulosis type A and type B lesions for more than 25 years developed Hodgkin's disease (nodular sclerosing type) in the para-aortic and para-iliac lymph nodes. Histologic examination of the skin lesions in the second patient, who had Hodgkin's disease (nodular sclerosing type) in many supradiaphragmatic lymph nodes, showed the characteristic features of lymphomatoid papulosis type A.
These findings, together with the results of recent immunohistochemical investigations showing many similarities between the large atypical cells in lymphomatoid papulosis type A lesions and Reed-Sternberg cells in Hodgkin's disease, support the view that lymphomatoid papulosis type A and Hodgkin's disease are closely related conditions.
The results of recent studies indicate a close relationship between lymphomatoid papulosis type B and the early stages of mycosis fungoides. Accordingly, the possible relationship between lymphomatoid papulosis types A and B, mycosis fungoides, and Hodgkin's disease is discussed.
MYCOSIS FUNGOIDES
Lymphomatoid papulosis associated with mycosis fungoides: a study of 21 patients including analyses for clonality.
Zackheim HS, Jones C, Leboit PE, Kashani-Sabet M, McCalmont TH, Zehnder J.
Department of Dermatology, University of California, San Francisco, CA, USA.
J Am Acad Dermatol. 2003 Oct;49(4):620-3 Abstract quote.
BACKGROUND: Although an association of lymphomatoid papulosis (LyP) with mycosis fungoides (MF) is recognized, our understanding of this relation is limited.
OBJECTIVE: We sought to document the clinical experience at the University of California, San Francisco, in 21 patients who had both LyP and MF and to do clonality studies in 7 of those patients in whom this was possible.
METHODS: We conducted chart review of the 21 patients and analysis for T-cell receptor-gamma gene rearrangements by the polymerase chain reaction.
RESULTS: Of 54 patients, 21 (39%) with LyP had associated MF. LyP preceded MF in 14 (67%), MF preceded LyP in 4 (19%), and there was concurrent appearance in 3 (14%). Of the 21 patients, 20 (95%) were type A and only 1 (5%) was type B. An identical clone was found in lesions of both LyP and MF in all 7 patients in whom analysis was possible.
CONCLUSION: Findings of this study strengthen the idea that LyP and MF are related T-cell lymphoproliferative disorders.PREGNANCY
Lymphomatoid papulosis associated with pregnancy.Yamamoto O, Tajiri M, Asahi M.
Department of Dermatology and Occupational Dermatopathology, University of Occupational and Environmental Health, Kitakyushu, Japan.
Clin Exp Dermatol 1997 May;22(3):141-3 Abstract quote We report a case of lymphomatoid papulosis which developed in a 29-year-old pregnant woman. She had numerous papules scattered over the inner aspect of the left thigh. Histology of the biopsy specimen demonstrated an atypical mononuclear cell infiltration of the dermis.
Spontaneous regression of the lesions occurred after termination of gestation. A possible effect of hormonal changes and alterations in T lymphocyte activity during pregnancy on the occurrence of lymphomatoid papulosis is discussed.
In 1968, Macaulay introduced the term lymphomatoid papulosis for a chronic self-healing skin lesion which was clinically benign and histologically malignant. Clinically, lymphomatoid papulosis consists of involuting and recurring papules, plaques and nodules. Histopathologically, the lesion is characterized by an atypical lymphoid infiltrate which resembles malignant lymphoma. Immunohistochemically, the atypical lymphoid cells bear T-cell markers and are characterized by the expression of Ki-1 or CD30.
We describe the first case of typical lymphomatoid papulosis which developed during pregnancy.
PATHOGENESIS CHARACTERIZATION APOPTOSIS
- Death Receptor Apoptosis Signaling Mediated by FADD in CD30-Positive Lymphoproliferative Disorders Involving the Skin.
Clarke LE, Bayerl MG, Bruggeman RD, Mauger D, Ioffreda MD, Abou-Elella A, Helm KF.
From the Departments of *Pathology, daggerDermatology, and double daggerHealth Evaluation Sciences, Penn State University College of Medicine/Milton S. Hershey Medical Center, Hershey, PA.
Am J Surg Pathol. 2005 Apr;29(4):452-459. Abstract quote
BACKGROUND:: The CD30-positive lymphoproliferative disorders lymphomatoid papulosis (LyP), primary cutaneous anaplastic large cell lymphoma (C-ALCL), and systemic anaplastic large cell lymphoma (S-ALCL) are lesions that overlap clinically, histopathologically, and immunophenotypically. Their biologic behaviors, however, vary considerably. In particular, lesions of LyP regress spontaneously while those of S-ALCL persist and often progress. Apoptosis has been suggested as the mechanism by which the lesions of LyP regress, but the underlying signaling pathways remain unclear. In this study, we used newly developed activation state-specific antibodies to demonstrate apoptosis signaling through the death receptor-mediated pathway regulated by FADD and caspase 3.
METHODS:: Dual immunohistochemistry for CD30 and activated forms of FADD and caspase 3 was performed on cutaneous biopsy specimens from 27 patients with CD30-positive lymphoproliferative disorders involving the skin. The patients included 18 with primary cutaneous CD30-positive LPDs (15 with LyP and 3 with C-ALCL) and 9 with S-ALCL.
RESULTS:: The proportion of CD30-positive cells expressing activated FADD was significantly different between primary cutaneous CD30-positive lymphoproliferative disorders and S-ALCL (36.4% vs. 14.5%, P = 0.0083). Expression of cleaved caspase 3 was also significantly different between primary cutaneous lesions and S-ALCL (9.2% vs. 1.9%, P = 0.048).
CONCLUSIONS:: Although a larger number of cases should be studied to validate these results, these data provide evidence that differences in signaling through the death-receptor apoptosis pathway mediated by FADD may be responsible for the varying biologic behaviors of CD30-positive lymphoproliferative disorders involving the skin.Loss of growth regulation for LyP Mol Cell Biol 1996;16:3480-3489
Blood 1999;94:2854-2861
Progression of the T-cell clone associated with loss of growth regulation by transforming growth factor beta because of mutations within the transforming growth factor beta receptor complex
Proapoptotic and antiapoptotic markers in cutaneous T-cell lymphoma skin infiltrates and lymphomatoid papulosis.Nevala H, Karenko L, Vakeva L, Ranki A.
Department of Dermatology and Venereal Diseases, Helsinki University Central Hospital, Finland.
Br J Dermatol 2001 Dec;145(6):928-37 Abstract quote BACKGROUND: In cutaneous T-cell lymphoma (CTCL) lesions, both reactive T cells and malignant T cells intermingle. The disease progression is mostly slow. Recent evidence suggests that even if clinical remission is reached, malignant cells persist and a relapse follows sooner or later. To wha extent tumour cell apoptosis occurs in the skin lesions either due to the reactive T cells or t therapeutic efforts is not known.
OBJECTIVES: To determine the extent of tumour cell apoptosis and the expression of proapoptotic an antiapoptotic markers in serial skin lesion samples from patients with CTCL, and to compare th findings with those in patients with lymphomatoid papulosis (LyP).
METHODS: Thirty-four skin samples were obtained from 12 patients with CTCL at the time o diagnosis and at a mean of 1.6, 3 and 6 years later. The patients received psoralen plus ultraviolet (PUVA), electron beam or cytostatic treatments. In addition, fresh post-treatment samples fro three patients with CTCL undergoing PUVA therapy were obtained. For comparison, skin biopsies o five patients with LyP were studied. Immunohistochemical demonstration of the expression of th following markers was performed on formalin-fixed skin sections: Fas (CD95), Fas ligand (FasL) bcl-2, granzyme B, the tumour-suppressor protein PTEN and the effector caspase, caspase-3. Th malignant cells were identified morphologically, and apoptotic cells were identified with th terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling method on parallel sections.
RESULTS: In untreated CTCL lesions, apoptotic lymphocytes were extremely rare, and no increase in the number of apoptotic cells was observed after any of the treatments used. In LyP, apoptotic cell were more frequent, comprising on average 5% of the infiltrate. The apoptosis-associated marker Fas, FasL, caspase-3 and granzyme B were expressed by morphologically neoplastic cells in CTCL and by large atypical cells in LyP, with no significant differences. However, only a few reactive cell in CTCL infiltrates expressed granzyme B while about 10% of the corresponding cells were positive in LyP. The expression of antiapoptotic bcl-2 was more frequent in CTCL than in LyP, while PTE expression was high in both instances. The number of bcl-2 + cells tended to decrease after therapy When comparing the findings between the first and the last samples, a decrease in the number of bcl-2+ cells and an increase in Fas+ cells was associated with disease progression, despite therapy, while the opposite was true for remissions.
CONCLUSIONS: Apoptosis was found to be a rare event in CTCL lesions irrespective of precedin therapy During patient follow-up, no significant differences in the expression of apoptotic marker was observed while in most cases a lower level of antiapoptotic bcl-2 expression was observed after all types of therapies and in association with disease progression when compared with high expression in the untreated lesions. The absence of apoptosis and high expression of bcl-2 together with a low expression of apoptosis-inducing granzyme B in the reactive lymphocytes in CTC could explain the chronic nature of the disease and the poor response to therapy, while th more frequent occurrence of granzyme B and apoptosis together with a lower level of expressio of bcl-2 by the large atypical cells in LyP could contribute to the favourable outcome of the latter.
VIRAL ETIOLOGY Am J Pathol 1985;119:315
Viral like particles have been identified in LyP lesionsHuman Herpesvirus 6,7, and 8 in LyP J Cutan Pathol 2001;28:29-33
No evidence for etiologic role
These viruses were suspected because HHV6 and 7 and T-lymphotropic viruses and both have been found in Hodgkin's lymphoma tissue, a disease that occurs in 5% of LyP patientsStudy performed using PCR
Human Herpesvirus 8 in LyP Lancet 1997;348:475
PCR amplified sequences of this virus in 2/4 cases of LyPEPSTEIN-BARR VIRUS Arch Dermatol 1996;132:279
No etiologic roleExpression of cutaneous lymphocyte-associated antigen and TIA-1 by lymphocytes in pityriasis lichenoides et varioliformis acuta and lymphomatoid papulosis: immunohistochemical study
Kyoung-Ae Jang1, Jung-Chul Choi2 and Jee-Ho Choi2 1
Department of Dermatology, Seoul Paik Hospital, Inje-Univeristy, Seoul, Korea, 2 Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea
J Cutan Pathol 2001;28 (9), 453-459 Abstract quote
Background: Pityriasis lichenoides et varioliformis acuta (PLEVA) and lymphomatoid papulosis (LyP) are benign self-healing cutaneous eruptions that may be clinically and histologically similar. The purposes of this study were to evaluate immunohistological characteristics of PLEVA and LyP and to investigate whether Epstein-Barr virus (EBV) may be present in PLEVA and LyP.
Methods: We performed an immunohistochemical staining in 12 cases of PLEVA and 8 cases of LyP using nine antibodies for CD3, CD4, CD8, CD30, CD45RO, CD56, CD79, cutaneous lymphocyte-associated antigen (CLA), and TIA-1. In situ hybridization was performed using fluorescein-conjugated oligonucleotide probes for EBV early regions (EBER).
Results: In PLEVA, immunohistochemical studies revealed that infiltrated lymphocytes consisted of mainly CD3-positive (5+), CD8-positive (4+~5+), CLA-positive (4+~5+) T cells and partly CD79 positive (+~2+) B cells. CD4-positive T cells were less than 25%. In LyP, immunohistochemical studies revealed that infiltrated lymphocytes consisted of partly CD3-positive (5+), CD8-positive (2+~3+), CLA-positive (3+~4+) T cells and partly CD79-positive (2+~3+) B cells. CD4-positive T cells were less than 10%. CD8 and CLA were more strongly expressed in PLEVA than in LyP. CD30 was strongly expressed in LyP but not expressed in PLEVA. CD79 was more expressed in LyP than in PLEVA. TIA-1 was not expressed in any cases. In situ hybridization using antisense EBER probe showed negative reaction in all cases.
Conclusions: Immunohistochemical stains for CD8, CD30, CD79 and CLA may be valuable tools in the differential diagnosis between PLEVA and LyP. TIA-1 was negative in LyP, which means cytotoxic cells may not be implicated in the pathogenesis of LyP. It was a contradictory result to the previous results. The absence of EBV in PLEVA and LyP suggests that this virus may not be operative in the pathogenesis of these diseases. These results suggest that LyP and PLEVA are separate disorders, thus accounting for their variable prognosis.
Jun B
- JunB expression is a common feature of CD30+ lymphomas and lymphomatoid papulosis.
Rassidakis GZ, Thomaides A, Atwell C, Ford R, Jones D, Claret FX, Medeiros LJ.
1Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Mod Pathol. 2005 Oct;18(10):1365-70. Abstract quote
JunB is a member of the Jun family of proteins that are components of the AP-1 transcription factor complex. AP-1 is involved in cell proliferation and apoptosis. Recent evidence suggests that Hodgkin and Reed-Sternberg cells overexpress JunB and that JunB facilitates constitutive CD30 expression by binding to an AP-1 site in the CD30 promoter.
In this study we surveyed JunB expression in a variety of CD30+ lymphoma types including 42 cases of anaplastic large cell lymphoma, 36 classical Hodgkin lymphoma, 15 cutaneous anaplastic large cell lymphoma, and 11 CD30+ diffuse large B-cell lymphoma. In addition, seven cases of nodular lymphocyte-predominant Hodgkin lymphoma and 42 diffuse large B-cell lymphoma, known to be CD30-, were analyzed. JunB expression was assessed using tissue microarrays, immunohistochemistry and a monoclonal antibody specific for JunB. Expression of JunB was observed in 41 of 42 cases of anaplastic large cell lymphoma, including all 21 cases positive for anaplastic lymphoma kinase and 20 of 21 (95%) negative for anaplastic lymphoma kinase. JunB was also expressed in all cases of classical Hodgkin lymphoma, cutaneous anaplastic large cell lymphoma and CD30+ diffuse large B-cell lymphoma, and in lymphomatoid papulosis. By contrast, all nodular lymphocyte-predominant Hodgkin lymphomas and diffuse large B-cell lymphomas that were CD30- were also JunB-.
We conclude that JunB is expressed in virtually all CD30+ lymphomas and is a potential target for experimental therapy in patients with these tumors.PROGRESSION OF DISEASE FROM Lyp TO SYSTEMIC LYMPHOMA
Fascin expression in CD30-positive cutaneous lymphoproliferative disorders.Kempf W, Levi E, Kamarashev J, Kutzner H, Pfeifer W, Petrogiannis-Haliotis T, Burg G, Kadin ME.
Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA 02215, USA, Department of Dermatology, University Hospital, Zurich, Switzerland, Dermatopathologisches Gemeinschaftlabor, Friedrichshafen, Germany.
J Cutan Pathol 2002 May;29(5):295-300 Abstract quote Background: CD30-positive cutaneous lymphoproliferative disorders (LPD) represent a spectrum of diseases ranging from low-grade (lymphomatoid papulosis; LyP) to high-grade (pleomorphic and anaplastic large-cell lymphoma; PTL, ALCL) with overlapping morphologic and immunophenotypic features. The common phenotypic hallmark is the expression of CD30-antigen by the tumor cells which morphologically resemble Reed-Sternberg cells. Although LyP is a non-fatal recurring disorder, it is associated with systemic lymphomas including Hodgkin's lymphoma (HL), mycosis fungoides (MF) and ALCL in 5-20% of the cases. Currently there is no marker to predict the development of systemic lymphomas in patients with LyP. Fascin, an actin bundling protein, has recently been shown to be a unique marker found in almost 100% of classical HL.
Methods: Because of the association of LyP with HL, fascin expression was analyzed by immunohistochemistry in LyP (n = 45), cutaneous CD30+ ALCL (n = 17) and pleomorphic T-cell lymphoma (n = 9) (PTL) and LyP associated with systemic lymphomas (7 HL, 2 ALCL, 1 MF), with the intent to determine if fascin expression can predict disease progression.
Results: Fascin was expressed by tumor cells in 11/45 (24%) cases of LyP, 11/17 (64%) cases of ALCL, 7/9 (77%) cases of PTL and 6/10 (60%) cases of LyP associated with systemic lymphomas. Fascin expression in LyP was significantly less frequent than in ALCL (p < 0.001) and also than in LyP associated with lymphomas (p < 0.05). There was no significant difference of fascin expression within the histological subtypes of LyP. We found no evidence of ALK expression nor of Epstein-Barr virus expression in any case either by in situ hybridization or immunohistochemistry in the LyP cases associated with HL.
Conclusions: This is the first study to demonstrate that fascin is expressed in cutaneous CD30+ LPD and that it is a candidate marker of disease progression in LyP.
Progression of lymphomatoid papulosis to systemic lymphoma is associated with escape from growth inhibition by transforming growth factor-beta and CD30 ligand.
Kadin ME, Levi E, Kempf W.
Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
Ann N Y Acad Sci 2001 Sep;941:59-68 Abstract quote
Our objective is to understand the mechanism of progression of lymphomatoid papulosis (LyP) to CD30+ systemic lymphoma. LyP lesions appear in recurrent crops that regress, only to reappear at a later date in the same or different locations. About 10% of patients develop systemic lymphoma.
Because transforming growth factor-beta (TGF-beta) and CD30 ligand inhibit the growth of normal lymphocytes and can be detected in regressing lesions of LyP, we tested the effect of these cytokines on cell lines clonally derived from LyP in the progression to systemic lymphoma. TGF-beta failed to inhibit the growth of lymphoma cells from advanced disease due to mutations of the TGF-beta receptor complex that prevented binding of the ligand to tumor cells. A CD30 ligand agonist antibody caused proliferation of tumor cells from one patient and had no effect on tumor cells of another. In contrast, a Fas agonist antibody caused significant growth inhibition of all cell lines.
The results suggest that progression of LyP to lymphoma is associated with escape of lymphoma cells from growth regulation by TGF-beta and CD30 ligand.
LABORATORY/
RADIOLOGIC/
OTHER TESTSCHARACTERIZATION RADIOLOGIC LABORATORY MARKERS T-CELL CLONALITY
- T-cell clonality of peripheral blood lymphocytes in patients with lymphomatoid papulosis.
Schultz JC, Granados S, Vonderheid EC, Hwang ST.
Dermatology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA.
J Am Acad Dermatol. 2005 Jul;53(1):152-5. Abstract quote
Six patients with lymphomatoid papulosis demonstrated a clonal T-cell population in skin lesions by polymerase chain reaction methods.
Two of these patients showed identical T-cell clones in their peripheral blood T cells as well.
In one case, the clone persisted in the blood despite clearing of skin lesions with methotrexate.
GROSS APPEARANCE/
CLINICAL VARIANTSCHARACTERIZATION GENERAL VARIANTS ACRAL AND ANOGENITAL LyP occurring on the palms, soles, and anogenital areas Blood 1997;90:354-71.
Am J Dermatopathol 1996;18:221-35.
Pediatr Dermatol 1998;15:146-7.
Arch Dermatol 1997;133:1453-6.
Exceptionally occurs at other sites such as palms, soles, and anogenital area.2,3,6,7HYDROA VACCINIFORME-LIKE Hydroa vacciniforme-like lymphomatoid papulosis in a Japanese child: a new subset.
Tabata N, Aiba S, Ichinohazama R, Kikuchi K, Aoyama H, Watanabe M, Tagami H.
Department of Dermatology, Tohoku University School of Medicine, Sendai, Japan.
J Am Acad Dermatol 1995 Feb;32(2 Pt 2):378-81 Abstract quote
An 8-year-old Japanese girl had a 9-month history of a self-healing papulovesicular eruption on her face, scalp, and neck that resembled hydroa vacciniforme (HV). Histologically, there was a dense infiltration of small lymphocytic cells and scattered large atypical cells expressing CD30. Study of gene rearrangement showed no monoclonality in the infiltrating cells.
To our knowledge, this is the second case of lymphomatoid papulosis with clinical features resembling HV. However, we also found descriptions in the literature of two other Japanese children with malignant lymphoma who both initially had clinical features resembling HV.
These findings suggest that these cases of HV-like disease constitute a subset of lymphomatoid papulosis that is highly likely to progress to malignant lymphoma.
LOCALIZED
Localized lymphomatoid papulosis.Kagaya M, Kondo S, Kamada A, Yamada Y, Matsusaka H, Jimbow K.
Department of Dermatology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Dermatology 2002;204(1):72-4 Abstract quote A 50-year-old Japanese male visited our clinic in April 1999 with a 2-year history of self-healing, reddish papules on his right palm. On examination, there were grouped erythematous papules, 2-4 mm in size, which formed a relatively well-circumscribed erythematous plaque.
A biopsy specimen showed a wedge-shaped, dense dermal infiltrate consisting of variously sized mononuclear lymphoid cells mixed with few large CD30-positive cells and inflammatory cells, suggesting the diagnosis of regional lymphomatoid papulosis (LyP). Analysis of the T cell receptor gene revealed a polyclonal pattern on lesional skin.
Only 5 cases of LyP presenting in a regional distribution have been reported previously. Although the etiology of localized LyP remains unknown, considering that 2 of 5 reported patients developed widespread lesions regional LyP may be the initial presentation of typical LyP.
MUCOSAL Mucosal involvement in a patient with lymphomatoid papulosis J Am Acad Dermatol 2001;44:339-41
38-year-old woman with nodular and papulovesicular lesions develop on the genital area and oral commissure
Mucosal involvement in LyP is a rare event, and its clinical relevance is still unknown
Aggressive therapies are not recommended in patients with LyP with either cutaneous or mucosal involvement.
PERSISTENT AGMINATION
Yale Comprehensive Cancer Center, Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06519, USA.
BACKGROUND: Lymphomatoid papulosis (LyP) is a self-healing eruption in the spectrum of CD30+ lymphoproliferative disorders. The most common lymphoproliferative disorder associated with LyP is the most common form of cutaneous T-cell lymphoma: mycosis fungoides
. OBJECTIVE: We sought to describe a distinct entity on the spectrum of CD30+ lymphoproliferative disorders.
RESULTS: Seven patients presented with similar findings. Within a well-circumscribed area, the size and location of a patch of mycosis fungoides, these patients had continual eruptions of papulonodules that were histologically typical of LyP. The localized areas of involvement were treated as oligolesional mycosis fungoides and long-standing remissions occurred even after years of experiencing continuous localized eruptions. The clinical and histologic findings are reviewed and presented in a way to further the identification of patients with this entity.
LIMITATIONS: This distinct entity is only defined by 7 patients.
CONCLUSION: The agmination of LyP-like papulonodules confined to a discrete circumscribed area is a distinct clinical subset within the spectrum of CD30+ lymphoproliferative disorders. The behavior of this entity is that of a progressive lymphoma that warrants therapy.TOUNGE
Involvement of the tongue by lymphomatoid papulosis.Kato N, Tomita Y, Yoshida K, Hisai H.
Department of Dermatology and Research Institute, National Sapporo Hospital, Japan.
Am J Dermatopathol 1998 Oct;20(5):522-6 Abstract quote We report on a case of lymphomatoid papulosis (LyP) with involvement of the tongue.
The patient was a 34-year-old Japanese man. Three reddish, centrally depressed, slightly elevated nodules were evident on the dorsal tongue, along with lesions elsewhere on the skin. One of them was biopsied and exhibited a superficial and deep, perivascular and interstitial mixed cellular infiltrate including atypical lymphoid cells, lymphocytes, neutrophils, and histiocytes. The patient also showed rhythmical recurrence of reddish papules and ulcerated nodules on the trunk, extremities, and anogenital area.
Histologically, these papules showed a dense, wedge-shaped mixed cellular infiltrate in the dermis, which included medium and large atypical lymphoid cells, lymphocytes, neutrophils, and histiocytes. Immunoperoxidase staining for CD30 was positive in the cell membrane and cytoplasm of the atypical cells.
We could not find other reports of LyP involving the tongue. Systemic treatment with interferon (INF)-alpha2a was dramatically effective in inhibiting recurrence of the eruption.
HISTOLOGICAL TYPES CHARACTERIZATION TYPE MICROSCOPIC FINDINGS A Large atypical cells similar to the cells in CD 30+ cutaneous T cell lymphomas with inflammatory cells like neutrophils and eosinophils, CD 30+ cells are dispersed and not in cohesive sheets B CD 30- cells similar in morphology to the cerebriform mononuclear cells in mycosis fungoides C Sheets of large atypical cells concentrated in the upper dermis with little or no infiltration into the subcutis.
Lymphomatoid papulosis: reappraisal of clinicopathologic presentation and classification into subtypes A, B, and C.
El Shabrawi-Caelen L, Kerl H, Cerroni L.
Department of Dermatology, University of Graz, Graz, Austria.
Arch Dermatol. 2004 Apr;140(4):441-7. Abstract quote
OBJECTIVES: To analyze clinicopathologic features of lymphomatoid papulosis and delineate the characteristics of histopathologic variants (types A, B, and C).
DESIGN: Retrospective nonrandomized study.
SETTING: University-based dermatologic referral center.
PATIENTS: Eighty-five patients with lymphomatoid papulosis. Clinical data and 1 or more biopsy specimens were available for review in all cases. When possible, immunophenotypic and molecular analyses were carried out.
RESULTS: Of these patients, 78 presented only 1 histopathologic subtype of lymphomatoid papulosis (64 had type A, 3 had type B, and 11 had type C). The last 7 patients presented more than 1 subtype (1 had A and B, 5 had A and C, and 1 had A, B, and C). Two patients had regional lymphomatoid papulosis, an unusual clinical presentation characterized by groups of lesions localized to 1 anatomic region. We observed, we believe for the first time, that some histopathologic patterns, ie, follicular mucinosis (n = 1), syringotropic infiltrates (n = 1), epidermal vesicle formation (n = 2), and syringosquamous metaplasia (n = 1), were associated with lymphomatoid papulosis. A distribution along hair follicles, or follicular lymphomatoid papulosis, was observed in 5 biopsy specimens. A bandlike rather than a wedge distribution of the infiltrate was seen in 5 specimens from patients with lymphomatoid papulosis type A. Of 8 patients who had associated lymphoid malignancies, 4 had Hodgkin disease and 4 had mycosis fungoides.
CONCLUSIONS: Lymphomatoid papulosis is a cutaneous disorder with multiple clinicopathologic features. Differentiating between mycosis fungoides and anaplastic large cell lymphoma may be very difficult and sometimes impossible. In the spectrum of CD30(+) cutaneous lymphoproliferative disorders, boundaries between these 2 entities are not clear-cut.VARIANTS ANGIOCENTRIC Lymphomatoid papulosis histopathologically simulating angiocentric and cytotoxic T-cell lymphoma: a case report.
Wu WM, Tsai HJ.
Department of Dermatology, Chang Gung Memorial Hospital, Taipei, Taiwan
Am J Dermatopathol. 2004 Apr;26(2):133-5. Abstract quote
We report a patient presenting with a 20-year history of recurrent papulonecrotic lesions in which skin biopsy shows extensive vascular destruction. Atypical lymphoid cells surrounding the dermal vessels had a CD3+, CD4-, CD5-, CD8+, CD20-, CD30+, CD56+, TIA-1+, and granzyme B immunophenotype implicating a natural killer/T origin. In situ hybridization was negative for Epstein-Barr virus transcripts.
Analysis of T-cell receptor-gamma gene of 2 separate biopsy specimens detected an identical clone. The patient was treated with low-dose methotrexate and achieved complete resolution in a month. According to the clinical course, immunophenotype, clonality analysis and the excellent response to methotrexate, we conclude that this is an unusual case of lymphomatoid papulosis.
We believe that this unusual presentation needs to be distinguished from other aggressive lymphomas, including the natural killer/T-cell and cytotoxic T-cell subsetsGRANULOMATOUS ECCRINOTROPIC Granulomatous Eccrinotropic Lymphomatoid Papulosis
A. Neil CrowsonMD1, , Dmitry Y. BaschinskyMD2, , Al KovatichMSc3, , and Cynthia MagroMDAm J Clin Pathol 2003;119:731-739 Abstract quote We describe 9 patients with a novel variant of lymphomatoid papulosis characterized by prominent localization of the infiltrate around the eccrine coil, resulting in nodular expansion of the coil accompanied by variable granulomatous inflammation.
Light microscopy, immunohistochemical analysis using antibodies to CD2, CD3, CD4, CD5, CD7, CD8, and CD30 in 6 cases, and polymerase chain reaction–single-stranded conformational polymorphism analysis for T-cell receptor g chain gene rearrangement in 5 cases revealed 2 cytomorphologic patterns (large cell dominant with polymorphous inflammation, small cell lymphocyte-rich with an inconspicuous large cell component [phenotypes, CD30+/CD3+/CD4+/CD7– for large atypical cells; reactive for small lymphocytes]) and clonal restriction in 4 and polyclonality in 1 of the lymphocyte-dominant cases. During an average 6-year follow-up, no lymphomas developed.
Recognition of this variant is important—accentuation of the infiltrate around the eccrine coil and cutaneous nerves, presence of granulomatous inflammation, dominance of small lymphocytes in the dermis, and variable extension into the panniculus may lead to diagnostic confusion with entities such as discoid lupus erythematosus, Jessner lymphocytic infiltrate of skin, subcutaneous T-cell lymphoma, and persistent arthropod bite reaction.
Our findings suggest that pruritus, a younger age at diagnosis, and a more indolent course are defining clinical features.MYXOID CHANGE
A case of lymphomatoid papulosis with prominent myxoid change resembling a mesenchymal neoplasm.Atkins KA, Dahlem MM, Kohler S.
Am J Dermatopathol 2003 Feb;25(1):62-5 Abstract quote Lymphomatoid papulosis is a chronic recurrent eruption of self-regressing papules and nodules. Histologically this disorder is characterized by large atypical lymphoid cells resembling Reed-Sternberg (RS) cells that are set in a background of a mixed inflammatory infiltrate.
Depending on the architecture of the infiltrate and the percentage of atypical cells, the histologic appearance is subclassified as type A, B, or C. The different histologic patterns do not seem to correlate with distinct clinical appearances.
We report a case of lymphomatoid papulosis with unusual histologic features affecting a 14-year-old girl. The presence of anaplastic cells in a background of myxoid stroma closely resembled a sarcoma on histologic examination.
SPECIAL STAINS/
IMMUNOPEROXIDASE/
OTHERCHARACTERIZATION SPECIAL STAINS IMMUNOPEROXIDASE NATURAL KILLER PHENOTYPE Lymphomatoid papulosis with a natural killer-cell phenotype.
Bekkenk MW, Kluin PM, Jansen PM, Meijer CJ, Willemze R.
Department of Dermatology, Leiden University Medical Centre, Albinusdreef 2, 2300 RC Leiden, the Netherlands.
Br J Dermatol 2001 Aug;145(2):318-22 Abstract quote
Lymphomatoid papulosis (LyP) is defined as a recurrent self-healing papulonodular eruption with the histological features of a (CD30+) cutaneous T-cell lymphoma. The atypical cells usually have a CD3+/-, CD4+/-, CD8-, CD30+, CD56- T-cell phenotype.
We report an unusual case of LyP, in which the atypical cells expressed a CD3-, CD4-, CD8-, CD30+, CD56+ phenotype. Detailed phenotypic and genotypic analysis confirmed that these cells had a natural killer (NK)-cell phenotype. Lymphomas with an NK-cell phenotype usually have a poor prognosis.
However, the waxing and waning of papular lesions for more than 20 years and the excellent response to low-dose oral methotrexate in this patient suggest similar clinical behaviour to LyP cases with a T-cell phenotype.
ELECTRON MICROSCOPY
Immunological, cytochemical and ultrastructural studies in lymphomatoid papulosis.Willemze R, Scheffer E, Ruiter DJ, van Vloten WA, Meijer CJ.
Br J Dermatol 1983 Apr;108(4):381-94 Abstract quote In lymphomatoid papulosis two histological types can be distinguished, i.e. type A and type B. In the present study various immunological, enzyme-histochemical and ultrastructural techniques were used to investigate the cellular infiltrate in both types of lymphomatoid papulosis.
The type A lesions showed a predominance of large atypical cells, relatively few T cells and few or no Langerhans or related cells, as defined by a positive staining for OKT6 and NA I/34 antisera. The immunological, cytochemical and ultrastructural characteristics of these large atypical cells resembled those of the Langerhans cell/interdigitating reticulum cell series. The morphology and marker profile of these large cells resembled those of Reed-Sternberg cells, which suggests a relationship between lymphomatoid papulosis type A and Hodgkin's disease. The type B lesions showed a predominance of small, medium-sized and large cerebriform mononuclear cells with the phenotype of activated T helper cells, and numerous Langerhans and/or related cells.
Their cellular composition was similar to that observed in the early stages of mycosis fungoides.
DIFFERENTIAL DIAGNOSIS KEY DIFFERENTIATING FEATURES CTCL-CD30 POSITIVE Although there may be similarity to CD30+ lymphomas, usually the lymphomas have numerous large atypical cells which are present as cohesive groups which extend into the subcutis. Inflammatory cells are usually localized to the periphery of the lesion.
LANGERHANS CELL HISTIOCYTOSIS
Department of Pathology, University of Washington, Seattle, WA, USA.
Although CD1a+ dendritic cells (DC) in cutaneous T-cell lymphomas (CTCL) have been well documented, the presence of large numbers of DC within lymphoid infiltrates can pose a diagnostic difficulty.
We present a case of a 70-year-old man with a 3-year history of recurrent red papules and plaques on the extremities and trunk that was referred to our institution, with the diagnosis of Langerhans cell histiocytosis.
Skin biopsies showed a wedge-shaped cellular infiltrate in the superficial and deep dermis consisting of two cell populations. Most prominent were clusters of epithelioid cells with grooved nuclei and abundant eosinophilic cytoplasm, which stained with antibodies to CD1a and S-100. A second, less prominent population of atypical lymphocytes, some with enlarged, hyperchromatic and convoluted nuclei, were intermixed. The latter were positive for CD30, CD3 and CD5 and negative for CD20, CD34, CD68, ALK-1 and TdT. T-cell receptor gene rearrangement studies confirmed a clonal T-cell population, which with the clinical history was consistent with the diagnosis of lymphomatoid papulosis.
While previous studies have shown an increased density of dermal DC in CTCL, we believe that this represents the first report of an unusually florid DC proliferation mimicking Langerhans cell histiocytosis and masking a lymphoproliferative disorder.SCABIES
CD30 antigen expression in cutaneous inflammatory infiltrates of scabies: a dynamic immunophenotypic pattern that should be distinguished from lymphomatoid papulosis.Gallardo F, Toll A, Pujol RM; Carlos Barranco.
Department of Dermatology, Hospital del Mar, IMAS, Barcelona, Spain Department of Dermatology, Pathology, Hospital del Mar, IMAS, Barcelona, Spain.
J Cutan Pathol 2002 Jul;29(6):368-73 Abstract quote Background: Expression of CD30 antigen is a distinct marker of lymphocyte activation that was originally described in the Reed-Sternberg cells of Hodgkin's disease. The observation of CD30+ cells has been considered a diagnostic feature of cutaneous CD30 lymphoid proliferations. However, CD30 expression has also been reported in some cutaneous benign inflammatory infiltrates.
Methods: Eleven skin biopsies from patients with scabies were double-blindly and retrospectively analysed. A panel of histopathological parameters and immunophenotypic expression of CD4, CD8, CD30 and S-100 antigens was studied. CD30 and S-100 antigens expression were related to clinical features.
Results: Large CD30+ cells were demonstrated in eight (8/11) biopsies, corresponding to patients with long-standing lesions (3 months or longer). However, no expression of the CD30 antigen was observed in all biopsy specimens (3/11) corresponding to early lesions (2 months or less). The presence of S-100 positive cells in the papillary dermis was an almost constant feature.
Conclusions: CD30+ large cells seem to be a common feature in long-standing infiltrates of scabies. CD30 expression in scattered cells of a cutaneous lymphoid infiltrate cannot be assessed as a strong diagnostic argument of neoplastic cutaneous CD30+ lymphoid proliferation (lymphomatoid papulosis/cutaneous CD30+ lymphoma). Therefore, the possibility that large atypical CD30+ cells may be also present in several benign inflammatory diseases should be always considered.
PROGNOSIS CHARACTERIZATION GENERAL Recurrences and relapses common
CD30+ cutaneous lymphoproliferative disorders: the Stanford experience in lymphomatoid papulosis and primary cutaneous anaplastic large cell lymphoma.
Liu HL, Hoppe RT, Kohler S, Harvell JD, Reddy S, Kim YH.
Department of Dermatology, Stanford University, 900 Blake Wilbur Drive, Stanford, CA 94305, USA.
J Am Acad Dermatol. 2003 Dec;49(6):1049-58. Abstract quote
BACKGROUND: CD30+ cutaneous lymphoproliferative disorders (CLPDs) include lymphomatoid papulosis, borderline cases of CD30+CLPDs, and primary cutaneous anaplastic large cell lymphoma (PCALCL). Prior studies have shown CD30+CLPDs have an excellent prognosis.
OBJECTIVE: We sought to present the single-center experience of Stanford University, Stanford, Calif, in the management of CD30+CLPDs.
METHODS: A retrospective cohort analysis of 56 patients with CD30+CLPDs treated at our institution was performed.
RESULTS: No patients with lymphomatoid papulosis died of disease, and overall survival was 92% at 5 and 10 years. Disease-specific survivals at 5 and 10 years for PCALCL were 85%. Disease-specific survival at 5 years for localized versus generalized PCALCL was 91% versus 50% (P =.31). PCALCL was highly responsive to treatment, but the relapse rate was 42%. In all, 3 patients progressed to extracutaneous stage of disease. No clinical or histologic factors analyzed were predictive of worse outcome in lymphomatoid papulosis and PCALCL.
CONCLUSION: Similar to prior reports from multicenter European groups, the single-center experience at our institution demonstrates CD30+CLPDs have an overall excellent prognosis; however, cases of PCALCL with poor outcome do exist.
Lymphomatoid papulosis: a follow-up study of 41 patients.Christensen HK, Thomsen K, Vejlsgaard GL.
Dermatological Department, Rigshospitalet, Copenhagen, Denmark.
Semin Dermatol 1994 Sep;13(3):197-201 Abstract quote Forty-one patients with lymphomatoid papulosis have been followed from 1 to 22 years (mean 11.4 years, median 10 years). Six patients developed malignant lymphoma, 3 cutaneous T-cell lymphoma, 2 Ki-1 large cell lymphoma, and 1 Hodgkin's disease.
A clinical malignant presentation combined with the finding of aneuploidy in skin lesions seem to be indications of a malignant potential.
Treatment with methotrexate in low dosage is an efficient treatment of lymphomatoid papulosis and probably diminishes the risk of malignancy.
TREATMENT CHARACTERIZATION GENERAL J Am Acad Dermatol 1996;34:470-81.
For patients with more severe manifestations of LyP, several treatment modalities:
UVB
Interferon -2a
PUVA
Low-dose oral methotrexate
Systemic corticosteroids
Topical chemotherapySuccess in minimizing the frequency of recurrences is still controversial
EXTRACORPOREAL PHOTOCHEMOTHERAPY
Lymphomatoid papulosis treated with extracorporeal photochemotherapy.Wollina U.
Department of Dermatology, University of Jena, 07740 Jena, Germany.
Oncol Rep 1998 Jan-Feb;5(1):57-9 Abstract quote Lymphomatoid papulosis (LP) is a rare low-grade T-cell lymphoma which may respond to cytotoxic drugs and PUVA irradiation but long-term remission has not been achieved.
Extracorporeal photochemotherapy (ECP) is an immunomodulating therapy used successfully for several types of CTCL, no experience with LP has been reported yet. ECP therapy with 8-methoxypsoralen was introduced on two subsequent days once per month for half a year in a 42-year old women with a 20-year history of LP.
Disseminated papules disappeared rapidly after 3 cycles of ECP treatment but metastatic spread continued, which made necessary a subsequent polychemotherapy.
One year later, the patient died of central nervous system metastasis. ECP monotherapy seems unable to control disease progression in LP despite beneficial effects on skin lesions.
INTERFERON ALPHA
Therapeutic use of interferon-alpha for lymphomatoid papulosis.Schmuth M, Topar G, Illersperger B, Kowald E, Fritsch PO, Sepp NT.
Department of Dermatology, University of Innsbruck, Innsbruck, Austria.
Cancer 2000 Oct 1;89(7):1603-10 Abstract quote BACKGROUND: Lymphomatoid papulosis is a primary cutaneous, CD30 positive lymphoproliferative disorder with the potential to transform into systemic, malignant lymphoma. Therapeutic strategies for patients with lymphomatoid papulosis have been designed to prevent transformation but have proved to be either inefficacious or limited by side effects.
METHODS: The authors compared the clinical, histologic, and immunohistochemical features from a group of five patients receiving interferon-alpha (IFN-alpha) subcutaneously three times per week with the same features from a group of six patients receiving conventional therapy, including photochemotherapy, antibiotics, topical corticosteroids, or surgery, in an open trial.
RESULTS: In the IFN-alpha group, four patients showed a complete remission, and one patient showed a partial remission within a time period of 6 weeks. Two patients developed disease recurrences after discontinuation of short term IFN-alpha therapy (5-7 months). Thereof, one patient went into stable remission after long term IFN-alpha therapy (17 months), and one patient remains in partial remission. In the control group, one patient went into spontaneous remission, two patients showed partial remission, of which one patient developed progressive disease at a later time point, whereas three patients have recurrent disease despite of treatment.
CONCLUSIONS: The current results indicate that the treatment with IFN-alpha of patients with lymphomatoid papulosis alters the clinical course of the disease with fewer side effects than previous regimens; however, short term treatment does not induce stable remission. Therefore, prolonged treatment appears to be warranted for these patients.
METHOTREXATE
Successful treatment of a patient with lymphomatoid papulosis by methotrexate.Yazawa N, Kondo S, Kagaya M, Yazawa H, Minamitsuji Y, Jimbow K.
Department of Dermatology, Sapporo Medical University School of Medicine, Japan.
J Dermatol 2001 Jul;28(7):373-8 Abstract quote We report a case of lymphomatoid papulosis (LyP) that occurred in a 44-year-old Japanese male patient. Reddish papules with a small number of pustules and nodules were observed on the extremities, chest and upper back. Most lesions were also associated with central necrosis, ulceration and crusting, and regressed spontaneously within 4 to 6 weeks.
Histopathological examination revealed wedge-shaped dense cellular infiltrate in the dermis, which was mixed with large atypical lymphoid cells, small lymphocytes, eosinophils and neutrophils. These large atypical cells expressed CD30 on their cell membrane and cytoplasm. Rearrangement of the T-cell receptor (TcR) beta-chain gene was detected in the skin lesion. Lymphadenopathy with histopathologic change similar to the skin lesions, but without TcR gene rearrangement, was found at the left inguinal area.
Systemic administration of methotrexate (7.5-15.0 mg/week) was found to be dramatically effective in resolution of skin lesions and prevention of their recurrence.
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