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Background
This is an uncommon skin rash characterized by recurrent papules and plaques usually on the trunk.
OUTLINE
EPIDEMIOLOGY CHARACTERIZATION SYNONYMS Jessner's lymphocytic infiltrate of Jessner and Kanof INCIDENCE Uncommon AGE Adults
4th-6th decadesMales favored
DISEASE ASSOCIATIONS CHARACTERIZATION DISCOID LUPUS ERYTHEMATOSUS Jessner's lymphocytic infiltrate and probable discoid lupus erythematosus occurring separately in two sisters.
O'Toole EA, Powell F, Barnes L.
Department of Dermatology, St. James's Hospital, Dublin, Ireland.
Clin Exp Dermatol 1999 Mar;24(2):90-3 Abstract quote
We describe two sisters with clinical and histological features suggestive of Jessner's lymphocytic infiltrate in one and discoid lupus erythematosus in the other.
The occurrence of these two entities in one family now gives credence to the theory that Jessner's lymphocytic infiltrate is in the same disease spectrum as lupus and probably also polymorphic light eruption.
LABORATORY/RADIOLOGIC/
OTHER TESTSCHARACTERIZATION LABORATORY MARKERS FLOW CYTOMETRY Single cell DNA measurements in benign cutaneous lymphoid infiltrates and in positive patch tests.
Ralfkiaer E, Wantzin GL, Larsen JK, Christensen IJ, Thomsen K.
Br J Dermatol 1985 Mar;112(3):253-62 Abstract quote Cellular DNA in skin biopsies from eighteen patients with positive patch tests and eleven patients with benign lymphocytic skin infiltates (cutaneous lymphocytoma, lymphoplasia or Jessner's lymphotic infiltrate) was estimated by flow cytometry of propidium iodide-stained dermal cells.
Specimens from three patients with patch tests and one with cutaneous lymphocytoma had DNA histograms similar to those of normal blood mononuclear cells. The remaining patients demonstrated DNA histogram abnormalities in the form of hyperdiploid peaks in forty-two of forty-five specimens. The estimated proportion of cells in the S-phase was similar in patch tests (median: 9.2%) and in benign lymphocytic skin infiltrates (median: 9.6%). The median number of cells in the G2/M-phase was 3.1% in both groups of disorders.
These data indicate DNA content heterogeneity of the dermal cells in benign lymphocytic skin infiltrates. This may be attributed to DNA replication and/or chromatin dispersion during cellular activation and proliferation. The data also emphasize that hyperdiploid peaks are not necessarily indicative of the presence of separate cell clones.
GROSS APPEARANCE/
CLINICAL VARIANTSCHARACTERIZATION GENERAL VARIANTS CHILDHOOD Childhood Jessner's lymphocytic infiltrate of the skin.
Higgins CR, Wakeel RA, Cerio R.
Royal London Hospital, U.K.
Br J Dermatol 1994 Jul;131(1):99-101 Abstract quote We report a case of Jessner's lymphocytic infiltrate of the skin in an 11-year-old boy. This benign lymphocytic infiltrate was originally described in 1953, and classically occurs in middle-aged men.
Its occurrence in children appears to be very rare, and there are only two other case reports in the literature.
FAMILIAL Familial Lymphocytic Infiltration of the Skin: Histochemical and Molecular Analysis in Three Brothers.
Dippel E, Poenitz N, Klemke CD, Orfanos CE, Goerdt S.
Department of Dermatology, University Medical Center Benjamin Franklin, Free University of Berlin, Germany.
Dermatology 2002;204(1):12-16 Abstract quote Background: Lymphocytic infiltration of the skin (Jessner and Kanof) is a T cell pseudolymphoma characterized by the occurrence of recurrent asymptomatic papules and plaques and by a coat-sleeve-like perivascular lymphoid infiltrate. Rarely, familial cases have been reported.
Objectives: Our study was performed to address the question of a genetic predisposition in a case of familial lymphocytic infiltration by histochemical and molecular analysis.
Results: We report on 3 brothers with typical clinical and histological features of Jessner's lymphocytic infiltration of the skin. Immunohistochemical analysis revealed a mixed lymphocytic infiltrate with a predominance of CD8+ T cells in all 3 patients. Molecular determination of T cell clonality by PCR-based GeneScan analysis of the T cell receptor (TCR)-[gamma]-chain showed oligoclonal, pseudomonoclonal or polyclonal TCR-[gamma] rearrangement patterns in lesional skin and in peripheral blood of all 3 brothers, while no common TCR idiotype was detected.
Conclusion: Inherited deviations in TCR usage seem unlikely as a special cause of familial Jessner's lymphocytic infiltration of the skin; lack of clonality furthermore supports the notion that this variant of the disease is as true a pseudo-T-cell lymphoma as are the spontaneous cases.
FEMALES Jessner's lymphocytic infiltrate in two girls.
Mullen RH, Jacobs AH.
Department of Dermatology, Stanford (Calif) University Medical Center 94303.
Arch Dermatol 1988 Jul;124(7):1091-3 Abstract quote Two girls demonstrated waxing and waning predominantly facial eruptions. Clinically as well as histologically, the lesions are consistent with lymphocytic infiltrate to Jessner and Kanof and constitute the first reported childhood cases.
Although primarily a disease of male adults, this entity should be included in the differential diagnosis of facial plaques in children.
HISTOLOGICAL TYPES CHARACTERIZATION GENERAL Superficial and deep perivascular lymphocytic infiltrate VARIANTS
SPECIAL STAINS/IMMUNOPEROXIDASE/
OTHERCHARACTERIZATION SPECIAL STAINS IMMUNOPEROXIDASE Lymphocyte markers on formalin-fixed tissue in Jessner's lymphocytic infiltrate and lupus erythematosus.
Akasu R, Kahn HJ, From L.
Department of Pathology, Women's College Hospital, University of Toronto, Ontario, Canada.
J Cutan Pathol 1992 Feb;19(1):59-65 Abstract quote Clinical and histological differentiation between Jessner's lymphocytic infiltration of the skin (JLI) and lupus erythematosus (LE) may be difficult. Previous immunohistochemical studies using monoclonal antibodies on frozen sections have shown that the majority of inflammatory cells in JLI and LE are T lymphocytes, whereas B lymphocytes are few or absent.
We have performed an immunohistochemical study on formalin-fixed, paraffin-embedded tissue sections from seven patients with JLI and five with LE using monoclonal antibodies MT1 (pan T-cells), OPD4 (helper/inducer T-cells CD4), MT2 (mantle zone B and some T-cells), MB2 (pan B-cells), L26 (pan B-cells), and LN1 (germinal centre B-cells). In both diseases, the-majority of the inflammatory cells were T lymphocytes (MT1 positive), confirming the results others have obtained on frozen material. OPD4 positive cells were detected in varying numbers in all cases. However, the percentage of B lymphocytes tended to be higher in JLI than LE. LN1 was the most useful B-cell marker in distinguishing JLI from LE. However, a combination of MT2 and LN1 gave the most significant difference.
We conclude that immunohistochemical analysis using a panel of monoclonal antibodies to T and B lymphocytes may be useful in differentiating JLI from LE, although there is still considerable overlap.
Clinical and immunologic studies in reticular erythematous mucinosis and Jessner's lymphocytic infiltrate of skin.
Braddock SW, Kay HD, Maennle D, McDonald TL, Pirruccello SJ, Masih A, Klassen LW, Sawka AR.
Department of Internal Medicine, University of Nebraska Medical Center, Omaha 68198-4360.
J Am Acad Dermatol 1993 May;28(5 Pt 1):691-5 Related Articles, Books, LinkOut
Clinical and immunologic studies in reticular erythematous mucinosis and Jessner's lymphocytic infiltrate of skin.Braddock SW, Kay HD, Maennle D, McDonald TL, Pirruccello SJ, Masih A, Klassen LW, Sawka AR.
Department of Internal Medicine, University of Nebraska Medical Center, Omaha 68198-4360.
BACKGROUND: Little is understood about reticular erythematous mucinosis and Jessner's lymphocytic infiltrate of skin.
OBJECTIVE: Our purpose was to define reticular erythematous mucinosis and Jessner's lymphocytic infiltrate of skin further with focus on immunologic studies.
METHODS: In patients with reticular erythematous mucinosis and Jessner's lymphocytic infiltrate of skin, we measured circulating immune complexes before, during, and after therapy. We examined natural killer cells in a functional assay; we performed direct immunofluorescence and T- and B-cell marker studies in skin biopsy specimens.
RESULTS: The infiltrate in reticular erythematous mucinosis is composed of helper T cells. Circulating immune complexes are increased in both reticular erythematous mucinosis and Jessner's lymphocytic infiltrate of skin and decrease with hydroxychloroquine therapy and clinical clearing. Natural killer cell function is decreased in reticular erythematous mucinosis and Jessner's lymphocytic infiltrate of skin.
CONCLUSION: Changes in circulating immune complex titers accompanying therapy with hydroxychloroquine and clinical clearing, with recurrence of the condition and increase in circulating immune complexes on discontinuation of treatment, point to a possible relation between these events.
DIFFERENTIAL DIAGNOSIS KEY DIFFERENTIATING FEATURES GENERAL Nodular lymphoid disease of the head and neck: lymphocytoma cutis, benign lymphocytic infiltrate of Jessner, and their distinction from malignant lymphoma.
Van Hale HM, Winkelmann RK.
J Am Acad Dermatol 1985 Mar;12(3):455-61 Abstract quote Skin biopsy specimens from six patients with nodular lymphoid disease of the head and neck were studied by routine histology, direct immunofluorescence microscopy, and leukocyte monoclonal antibodies to T and B cell subsets and monocytes.
Initially, these lesions were clinically considered to be benign lymphocytic infiltrates of Jessner, lymphocytoma, or lymphoma. Direct immunofluorescence was negative or showed nonspecific staining in all four patients in whom it was performed. Leukocyte monoclonal antibody stains revealed two distinct patterns of lymphocytes. Lymphocytoma was represented by nodular masses of B lymphocytes with peripheral and intervening zones of T cells. The second pattern consisted of solid nodular masses of T lymphocytes occupying the dermis and subcutaneous tissue.
In the specimens interpreted as benign lymphocytic infiltration, the T cells were composed equally of helper and suppressor cells.
PALPABLE MIGRATORY ARCIFORM ERYTHEMA
Palpable migratory arciform erythema. Clinical morphology, histopathology, immunohistochemistry, and response to treatment.Abeck D, Ollert MW, Eckert F, Szeimies RM, Tiemann M, Braun-Falco O, Steinkraus V, Ring J.
Department of Dermatology, Universitat-Krankenhaus Eppendorf, Hamburg,Germany.
Arch Dermatol 1997 Jun;133(6):763-6 Abstract quote BACKGROUND: Palpable migratory arciform erythema is clinically characterized by sharply circumscribed, infiltrated erythematous patches that tend to spread irregularly, resulting in arciform morphologic features. The histopathologic features are characterized by a patchy inflammatory perivascular and periadnexal T-lymphocytic infiltrate throughout the dermis. The disease runs a chronic course and is rarely described in the literature.
OBSERVATION: Three middle-aged patients of both sexes had palpable migratory arciform erythema with 1, several, or multiple lesions on the trunk. There was a dense perivascular and periadnexal, predominantly lymphocytic infiltrate of the reticular dermis without any interstitial distribution of inflammatory cells. Absence of mucin deposits and plasma cells was a striking feature. The immunohistochemical profile showed an infiltrate dominated by T cells of polyclonal origin. In addition, polyclonal B cells and histiocytes were present in small numbers. In all 3 cases, oral antibacterial treatment resulted in a complete (2 patients) or temporary (1 patient) resolution of skin lesions.
CONCLUSIONS: Palpable migratory arciform erythema shows distinctive differences in clinical and pathological features and treatment in contrast to other diseases with cutaneous lymphocytic infiltrates, including lymphocytic infiltration of Jessner and Kanof. Therefore, it is likely a distinct disease entity.
PROGNOSIS AND TREATMENT CHARACTERIZATION PROGNOSTIC FACTORS TREATMENT AURANOFIN Jessner's lymphocytic infiltrate treated with auranofin.
Farrell AM, McGregor JM, Staughton RC, Bunker CB.
Clin Exp Dermatol 1999 Nov;24(6):500 Abstract quote Weedon D. Weedon's Skin Pathology. Churchill Livingstone. 1997.
Fitzpatrick's Dermatology in General Medicine. 5th Edition. McGraw-Hill. 1999.
Last Updated 3/4/2002
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