Jessner lymphocytic infiltration of the skin is a rare chronic dermatosis characterized by benign infiltration of the skin by lymphocytes. The disease has a wave-like course, prone to self-resolution. Clinically manifested by a rash on the unchanged skin of flat smooth bluish-pink plaques or papules that merge into foci the size of the palm of a child or adult. Primary elements have clear boundaries, peel off. Plaques are usually single, located on the face, neck, trunk, limbs. It is diagnosed clinically with histological confirmation, sometimes molecular biological studies are carried out. Treatment – NSAIDs, hormone therapy, topical medications.
Jessner lymphocytic infiltration of the skin is a benign pseudolymphoma of the skin with a chronic wave–like recurrent course. It is rare. It occurs more often in men over 20 years of age. It has no seasonal, racial differences, and is not endemic. Sometimes there is an improvement in the summer. For the first time this pathology was described in 1953, when M. Jessner and N. Kanof considered it as an independent disease with through infiltration by lymphocytes of all layers of the dermis. The name “pseudolymphoma” was introduced in 1965 by K. Mach, which combined the Jessner-Kanof infiltration into one group with other types of lymphocytic infiltration.
In 1975, O. Brown differentiated the type of the disease by attributing infiltration by lymphocytes to B-cell pseudolymphomes, but later specialists began to consider the pathology as a T-pseudolymphoma. It is T-lymphocytes that provide a benign course of pathology and the possibility of spontaneous involution of primary elements. Further studies have shown that the immune system of the body plays an essential role in the occurrence and course of Jessner lymphocytic infiltration. Perhaps this is due to the fact that the cells of the immune system are located in the digestive tract, and it is affected in 70% of cases of the disease. The study of Jessner lymphocytic infiltration of the skin continues at the present time. Understanding the causes of the occurrence and development of T-lymphoid processes is of great importance in the development of pathogenetic treatment of pseudolymph.
The most likely causes of Jessner lymphocytic infiltration of the skin are considered to be hyperinsolation, tick bites, infections, pathology of the gastrointestinal tract, the use of dermatogenic cosmetics and irrational use of medications that provoke systemic immune disorders, visually represented by infiltrative changes in the skin. The mechanism of Jessner lymphocytic infiltration of the skin is as follows: intact epidermis gives T-lymphocytes the opportunity to infiltrate the deep layers of the dermis, located in the papillary outgrowths and around the vascular plexuses throughout the thickness of the skin. Triggers of the disease trigger inflammation, to which skin cells and cells of the immune system react directly. T-lymphocytes are involved in the process of relieving inflammation, providing a benign response of the immune system in the form of proliferation of epithelial cells of the dermis.
At the same time, banal inflammation develops in the skin, passing through three stages: alterations, exudation and proliferation with the participation of histiocytes – cells of reticular tissue. Histiocytes cluster and form islets resembling lymphoid follicles. At the final stage of inflammation relief, two parallel proliferation processes complement and reinforce each other. So there is a focus of lymphocytic infiltration. Since lymphocytes are heterogeneous, the evaluation of their histochemical properties using immunological markers and monoclonal antibodies formed the basis of immunophenotyping. This analysis is of great diagnostic importance in modern dermatology.
The primary element of a skin rash with Jessner lymphocytic infiltration of the skin is a large flat pink-cyanotic plaque or papule with clear borders and a smooth surface, which tends to peripheral growth. Merging with each other, the primary elements form ring-shaped or arc-shaped “islands” with peeling areas. The resolution of the precipitated elements begins from the center, so the drain foci may have a sinking in the central part. The typical localization is considered to be the face, neck, parotid space, occiput, forehead, cheeks and cheekbones. Rarely rashes appear on the skin of the trunk and limbs. Usually the primary element is single, less often there is a tendency for the process to spread.
Jessner lymphocytic infiltration of the skin is characterized by a wave-like recurrent course. Resistant to ongoing therapy, capable of spontaneous self-resolution. Relapses usually occur in places of the previous localization, but they can also capture new areas of the skin. Despite the long-term chronic course, the internal organs are not involved in the process.
The disease is diagnosed by a dermatologist on the basis of anamnesis, clinic, histology and luminescent microscopy (the typical glow at the border of the dermoepidermal junction is not determined) with the obligatory consultation of an immunologist and oncologist. Histologically, Jessner lymphocytic infiltration of the skin reveals an unchanged surface layer of the skin. In the thickness of the dermal layers, a grouping of lymphocytes and connective tissue cells around the vessels is found.
In difficult cases, tumor immunotyping, histochemical and molecular testing are carried out. K. Fan and co-authors recommend basing the diagnosis on the results of DNA cytofluorimetry with an analysis of the number of normal cells (with Jessner lymphocytic infiltration of the skin of more than 97%). Differential diagnosis is carried out with sarcoidosis, systemic lupus erythematosus, centrifugal erythema Bietta, annular granuloma, a group of lymphocytic tumors, toxicoderma and syphilis.
Treatment is aimed at relieving the acute phase of Jessner lymphocytic infiltration of the skin and increasing the duration of light intervals. Pathology therapy is non-specific. There is a good therapeutic effect when prescribing antimalarial drugs (chloroquine, hydroxychloroquine) and nonsteroidal anti-inflammatory drugs (diclofenac, indomethacin) after preliminary treatment of concomitant pathology of the gastrointestinal tract. If the state of the digestive system allows, enterosorbents are used. Hormonal corticosteroid ointments and creams are locally indicated, as well as injectable blockages of rash foci with triamcinolone and betamethasone. In case of resistance, plasmapheresis is connected to the therapy (up to 10 sessions).