Year : 2006 | Volume
: 51 | Issue : 1 | Page : 62--63
Disseminated lymphadenosis benigna cutis
Emy Aby Thomas, Kanwal Masih, Soniya Sadiq
Department of Dermatology, Christian Medical College and Hospital, Ludhiana - 141 008, Punjab, India
Emy Aby Thomas
Department of Dermatology, Christian Medical College and Hospital, Ludhiana - 141 008, Punjab
|How to cite this article:|
Thomas EA, Masih K, Sadiq S. Disseminated lymphadenosis benigna cutis.Indian J Dermatol 2006;51:62-63
|How to cite this URL:|
Thomas EA, Masih K, Sadiq S. Disseminated lymphadenosis benigna cutis. Indian J Dermatol [serial online] 2006 [cited 2019 Dec 10 ];51:62-63
Available from: http://www.e-ijd.org/text.asp?2006/51/1/62/25206
Lymphadenosis benigna cutis (LBC) denotes a group of skin disorders defined as benign lymphoproliferative reaction that may simulate cutaneous malignant lymphomas clinically and/or histologically. As they mimic cutaneous T cell lymphomas (CTCL) or cutaneous B cell lymphomas (CBCL), they are also designated as cutaneous pseudolymphomas. There are many known causes for the development of LBC, such as infectious agents, foreign bodies, drug and antigenic reaction, depending upon which lymphocytic infiltrate many consist predominantly of B cells or T cells. Patients with LBC usually present with solitary erythematous nodule or a plaque. In about 10-15% of patients more generalized or multifocal skin lesions may be observed. In majority of the patients a definite cause of LBC can not be ascertained.
A 48 year old male presented with skin coloured nodular and papular lesions on the face for the last 2 years which later spread to involve the neck and forearms over a period of time. There was no associated photosensitivity or any other known exacerbating factors. Patient did not give any history of drug intake or a known antigenic stimulus such as vaccination, trauma, tattoo, insect bite, infection or application of leeches at the site of the lesions. There was no similar lesion in any other members in the family. Cutaneous examination revealed multiple translucent papules and nodules on the face, eyelids [Figure 1] sides of the neck, flexor aspects of both the arms and forearms with few erythematous, papular lesions on the abdomen. Mucosae nails and scalp were normal. Systemic examination was unremarkable. Complete hemogram, X-ray chest, liver function tests, renal function tests and serum electrolytes did not reveal any abnormality. Serological test for Borrelia burgdorferi was negative. Clinical diagnosis of disseminated LBC was made which was confirmed by histopathological evaluation of skin biopsy. The microscopic examination showed a dense cellular infiltrate in the dermis, comprised of a mixture of mature lymphocytes and histiocytes with a predominance of lymphocytes resulting in lymphoid follicle formation [Figure 2]. No atypical cells were seen. Skin appendages and blood vessels were normal. Overlying epidermis was thinned out with flattened rete ridges.
LBC is an infiltrative condition of the skin, especially of the head and neck region, usually presenting as erythematous or violaceous nodules or plaques. Patients with LBC mostly present as a solitary erythematous nodule or plaque. More generalized or multifocal translucent skin lesions may be observed in about 10-15% of patients, as was noted in our patient. The condition occurs two to three times more frequently in females than males and characteristically develops in early adult life, although it may occur at any age. LBC is the stereotypical example of the cutaneous B-cell pseudolymphomas. In majority of the patients the condition is idiopathic; however, it has been described in association with various antigenic stimuli including arthropod bites, ingestion of drugs, injection or vaccination, chronic infections, cobalt, gold, tattoo pigment and treatment with leeches (Hirudo medicinalis). The most common causative factor of LBC seems to be Borrelia burgdorferi infection, especially in countries with endemic infection. In cases of infection with Borrelia burgdorferi and drug reactions the skin lesion usually resolve within 1-8 weeks. In our patient no etiological factor could be ascertained and the lesions were persisting as such for the last 2 years. Procession of B-cell pseudolymphoma into cutaneous B-cell lymphoma has been reported. In our patient, follicle formation within the lymphocytic infiltrate and absence of cellular atypia helped us to differentiate it from primary lymphoma or leukemic infiltration of the skin. There is no treatment of established value for LBC. Penicillin and radiotherapy have been advocated in thepat without adequate substantiation. Intralesional steroids have also been advocated. Miliary lesions may respond to topical steroids. LBC, both in localized and disseminated form is a benign disorder; however, it may run a protracted, sometimes even life-long course especially in the disseminated form. Systemic symptoms are exceptional and disseminated lesions very occasionally may undergo malignant change.
|1||Wa Van Vloten, R Willemze. The many faces of lymphocytoma cutis. J Eur Acad Dermatol Venereol 2003; 17:3-6.|
|2||Greaves WW. Benign Lymphoplasias of the skin. In: Arthur Rook, Wilkinson DS, Ebling FJG, Champion RH, eds. Textbook of Dermatology, 4th ed. Oxford University Press 1987:1713-17.|
|3||Cerroni L, Kerl H, Gatter K. An illustrate guide to skin lymphomas. Oxford: Blackwell sciences 1998; 101.|
|4||Claudia Colli, Bernd Leinweber, Robert Mulleger andras Chott, et al. Borrelia burgdorferi - associated lymphocytoma cutis: clinicopathologic, immunophenotypic and molecular study of 106 cases. Journal of cutaneous pathology 2004; 31:232-40.|
|5||Crowson AN, Magro CM. Antidepressant therapy. A possible cause of atypical cutaneous lymphoid hyperplasia. Arch Dermatol 1995; 131:925.|
|6||Goerdt S, Speiker T, Wolffer LU, et al. Multiple cutaneous B-cell pseudolymphoma after allergen injection. J Am acad Dermatol 1996; 34:1072.|
|7||Bafverstedt BO. Lymphadenosis benigna cutis. Acta Derm Venereol 1968; 48:1-6.|