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T Cell Large Granular Lymphocyte Leukaemia with Cutaneous Infiltration.

Sir, A 63-year-old woman was referred to the Department of Dermatology of the Complejo Hospitalario de Granada, Granada, Spain, in 2016 with painful erythematous desquamative nodules and papules of three weeks’ duration. She had a history of stage I infiltrating ductal carcinoma of the breast, unilinear myelodysplastic syndrome with granulocytic involvement, chronic neutropaenia and a diagnosis of T cell (cluster of differentiation [CD]8+) large granular lymphocyte (LGL) leukaemia. Upon examination, the papules were distributed mainly on the forehead and right upper and lower limbs [Figures 1A–C]. Some of the lesions were fluctuating and suppurative, while the others were of a solid consistency. The examination also revealed oral aphthae which were causing dysphagia [Figure 1D]. At referral, the patient was receiving treatment with 50 mg of low-dose cyclosporine on alternate days and 300 μg of granulocyte-colony stimulating factor per week, to which a partial response was noted. Given the suspicion of leukaemia cutis, a biopsy of the lesions was taken. The findings were compatible with a diagnosis of folliculitis, with polymerase chain reaction and direct immunofluorescence tests negative for Mycobacterium tuberculosis and immunoglobulin (Ig) G, IgA, IgM and complement 3 deposits, respectively. Consequently, treatment with 500 mg of cloxacillin every six hours and 15 mg of prednisone per day was initiated; however, there was no evidence of clinical improvement. Successive biopsies indicated systemic vasculitis caused by granulomatosis with polyangiitis. Eventually, nine months after the onset of the symptoms, a final biopsy revealed that the papules represented the cutaneous infiltration of LGL leukaemia [Figure 2], associated with secondary interstitial granulomatous dermatitis. At the time of writing, the patient was being treated with combined cyclophosphamide, vincristine, doxorubicin and prednisone (CHOP) therapy which resulted in the resolution of her cutaneous symptoms [Figure 3]. There was no evidence on computed tomography of any systemic progression to other organs. LGL leukaemia is a low-grade lymphoproliferative disorder characterised by monoclonal expansion in the peripheral blood and bone marrow with either an activated cytotoxic T lymphocyte (i.e. CD8 or CD57+ cells) or, less frequently, a natural killer (CD3-, CD8or CD56+ cells) phenotype.1 Generally, LGLs represent 10–15% of circulating mononuclear cells and are identified morphologically by their large size and rounded or dentate nuclei and abundant cytoplasm with azurophilic granules.2 Clonality has been confirmed by T cell receptor gene letter to the editor Sultan Qaboos University Med J, November 2017, Vol. 17, Iss. 4, pp. e489–490, Epub. 10 Jan 18 Submitted 31 May 17 Peer-Reviewed Accepted 10 Aug 17 doi: 10.18295/squmj.2017.17.04.022