transferase-positive, CD34– and, interestingly, CD10+, but showed no clonal rearrangement in immunoglobulin and T-cell receptor genes. 2 As discussed by Petrella et al., 1 recent studies 3–9 suggest that a plasmacytoid dendritic cell precursor 10 is the most likely normal counterpart of blastic NK-cell lymphoma. Plasmacytoid dendritic cell precursors are of lymphoid origin and differenti- ate into mature dendritic cells with interleukin-3 and CD40 ligand, or microbial stimuli. 10 Therefore, the reported hetero- geneity in phenotype of blastic NK-cell lymphoma may reflect maturational states of this lineage rather than separate subline- ages. Because plasmacytoid dendritic cell precursors are nor- mally CD56–, 10 the presence of the CD56– cases of blastic NK-cell lymphoma 1,2 is not ‘surprising’. However, the name blastic NK-cell lymphoma (and agranular CD4+ ⁄ CD56+ hae- matodermic neoplasm) should be replaced by the term that is more appropriate for this entity, because both have been termed based on the expression of CD56. 11,12 I propose the name ‘plasmacytoid dendritic cell precursor sarcoma ⁄ leukae- mia’, which may be useful to denote the heterogeneous tumours in this entity including CD56– cases. Division of Dermatology, Graduate School of Medical and Dental Sciences, Niigata University, 1–757 Asahimachi-dori, Niigata 951-8510, Japan E-mail: kawai@med.niigata-u.ac.jp K. K AWAI References 1 Petrella T, Teitell MA, Spiekermann C et al. A CD56-negative case of blastic natural killer-cell lymphoma (agranular CD4+ ⁄ CD56+ haematodermic neoplasm). Br J Dermatol 2004; 150:174–6. 2 Momoi A, Toba K, Kawai K et al. Cutaneous lymphoblastic lym- phoma of putative plasmacytoid dendritic cell-precursor origin: two cases. Leuk Res 2002; 26:693–8. 3 Chaperot L, Bendriss N, Manches O et al. Identification of a leuke- mic counterpart of the plasmacytoid dendritic cells. Blood 2001; 97:3210–17. 4 Petrella T, Comeau MR, Maynadie M et al. ‘Agranular CD4+ CD56+ hematodermic neoplasm’ (blastic NK-cell lymphoma) ori- ginates from a population of CD56+ precursor cells related to plas- macytoid monocytes. Am J Surg Pathol 2002; 26:852–62. 5 Feuillard J, Jacob MC, Valensi F et al. Clinical and biologic features of CD4+ CD56+ malignancies. Blood 2002; 99:1556–63. 6 Briere F, Bendriss-Vermare N, Delale T et al. Origin and filiation of human plasmacytoid dendritic cells. Hum Immunol 2002; 63:1081– 93. 7 Jacob MC, Chaperot L, Mossuz P et al. CD4+ CD56+ lineage negat- ive malignancies: a new entity developed from malignant early plasmacytoid dendritic cells. Haematologica 2003; 88:941–55. 8 Herling M, Teitell MA, Shen RR et al. TCL1 expression in plasmacy- toid dendritic cells (DC2s) and the related CD4+ CD56+ blastic tumors of skin. Blood 2003; 101:5007–9. 9 Chaperot L, Perrot I, Jacob MC et al. Leukemic plasmacytoid dend- ritic cells share phenotypic and functional features with their nor- mal counterparts. Eur J Immunol 2004; 34:418–26. 10 Shortman K, Liu YJ. Mouse and human dendritic cell subtypes. Nat Rev Immunol 2002; 2:151–61. 11 Chan JKC, Jaffe ES, Ralfkiaer E. Blastic NK-cell lymphoma. In: World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues (Jaffe ES, Harris NL, Stein H, Vardiman JW, eds). Lyon: IARC Press, 2001; 214–15. 12 Petrella T, Dalac S, Maynadie M et al. CD4+ CD56+ cutaneous neoplasms: a distinct hematological entity? Groupe Franc ¸ais d’E ´ tude des Lymphomes Cutane ´s (GFELC). Am J Surg Pathol 1999; 23:137–46. Conflicts of interest: none declared. Erythema multiforme due to progesterone in a low-dose oral contraceptive pill DOI: 10.1111/j.1365-2133.2004.06313.x SIR, Despite the widespread use of low-dose oral contracep- tives consisting of progesterone and oestrogen derivatives, drug eruptions, which have included erythema nodosum, 1 Sweet’s syndrome, 2 solar urticaria, 3 photosensitivity reaction 4 and alopecia, 5 evoked by the pills have rarely been reported. Here we describe a woman who developed erythema multi- forme (EM) due to oral contraceptives; a further challenge test suggested that a progesterone derivative contained in the drug was the causative agent. A 34-year-old woman was referred to the Department of Dermatology, Kyoto University Graduate School of Medicine with a 3-week history of itching and oedematous multiple erythema on the body and extremities (Fig. 1), which had not responded to either oral prednisolone or intravascular hydro- cortisone sodium succinate. She had been taking low-dose oral contraceptives consisting of ethinyl-oestradiol and levonor- gestrel for 2 years, polaprezinc and nizatidine for 1 year due to gastric ulcer, and cetirizine hydrochloride and clarithromy- cin for 1 month due to allergic rhinitis. A skin biopsy from the fresh erythema on the arm showed epidermal spongiosis Fig 1. Oedematous multiple erythema on the dorsal side of the hand. Ó 2005 British Association of Dermatologists • British Journal of Dermatology 2005 152, pp368–403 370 Correspondence