378 tional stabilization of the protein which may also abolish its function; c) overexpression of wild-type protein in response to spontaneous genetic errors occurring at a higher frequency in neoplastic tissue; d) the effect of antigen retrieval techniques which can alter detection thresholds; e) mutations occur out- side the exons studied. Several repo rts have described that p53 alteratio ns are no t o bserved in mo re benign MDS cases. 2-6 How- ever, this study, in keeping with a study do ne by Kita- gawa et al. 9 revealed two RA cases sho wing p53 o ver- expression suggesting that p53 abnormality may not be a terminal genetic event during leukemia develop- ment. To the best of our knowledge only one other study has described p53 alteratio n in the RA phase. 10 The presence of DNA from normal cells in less advanced subtypes is likely to affect the sensitivity o f the mutation detection and may underestimate the rate o f p53 mutatio n in RA phase. Taking into account the shorter interval between RA phase and progression, p53 overexpression may have contributed to the pathogenetic process in the progression of MDS in our cases. However, addi- tional and more extended studies are necessary to determine the genetic basis for this immunoreactivi- ty and to clarify the prognostic value of such find- ings. Sílvia M.M. Magalhães, Larissa P. Ponte, Francisco Valdeci A. Ferreira, Francisco Dário Rocha Filho Hematology and Hemotherapy Center of Ceará – HEMOCE, Department of Clinical Medicine, Department of Pathology, Labtech Federal University of Ceará, Fortaleza, Brazil Key words p53 overexpression, refractory anemia Correspondence Sílvia M.M. Magalhães, Federal University of Ceará – Av. José Bastos 3390 – CEP 60.436-160, Fortaleza, CE – Brazil. Phone/Fax: international +55-85-2816221/+55- 85-2831854 References 1. Gallagher A, Darley RL, Padua R. The molecular basis of myelodysplastic syndromes. Haematologica 1997; 82:191-204. 2. Adamson DJA, Dawson AA, Bennett B, King DJ, Haites NE. P53 mutation in the myelodysplastic syn- dromes. Br J Haematol 1995; 89:61-6. 3. Jonveaux Ph, Fenaux P, Quiquandon I, et al. Muta- tions in the p53 gene in myelodysplastic syndromes. Oncogene 1991; 6:2243-7. 4. Ludwig L, Schulz AS, Janssen JWG, Kurt G, Bartram CR. P53 mutations in myelodysplastic syndromes. Leukemia 1992; 6:1302-4. 5. Mo ri N, Hidai H, Yo ko ta J, et al. Mutatio ns o f the p53 gene in myelodysplastic syndrome and overt leukaemia. Leuk Res 1995; 19:869-75. 6. Sugimoto K, Hirano N, Toyoshuima H, et al. Muta- tions of the p53 gene in myelodysplastic syndrome (MDS) and MDS-derived leukemia. Blood 1993; 81: 3022-6. 7. Hall PA, Lane DP. P53 in tumor pathology: can we trust immuno histo chemistry? – revisited! J Patho l 1994; 172:1-4. 8. Lepelley P, Preudhomme C, Vanrumbeke M, Quesnel B, Co sso n A, Fenaux P. Detectio n o f p53 mutatio ns in hematological malignancies: comparison between immunocytochemistry and DNA analysis. Leukemia 1994; 8:1342-9. 9. Kitagawa M, Yoshida S, Kuwata T, Tanizawa T, Kamiyama R. P53 expressio n in myelo id cells o f myelo - dysplastic syndromes - association with evolution of overt leukemia. Am J Pathol 1994; 145:338-44. 10. Kikukawa M, Aoki N, Mori M. A case of refractory anaemia with p53 point mutation at codon 249 (AGG to ATG). Br J Haematol 1996; 92:831-3. A complex immunodeficiency. Idiopathic CD4 + T-lymphocytopenia and hypogammaglobulinemia associated with HHV8 infection, Kaposi’s sarcoma and gastric cancer Sir, We report a case of idiopathic CD4 + T-lymphocy- topenia (ICL) associated with hypogammaglobu- linemia in a 70-year-old woman. She developed Kaposi’s sarcoma (KS) and her mononuclear cells were found to be positive for Herpes virus type 8 (HHV8). In 1997 she developed gastric cancer and died fro m septic sho ck. At the beginning o f 1990 unusual cases o f CD4 + T- lympho cyto penia in the absence o f human immuno - deficiency virus (HIV) infection were reported. 1,2 In 1993 the CDC defined the criteria for a new syn- drome: ICL. The criteria are lo w CD4 + T-lymphocytes (less than 300/ μL o r belo w 20% o f the to tal lympho - cyte count), no serologic evidence of HIV infection and no defined immuno deficiency diseases o r thera- py asso ciated with T-cell depletio n. 3 In 1994 a 70-year-old woman with hypertension and herpes zoster virus infection was admitted to our sectio n because o f fever, skin abscesses due to Serra- tia marcescens and angio mato us abscesses o n the left leg. There was no epidemiology suggestive of HIV Scientific correspondence Figure 1. Nuclear staining for p53 (red) in the bone marrow of a patient with MDS before (left, x200) and after pro- gression (right, x400). ©Ferrata Storti Foundation