103 APLASTIC ANAEMIA WITH PNH-LIKE RED CELLS Haema 2003; 6(1): 103-106 Brief report Aplastic anaemia with large PNH-like red cell population John Meletis, Evangelos Terpos, Despina Mavrogianni, Konstantinos Lilakos, Effie Apostolidou, Maria Tsironi, Konstantinos Korovessis, Veroniki Komninaka, Angelos Sarantopoulos, Michalis Samarkos, Konstantinos Konstantopoulos 1 st Department of Internal Medicine, University of Athens School of Medicine, Laiko Hospital, Athens, Greece Abstract. Paroxysmal nocturnal haemoglobinuria (PNH) has been inaccurately viewed as a late com- plication of aplastic anaemia due to insensitivity of Ham and sucrose lysis tests. Patients with AA show a deficiency of glycosyl-phosphatidylinositol (GPI)-ancored proteins (PNH phenotype) on their periph- eral blood at a proportion of between 10%-60%, at diagnosis. This deficiency usually affects a small proportion of the studied blood cells. In serial studies, PNH phenotype did not change up to 15 years after diagnosis. We present here a case of a 27-year-old patient with acquired AA, who presented with a high proportion of PNH-like red cell population, which was decreased after immunosuppressive treat- ment. Key words: aplastic anemia  paroxysmal nocturnal hemoglobinuria  PNH  CD55 (DAF)  CD59 (MIRL)  red cells * Correspondence: John Meletis, MD, First Department of Internal Medicine, University of Athens School of Medicine, Laiko General Hospital, Athens, Greece, FAX:+30210.7788830, e-mail: imeletis@cc.uoa.gr count: neutrophils 18%, lymphocytes 76%, monocytes 5% and eosinophils 1%) and a mild thrombocytope- nia with large platelets (78x10 9 /l) although MPV was within normal range (Figure 1). There were no imma- ture forms of red or white series in the blood smears. The reticulocyte count was 0.1%. Coombs reaction was negative and serum haptoglobins levels were normal as well as the coagulation parameters. The erythro- cyte sedimentation rate was 38 mm/1h. Serum bio- chemistry was as follows: SGOT 50 IU/l, SGPT 52 IU/l, LDH 263 IU/l, ãGT 29 IU/l, ALP 128 IU/l, Bil 1.12 mg/dl, Fe 180 ìg/dl. Serum proteins, ferritin, B 12 and folate levels, serum electrophoresis and quantitative analysis of immunoglobulins were within normal range. Ham and sucrose lysis tests were negative. Chest X-rays revealed no abnormality. Blood and urine cul- A 27-year-old Greek male presented to the outpa- tient department because of progressive weakness and fatigue, dyspnoea on slight exertion and fever. Fever has started seven days before admission, reached 38.5 o C, often peaking twice daily; there were also chills, sweating, and sometimes dry cough. The administra- tion of ampicilline initially and cefuroxime afterwards had no effect. His past medical history was unremark- able. Physical examination on admission revealed only pallor without any sign of infection. There were no hepatosplenomegaly or lymphadenopathy. The body temperature was 37.6 o C, the pulse rate was 125/min and the blood pressure was 110/70 mmHg. His hematological tests showed severe normochro- mic and normocytic anaemia (Ht 19.8%, Hb 6.4 g/dl), leukopenia (white blood cells 1.2x10 9 /l; differential