Chronic lymphocytic leukemia (CLL) is the most common adult leukemia one may encounter in the Western World (25-30%) (1). The standardized incidence rate is 4/100 000 people per annum and increases with age (2). The median age at diagnosis is 65. Men get sick twice as often as women (2).

Monoclonal CLL is a disease characterized by the accumulation of morphologically mature but not functionally B cells (rare T or NK) in peripheral blood, bone marrow, lymph nodes, spleen and, very rarely, in skin (2, 3). Neoplastic cells express the following surface antigens: CD19+, CD5+, CD23+, CD20+/-, slg +/- (4). The moment of the initiation of the treatment depends on the severity of the disease and the choice of treatment depends on the correct assessment of the expectancy of patient survival independent of CLL as well as the biological state of the patient and his comorbidities. The goal of treatment, especially in younger patients, should be putting them into deep remission, without a minimal residual disease (MRD – minimal residual disease). By default, the monitoring response to treatment is carried out in accordance with the criteria of the NCI (National Cancer Institute, 1988) (5), which do not take into account the condition of minimal residual disease.

A 38 year-old man was hospitalized for the first time in the Department of Hematology and Bone Marrow Transplantation, Medical University of Silesia, Katowice in August 2002. In an interview in June 2002 he said that he had noticed a significant reduction in body weight (10% within 3 months), night sweats, and recurrent infections. With comorbidities Gilbert’s syndrome diagnosed in adolescence.

On admission he was in a generally good condition, ECOG = 0. On physical examination lymphadenopathy was revealed: bilaterally enlarged cervical lymph nodes, axillary and inguinal to about 3 cm. An abdominal ultrasonography showed hepatosplenomegaly (the longitudinal span of the right hepatic lobe was 16 cm, and that of the spleen 13 cm). In the peripheral blood examination we observed hyperleukocytosis: WBC – 15.2 G/L (N: 4-10 G/L) with 12.7 G/L morphology mature lymphocytes displaying the following phenotypes: CD5+, CD19+, CD20+, CD23+, CD79b+, CD22+, CD38+ (70% of the cells), CD43+, ZAP70+ (50% of the cells). In addition, we did not observe anemia, Hgb – 14 g/dl (N: 11.2-15.8 g/dl) and thrombocytopenia, PLT – 235 G/L (N: 130-400 G/L). The relevant laboratory findings included: alanine aminotransferases; Alat – 19 IU/L (N: 10-40 IU/L), asparate aminotransferases; Aspat – 22 IU/L (N: 10-42 IU/L), lactate dehydrogenase; LDH – 201 IU/L (91-180 IU/L), serum bilirubin level – 38 umol/L (N: 3.4-17.1 umol/l), creatinine – 78 umol/L (N: 55-113 umol/l), beta2-micro-globulin – 1975 ug/l (N: 1500-3000 ug/l), immuno-globulin; IgG – 7.2 g/L (N: 7-16 g/L), the negative direct and the indirect Coombs antiglobulin test. In the study of peripheral blood FISH stated did not reveal: deletion of the short arm of chromosome 17p, deletion of the long arm of chromosome 11q, deletion of the long arm of chromosome 13q and trisomy of the chromosome 12. The trephine biopsy showed: diffuse infiltration of the small lymphoid B cells (CD20+, CD23+, CD5+, cyclin D1 occupying 30% of the bone marrow. Ki67 proliferative index in CLL cells were 2-35%. Hematopoiesis preserved. Islands of granulopoiesis MPO(+) and erythropoiesis poorly and rich-cells. Megacaryocytes numerous and scattered.