• 2018-07
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  • 2019-06
  • br Case report A year old


    Case report A 73 year-old man was diagnosed with chronic lymphocytic lymphoma (CLL) in December 2009, where he presented with a servical mass at another state hospital. He was treated with 6 cycles of cyclophosphamide, vincristine and prednisone (CVP). On follow-up he received 6 cycles of fludarabine because of relapsed disease. His past history showed a 60 year/pack cigarette usage. His family and social histories were unremarkable. He was referred to our center with B symptoms, and axillary lymphadenopathies in December 2012. His physical examination was unremarkable except bilateral axillary and left posterior servical lymphadenopathies. His blood count parameters were as follows: EMD638683 (Hb): 14.5g/dL, MCV: 90.3fL, leukocyte: 20.08×103/mm3, lymphocyte: 14.19×103/mm3, platelet count (Plt): 168×103/mm3. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) values were 71mm/h and 6mg/L (normal range: 0–5), respectively. All other laboratory tests including serum electrolytes, liver and renal function tests, and coagulation profile were normal. Bilateral multiple axillary lymphadenopathies (7×3.5cm2 in the right, 6×3.5cm2 in the left) were noted in the superficial ultrasonography. Six cycles of fludarabine and cyclophosphamide (FC) combination were applied from December 11, 2012 to April 30, 2013, resulting in relief from symptoms and achieving a partial remission in lymphadenopathies. The patient applied with deep anemia (Hb: 3.6g/dL) and thrombocytopenia (Plt: 35×103/mm3) in April 2014, one year from the last chemotherapy. However, erythropoietin (EPO) level was 2030mIU/mL (normal range: 4.3–20). ESR and CRP values were 136mm/h and 221mg/L, respectively. Bone marrow biopsy revealed hypercellularity (%60), and grade III increment for iron and reticular fibers. There were no abnormality in erythrocytic and granulocytic series in terms of differentiation and maturation. No infiltration or granuloma was noted. In addition, dismegacaryopoiesis and an increase in the number of the megacaryocytes were also reported (Fig. 1). Direct and indirect antiglobulins tests (initial and repeated) were negative, and reticulocyte correction index was 0.04. Detailed laboratory investigations including viral aetiology, rheumatological parameters, and tumor markers were unremarkable. JAK2 (V617F) mutation was negative. A computed tomography (CT) of the abdomen, in September 2014, revealed a mild splenomegaly (13.3cm) without hepatomegaly, and a heterogen solid mass in 7×7×8cm diameter bearing cystic areas in the medial lower pole of the left kidney. Tru-cut biopsy of the renal mass showed vimentin (+), CD10 (+), Ki-67: 10–20%, EMA (+), LMWK (+) cells which were consistent with clear cell type RCC (Fig. 2a–d). Torax CT to rule out a probable metastasis of RCC was found to be negative. Surgical removal of the aforementioned lesion was planned. Unfortunately, on-follow up, he developed tonic-clonic seizures for two times every other day. Electroencephalography recorded normal brain activities. Brain magnetic resonance imaging did not detect any bleeding or mass lesion. Intravenous administration of sodium valproate was initiated following improvement in seizures. However, the general condition of the patient worsened and he expired on December 2014 with active RCC.
    Conflict of interests
    Chronic lymphocytic leukemia (CLL) is the most frequent hematologic neoplasm in Western countries. The clinical course of chronic lymphocytic leukemia ranges from a very indolent disorder with a normal lifespan, to a rapidly progressive disease leading to death. The variable clinical course of CLL is driven, at least in part, by the disease molecular heterogeneity. This makes it difficult to select treatment choice and estimate survival . Most common chromosome abnormalities of CLL are deletions (6q, 11q, 13q, or 17p) and less frequently chromosomal gains (trisomy 12). Molecular markers with prognostic impact include inactivating mutations of 3, , and baculoviral IAP repeat containing 3 () genes. Molecular genotyping of CLL enhances our understanding of the clinical heterogeneity of the disease and provides new insights useful for treatment decision making .