Case study: SLL and CLL
A 72-year-old man with a history of diabetes mellitus, hypertension, and hypercholesterolemia self-palpated a left submandibular lump in 2012. Complete blood count (CBC) in his internist’s office showed solitary leukocytosis (white count 22) with predominant lymphocytes for which he was referred to a hematologist. Peripheral blood flow cytometry on 04/11/12 confirmed chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL): abnormal cell population comprising 63% of CD45 positive leukocytes, co-expressing CD5 and CD23 in CD19-positive B cells. CD38 was negative but other prognostic markers were not assessed at that time. The patient was observed regularly for the next 3 years and his white count trend was as follows: 22.8 (4/2012) --> 28.5 (07/2012) --> 32.2 (12/2012) --> 36.5 (02/2013) --> 42 (09/2013) --> 44.9 (01/2014) --> 75.8 (2/2015). His other counts stayed normal until early 2015 when he also developed anemia (hemoglobin [HGB] 10.9) although platelets remained normal at 215. He had been noticing enlargement of his cervical, submandibular, supraclavicular, and axillary lymphadenopathy for several months since 2014 and a positron emission tomography (PET)/computed tomography (CT) scan done in 12/2014 had shown extensive diffuse lymphadenopathy within the neck, chest, abdomen, and pelvis. Maximum standardized uptake value (SUV max) was similar to low baseline activity within the vasculature of the neck and chest. In the abdomen and pelvis, however, there was mild to moderately hypermetabolic adenopathy measuring up to SUV of 4. The largest right neck nodes measured up to 2.3 x 3 cm and left neck nodes measured up to 2.3 x 1.5 cm. His right axillary lymphadenopathy measured up to 5.5 x 2.6 cm and on the left measured up to 4.8 x 3.4 cm. Lymph nodes on the right abdomen and pelvis measured up to 6.7 cm and seemed to have some mass effect with compression on the urinary bladder without symptoms. He underwent a bone marrow biopsy on 02/03/15, which revealed hypercellular marrow (60%) with involvement by CLL (30%); flow cytometry showed CD38 and ZAP-70 positivity; fluorescence in situ hybridization (FISH) analysis showed 13q deletion/monosomy 13; IgVH was unmutated; karyotype was 46XY.