A 22-year-old previously healthy male presented with nocturnal lower back ache, pleuritic central chest pain, and intermittent fever for two weeks. He did not have other constitutional symptoms or bleeding manifestations. Prior to admission, he had been treated with antibiotics and steroids by a general practitioner. His symptoms have subsided temporarily during this treatment. On admission, he was not pale and his vital parameters were stable. He had bone tenderness over the sternum and lower lumbar spine. His cardiovascular, respiratory, abdominal, and neurological examination was normal.
On investigation, his white blood cell count (WBC) was 2.91 x 103/muL with 51% neutrophils, heamoglobin was 13.6 g/dL, and platelet count was 28 x 103/muL. Blood picture revealed bicytopenia with leucoerythroblastic picture and occasional atypical cells. Reticulocyte count was 0.8%. Initial C-reactive protein was 520 mg/L, erythrocyte sediment rate was 110 mm/1st hour, and lactate dehydrogenase (LDH) was 4834 U/L. His alkaline phosphatase was 803 U/L (30-120 U/L), gamma glutamyl transferase was 171 U/L (<55 U/L), and total bilirubin was 67 mumol/L (5-21 mumol/L) with increased direct fraction. His renal function and coagulation profile were normal. During the hospital stay, his WBC dropped to 0.69 x 103/muL with an absolute neutrophil count of 0.04 x 103/muL. Haemoglobin and platelets dropped to 7.4 g/dL and 6 x 103/muL, respectively. His viral studies including hepatitis A, hepatitis B, cytomegalovirus, Epstein-Barr, and human immunodeficiency were negative. Blood, urine, and sputum cultures were sterile. BM tuberculosis polymerase chain reaction and culture was negative.
BM aspiration and trephine biopsy revealed extensive necrosis with absence of cells. Repeated BM biopsy showed marrow spaces contained amorphous eosinophilic debris mixed with poorly demarcated cells (Figures 1 and 2). Nuclear details could not be appreciated. A clearly visible focus of immature lymphoid cells, which demonstrated nuclear terminal deoxynucleotidyl transferase (TdT) positivity on immunohistochemistry, was detected leading to the diagnosis of ALL. Immunophenotyping of peripheral blood by flow cytometry concluded 1-2% blasts of B lymphobast phenotype.
He was started on broad-spectrum antibiotics and high-dose steroids and required transfusion of several packed red cells and platelets before transfer to National Cancer Institute, Maharagama, for further management. ALL treatment protocol adapted from Hoelzer's (GMALL/BFM) 5/93 treatment regimen was started, and he has undergone the induction, consolidation 1, reinduction, and halfway of the consolidation 2 phase. He is responding well to treatment.