Ticle distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Salomon et al. Experimental Hematology Oncology 2012, 1:24 http://www.ehoonline.org/content/1/1/Page 2 ofAt that point, the patient’s diagnosis was Philadelphia negative (Ph neg) chronic myelogenous leukemia (CML) with+8. Of note that Bcr/Abl negative CML is clinically distinct from Bcr/Abl positive CML, myelodysplastic syndrome and chronic myelomonocytic leukemia [6] and usually, is associated with poor prognosis [7,8]. One could argue whether atypical CML, Bcr/Abl negative according to WHO classification could represent chronic neutrophilic leukemia as in the presented case. A year and a half after diagnosis of Phneg CML was established, the patient complained of persistent discomfort and pain in the upper left abdomen lasting three days without fever. Laboratory work-up showed creatinine of 1.9 mg/dL, uric acid 13.5 mg/dL, phosphor 5.9 mg/dL, potassium 4.8 meq/L and LDH 403 IU/L. White blood cell were 38,000/ L with 76 neutrophils, 7 lymphocytes, 17 monocytes , 1 blasts, 4 metamyelocytes, 10 myelocytes and 9 segments. The hemoglobin was 10 gr/dL and platelet count was 243 k/ L. Abdominal ultrasound (US) Doppler revealed splenomegaly with several peripheral hypoechogenic areas compatible with spleen infarcts (Figure 1a). Also, a small calculus in lower calices of left kidney was noted. Abdominal CT scan demonstrated few peripheral hypodense areas compatible with spleen infarcts (Figure 1b).No enlargement of retroperitoneal lymph nodes or bulky mass was observed. A month earlier, the patient went through colonoscopy and a villous adenoma polyp was found. Urianalysis of sediment revealed amorphous urates and 30 erythrocytes/ high-power field (HPF). A rise in creatinine at the time of presentation from 0.65 to 1.9 mg/dL, uric acid up to 13.5 mg/dL, phosphate up to 5.9 with calcium 9.6 mg/dL, LDH 403 IU/L and alkaline phosphatase 57 IU/L support a diagnosis of acute urate nephropathy. The latter is the outcome of precipitation of uric acid in distal tubules and collecting ducts because of increased filtered load of urate due to excessive production of purines as occurs in tumor lysis syndrome (TLS) [9]. TLS can occur spontaneously [10], but it is commonly seen following the initiation of anticancer treatment [9]. It occurs in both hematological malignancies and in solid tumors, which harbor PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27689333 high proliferative rates and tumor burden. The patient’s creatinine continued to rise, and the phosphor reached a value of 9.6 mg/dL. At that point the patient was started on hemodialysis and received 5 treatments, before further deterioration occurred. The patient was also treated with aluminum hydroxide (950 mg tid).abcCreatinin, Phosphor (mg/dl)12 10 8 6 4 2 0 1 14 26 33 34 36 37 38 39 40 41 42 dialy sis Phosporus Creatinine WBC 100 90 80 70 60 50 40 30 20 10WBC x 10 /LDayFigure 1 a: Grey scale image of ultrasound of the spleen Necrostatin-1 supplier demonstrate small peripheral hypo echoic area compatible with infarcts (short arrow). b: Non enhanced CT image of the spleen demonstrate hypodense peripheral areas compatible with splenic infarcts (arrow). c: Level of phosphor in peripheral blood in correlation to white cell counts. The extreme shift from hyperhsophatemia to severe hypophsphatemia is demonstrated.Salomon et.
