Summary We describe a case of canine thymoma in an 11‐year‐old pure‐bred female Spanish Mastiff. On postmortem examination a big mass was found in the thoracic cavity. Histologically the neoplastic parenchyma showed great structural variability; the principal findings included the presence of tumour cells forming cords or sheets, cystic formations, Hassall‐corpuscle like squamous formations, and small or intermediate calibre vessels encircled by areas with eosinophilic material and lymphocytes. In order to determine the histogenesis of the thymic neoplasia we used immunohistochemical techniques specific for different markers: cytokeratins, vimentin, desmin and neuron specific enolase. A strong positive immunoreaction of rumour cells to wide spectrum cytokeratins confirmed the epithelial origin of the neoplasia.

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Renal dysfunction often complicates the course of orthotopic liver transplant (OLT) recipients and is associated with an increase morbidity and mortality. The aim of this study was to determine the incidence of renal disease (acute and chronic), possible risk factors and to determine the impact on the patient survival. Clinical data included age, gender, aetiology for hepatic failure, presence of diabetes mellitus, hypertension, hepatitis B and C infection, renal dysfunction pre transplant (RD pre) and immunosuppression. Laboratorial data included serum creatinine at day 1, 7, 21, month 6, and every year. The glomerular fi ltration rate (GFR) was determined by Cockcroft-Gault equation. We studied, retrospectively, from September 1992 to March 2007, 708 OLT recipients, 82 being retransplanted. Mean age 44 ±12.6 years, 64% males, 17% diabetic, 18.8% with hypertension, 19.9% with C hepatitis and 3.8% B hepatitis. Renal dysfunction was known in 21.6%. Mean follow-up was 3.6 years (0-15). Mean transplant survival was 75% at 12 months and 69% at 3 years. 152 patients died. Uni and multivariate analysis were performed and a p<0.05 was considered signifi cant. Renal dysfunction in this population was observed in more than 50% and was divided in 2 groups: acute renal failure (ARF) in the immediate post transplant period (33.8%) and chronic kidney disease (CKD) according to KDIGO defi nition (50.2%). ARF occurred in 33.8% of the patients. Only 14% recovered the renal function with GFR > 60 ml/min (r = 0.686, p <0.001), 15.5% did not recovered renal function and are on dialysis (r= 0.454, p <0.001), 30.5% died (r= 0.222, p<0.001).In the time of this study, half of the population had CKD 3, 29% with a GFR< 45 ml/min, 9% had CKD 4 and 5.6% CKD5d. Persisting renal failure (GFR < 45 ml/min) was positively correlated with age (r=0.199, p<0.001), diabetes (r=0.88, p=0.032), alcohol (r=0.097, p=0.015), RD pre (r=0.279, p<0.0001), ARF post transplant (r=0,319 p<0.0001) and with high mortality (r=0.188, p<0.0001). On multivariate analysis, it was positively correlated with age (p<0.001), RD pre (p<0.001), ARF post transplant (p=0.03) and with mortality (p=0.015). It was not correlated with aetiology of hepatic failure. Mortality was also correlated, on multivariate analysis, with RD pre (p=0.006), ARF post transplant (p<0.001), CKD stage 3 post transplant (p=0.002), CKD 5d (p<0.001) and haemodialysis treatment (p<0.001). There was no correlation between mortality and need of re transplant. In conclusion, OLT recipients are disposed to renal complications that have a negative impact in the survival of these patients. Renal dysfunction seems to be more important than the need of re transplant in what concerns clinical prognostic. POSTER BOARD NUMBER P4 -37CHRONIC KIDNEY DISEASE FOLLOWING 1987 ORTHOTOPIC LIVER TRANSPLANTATION.

AEL is a uncommon type of acute leukemia. The subjects in this retrospective study were 69 patients diagnosed as having AEL to assess the incidence of different subtypes, detect prognostic factors, and compare there profile with others AML. 63 patients (82,5%) were diagnosed of erythroleukemia (EL) and 7 (17,5%) were pure erythroid leukemia according to WHO classification. 63,6% of EL presented erythroid maturation (immature/mature erythroid ratio &lt;25%), and 36,4% &gt;25%. Three of seven pure erythroid leukemia showed immature erythroid precursors identified by ultrastructural methods, and four had erythroid cells at all maturation stage. 49 (71%) were de novo AEL, only 3 pure erythroid leukemia, 9 (13%) were therapy related, in nine (13%) was preceded by a MDS, and 2 suffer a BC-CML, all of this later, pure erythroid leukemia. The three cases of pure erythroid proliferations with only immature precursors were two Down’s syndrome, both 2 years old, and one BC-CML. The chromosomal abnormalities were classified by SWOG and MRC. BC-CML were excluded from survival analyses. A p value &lt;0.01 was considered significant. There were 38 males and 31 females. The median age was 62 years. The medians hemoglobin 80 g/l; white cell 3,8x109/L; absolute neutrophil 1,0x109/L and platelet 36,0x109/L. Multilineage dysplasia were present in 74,5% (41/55). The overall incidence of chromosomal abnormalities was 79,7%(55/69). 35(50,7%) patients had complex karyotype, 26/49(53,1%) in de novo acute erythroid leukemia. Single abnormalities include 4 monosomy 7, 2 del(5q), two +8, two + 21. 39/64 patients (60,9%) received intensive chemotherapy (9 were consolidated with SCT) and 19/39 (48,7%) achieved CR. Remission rate was 83,3% for normal karyotype and 85,7% and 62,5% for intermediate cytogenetic groups according SWOG (p=0,003) and MCR(p=0,037). The median OS was 4 months with a projected actuarial DFS at 12 months 32,5%. Patients under 40 years (p=0,0001) with normal karyotype (p=0.0003) or intermediate SWOG (p=0.0002) or MRC (p=0.0019) citogenetic groups, who received intensive chemotherapy (p&lt;0.0001) had a longer OS, and younger patients (p=0.0056) with normal karyotype (p=0.0038), or intermediate SWOG (p=0.0006) or MRC (p=0.039) citogenetic groups, consolidated with SCT (p=0.0023) showed the longest DFS. Multivariate analysis showed that only karyotype, is a powerful prognostic indicator both for OS and DFS, besides treatment for OS and age for DFS. The higher risk of relapse is for ≥65 years old patients (OR=2,84) with unknown (OR=7,86) or unfavourable (OR=4,29) SWOG groups and the higher risk of death is for unfavourable (OR=4,33) SWOG groups and those treat with supportive care (OR =3,31). When AEL were compared with a consecutive series of 339 de novo AML, 109 of them ≥ 65 years, and 68 therapy related AML, EL excluded, these series are similar for age and sex but AEL present more frequent multilineage dysplasia (p&lt;0,001), and SWOG or MRC unfavourable citogenetic groups (p&lt;0,001), beside the low remission rate, high risk of relapse and death, was similar at elderly patients AML and therapy related AML.

Aim: Investigate other chromosome abnormalities (OCAs) in Ph-cells of CML imatinib treated patients and analyze whether these changes have some implication to establish clonal disorders. 44 patients, 31 males and 13 females. Median age 51 years (R 14–81). Two patients were in accelerated phase (AP) and one in blast crisis (BC) at the beginning of imatinib (IM). Dose: 400 mg daily with subsequent escalations. 25 received IM up-front but 6 had a short outcome and 19 have been treated with prior CML therapy. Only one imatinib up-front failed to reach the hematological response. 89,5% of valuable cases IM up-front reached complete cytogenetic response (CCgR), 82% at 12 months vs 68% CCgR (31% at 12 mo) for patients with prior therapy(p=0,01). FISH was performed using LSI BCR/ABL ES probe. 500 cells were scored. Cases with +8, FISH was performed using simultaneous BCR/ABL and CEP8 probes. FISH was require to confirm CCgR, because conventional cytogenetic (CC) cannot theoretically detect disease <3–5% since usually 20–30 metaphases are evaluated. Two had a variant t(2;9;22) and t(16;22). 5 had additional chromosome abnormalities (ACAs): 2 at diagnosis, 1 in IM resistance and 2 in AP. Unexpectedly, a der del(9q) was detect in 2 patients when IM resistance and only a third at diagnosis. None of 4 mutation cases had ACAs. Three cases, above reported, developed clonal changes in Ph- cells. Case 1: A 72 years man diagnosed in December 2002 with CP-CML. He received IM 600 mg daily and achieved CCgR at 18 mo and molecular complete response (CMolR) at 30 mo. A routine BM at 36 mo, showed a isolated lymphoid proliferation resemble a normal lymph node. CC demonstrated a karyotype with 46,XY,add(14q),−19,+mar [2/29] and a derivative clone near-tetraploid [2/29]. No Ph was found. FISH confirmed BCR/ABL- and 15% hyperploid cells. RQ-PCR showed CMolR. After 30 days, he develops a B-DLCL with generalised lymphadenopathy. Lymphoid cells were CD20+, CD10−, 60% Ki67. CC showed the pseudodiploid Ph- clone before detect in BM but not hyperploidy. FISH confirmed a variant BCL2 rearrangement at 97% and BCR/ABL negativity. PCR demonstrated B clonatity. Retrospective FISH and PCR of previous BM showed 15% t(14;18), hyperploidy and B clonality. The patient died promptly. Necropsy confirmed B-NHL. Case 2: A 47 years woman diagnosed with CML in june 2000 received multiples therapy without CgR. No OCAs are detected at this time. In January 2003 started 400 mg IM daily. CCgR was reached at 12 mo and MMolR at 18 mo. BM at 36 mo didn’t show dysplasia. All 16 metaphases were Ph- and 44% of them had +8. By FISH bcr/abl was negative and 51% cells Ph- showed +8. At 54 mo, she hasn’t cytopenias but a loss of CCgR and MMolR are evident. IM dose was increased. Case 3: A 42 years woman with CML t(2;9;22) diagnosed in June 2006. At 6 months, a BM showed no dysplasia. CC showed t(2;9;22) in 5/20 metaphases and +8 in 3/15 Ph- metaphases. At 12 months, the Ph were present in 2/45 metaphases, 4/43 Ph- cells had +8, 2/43 had +8, −17 and 37/45 were 46,XX. At this time have myeloid dysplasia without cytopenias. Dasatinib treatment was started. Conclusion: Though the cause of this phenomenon remains to determined, our observations in this small series suggest that clonal OCAs are becoming more evident when more patients achieving CCgR with imatinib. This treatment may favour the manifestation of Ph-negative clonal disorders, even a B-NHL not previously reported. In two cases with trisomy 8 the Imatinib response was affected.