To study the role of BK virus(BK polyomavirus)in the development of the hemorrhagic cystitis(HC)after hematopoietic stem cell transplantation(HSCT)and analyze the risk fators for BK viruri4a and HC.Methods From August 2006 to November 2007,blood and urine samples were collected from 80 patients undergoing HSCT.BK virus DNA was detected with PCR.Cytomegalovirus (CMV)antigen was detected with immunofluorescence histochemical examination.A control group including 20 healthy individuals was established.Results Late-onset HC occurred in 15 of the 80 HSCT patients with an incidence of 18.8%.The median onset time of HC was 44(13-150)days after transplantation.BK viruria was detected in 30 of the 80 HSCT patients(37.5%)and the positive rate of viruria in the HC patients was 86.7%(13/15).The median time of BK viruria detection in HC patients wag 23(0-56)days after transplantation,being earlier than the onset time of HC.The persistence time of BK viruria was 7(2-14) weeks,being much longer than that of HC(11 days).CMV antigen viremia was detected in 12 of the 80 transplanted patients.with a positive rate of 36.7% in patients with BK viruria and 40.0% in HC patients.Nine of the 30 HC patients developed acute graft versus host disease(Agvhd)of grade Ⅱ-Ⅳ(30.0%).BK virus was not detected in the urine of the remainimg two HC patients and the 20 control subjects as well as in all the blood samples.Univariate analysis indicated that CMV viremia and Agvhd of grade Ⅱ-Ⅳ were agsociated with the occurrence of BK viruria.Condusions BK viruria is the main cauge of the late-onset HC after HSCT.CMV infection and Agvhd may contribute to the occurrence of HC agsociatieg with BK virus.

OBJECTIVE：To investigate the role of clinical pharmacists in the therapy of gefitinib-caused liver injury complicated with cholecystitis in a patient with lung adenocarcinoma ，and to provide reference for the therapy of similar type of patients. METHODS ： Clinical pharmacists participated in the treatment for gefitinib-caused liver injury complicated with cholecystitis in a patient with lung adenocarcinoma. The patient took Gefitinib tablets orally for a long time for anti-tumor treatment，and was hospitalized due to abnormal increase of transaminase. The doctors gave intravenous infusion of tiopronin sodium+ acetylcysteine+reduced glutathione+citicoline to protect liver ，but the effect was not good. After consulting the literature and analyzing the patient ’s condition ， clinical pharmacists suggested that gefitinib should be stopped ， and Magnesium isoglycyrrhizinate injection 0.2 g+5％ Glucose injection 250 mL，ivgtt，qd for liver protection treatment. After discharge ，the patient took Gefitinib tablets orally and was admitted to hospital again due to abnormal increase of transaminase ，and suffered from non-infectious and non-calculous cholecystitis. Clinical pharmacists suggested continuing intravenous drip of Magnesium isoglycyrrhizinate injection 0.2 g+5％ Glucose injection 250 mL，qd for liver protection treatment ，oral administration of Danshu capsules 0.9 g，tid for conservative treatment ；at the same time ，closely monitoring the changes of related indicators. After discharge，clinical pharmacists instructed patients to stop gefitinib ，and take Icotinib hydrochloride tablets 0.125 g，tid+Compound Taxus capsules 0.6 g，tid for anti-tumor treatment. RESULTS ：The doctors adopted the opinions of clinical pharmacists ，and the transaminase levels returned to normal ，and the symptoms of cholecystitis basically subsided. CON CLUSIONS：In the treatment of gefitinib-caused liver injury complicated with cholecystitis in patients with lung adenocarcinoma ， clinical pharmacists 135） assisted doctors to improve the treatment plan and ensure the effectiveness of drug use.

OBJECTIVETo revalidate the conversion factor（CF）for the conversion of BCR-ABL （P210）transcript levels to the international scale（BCR- ABLIS）in chronic myeloid leukemia（CML） which validated before.

METHODSPeking University People's Hospital（PKUPH）prepared the exchange samples for revalidation of CFs of 15 laboratories which validated nine or eighteen months ago. The fresh BCR-ABL（P210）（+）bone morrow or peripheral blood nucleated cells were diluted with BCR-ABL （P210）（-）cells to achieve different BCR- ABL levels, totally 16 sets and 24 samples per set were prepared. TRIzol reagent was added in each tube. Each laboratory tested BCR-ABL transcript levels of one set of samples. Agreement between BCR-ABLIS of each laboratory and PKUPH was assessed by the Bland- Altman method. For laboratories which did not meet the criteria of revalidation, linear regression equation was derived after the samples with maximum BCR-ABL deviation were removed until R²>0.98, then new CF was calculated.

RESULTS10 laboratories met the revalidation criteria with both bias within ±1.4 fold and 95% limits of agreement within ±6 folds, and their CFs still could be used for accurately conversion of BCR-ABLIS. New CFs were recalculated as of 1.8-6.3 folds of their previous CFs in 5 laboratories not met the criteria.

CONCLUSIONRevalidation of CF by sample exchange among laboratories was necessary for accurate and continuous application of BCR-ABLIS, which not only tested the validity of CF acquired before but also calculated new available CFs for those with invalid CFs.

Bone Marrow Cells ; Fusion Proteins, bcr-abl ; genetics ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; diagnosis ; genetics

Objective: To investigate the current status and real performance of the detection of RUNX1-RUNX1T1 fusion transcript levels and WT1 transcript levels in China through interlaboratory comparison. Methods: Peking University People’s Hospital (PKUPH) prepared the samples for comparison. That is, the fresh RUNX1-RUNX1T1 positive (+) bone morrow nucleated cells were serially diluted with RUNX1-RUNX1T1 negative (-) nucleated cells from different patients. Totally 23 sets with 14 different samples per set were prepared. TRIzol reagent was added in each tube and thoroughly mixed with cells for homogenization. Each laboratory simultaneously tested RUNX1-RUNX1T1 and WT1 transcript levels of one set of samples by real-time quantitative PCR method. All transcript levels were reported as the percentage of RUNX1-RUNX1T1 or WT1 transcript copies/ABL copies. Spearman correlation coefficient between the reported transcript levels of each participated laboratory and those of PKUPH was calculated. Results: ①RUNX1-RUNX1T1 comparison: 9 samples were (+) and 5 were (-) , the false negative and positive rates of the 20 participated laboratories were 0 (0/180) and 5% (5/100) , respectively. The reported transcript levels of all 9 positive samples were different among laboratories. The median reported transcript levels of 9 positive samples were from 0.060% to 176.7%, which covered 3.5-log. The ratios of each sample’s highest to the lowest reported transcript levels were from 5.5 to 12.3 (one result which obviously deviated from other laboratories’ results was not included) , 85% (17/20) of the laboratories had correlation coefficient ≥0.98. ②WT1 comparison: The median reported transcript levels of all 14 samples were from 0.17% to 67.6%, which covered 2.6-log. The ratios of each sample’s highest to the lowest reported transcript levels were from 5.3-13.7, 62% (13/21) of the laboratories had correlation coefficient ≥0.98. ③ The relative relationship of the reported RUNX1-RUNX1T1 transcript levels between the participants and PKUPH was not always consistent with that of WT1 transcript levels. Both RUNX1-RUNX1T1 and WT1 transcript levels from 2 and 7 laboratories were individually lower than and higher than those of PKUPH, whereas for the rest 11 laboratories, one transcript level was higher than and the other was lower than that of PKUPH. Conclusion The reported RUNX1-RUNX1T1 and WT1 transcript levels were different among laboratories for the same sample. Most of the participated laboratories reported highly consistent result with that of PKUPH. The relationship between laboratories of the different transcript levels may not be the same.