Establishment of a Korean Hepatitis B Surface Antigen Low Titer Performance Panel for Performance Validation of Hepatitis B Surface Antigen Immunoassays / 대한수혈학회지

BACKGROUND: A range of well characterized materials are needed for validating the performance of hepatitis B surface antigen (HBsAg) immunoassays. These materials are purchased currently from overseas manufacturers at a high cost and with limited quantity. This study was conducted to establish an HBsAg low titer performance panel for use as a national standard for validation of HBsAg immunoassays in Korea. METHODS: 476 plasma units reactive on blood donor screening were collected HBsAg was tested using 3 enzyme immunoassays (EIA) and 1 chemiluminescence immunoassay (CIA). Units reactive on the CIA assay or on 2 or more immunoassays were subjected to hepatitis B virus (HBV) DNA quantification, HBV genotyping and subtyping. Units reactive on HBV DNA quantification were confirmed for HBsAg by neutralization. Candidates for the panel were subjected to a collaborative study performed at 7 laboratories using 7 immunoassays. RESULTS: Eleven HBsAg positive units were selected for the low titer performance panel based on HBsAg immunoassay, HBV DNA quantification, HBV genotyping and subtyping results. The range of the HBsAg concentration of the panel members was 0.05~1.28 IU/mL. Two HBsAg negative units were also included as negative controls. CONCLUSION: As a result of this study, a low titer performance panel [KFDA standard (08/028); HBsAg low titer performance panel (BTRL HBV/LP)] for validation of HBsAg immunoassays has been established as a Korean national standard. Use of this panel will improve performance assessment of HBsAg immunoassays. Because the performance of immunoassays cannot be assessed properly with a limited number of panels, continuous efforts are needed to develop a range of performance panels.

Evaluation of a Blood Coagulation Factor XIII Assay Kit

BACKGROUND: Plasma coagulation factor XIII (FXIII) catalyzes the formation of covalent bounds between fibrin monomers, thus stabilizing the fibrin clot and increasing its resistance to fibrinolysis. Alteration of FXIII may contribute to bleeding, wound dehiscence and recurrent abortion. However, standard clotting tests cannot detect the FXIII deficiency. In this study, we evaluated a newly developed FXIII test kit (CoalinkTM, PeopleBio Inc., Seoul, Korea) in patients with various clinical conditions. METHODS: We evaluated the linearity and precision of the new FXIII test kit and compared the results of the new kit and the Pefakit FXIII assay. The FXIII was tested in idiopathic thrombocytopenic purpura (ITP) (n=40) patients, chronic renal failure (CRF) (n=20) patients, liver cirrhosis (LC) (n=40) patients, EDTA-induced pseudothrombocytopenia (EDTAIP) (n=10) patients, and in normal healthy persons (n=50). In the normal healthy persons, we determined a complete blood count (CBC), Ed-highlight-the second (n=50) is redundant. prothrombin time (PT) measurement and activated partial prothrombin time (aPTT) measurement and evaluated the results using the two assays. RESULTS: Serial dilution experiments with five samples provided good linearity (r2=0.9717). The intra- and inter assay precisions (CV) were 2.3~8.6% and 3.9~14.9%, respectively (n=20). There was a significant correlation between the use of the new kit and the Pefakit FXIII assay (r=0.8798, n=50). The FXIII activities of the normal healthy persons, ITP, CRF, LC and EDTAIP patients were 103.3+/-23.3%, 79.7+/-41.0%, 117.9+/-82.3%, 56.9+/-23.7% and 130.0+/-29.0%, respectively and they were significantly decreased in the ITP and LC patients (P<0.05). The rates below 80% of the FXIII level were 67.5% in the ITP patients, 90.0% in the LC patients, 35.0% in the CRF patients and 0.0% in the EDTAIP patients. FXIII activities were closely related to platelet count (r=0.832, P<0.05) and negatively correlated with PT (r=-0.389, P<0.05) and aPTT (r=-0.326, P<0.05). CONCLUSION: The new kit was determined to have good linearity and precision. Moreover, it was simple and rapid to perform. This method may prove useful for the evaluation of FXIII.

Two Cases of Myelofibrosis Mimicking Malignant Lymphoma in Computed Tomography of Abdomen: A Case of Autoimmune Myelofibrosis associated with Systemic Lupus Erythematosus Showing Extensive Lymphadenopathy and A Case of Chronic Idiopathic Myelofibrosis wit / 대한진단검사의학회지

Myelofibrosis results from stimulation of bone marrow stromal fibroblasts by fibrogenic cytokines elaborated by neoplastic or reactive cells in the marrow. Chronic idiopathic myelofibrosis should be differentiated from secondary myelofibrosis resulting from bone marrow involvement of malignant lymphoma because these diseases have different therapeutic strategies. Myelofibrosis in systemic lupus erythematosus is an uncommon but well-recognized complication, and identifying an autoimmune myelofibrosis is important in diagnosing this benign cause of myelofibrosis. We report two cases of myelofibrosis presenting the clinical and radiologic findings that mimicked malignant lymphoma -a case of autoimmune myelofibrosis associated with systemic lupus erythematosus showing extensive lymphadenopathy and a case of chronic idiopathic myelofibrosis with focal intrasplenic extramedullary hematopoiesis- and discuss the importance of the clinical information and radiologic findings for the pathologic diagnosis of myelofibrosis.

A Case of Chronic Myelogenous Leukemia with Abnormal Expression of N-CAM (CD56) Adhesion Molecule on CD34-negative Non-blastic Myeloid Cells / 대한진단검사의학회지

The CD56 antigen is a cell adhesion molecule and its expression on tumor cells is thought to play a role in CD56-positive lymphomas and leukemias with unusual sites of involvement. As to chronic myelogenous leukemia (CML) and related blastic crisis, CD56 expression is not generally considered as a part of the CML phenotype and has rarely been reported in CML and other chronic myeloproliferative dirsorders (CMPD). We reported a case of CML expressing the CD56 antigen on the CD34-negative myeloid cells presented with extramedullary granulocytic sarcoma and examined the CD56 reactivity on bone marrow biopsy sections in 9 patients with CMPD. To assess the abnormal expression of the CD56 antigen on myeloid and progenitor cells from CMPD, immunohistochemical staining and flow cytometric analysis were performed on bone marrow biopsy sections and aspirate specimens, respectively. Of nine patients with CMPD, a case of CML in blastic crisis with extramedullary granulocytic sarcoma showed an abnormal expression of CD56 on CD34-negative myeloid cells. The expression of CD56 on CML myeloid elements seems to represent an aberrant phenomenon that could affect the pattern of tumor cell dissemination.