High-protein anti-D reagents prepared from pools of human serum have been used for routine RhD typing but, low-protein, saline reactive anti-D reagents formulated predominantly with monoclonal antibodies are in current use. Because some of the high-protein reagents contain macromolecular additives that may cause red cells coated with immunoglobulin to aggregate spontaneously, antisera with these additives may produce a false-positive reaction. A four-day old male was admitted due to severe jaundice. Initially, the RhD type of the newborn using a high-protein reagent was D-positive and then, using two low-protein reagents, it was D-negative. The blood type of the mother was B, CDe, and that of the newborn was B, CcdEe. The direct antiglobulin test on the newborn's RBC was positive. Anti-E and anti-c were identified in the mother's serum and anti-E only was identified in the newborn's serum. The newborn was treated with phototherapy for 10 days and discharged as recovered. We present a case of hemolytic disease of the D negative newborn, which showed a discrepancy between high protein anti-D and low protein anti-D. With a review of literature, the newborn was possibly misinterpreted as D positive.
Antibodies, Monoclonal ; Coombs Test ; Humans ; Immune Sera ; Immunoglobulins ; Indicators and Reagents ; Infant, Newborn* ; Jaundice ; Male ; Mothers ; Phototherapy

BACKGROUND: Recently, a new EIA method for pancreatic amylase was introduced that was assayed by inhibition of the salivary amylase using the synergistic action of two monoclonal antibodies. We evaluated the clinical usefulness of the pancreatic amylase by using the sensitivity, the specificity and diagnostic accuracy of the receiver-operator characteristics (ROC) curve. METHODS: We divided into 3 groups: acute pancreatitis (n=26) diagnosed by ultrasonography and computed tomography, control patients (n=105), and healthy controls (n=95). Serum total amylase, pancreatic amylase, and lipase were assayed by the Hitachi 7170. The upper limit of the reference range of the total amylase, pancreatic amylase, and lipase was respectively 216 U/L, 115 U/L and 200 U/L in this hospital. RESULTS: The sensitivity of total amylase, pancreatic amylase, and lipase for the diagnosis of acute pancreatitis was 73.1%, 88.5%, and 92.3%, respectively. The specificity of total amylase, pancreatic amylase, and lipase was 70.5%, 81.9%, and 82.9%, respectively. The diagnostic accuracy, determined as the area under the curve, was 0.795 for total amylase, 0.868 for pancreatic amylase, and 0.886 for lipase. There was a significant difference between the total amylase and pancreatic amylase (P=0.045), but not a significant difference between the pancreatic amylase and lipase (P=0.613) by ROC curve. CONCLUSIONS: Pancreatic amylase had a higher sensitivity, specificity, and diagnostic accuracy than the total amylase, and showed a similar diagnostic performance as lipase. Therefore, we concluded that the pancreatic amylase was a better diagnostic tool than the total amylase in the diagnosis of acute pancreatitis.
Amylases* ; Antibodies, Monoclonal ; Diagnosis ; Humans ; Lipase ; Pancreatitis* ; Reference Values ; ROC Curve ; Sensitivity and Specificity ; Ultrasonography

Typing of cryptococcal varieties and antifungal susceptibility testing were performed on two strains which were isolated from a nonimmunosuppressed host with cryptococcal meningitis and another from a patient with systemic cryptococcosis with underlying liver cirrhosis. Both varieties of clinical isolates were identified by the use of the glycin-cycloheximide-bromothymol blue agar medium as Cryptococcus neoformans variety neoformans. For the two isolates of Cryptococcus neoformans, the minimal inhibitory concentrations (MIC) of amphotericin B were 0.25 g/mL and the MICs of fluconazole were 8 g/mL.
Agar ; Amphotericin B ; Cryptococcosis ; Cryptococcus neoformans* ; Cryptococcus* ; Fluconazole ; Humans ; Liver Cirrhosis ; Meningitis, Cryptococcal

Histiocytic sarcoma is a malignant proliferation of cells showing morphologic and immunophenotypic features similar to those of mature tissue histiocytes and is known for its rapid progression and poor prognosis. We describe a case of histiocytic sarcoma diagnosed by bone marrow biopsy. A 64-yr-old male was admitted for fever and weight loss that persisted for 8 months. The patient died undiagnosed on the 7th hospitalization day. A bone marrow biopsy performed just before the patient's death revealed diffuse proliferation of large pleomorphic neoplastic cells with large, round to oval nuclei, vesicular chromatin, and abundant foamy cytoplasm. These cells were positive for histiocytic markers, CD68, lysozyme, CD21, and S-100 protein, but negative for B-cell, T/NK-cell, and epithelial cell markers, thus confirming the presence of histiocytic sarcoma.
Antigens, CD/metabolism ; Antigens, CD31/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Bone Marrow/*pathology ; Fever/diagnosis ; Histiocytic Sarcoma/*diagnosis/pathology/radiography ; Humans ; Male ; Middle Aged ; Muramidase/metabolism ; S100 Proteins/metabolism ; Tomography, X-Ray Computed

Disseminated intravascular coagulation (DIC) is a major complication in sepsis patients. We compared the performance of five DIC diagnostic criteria, focusing on the prediction of mortality. One hundred patients with severe sepsis or septic shock admitted to intensive care unit (ICU) were enrolled. Routine DIC laboratory tests were performed over the first 4 days after admission. The overall ICU and 28-day mortality in DIC patients diagnosed from five criteria (International Society on Thrombosis and Haemostasis [ISTH], the Japanese Association for Acute Medicine [JAAM], the revised JAAM [R-JAAM], the Japanese Ministry of Health and Welfare [JMHW] and the Korean Society on Thrombosis and Hemostasis [KSTH]) were compared. Both KSTH and JMHW criteria showed superior performance than ISTH, JAAM and R-JAAM criteria in the prediction of overall ICU mortality in DIC patients (odds ratio 3.828 and 5.181, P = 0.018 and 0.006, 95% confidence interval 1.256–11.667 and 1.622–16.554, respectively) when applied at day 1 after admission, and survival analysis demonstrated significant prognostic impact of KSTH and JMHW criteria on the prediction of 28-day mortality (P = 0.007 and 0.049, respectively) when applied at day 1 after admission. In conclusion, both KSTH and JMHW criteria would be more useful than other three criteria in predicting prognosis in DIC patients with severe sepsis or septic shock.
Asian Continental Ancestry Group ; Dacarbazine ; Diagnosis ; Disseminated Intravascular Coagulation* ; Hemostasis ; Humans ; Intensive Care Units ; Mortality* ; Prognosis ; Sepsis* ; Shock, Septic ; Thrombosis

BACKGROUND: Kidney transplantation(KT) from unrelated donors has been increasing in Korea in recent years. However, the number of HLA antigen mismatches in unrelated donor KTis larger compare with that in related donor KT. Recently, some studies have reported that cross-reactive group(CREG) matching would improve graft outcome. METHODS: We studied a total of 277 cases of kidney transplants from unrelated donors(cadaver donor 195 cases, living unrelated donor 82 cases) in our center from March 1992 to August 1998. HLA class I antigens were assigned to 10 CREG antigens based on the amino acid residue system of Takemoto. HLA-DR antigens were assigned to 10 broad HLA antigens. Antigens present in donor but not in recipient were considered as mismatches. The survival analysis was carried out by Kaplan-Meier method and differences in survival rates were tested by log-rank test. RESULTS: Mean numbers of mismatches in HLA and CREGs were 4.0 and 2.9. Mismatched numbers of CREG-A,B and 5 year survival rates showed a linear association(P=0.01), but those of HLA-A,B did not show a linear association(P=0.88). Probability of finding zero or one CREG mismatched recipients in unrelated KT was 53%(146 cases). A significant statistic difference was noted in survival rates between zero or one and two or more CREG mismatched group(P=0.01). CONCLUSION: Zero or one CREG mismatched group had better survival in unrelated living or cadaveric KT. Applying CREG matching strategy to recipient selection, graft survival will be significantly improved in unrelated living or cadaveric KT.
Cadaver ; Graft Survival* ; Histocompatibility Antigens Class I ; HLA Antigens ; HLA-DR Antigens ; Humans ; Kidney Transplantation* ; Kidney* ; Korea ; Survival Rate ; Tissue Donors ; Transplants* ; Unrelated Donors

BACKGROUND: AML with myelodysplasia related changes (AML MRC) is known to show a poor prognosis compared with de novo AML, but controversies exist about the prognostic impact of multilineage dysplasia (MLD) among MRC. We investigated the prognostic impact of MLD in AML MRC. METHODS: A total of 357 patients newly diagnosed as AML at Asan Medical Center from January 2001 to December 2005 were analyzed. They were diagnosed and classified as AML with recurrent genetic abnormalities, AML MRC, and AML not otherwise specified (AML NOS). Prognostic markers including overall survival (OS) and event free survival (EFS) were obtained through retrospective analysis of electronic medical records. RESULTS: AML MRC patients showed a lower complete remission (CR) rate (44.7% vs. 64.9%, P=0.002) and shorter OS (297 vs. 561 days, P=0.004) and EFS (229 vs. 374 days, P=0.004) than AML NOS patients. Patients with MLD among AML MRC also showed a lower CR rate (37.7%, P=0.001) and shorter OS (351 days, P=0.036) and EFS (242 days, P=0.076) than AML NOS patients. However, among AML MRC patients, there were no differences in OS, EFS and CR between patients with and without MLD. CONCLUSIONS: AML MRC patients showed a lower CR rate and shorter OS and EFS than AML NOS patients. AML MRC patients with MLD showed similar results and their prognosis was not different from those without MLD. MLD findings among AML MRC could be an independent poor prognostic factor in de novo AML.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Cell Lineage ; Child ; Child, Preschool ; Data Interpretation, Statistical ; Disease-Free Survival ; Female ; Humans ; Infant ; Leukemia, Myeloid, Acute/complications/diagnosis/*mortality ; Male ; Middle Aged ; Myelodysplastic Syndromes/complications/*diagnosis ; Prognosis ; Retrospective Studies ; Survival Analysis

BACKGROUND: Therapy-related AML (t-AML) occurs as a late complication of chemotherapy administered to treat a prior disorder. Prognostic factors affecting the clinical outcome in t-AML have not yet been clearly defined; therefore, we evaluated these factors in this study. METHODS: Forty-eight patients diagnosed with t-AML within the past 10 years were enrolled, and their chemotherapy regimens categorized into 4 groups: alkylating agents (AK) only, topoisomerase II inhibitors (TI) and AK, TI only, and others. The prognostic factors affecting clinical outcome were evaluated. RESULTS: Five (10.4%), 21 (43.8%), 9 (18.8%), and 13 (27.0%) patients were treated with AK only, AK and TI, TI only, and others, respectively. Patients with an AML M3 phenotype showed significantly longer overall survival (OS; 55.1 vs. 14.3 months, P=0.040) and disease-free survival (DFS; 61.2 vs. 17.5 months, P=0.049) than other phenotypes. In contrast, patients with a complex karyotype showed significantly shorter OS (7.9 vs. 31.3 months, P=0.008) and DFS (9.5 vs. 38.6 months, P=0.046); additionally, patients with chromosome 5 or 7 abnormalities showed significantly shorter OS (9.1 vs. 30.7 months, P=0.011) than other phenotypes. Only the presence of a complex karyotype or AML M3 phenotype retained prognostic impact in a multivariate analysis. CONCLUSION: Only the AML M3 phenotype was identified as having a good prognosis, and this might suggest that it exhibits unique clinical features in t-AML patients. Moreover, our findings indicated that karyotype was the strongest prognostic indicator and predicted a poor prognosis for t-AML patients with a complex karyotype.
Alkylating Agents ; Chromosomes, Human, Pair 5 ; Disease-Free Survival ; Humans ; Karyotype ; Leukemia, Myeloid, Acute ; Phenotype ; Prognosis ; Topoisomerase II Inhibitors

Multiplex reverse transcription polymerase chain reaction (mRT-PCR) has recently emerged as an alternative to cytogenetics. We designed and used simplified mRT-PCR system as a molecular screen for acute leukemia. Fifteen fusion transcripts were included: BCR-ABL1, PML-RARA, ZBTB16-RARA, RUNX1-RUNX1T1, CBFB-MYH11, DEK-NUP214, TCF3-PBX1, ETV6-RUNX1, MLL-AFF1, MLL-MLLT4, MLL-MLLT3, MLL-MLLT10, MLL-ELL, MLL-MLLT1, and MLL-MLLT6. A total of 121 diagnostic acute leukemia specimens were studied, comparing the mRT-PCR system with standard cytogenetics. Fifty-six cases (46.3%) had fusion transcripts revealed by our mRT-PCR assay. The concordance rate between mRT-PCR and cytogenetics was 91.7%. However, false negative results were found in three cases who have inv(16), t(4;11) or t(11;19)(q23;p13.1), respectively. Seven cryptic translocations including ETV6-RUNX1, MLL-MLLT3, MLL-MLLT4, and PML-RARA were detected. This mRT-PCR assay is a useful screening tool in acute leukemia because it provides rapid and reliable detection of clinically important chimeric transcripts. In addition, cryptic translocations provide additional genetic information that could be clinically useful.
Acute Disease ; Adolescent ; Adult ; Aged ; Child ; Child, Preschool ; Chromosome Inversion ; Cytogenetics ; Female ; Humans ; Infant ; Leukemia/*diagnosis/genetics/metabolism ; Male ; Middle Aged ; *Multiplex Polymerase Chain Reaction ; Oncogene Proteins, Fusion/*genetics ; Prognosis ; Translocation, Genetic ; Young Adult

BACKGROUND: Coronary artery disease is an important cause of death in adults and stent insertion is one of the treatment modalities. The most severe adverse effect of a stent insertion is the formation of a thrombus; therefore, antiplatelet agents are used. The addition of cilostazol to low-dose aspirin and clopidogrel results in a better antiplatelet effect. However, laboratory tests to monitor the effect of cilostazol are insufficient. METHODS: We tested the inhibitory effect of cilostazol using maximal platelet aggregation in 20 healthy volunteers. Conditions for incubation and concentrations of cilostazol and prostaglandin E1 (PGE1) were established and aggregation was induced by 5'-adenosine diphosphate (ADP) and measured with light transmission aggregometry (LTA). Blood samples were incubated with 1 µM and 2 µM cilostazol for 10 minutes at room temperature, and 80 nM PGE1 was added and incubated for an additional 10 minutes. Aggregation was induced by ADP and reactivity was evaluated. RESULTS: The average maximum aggregation (MA) was 58.1% at 1 µM cilostazol and 22.0% when PGE1 was added. The average MA was 42.8% when cilostazol concentration was increased to 2 µM and 21.2% when PGE1 was added. Average inhibition of aggregation at 1 µM cilostazol was not statistically significant (P=0.085), but was significant (P=0.004) at 2 µM cilostazol. Aggregation was not inhibited even with 2 µM cilostazol and PGE1 in 2 volunteers, which suggests possible resistance to cilostazol. CONCLUSIONS: We designed a method to monitor the effect of cilostazol using in vitro incubation with PGE1.
Adenosine Diphosphate ; Adult ; Alprostadil ; Aspirin ; Cause of Death ; Coronary Artery Disease ; Healthy Volunteers ; Humans ; In Vitro Techniques ; Methods ; Platelet Aggregation ; Platelet Aggregation Inhibitors ; Stents ; Thrombosis ; Volunteers