E Rettinger, M Schumm, M Pfeiffer, S Kuçi, A Willasch, R Handgretinger, D Niethammer, P Lang
{"title":"Identification and selective depletion of alloreactive T-cells for adoptive immunotherapy.","authors":"E Rettinger, M Schumm, M Pfeiffer, S Kuçi, A Willasch, R Handgretinger, D Niethammer, P Lang","doi":"10.1532/LH96.09010","DOIUrl":"https://doi.org/10.1532/LH96.09010","url":null,"abstract":"<p><strong>Background: </strong>T-cell-depleted allografts may exhibit delayed T-cell recovery, severe infections, and relapse after haploidentical hematopoietic stem cell transplantation (HSCT). Required donor lymphocyte infusions containing nonalloreactive cells may transfer immune function without causing graft-versus-host disease.</p><p><strong>Methods: </strong>We developed an ex vivo approach for the immunomagnetic depletion of alloreactive CD25+, CD69+, and HLA-DR+ T-cells. To achieve highest rates of alloantigen expression, we cocultured peripheral blood mononuclear cells (PBMNCs) with PBMNCs (A/B*), dendritic cells (A/B* DCs), or cytokine-pretreated PBMNCs (A/B* cyt cells). Functional analyses were performed after depletion.</p><p><strong>Results: </strong>After coculture with PBMNCs (A/B* cells), 29% of T-cells became CD25+, CD69+, and HLA-DR+. In modified mixed lymphocyte reactions (MLR) (A/B* cyt cells and A/B* DCs), 35% and 37% of T-cells became CD25+, CD69+, and HLA-DR+. Alloactivation was confirmed by interferon gamma release and proliferation. Immuno-magnetic depletion produced <1% alloactivated cells. Furthermore, this depletion strategy was allospecific and hardly impaired the immune function of the retained cells.</p><p><strong>Discussion: </strong>The efficiency of immunomagnetic depletion depended on the stimulatory capacity of stimulator cells and was improved by using cytokine-pretreated PBMNCs for alloactivation. Overall, this approach might be a promising strategy for restoration of the immune system, particularly after haploidentical HSCT.</p>","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"16 1","pages":"8-22"},"PeriodicalIF":0.0,"publicationDate":"2010-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28771883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Time to drop routine reporting of differential percentage values from CBC reports.","authors":"David L Zwick","doi":"10.1532/LH96.09017","DOIUrl":"https://doi.org/10.1532/LH96.09017","url":null,"abstract":"","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"16 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2010-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28771881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Book Review: Comments on the 2008 WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues by a Practicing Hematopathologist","authors":"G. Shaw","doi":"10.1532/LH96.09006","DOIUrl":"https://doi.org/10.1532/LH96.09006","url":null,"abstract":"","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"15 1","pages":"17-19"},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67384042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ethnic and genetic causes of neutropenia: clinical and therapeutic implications.","authors":"Guido D'Angelo","doi":"10.1532/LH96.09005","DOIUrl":"https://doi.org/10.1532/LH96.09005","url":null,"abstract":"<p><p>The white blood cell count represents clinical data linked with different pathologic conditions, as well as with lifestyle. Another very important condition that affects the number of leukocytes is race and ethnic group-the geographic zone of origin. Genetic studies have identified the gene that controls the expression of the Duffy antigen receptor for chemokine (DARC), which is associated with the ethnic group to which individuals belong. The single-nucleotide polymorphism strongly associated with race is DARC rs2814778. Currently, it is the only condition that can explain the difference in white blood cell count between different ethnic groups. In a society increasingly characterized by multiracial issues, the leukopenia and/or neutropenia in ethnic groups must be known and accurately assessed clinically. Improved knowledge of this association may help in optimizing therapeutic approaches, mainly for African patients with severe diseases, cancer in particular. Recently, preclinical data have also suggested a link between the Duffy antigen and coagulation. This review also discusses the main causes of genetic neutropenia.</p>","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"15 3","pages":"25-9"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28479207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kelley J Mast, Sue Hammond, Stephen J Qualman, Samir B Kahwash
{"title":"The coinheritance of beta- and alpha- thalassemia: a review of one patient and her family.","authors":"Kelley J Mast, Sue Hammond, Stephen J Qualman, Samir B Kahwash","doi":"10.1532/LH96.09002","DOIUrl":"https://doi.org/10.1532/LH96.09002","url":null,"abstract":"<p><p>The diagnosis and management of alpha-thalassemia may be complicated by the variability of the phenotype, which is due to the interaction of coinherited alpha-thalassemia and the variable severity of beta-thalassemia mutations. A well-documented case of complex beta- and alpha-thalassemia coinheritance is described. Laboratory and clinical data for the patient and her family are reviewed. The patient is an asymptomatic girl, one of identical twins. She presented at 1 month of age for follow-up of an abnormal newborn-screening result (hemoglobin F only), which initially suggested homozygosity for beta-thalassemia. Extensive studies on the patient and family revealed that she had coinherited alpha-thalassemia traits and homozygous beta-thalassemia. This case demonstrates the interaction of coinherited alpha- and beta-thalassemia with the resultant amelioration of the clinical phenotype. It also highlights the importance of family studies and close follow-up in diagnosing complex hemoglobinopathies.</p>","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"15 3","pages":"30-3"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28479208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fabio Stagno, Anna Triolo, Vittorio Del Fabro, Salvatore Berretta, Nunziatina Laura Parrinello, Giovannella Fargione, Francesco Di Raimondo
{"title":"Aberrant phenotypic expression of the T-cell-associated antigen CD8 on B-cell chronic lymphocytic leukemia cells.","authors":"Fabio Stagno, Anna Triolo, Vittorio Del Fabro, Salvatore Berretta, Nunziatina Laura Parrinello, Giovannella Fargione, Francesco Di Raimondo","doi":"10.1532/LH96.08015","DOIUrl":"https://doi.org/10.1532/LH96.08015","url":null,"abstract":"<p><p>B-cell chronic lymphocytic leukemia (B-CLL) is a heterogeneous hematologic malignancy caused by a clonally expanded B-cell population that recirculates between the blood and tissues. Described is the case of an 81-year-old female B-CLL patient with aberrant expression of a T-cell-associated antigen, CD8, on CD19+ B-CLL cells. Despite chlorambucil therapy and a subsequent salvage regimen, the patient rapidly entered progressive disease and died 9 months later. Flow cytometric immunophenotyping of the B-CLL cells for a number of antigens ruled out a mixed-lineage disorder. The implications of CD8 expression in B-CLL are discussed, and its expression in this case probably reflects an aberrant lineage infidelity. CD8 expression might be considered as a marker of aggressive disease.</p>","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"15 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28032634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pascale S Akl, Ferdane Kutlar, Niren Patel, Catherine L Salisbury, Peter Lane, Andrew N Young
{"title":"Compound heterozygosity for hemoglobin S [beta6(A3)Glu6Val] and hemoglobin Korle-Bu [beta73(E17)Asp73Asn].","authors":"Pascale S Akl, Ferdane Kutlar, Niren Patel, Catherine L Salisbury, Peter Lane, Andrew N Young","doi":"10.1532/LH96.09004","DOIUrl":"https://doi.org/10.1532/LH96.09004","url":null,"abstract":"<p><p>We report a case of compound heterozygous hemoglobins S [beta6(A3)Glu6Val] and Korle-Bu [beta73(E17)Asp73Asn] in a 2-year-old girl. This hemoglobin genotype is associated with a benign clinical course, much like the sickle cell trait; however, its laboratory characteristics are very similar to compound heterozygous hemoglobin S and hemoglobin D-Los Angeles [beta121(GH4)Glu121Gln], which produces severe sickling hemolytic anemia. We describe laboratory data used to resolve this important differential diagnosis and review the interactions between hemoglobin S and the variant hemoglobins that may account for the different clinical phenotypes in compound heterozygotes.</p>","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"15 3","pages":"20-4"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28479206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"False-positive crystals in urine from contamination by Multistix 10 SG reagent strips for urinalysis.","authors":"Ji Yeon Kim, Svetal Patel, Anand S Dighe","doi":"10.1532/LH96.09008","DOIUrl":"https://doi.org/10.1532/LH96.09008","url":null,"abstract":"<p><p>Dipstick testing of urine is commonly performed as part of point-of-care testing. Unless separate aliquots are used for dipstick testing, substances may be eluted from the test strip and contaminate patient samples. Such contamination has the potential to lead to interference in subsequent assays if the contaminated specimen is sent to the central laboratory for additional testing. We report our identification of refractile but not birefringent needle-shaped crystals as contaminants from prior contact of urine samples with the nitrite pad in the Multistix 10 SG Reagent Strips for Urinalysis (Siemens Healthcare Diagnostics, Deerfield, IL, USA). Educating clinicians who perform point-of-care testing outside the central laboratory is essential to eliminate this preanalytic artifact.</p>","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"15 4","pages":"35-7"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28516213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
John Blamoun, Maria Alfakir, Ashraf I R Sedfawy, Mahmoud Q Moammar, Michael Maroules, M Anees Khan, Vincent A DeBari
{"title":"The association of D-dimer levels with clinical outcomes in patients presenting with acute pulmonary embolism.","authors":"John Blamoun, Maria Alfakir, Ashraf I R Sedfawy, Mahmoud Q Moammar, Michael Maroules, M Anees Khan, Vincent A DeBari","doi":"10.1532/LH96.08014","DOIUrl":"https://doi.org/10.1532/LH96.08014","url":null,"abstract":"<p><p>The D-dimer fragment of fibrin degradation has been a useful adjunct in the diagnosis of venous thromboembolism (VTE). In conjunction with predictive algorithms, the high negative predictive value (NPV) of D-dimer measurements has provided this analyte with a prominent position in the diagnosis of pulmonary embolism (PE). The purpose of this study was to determine if D-dimer levels correlate with ventilation/perfusion (V/Q) derangements as assessed by the alveolar-arterial oxygen tension gradient (DeltaA-a) and to ascertain if quantitative measurements of D-dimer on admission have prognostic value in terms of during-admission mortality and recurrence over a 60-week period. The study utilized a retrospective cohort of 108 subjects admitted to a single institution and studied longitudinally. The cohort was divided into 4 groups representing degree of severity assessed by computed tomographic (CT) angiography: mild, moderate, severe, and very severe. Differences in D-dimer levels among these groups were strongly significant (P < .0001). A strong correlation was observed between D-dimer concentration and DeltaA-a (P < .0001). Logistic methods were used to calculate a \"cut-off\" level that would distinguish mild-moderate from severe-very severe PE. At a concentration of 12.35 mug/mL, this level yielded an odds ratio (OR) of 12.64 (P = .006) for during-admission mortality and a hazard ratio (HR) of 0.13 (P < .0001) for 60-week recurrence. These data suggest that D-dimer levels have utility beyond their NPV and should be considered as potential prognostic markers in subjects presenting with acute PE.</p>","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"15 1","pages":"4-9"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28032636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"An effective method for hemoglobin E detection: DEAE sepharose microcolumn.","authors":"Orathai Tangvarasittichai, Surapon Tangvarasittichai","doi":"10.1532/LH96.08011","DOIUrl":"https://doi.org/10.1532/LH96.08011","url":null,"abstract":"<p><p>Hemoglobin E (Hb E) is a variant hemoglobin that can lead to considerable morbidity when it occurs in a compound heterozygous state with beta-thalassemia. Therefore, its detection is important because it permits antenatal counseling. Hb E is prevalent in economically weaker regions of the world. Thus, its recognition is often hindered by the high costs of sophisticated Hb E-detection assays. We developed a simple visual test based on identifying Hb E in blood samples with DEAE Sepharose microcolumn chromatography. The diagnostic accuracy of our new Hb E microcolumn assay was 100% for sensitivity, specificity, and positive and negative predictive values. Furthermore, the Hb E microcolumn assay is rapid, reproducible, and economical; hence, it offers affordable screening for Hb E in less well-equipped laboratories.</p>","PeriodicalId":85078,"journal":{"name":"Laboratory hematology : official publication of the International Society for Laboratory Hematology","volume":"15 2","pages":"10-2"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28272470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}