bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reliability of automated platelet counts: Comparison with manual method and utility for prediction of clinical bleeding
Authors: Lawrence Jeffry B. , Yomtovian Roslyn A. , Dillman Christine , Masarik Susan R. , Chongkolwatana Viroje , Creger Richard J. , Manka Agnes , Hammons Terry , Lazarus Hillard M. 
Published: February 2007

AbstractThe 20 × 109/L (20,000/μl) threshold for prophylactic platelet transfusion may be unnecessarily high. The widespread use of this threshold may reflect lack of confidence in the reliability of low platelet counts. We evaluated the performance of automated platelet counts and their relation to clinical bleeding. First, we prepared serial blood dilutions with “target” platelet counts from 2 to 40 × 109/L For the 48 measurements on 2 × 109/L “target” dilutions, values of 1 or 2 × 109/L were obtained with the Sysmex NE‐8000 analyzer (mean 1.44 × 109/L; SD 0.31 × 109/L). Similarly, for 5 × 109/L “target” counts, automated counts were 3‐6 × 109/L (mean 4.42 × 109/L; SD 0.18 × 109/L). Similar results were observed with all other “target” levels, with coefficients of variation (CV) from 6.39% to 7.71% with 10‐40 × 109/L “target” values. Secondly, we compared triplicate automated and manual platelet counts on thrombocytopenic patients with platelet counts from 4–30 × 109/L. The triplicate automated platelet counts differed by no more than 5 × 109/L among themselves, whereas the manual counts varied by as much as 30 × 109/L. Mean platelet counts: automated, 14.40 × 109/L (CV 10.12%); manual, 16.48 × 109/L (CV 30.39%) (P = 0.038 for counts; P < 0.001 for CV). Finally, we prospectively evaluated bleeding in thrombocytopenic patients (1,809 patient‐days of observation). Univariate and multivariate logistic regression analysis revealed highly significant correlations between the automated platelet count and major and minor bleeding manifestations. Thus, automated platelet counts are highly reliable and accurately predict clinical bleeding. The use of automated analyzers should facilitate improved prophylactic platelet transfusion protocols.
Durable complete remission of macroglobulinemia after splenectomy: A report of two cases and review of the literature
Authors: Humphrey Jeffrey S. , Conley C. Lockard 
Published: February 2007

AbstractTwo patients with macroglobulinemia (monoclonal lgM in the serum) and massive splenomegaly were incapacitated by progressive disease refractory to standard chemotherapy. In each case, palliative splenectomy was followed by a prompt, complete, and unexpected clinical remission with disappearance from the serum of the monoclonal IgM component. One patient remains free of disease 12 years after splenectomy. The other patient remained free of detectable macroglobulinemia for 13 years after splenectomy. A review of the literature revealed other cases of remission of macroglobulinemia attributable to splenectomy alone. Data in humans and animals suggest that the spleen may facilitate IgM secretion by normal and malignant B lymphocytes. Splenectomy should be considered a possible treatment option for patients with massive splenomegaly and macroglobulinemia who progress on chemotherapy. © 1995 Wiley‐Liss, Inc.
Decreased protein C inhibitor after percutaneous transluminal coronary angioplasty in patients with acute myocardial infarction
Authors: Tanigawa Motoaki , Wada Hideo , Minamikawa Kouzou , Wakita Yoshihiro , Nagaya Shozaburo , Mori Tateyuki , Tamaki Shigehisa , Nishikawa Hideo , Kakuta Yutaka , Nakano Takeshi , Hayashi Tatsuya , Suzuki Koji , Shiku Hiroshi 
Published: February 2007

AbstractPlasma thrombin‐antithrombin 111 complex (TAT), FDP‐D‐dimer, activated protein C (APC)‐protein C inhibitor (PCI) complex, and tissue type plasminogen activator (t‐PA), PA inhibitor‐1 (PAI‐I) were significantly increased in patients with acute myocardial infarction (AMI) at onset. These patients exhibited a hypercoagulable state and protein C activation at onset. The plasma PCI level at onset of AMI was within the normal range, but was significantly decreased after percutaneous transluminal coronary angioplasty (PTCA). After PTCA, plasma t‐PA, FDP‐D‐dimer, and plasmin‐a,‐plasmin inhibitor were increased but APC‐PCI complex and TAT were not. The decrease in PCI after PTCA may have been caused by the activation of fibrinolysis. PCI may play an important role in the inhibition of fibrinolysis in stimulated or damaged endothelial cells. These findings suggest that the protein C pathway plays an important role in the onset of AMI and after PTCA. © 1995 Wiley‐Liss, Inc.
Hemoglobin F‐Cincinnati, α2Gγ2 41(C7) Phe → Ser in a newborn with cyanosis
Authors: Kohli‐Kumar Mudra , Zwerdling Theodore , Rucknagel Donald L. 
Published: February 2007

AbstractA term infant presented with mild cyanosis without evidence of hypoxia. Cardiopulmonary disease, polycythemia, and methemoglobinemia were excluded. Standard hemoglobin electrophoresis, including isoelectric focusing, were normal. However, by reversephase C4 HPLC, an abnormal globin chain was detected. Analysis of tryptic peptides and amino acid sequence showed that the patient had an amino acid substitution Phe→Ser at residue 41(C7) in the Gγ chain. This was confirmed by DNA sequencing that demonstrated a point mutation at the expected site in exon 2 of the Gγ gene, accounting for the appropriate change in the codon. This substitution, hemoglobin F‐Cincinnati, α2 γ2 41(C7) Phe→Ser, not previously described, presumably decreased oxygen affinity of the hemoglobin. This substitution is very near the heme group and the α1 β2 interface and, hence, in a crucial area of the globin chain. Abnormalities of γ globin chains tend to be overlooked due to their transient presence and trivial clinical symptomatology, or due to “in utero” selection when physiologically abnormal. Mutant hemoglobins with altered oxygen affinity should be included in the differential diagnosis of newborns presenting with cyanosis, in whom all common causes have been excluded. © 1995 Wiley‐Liss, Inc.
Heterogeneity of the aggregation response of human platelets to arginine vasopressin
Authors: Lachant Neil A. , Smith Mary R. , Xie Zi‐Jian , Romani William R. , Zhou Jane 
Published: February 2007

AbstractPrevious reports have alluded to variability in the aggregation response of normal human platelets to the neuropeptide arginine vasopressin (AVP). Since it has not been well documented, the current studies were undertaken to characterize this response. AVP (1‐100 nM) produced a concentration‐dependent aggregation response. Although the aggregation response to 100 nM AVP did not correlate with age or sex, there was a bimodal response distribution based on the presence or absence of a second wave of aggregation. In kinetic studies, the apparent km of AVP was 18.3 ± 5.4 nM. There was a significant inverse relationship between the maximal aggregation response to 100 nM AVP and the km (r = −0.82). One hundred nanomolar AVP increased the intracellular calcium concentration of platelets by 406 ± 120 nM in calcium free buffer and by 658 ± 233 nM in the presence of 1.0 nM CaCl2. The aggregation response to 100 nM AVP correlated most strongly with the transmembrane influx of calcium (r = 0.84). In individuals whom 100 nM AVP was able to generate a second wave of aggregation, the selective protein kinase C inhibitor bis‐indolylmaleimide significantly decreased the platelet aggregation response. Thus, there is significant heterogeneity in the aggregation response of normal human platelets to AVP. Based on our kinetic studies and the effects of PKC inhibition on the aggregation response to AVP, we would hypothesize that the variability of the aggregation response of normal human platelets to AVP is related to a polymorphism of the platelet AVP V1 receptor. © 1995 Wlley‐Liss, Inc.
Leu110Pro substitution in the RhD polypeptide is responsible for the DVII category blood group phenotype
Authors: Rouillac Christelle , Le Van Kim Caroline , Beolet Marylise , Cartron Jean‐Pierre , Colin Yves 
Published: February 2007

AbstractThe nucleotide sequence of the RhD transcripts from the reticulocytes of three unrelated variants with the DVII category blood group phenotype has been determined. Our results indicate that the expression of the low frequency antigen Rh40 and the lack of epD8 at the surface of these variant RhD positive red cells are associated with a single point mutation, T329C, in exon 2 of the RHD gene. This nucleotide polymorphism results in a leucine to proline substitution at amino acid position 110 of the RhD polypeptide. © 1995 Wiley‐Liss, Inc.
Safety of high doses of a monoclonal antibody‐purified factor IX concentrate
Authors: Warrier Indira , Kasper Carol K. , White Gilbert C. , Shapiro Amy D. , Bergman Garrett E. 
Published: February 2007

AbstractThis report summarizes safety and efficacy information among patients treated with high doses (>75 U/kg) of a monoclonal antibody‐purified factor IX concentrate [coagulation factor IX (human) monoclonal antibody purified)] in two clinical trials. One hundred infusions of this factor IX concentrate at doses >75 U/kg were administered to 35 patients, six of whom had experienced thrombotic complications during previous treatment with prothrombin complex concentrate. Hemostasis in all patients was rated as “excellent,” and there were no thrombotic complications. © 1995 wiley‐Liss, Inc.
Pretreatment fibrinogen levels are associated with response to chemotherapy in patients with small cell carcinoma of the lung: Department of veterans affairs cooperative study 188
Authors: Meehan Kenneth R. , Zacharski Leo R. , Moritz Thomas E. , Rickles Frederick R. 
Published: February 2007

AbstractSmall cell carcinoma of the lung (SCCL) responds commonly to combination chemotherapy but resistance to therapy follows. Prior reports have suggested that a relationship may exist between plasma fibrinogen levels and response to therapy in SCCL. This study was designed to determine the possible predictive value of the fibrinogen level for tumor response (chemoresistance) in SCCL. Pretreatment fibrinogen levels were correlated with outcome and response to therapy in a cohort of 119 previously untreated patients with SCCL who were admitted to VA Cooperative Study 188. Higher pretreatment fibrinogen levels at diagnosis correlated significantly with more advanced stage of disease at entry (P 0.001) and with reduced overall survival (P 0.030). In addition, higher pretreatment fibrinogen levels were correlated significantly with a reduced likelihood of achieving subsequent disease regression with combination chemotherapy (P = 0.005). Because several clinical trials have shown that anticoagulant therapy improves tumor response rates and survival of SCCL, we postulate that tumor cell thrombin generation not only promotes SCCL growth but may also be primarily responsible for both increased fibrinogen levels and for resistance to chemotherapy. These findings provide incentive for studies of thrombin effects on the development of multidrug esistance, and for new clinical trials of more potent and specific inhibitors of thrombin that may further improve tumor response and survival in SCCL. ©1995 Wiley‐Liss, Inc.
Hyperferritinemia in reactive hemophagocytic syndrome report of four adult cases
Authors: Koduri Prasad Rao , Carandang Godofredo , Demarais Patricia , Patel Ashok R. 
Published: February 2007

AbstractFour patients were diagnosed with reactive hemophagocytic syndrome (RHPS) during a 7 month period. Of these, three patients were diagnosed with acquired immunodeficiency syndrome complicated by disseminated Mycobacterium tuberculosis infection, incompletely treated Pneumocystis carinii pneumonia and disseminated histoplasmosis respectively. The fourth patient had non‐Hodgkin's lymphoma of the mature T‐cell phenotype. Fever, bicytopenia, or pancytopenia, elevated serum lactate dehydrogenase (LDH) level (>1,000 IU/L), and hemophagocytic histiocytosis in smears of bone marrow aspirate were present in all patients. Hyperferritinemia (>10,000 ng/ml) was present in all (range 34,976 to 425,984 ng/mL) and showed a decrease in the two patients who responded to therapy. Hyperferritinemia (>10,000 ng/ml) and elevated serum LDH (>1,000 IU/L) are important clues to the diagnosis of RHPS in the febrile cytopenic patient with immunodeficiency. © 1995 Wiley‐Liss, Inc.
Clinical correlates of subnormal vitamin B12 levels in patients infected with the human immunodeficiency virus
Authors: Paltiel Ora , Falutz Julian , Veilleux Martin , Rosenblatt David S. , Gordon Kathleen 
Published: February 2007

AbstractObjectives: To determine the prevalence and describe the clinical correlates of subnormal cobalamin levels in subjects infected with the human immunodeficiency virus (HIV), and to assess its relationship to virus‐mediated immunosuppression and/or anti‐viral therapy.Setting: Outpatient referral clinic in tertiary care hospital.Patient population: 200 HIV infected individuals.Study design: Descriptive cross sectional survey, with prospective follow‐up in a subgroup of patients before and after initiation of zidovudine therap.Measures: Routine complete blood count, serum B12 assay, CD4 counts. Serum homocysteine levels, and Schilling tests were performed on subgroups of study subjects.Results: Subnormal serum B12 levels were found in 61 subjects (30.5%). B12 deficient subjects were more likely to be taking zidovudine. (P = .007). Serum homocysteine levels were significantly higher in patients with subnormal cobalamin levels but were unrelated to CD4 counts or zidovudine use, and were rarely outside of the normal range. Malabsorption of vitamin B12 as evidenced by abnormal Schilling tests was more likely among patients with more advanced HIV disease, or gastrointestinal symptoms but was not necessarily associated with low B12 levels.Conclusions: Decreased cobalamin levels are found frequently in HIV disease, especially among those treated with zidovudine. Evidence of B12 malabsorption is found among those with more advanced disease and gastrointestinal symptoms.
Antibody to annexin V has anti‐phospholipid and lupus anticoagulant properties
Authors: Nakamura Norihiko , Kuragaki Chie , Shidara Yoshihiro , Yamaji Kenji , Wada Yoshinao 
Published: February 2007

AbstractAnti‐annexin V (anti‐ANXV) IgG and lupus anticoagulant (LAC) were both shown to be capable of inducing apoptosis in umbilical vein endothelial cells [Nakamura et al.:Biochem Biophys Res Commun 205:1488‐1493,1994]. In the present study, we have demonstrated that anti‐ANXV lgG prolongs the activated partial thromboplastin time and has an affinity for phospholipids in enzyme‐linked immunosorbent assay. This indicates overlapping of anti‐ANXV and LAC activities, suggesting that ANXV may be involved in the autoimmune mechanism for LAC production. © 1995 Wiley‐Liss, Inc.
Bone marrow of patients with active multiple myeloma: Angiogenesis and plasma cell adhesion molecules LFA‐1, VLA‐4, LAM‐1, and CD44
Authors: Vacca Angelo , Loreto Michela Di , Ribatti Domenico , Stefano Rita Di , Gadaleta‐Caldarola Gennaro , Iodice Giuseppe , Caloro Daniela , Dammacco Franco 
Published: February 2007

AbstractBone marrow plasma cells and stromal cells in multiple myeloma (MM) have been shown to be capable of releasing cytokines with angiogenic properties. Plasma cells can also express adhesion molecules controlling their adhesive interactions with endothelial cells. In the present study, we have evaluated by immunohistochemistry the extent of angiogenesis in the bone marrow of: a) 51 patients with active and non‐active MM; b) 25 patients with monoclonal gammopathy of undetermined significance (MGUS). Plasma cells were investigated by flow cytometry for the expression of the adhesion molecules LFA‐1, VLA‐4, LAM‐1, and CD44. The results showed that, while angiogenesis was very low or absent in patients with MGUS and non‐active MM, it increased markedly in those with active MM. The highest detectability of plasma cell adhesion molecules, except LAM‐1, was also found in these patients. The functional significance of these findings is unknown. Their consistent occurrence in the bone marrow of active myeloma patients, however, strongly suggests that more frequent adhesive interactions between plasma cells and their microvasculature underlie tumor dissemination.
Use of recombinant hirudin as antithrombotic treatment in patients with heparin‐induced thrombocytopenia
Authors: Schiele F. , Vuillemenot A. , Kramarz P. , Kieffer Y. , Anguenot T. , Bernard Y. , Bassand J. P. 
Published: February 2007

AbstractHeparin‐induced thrombocytopenia is a rare but severe complication of heparin therapy that can result in severe venous or arterial thromboembolic events and whose treatment remains partially unanswered. Recombinant hirudin is potentially effective as an antithrombotic treatment in the management of heparin‐induced thrombocytopenia, given its potent antithrombin effects without known interaction with platelets. We report the results obtained with intravenous recombinant hirudin (HBW 023) administered on a compassionate basis to patients suffering from heparin‐induced thrombocytopenia.Six patients suffering from heparin‐induced thrombocytopenia were submitted to intravenous recombinant hirudin (HBW 023) administered at a dose of 0.05 mg/kg/hr after an initial bolus injection of 0.07 mg/kg in the case of a venous thromboembolic event, and at a dose of 0.15 mg/kg/hr with the same initial bolus injection in the case of an arterial thromboembolic event. Whenever possible, oral anticoagulation with acenocoumarol was introduced at the same time as recombinant hirudin, which was interrupted as soon as the international normalized ratio reached 3. Clinical events, particularly thromboembolism and bleeding, were noted; activated partial thromboplastin time (aPTT), and platelet count were assessed throughout the administration of recombinant hirudin.Heparins responsible for heparin‐induced thrombocytopenia were porcine sodium or calcium heparinate in four cases, nadroparin in one case, and enoxaparin in one case. Thrombocytopenia was discovered on routine systematic platelet count in two patients and after the occurrence of arterial and venous thromboembolism in two patients, respectively. After discontinuation of heparin and the onset of recombinant hirudin, clinical evolution was uneventful in all patients, with no recurrence of thromboembolism, limb amputation, or hemorrhagic complication. The aPTT ratio varied from 1.8 to 3.5 (median 2.4) throughout administration of recombinant hirudin. Platelet count rose from nadir (median value 60 × 109 15 to 90) to above 100 × 109/L in every patient within 3–6 days (median 5), after discontinuation of heparin.Intravenous administration of recombinant hirudin ensured safe anticoagulation in patients with heparin‐induced thrombocytopenia and made it possible to wait for oral anticoagulation to become efficient and platelet count to return to normal values without occurrence or recurrence of thromboembolism.
Pancytopenia due to hemophagocytic syndrome as the presenting manifestation of babesiosis
Authors: Gupta Pankaj , Hurley Randolph W. , Helseth Peter H. , Goodman Jesse L. , Hammerschmidt Dale E. 
Published: February 2007

AbstractWe present a case of hemophagocytosis during infection with the intraërythrocytic protozoanBabesia microtiin a 47‐year‐old splenectomized renal allograft recipient. After therapy with clindamycin and quinine a relapse responded to atovaquone; durable remission was not achieved until trimethoprim/sulfa was added. We postulate the severity of our patient's syndrome was due to splenectomy and chronic immunosuppression. Babesiosis should be considered when immunocompromised patients develop pancytopenia.
Coagulant proteins and thrombin generation in synovial fluid: A model for extravascular coagulation
Authors: Chang Ping , Aronson David L. , Borenstein David G. , Kessler Craig M. 
Published: February 2007

AbstractThe coagulant content and thrombin generating potential of synovial fluid from patients with osteoarthritis were studied as a model of extravascular coagulation. The concentrations of individual coagulant proteins were partially correlated with their molecular weight. The levels of the very large coagulants factor V, factor VIII and von Willebrand factor antigen (vWF:ag) are less than 1% of the activities found in a normal pooled reference plasma while smaller coagulants including factors IX, XI and prothrombin range between 9 and 30%. The protease inhibitors antithrombin‐III (AT‐III) and Alpha‐2 macroglobulin in synovial fluid were present at levels of 74% and 13% of plasma, higher than expected based on their molecular weights. Prothrombin was more rapidly activated by tissue thromboplastin than by aPTT reagent. The thrombin activity formed in synovial fluid decreased more rapidly than that formed in dilute plasma. The addition of recombinant factor VIII or bovine factor V to synovial fluid accelerated the thrombin production by APTT but not by tissue thromboplastin. Indicating that the low levels of factor VIII and factor V did limit the rate of thrombin production. The addition of specific antibodies to factor VIII or factor V strongly inhibited thrombin production by aPTT.These data confirm a roughly inverse relationship between the concentrations of coagulation proteins and their molecular weight in synovial fluid and indicate that thrombin can be generated in synovial fluid. The inactivation of thrombin in synovial fluid may be more dependent on antithrombin‐III than in plasma because of the increased AT‐III/alpha‐2 macroglobulin ratio seen in synovial fluid.
Serum concentrations of IL‐5, GM‐CSF, and IL‐3 and the production by lymphocytes in various eosinophilia
Authors: Koike Toshiyuki , Enokihara Hideo , Arimura Hironari , Ninomiya Haruhiko , Yamashiro Kyoko , Tsuruoka Nobuo , Tsujimoto Masafumi , Aoyagi Masakuni , Watanabe Kanji , Nakamura Yuuichi , Saitou Kenji , Furusawa Shimpei , Shishido Hideo 
Published: February 2007

AbstractThe concentrations of interleukin‐5 (IL‐5), granulocyte‐macrophage colony‐stimulating factor GM‐CSF, and interleukin‐3 (IL‐3) in serum and in IL‐2‐stimulated lymphocyte culture medium (L‐IL2‐CM) prepared from patients with reactive eosinophilia were measured by enzyme‐linked immunosorbent assay (ELISA). Serum IL‐5 levels were increased in 16 out of 42 cases. GM‐CSF and IL‐3 were below the detectable levels in all sera examined. The concentrations of IL‐5 and GM‐CSF in L‐IL2‐CM were increased in 10 out of 29 patients. IL‐3 was below the detectable levels in all L‐IL2‐CM.