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Biomedical subjects

J Lazarchick

Publications and source records attributed to J Lazarchick.

At least 19 recordsLinked to original sources
PubMed2003

Autologous bone marrow transplant in a patient with sickle cell disease and diffuse large B-cell lymphoma.

As the life expectancy of patients with homozygous sickle cell anemia (SCA) improves, SCA care providers are confronted with diseases of the adult SCA population rarely seen before. We report here a 40-year-old woman with SCA who developed diffuse large B-cell non-Hodgkin's lymphoma (NHL) that was treated with eight cycles of chemotherapy consisting of cyclophosphamide, doxorubicin, vincristine, prednisone, and etoposide (CHOPE), without complete remission. She subsequently underwent high-dose cyclophosphamide and total-body irradiation followed by autologous bone marrow transplantation (BMT). To reduce the risk of sickle cell crisis precipitated by G-CSF, she underwent hypertransfusion to maintain a low % hemoglobin S throughout her treatment course. Although she has required iron chelation therapy and shows no sign of modification of her underlying SCA, she remains in remission from NHL 12 years posttransplant. To our knowledge, this is the first reported case of autologous BMT in a patient with SCA. Our patient illustrates that SCA in itself does not preclude autologous stem cell transplantation for lymphoma in selected patients, and this report should encourage others to consider autologous BMT in adults with SCA where it represents a lifesaving therapy for malignant diseases.

Adult↗
PubMed2000

Acute renal artery and vein thrombosis after renal transplant, associated with a short partial thromboplastin time and factor V Leiden mutation.

Renal graft thrombosis is a rare but devastating complication of renal transplantation. It accounts for one-third to one-half of early graft losses. We report a patient with acute renal artery and vein thrombosis associated with abnormally short activated partial thromboplastin time (aPTT) and factor V Leiden mutation. Vascular thrombosis developed on the ninth post-transplant day and led to a graft loss. Before transplantation, the patient had three episodes of thrombosis of arteriovenous access for hemodialysis. Our case illustrates the importance of investigating pretransplant patients for hypercoagulable states, particularly those with short aPTT.

Acute Disease↗
PubMed1999

Mesenteric vein thrombosis secondary to protein S deficiency.

Mesenteric vein thrombosis is an uncommon condition. Diagnosis is often difficult because of the nonspecific clinical presentation and findings on routine laboratory and radiological evaluation. Endoscopy is usually unrevealing. An underlying hypercoagulable state is often present, but protein S deficiency has rarely been implicated. We describe a case in which chronic inferior mesenteric vein thrombosis, with remarkable endoscopic findings, occurred as the initial presentation of type I protein S deficiency.

Angiography↗
PubMed1999

Primary hepatic B-cell lymphoma of mucosa-associated lymphoid tissue.

Mucosa-associated lymphoid tissue (MALT) lymphomas are low-grade B-cell lymphomas that occur in a variety of extranodal sites but rarely as a primary hepatic lymphoma. We describe the histological findings, immunophenotype, and immunohistochemistry of one such lymphoma found incidentally in a 69-year-old woman. The lymphoid infiltrate invaded the liver in a serpiginous configuration with entrapment of nodules of normal liver. Reactive follicles were surrounded by intermediate-sized lymphoid cells with slightly irregular nuclei and pale cytoplasm. Only a few scattered lymphoepithelial lesions were identified since most of the bile ducts were destroyed. The immunophenotype determined by flow cytometry identified the lymphoid cells as being CD19, CD20 positive and exhibiting lambda light chain restriction. CD5, CD10, and CD23 were negative. Immunohistochemistry showed the neoplastic cells to be positive for CD20 (L-26) and bcl-2. The reactive follicles were negative for bcl-2. CD3 showed only a few scattered T cells. Cyclin D1 did not stain the neoplastic cells. Cytokeratin (AE1/AE3) highlighted the lymphoepithelial lesions and residual bile ducts. MALT lymphomas need to be recognized and distinguished from other B-cell lymphomas, particularly mantle cell lymphomas, because of the difference in behavior and treatment.

Aged↗
PubMed1999

Laboratory recognition of a rare hemoglobinopathy: hemoglobins SS and SG(Philadelphia) associated with alpha-thalassemia-2.

This article describes the laboratory investigation of an unusual hemoglobinopathy involving hemoglobin (Hb) S, HbSG(Philadelphia), and alpha-thalassemia-2 in a patient whose phenotype was HbSC by alkaline electrophoresis. Findings of a mean corpuscular volume of 62 fL and microcytes on the blood smear were inconsistent with HbSC disease. The patient's clinical course over several years had been mildly symptomatic. Testing in our hospital laboratory using isoelectric focusing and cation-exchange high-performance liquid chromatography to separate hemoglobins showed an unknown variant. Additional studies, including globin chain electrophoresis, reverse-phase high-performance liquid chromatography, and polymerase chain reaction-based DNA analysis were performed at reference laboratories, which reported the following findings: HbG(Philadelphia) associated with alpha-thalassemia-2, HbS and HbG(Philadelphia), and the alpha-globin deletions defining the -alpha3.7/-alpha3.7 genotype. The hemoglobin molecular defects, alpha-thalassemia-2, and the pattern of inheritance are discussed.

Adult↗
PubMed1998

Inhibitory anti-factor V antibodies bind to the factor V C2 domain and are associated with hemorrhagic manifestations.

Factor V inhibitors may develop as spontaneous autoantibodies, as alloantibodies after exposure to bovine thrombin preparations, or in factor V-deficient patients after plasma therapy. Clinical manifestations range from asymptomatic laboratory abnormalities to life-threatening hemorrhage. We have characterized the anti-factor V antibodies from 12 patients diagnosed with factor V inhibitors. In 8 patients, hemorrhagic complications (5 autoantibodies and 3 bovine thrombin-induced alloantibodies) developed, and 4 were asymptomatic (2 autoantibodies and 2 alloantibodies). The IgG fractions from all 12 patients immunoprecipitated the factor Va light chain, but only the 8 IgG fractions associated with hemorrhage inhibited factor V activity in a prothrombinase assay. Nine IgG fractions, including the 8 patients with hemorrhage, immunoprecipitated the isolated second C-type domain (C2). The 8 IgG fractions from the symptomatic patients also immunoprecipitated recombinant chimeras containing only the N-terminal third of the factor V C2 domain, and isolated recombinant C2 domain abrogated the inhibitory effect of the antibodies. Five of the inhibitory IgG fractions blocked binding of factor V to phosphatidylserine. These results suggest that inhibitory anti-factor V antibodies are associated with hemorrhagic manifestations and frequently bind to a common region within the C2 domain, whether originating spontaneously or after exposure to bovine thrombin.

Adolescent↗
PubMed1996

The effects of desmopressin and 6% hydroxyethyl starch on factor VIII:C.

In moderate doses of 20 mL/kg (1.2 g/kg), hydroxyethyl starch (HES) 6% decreases factor VIII:C activity. Desmopressin (DDAVP) increases circulating levels of factor VIII:C by stimulating the release of factor VIII:C from peripheral storage sites. The objective of this study was to monitor the changes in factor VIII:C associated with sequential HES and DDAVP administration. Thirty patients undergoing surgical procedures with a predicted blood loss of less than 750 mL were enrolled. After induction of anesthesia, HES was administered, 20 mL/kg, to a maximum of 1500 mL, at a rate to meet intraoperative fluid requirements. Patients then randomly received either a 10-mL solution containing 0.3 microgram/kg of DDAVP (Group 1) or 10 mL of normal saline (Group 2). After HES administration, factor VIII:C levels decreased significantly, to 69% of baseline, in both groups. After study drug administration, factor VIII:C in Group 1 increased significantly to 135% of baseline at 30 min and 115% of baseline at 60 min while in Group 2 average factor VIII:C levels remained below baseline at 30 and 60 min. DDAVP produced an increase in factor VIII:C activity despite HES administration and should be considered a treatment option for the mild coagulopathy infrequently associated with HES administration.

Adolescent↗
PubMed1996

Myelodysplasia associated with Turner syndrome.

PURPOSE: This study reports the association of myelodysplasia with Turner syndrome. PATIENT AND METHODS: An 11-year-old girl with Turner syndrome was found to have mild macrocytic anemia that persisted during 2 years. RESULTS: Examination of the bone marrow revealed dyserythropoietic features with multinucleation consistent with refractory anemia. Levels of hemoglobin F were also markedly elevated (57%). She also had transient neutropenia and thrombocytopenia, as well as abnormal platelet function studies. The hematopoietic abnormalities were mild and may have been missed were she not followed for her hypertension and aortic coarctation. CONCLUSIONS: Myelodysplastic syndromes in children are frequently associated with chromosomal abnormalities, but an association with Turner syndrome has not been previously described. This could be due to the fact that mild hematopoietic abnormalities in these patients may not be investigated.

Anemia↗
PubMed1994

Antenatal vitamin K therapy of the low-birth-weight infant.

OBJECTIVE: The purpose of our study was to determine whether maternal vitamin K1 administered antenatally improved global coagulation parameters and the levels of specific vitamin K-dependent proteins in low-birth-weight infants. STUDY DESIGN: Thirty-three preterm mothers admitted in labor were assigned in a prospective, blinded fashion to receive either intramuscular vitamin K1 (17) or placebo (16). At delivery cord blood samples were tested for prothrombin time, activated partial thromboplastin time, factor II and protein C activity, and antigen levels. Statistical analysis was by Student t test. RESULTS: No statistically significant differences could be demonstrated with regard to group mean values for global tests (prothrombin time, activated partial thromboplastin time) or specific vitamin K-dependent protein levels (factor II, protein C) in newborns whose mothers received antenatal vitamin K compared with those who did not. CONCLUSION: These results would suggest that antenatal vitamin K1 therapy to mothers < 32 weeks' gestation has no significant effect on the level of vitamin K-dependent factors in the fetus.

Adolescent↗
PubMed1993

Intrapleural streptokinase in experimental empyema.

Intrapleural streptokinase has been used in multiloculated empyemas to enhance pleural space drainage, presumably by causing fibrinolysis of the interlocular septae. We evaluated the efficacy and safety of daily administration of 10,000 U intrapleural streptokinase or equal volumes of saline to enhance resolution of experimental empyema in the rabbit pleural space. Seventy-two hours after intrapleural turpentine, 10(8) colony-forming units each of Escherichia coli, Peptostreptococcus anaerobius, and Bacteroides fragilis were injected into the sterile pleural effusion of all animals. Immediately after bacterial inoculation, and daily for 3 days, animals received 10,000 U streptokinase or saline intrapleurally. Animals that achieved a pleural fluid pH < 7.30 and either glucose < 50 mg/dl or LDH > 500 IU/L were included for data analysis. At Day 4 after bacterial inoculation, the streptokinase-treated empyemic rabbits had more pleural fluid (18.8 +/- 5.1 ml) (mean +/- SEM) than did saline-treated control animals (4.8 +/- 1.7 ml) (p = 0.015), fewer interpleural adhesions (8.2 +/- 2.7) than did saline-treated control animals (25.1 +/- 3.6) (p = 0.002), and comparable amounts of visceral and parietal pleural plaque than did saline-treated control animals (p = NS). No evidence of systemic fibrinolysis was observed at 1 h after intrapleural streptokinase administration. We conclude that intrapleural streptokinase decreases interpleural adhesion numbers but fails to reduce the amount of pleural plaque observed in experimental empyema in rabbits. The increases in pleural fluid volume observed after streptokinase administration may be due to mechanisms other than fibrinolytic activity.

Animals↗
PubMed1992

Postfiltration factor VIII and fibrinogen levels in cryoprecipitate stored at room temperature and at 1 to 6 degrees C.

The 13th edition of the standards of the American Association of Blood Banks specified storage at 1 to 6 degrees C for cryoprecipitated anti-hemophilic factor (Cryo) administered up to 6 hours after thawing if the Cryo is used for factor VIII (FVIII) content (Standard J4.210). Previous editions specified room-temperature (RT) storage for up to 6 hours. Currently, the temperature specification has been deleted. There are few data addressing the optimal storage temperature and maximum storage time for FVIII and fibrinogen in thawed Cryo. Thirty bags of Cryo were assayed for FVIII and fibrinogen. Each bag was divided into two aliquots; one was stored at RT and the other at 1 to 6 degrees C. Assays were performed immediately after thawing (Base) and 6 and 24 hours after thawing, respectively. All samples were filtered through 200-mu blood component infusion sets before assay. Three hundred analyses were performed, 150 each for FVIII and fibrinogen by conventional clotting technique. Data were analyzed by using a paired t test. Cryo stored at 1 to 6 degrees C for 6 and 24 hours showed an FVIII loss of 35 percent (p less than 0.0001) and 63 percent (p less than 0.0001), respectively. Cryo stored at RT for 6 and 24 hours had an FVIII loss of 8 percent (p greater than 0.05) and 20 percent (p less than 0.0001). Cryo stored at 1 to 6 degrees C for 6 and 24 hours had a fibrinogen loss of 20 percent (p less than 0.0001) and 43 percent (p less than 0.0001). Cryo stored at RT for 6 hours had no fibrinogen loss and a 2 percent loss at 24 hours (p greater than 0.05). These preliminary data show a significant loss of FVIII and fibrinogen activity in Cryo stored at 1 to 6 degrees C and filtered before assay. The FVIII and fibrinogen activity at RT is clearly maintained up to 6 hours after thawing.

Blood Coagulation Tests↗
PubMed1991

Platelet dysfunction in Noonan's syndrome. A case with a platelet cyclooxygenase-like deficiency and chronic idiopathic thrombocytopenic purpura.

Individuals with Noonan's syndrome are likely to have one or more coagulation abnormalities: complex platelet function defects, partial Factor XI deficiency, or von Willebrand's disease. A distinctive platelet function defect has not been identified. The authors describe a 24-year-old women with Noonan's syndrome, chronic idiopathic thrombocytopenic purpura (ITP), and a platelet function defect characterized by a greater than 15-minute bleeding time, failure of aggregation and release with 10 microM ADP, 10 microM epinephrine, 750 microM arachidonic acid or 0.019 g/L collagen. A mixture of aspirin-treated platelets with the patient's platelets failed to correct the defect. Addition of 2.5 microM U46619 (a PGG2 analogue) corrected the aggregation and release defect. An electron microscopic analysis failed to reveal structural abnormalities. Thus, the platelet function defect in this patient appears to be a functional deficiency of cyclooxygenase. The presence of autoantiplatelet antibodies in a clinical setting consistent with chronic ITP raises the possibility that the defect may be acquired.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

The effect of bacteremia on automated platelet measurements in neonates.

Platelet volume measurements have been used to differentiate consumptive and hypoplastic thrombocytopenia. Since thrombocytopenia is a frequent complication of neonatal sepsis, the authors explored the utility of correlating mean platelet volume (MVP) and platelet distribution width (PDW) with bacteremia. In a sample of 156 infants, there was a significantly increased presence of bacteremia in those infants with MPV greater than 10.8 fL and/or PDW greater than 19.1%. High MPV and PDW showed high specificity for detecting bacteremia (95% and 79%, respectively), and had good negative predictive value. Neonates with blood cultures positive at birth (early infection) tended to have normal platelet volumes, while those infected after three days of age (late infection) had dramatic increases in MPV and PDW. Changes in MPV and PDW should be noted when the diagnosis of late sepsis is considered.

Age Factors↗
PubMed1990

Hemostatic alterations with exercise conditioning in NIDDM.

Various parameters of coagulation and fibrinolysis were measured in 13 men (aged 54 +/- 3 yr) with non-insulin-dependent diabetes mellitus (NIDDM) before and after 12-14 wk of exercise training. Subjects exercised for 30 min 3 times/wk at 70% of maximum O2 consumption (VO2max). Training increased VO2max by 12.5% but did not alter body weight, relative body fat, blood pressure, cholesterol, triglycerides, or high-density lipoprotein cholesterol. Slight downward trends were apparent for fasting glucose and insulin, but glycosylated hemoglobin was unchanged. There were no changes in coagulation parameters of plasminogen, hematocrit, or alpha 2-antiplasmin. Plasma fibrinogen (303 +/- 24.2 vs. 256 +/- 12.3 mg/dl) and fibronectin (380 +/- 41.9 vs. 301 +/- 22.2 micrograms/ml) were significantly reduced (P less than 0.02) by exercise conditioning. Three assays of fibrinolytic activity (tissue plasminogen activator, euglobulin lysis time, and an isotopic measure of fibrinolysis) confirmed that neither basal fibrinolysis nor the fibrinolytic responses to venous occlusion and maximal exercise were significantly altered. Exercise conditioning may have antithrombotic effects in NIDDM by reducing plasma fibrinogen and fibronectin. Although the significance of the fall in fibronectin awaits further studies, the reduction in plasma fibrinogen gives a rationale for the use of exercise training in men with NIDDM.

Diabetes Mellitus, Type 2↗