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Antibody Negative (antibody + negative)
Selected AbstractsThe effect of biopsy-positive silent coeliac disease and treatment with a gluten-free diet on growth and glycaemic control in children with Type 1 diabetesDIABETIC MEDICINE, Issue 12 2009S. Sun Abstract Objective, To determine the effect of coeliac disease and treatment with a gluten-free diet on growth and glycaemic control in asymptomatic children with Type 1 diabetes. Methods, Data were compared in children with coeliac disease diagnosed by annual antibody screening and jejunal biopsy and treated with a gluten-free diet (n = 49) against individuals who were antibody negative (n = 49) matched for age, sex and duration of diabetes. Results, No differences in growth were observed. In the years prior to diagnosis of coeliac disease, mean glycated haemoglobin (HbA1c) was lower in cases compared with control subjects [8.3 ± 1.1% vs. 8.7 ± 0.9%, P = 0.02 (mean ± sd)]. In cases, HbA1c deteriorated 12 months from the start of a gluten-free diet to levels similar to control subjects (8.9 ± 1.5% vs. 8.8 ± 1.5%, P -value for analysis of variance = 0.9). In regression analysis, the diagnosis of coeliac disease and start of a gluten-free diet was associated with a rise in HbA1c in the first year of treatment [odds ratio 1.56 (95% confidence intervals 1.16,2.10), P = 0.003] after adjusting for insulin dose and regimen and other variables. Conclusions, In children with Type 1 diabetes, lower HbA1c prior to diagnosis of silent coeliac disease rises following treatment with a gluten-free diet to levels similar to those without coeliac disease. Although unproven, these observations may relate to abnormalities at the small bowel mucosa before the appearance of circulating coeliac antibodies. [source] Hepatitis C virus risk behaviors within the partnerships of young injecting drug usersADDICTION, Issue 7 2010Judith A. Hahn ABSTRACT Aims Young injection drug users (IDU) are at high risk for hepatitis C virus (HCV). We sought to determine whether perceiving one's injecting partner to be HCV positive was associated with decreased odds of engaging in receptive needle/syringe sharing (RNS) or ancillary equipment sharing (AES) with that partner. Design Cross sectional study. Setting 2003 to 2007 in San Francisco. Participants 212 young (under age 30) IDU who were HCV antibody negative reported on 492 injecting partnerships. Measurements Self-reported RNS and AES within injecting partnerships. Findings RNS and AES (in the absence of RNS) occurred in 23% and 64% of injecting partnerships in the prior month. The odds of engaging in RNS were significantly lower for relationships in which the participant reported that his/her partner was HCV positive (odds ratio [OR] 0.49; 95% confidence interval [CI] 0.25,0.95). This association was attenuated when adjusted for reusing one's own needle/syringe (adjusted OR 0.57; 95% CI 0.28,1.15). The odds of engaging in AES were lower for participants who did not know the HCV status of their partner, only among non-sexual partnerships (OR 0.47; 95% CI 0.29,0.76). Conclusions Because perceiving one's partner to be HCV positive was associated with decreased RNS, increased HCV testing and partner disclosure may be warranted. AES was common and was decreased only among non-sexual partnerships in which the HCV status of the partner was not known. This suggests that interventions to reduce AES in young IDU must be widespread. [source] Seronegative myasthenia gravis: disease severity and prognosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2005F. Romi Around 10,20% of myasthenia gravis (MG) patients do not have acetylcholine receptor (AChR) antibodies (seronegative), of whom some have antibodies to a membrane-linked muscle specific kinase (MuSK). To examine MG severity and long-term prognosis in seronegative MG compared with seropositive MG, and to look specifically at anti-AChR antibody negative and anti-MuSK antibody negative patients. Seventeen consecutive seronegative non-thymomatous MG patients and 34 age and sex matched contemporary seropositive non-thymomatous MG controls were included in a retrospective follow-up study for a total period of 40 years. Clinical criteria were assessed each year, and muscle antibodies were assayed. There was no difference in MG severity between seronegative and seropositive MG. However, when thymectomized patients were excluded from the study at the year of thymectomy, seropositive MG patients had more severe course than seronegative (P < 0.001). One seropositive patient died from MG related respiratory insufficiency. The need for thymectomy in seronegative MG was lower than in seropositive MG. None of the seronegative patients had MuSK antibodies. This study shows that the presence of AChR antibodies in MG patients correlates with a more severe MG. With proper treatment, especially early thymectomy for seropositive MG, the outcome and long-term prognosis is good in patients with and without AChR antibodies. [source] CMV antibody prevalence and seroincidence in plateletpheresis donorsJOURNAL OF CLINICAL APHERESIS, Issue 2 2008Caroline E. Boeke Abstract Objective: To determine the prevalence and seroincidence of CMV seropositivity in plateletpheresis donors of different ages and gender. Methods: CMV antibody serostatus, birthdate, and date of first and most recent donation between the years 1976 and 2006 were retrieved from 222 plateletpheresis donor records at the Johns Hopkins Hospital Donor Center. CMV antibody serostatus was obtained for 183 donors at the most recent donation for which CMV antibody data were available. CMV antibody status and time interval between first and most recent donation were also obtained from 97 repeat plateletpheresis donors who were CMV antibody negative at time of first donation. Results: Overall CMV antibody positivity was 35.5% for 183 donors (mean age = 46.0 years) at time of most recent donation. CMV seropositivity tended to increase with age, being 37.5, 17.9, 37.5, 39.0, and 61.5% for donors aged 20,29 years (n = 8), 30,39 years (n = 39), 40,49 years (n = 64), 50,59 years (n = 59), and 60+ years (n = 13), respectively. Overall CMV seroincidence was 1.6 seroconversions per 100 person years with a rate of 1.4 seroconversions per 100 years for men and 2.3 for women. Conclusion: CMV seroprevalence and seroincidence in this plateletpheresis donor population are relatively low so that a large percentage of donors are likely to be able to provide CMV seronegative platelet components for many years. Our data suggest that targeting groups with lower CMV seroprevalence and seroincidence rates such as young people and possibly men will likely yield the highest percentage of CMV seronegative donors. J. Clin. Apheresis, 2008. © 2008 Wiley-Liss, Inc. [source] Mucosal challenge of Macaca nemestrina with simian immunodeficiency virus (SIV) following SIV nucleocapsid mutant DNA vaccination*JOURNAL OF MEDICAL PRIMATOLOGY, Issue 3-4 2000Robert J. Gorelick A simian immunodeficiency virus (SIV)(Mne) DNA clone was constructed that produces viruses containing a four amino acid deletion in the second zinc finger of the nucleocapsid (NC) domain of the Gag polyprotein. Viruses produced from this clone, although non-infectious both in vitro and in vivo, complete a majority of the steps in a single retroviral infection cycle. Eight pig-tailed macaques (Macaca nemestrina) were inoculated intramuscularly and subcutaneously three times over the course of 24 weeks with the NC mutant expressing DNA. These macaques, and four controls, were then challenged mucosally (intrarectally) with the homologous virus (SIV Mne CL E11S) and monitored for evidence of infection and clinical disease. Prior to challenge, a measurable humoral immune response was noted in four of eight immunized macaques. After challenge, all 12 macaques became infected, although four immunized animals greatly restricted their viral replication, and one immunized animal that controlled replication remains antibody negative. No disease has been evidence during the 46-week period of monitoring after challenge. [source] Evaluation of a new, fully automated immunoassay for detection of HTLV-I and HTLV-II antibodiesJOURNAL OF MEDICAL VIROLOGY, Issue 3 2008Xiaoxing Qiu Abstract Screening blood donations for human T-lymphotropic virus types I and II (HTLV-I/II) continues to be important in protecting the safety of blood products and controlling the global spread of these retroviruses. We have developed a fully automated, third generation chemiluminescent immunoassay, ARCHITECT rHTLV-I/II, for detection of antibodies to HTLV-I/II. The assay utilizes recombinant proteins and synthetic peptides and is configured in a double antigen sandwich assay format. Specificity of the assay was 99.98% (9,254/9,256, 95% CI,=,99.92,100%) with the negative specimens from the general population including blood donors, hospital patients and pregnant women from the US, Japan and Nicaragua. The assay demonstrated 100% sensitivity by detecting 498 specimens from individuals infected with HTLV-I (n,=,385) and HTLV-II (n,=,113). ARCHITECT rHTLV-I/II results were in complete agreement with the Murex HTLV-I/II reference assay and 99.7% agreement with the Genelabs HTLV Blot 2.4 confirmatory assay. Analytical sensitivity of the assay was equivalent to Murex HTLV-I/II assay based on end point dilutions. Furthermore, using a panel of 397 specimens from Japan, the ARCHITECT rHTLV-I/II assay exhibited distinct discrimination between the antibody negative (Delta Value,=,,7.6) and positive (Delta Value,=,7.6) populations. Based on the excellent specificity and sensitivity, the new ARCHITECT rHTLV-I/II assay should be an effective test for the diagnosis of HTLV-I/II infection and also for blood donor screening. J. Med. Virol. 80:484,493, 2008. © 2008 Wiley-Liss, Inc. [source] IgG classification of anti-PF4/heparin antibodies to identify patients with heparin-induced thrombocytopenia during mechanical circulatory supportJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2 2007S. SCHENK Summary., Commercial immunoassays frequently detect anti-PF4/heparin antibodies during mechanical circulatory support (MCS), but only a small minority of patients develops heparin-induced thrombocytopenia (HIT). Whereas platelet functional tests can distinguish between platelet-activating and non-platelet-activating antibodies, commercial PF4-dependent immunoassays do not. Between 2003 and 2004, 113 patients were placed on MCS. Blood samples were obtained on postimplant day 5,7 for analyses by antibody assays and the functional heparin-induced platelet activation (HIPA) assay. Three distinct groups of patient sera were identified: platelet-activating anti-PF4/heparin antibodies (n = 10), non-platelet-activating anti-PF4/heparin antibodies (n = 53), and anti-PF4/heparin antibody negative (n = 50). Patients with platelet-activating antibodies had the highest risk for thromboembolic events (P < 0.005), whereas those with non-platelet-activating antibodies did not differ from antibody negative patients (P = 0.369). The enzyme-immunoassay and column agglutination assays, which cover all immunoglobulin classes, demonstrated adequate sensitivity and negative predictive value; yet, both lacked specificity with respect to the platelet-activating antibodies. If all antibody positive patients were further classified by an IgG-specific anti-PF4/heparin enzyme-immuno assay, specificity for platelet-activating antibodies increased. Whereas IgG-specific optical density (OD) values below 1.0 were likely for non-platelet-activating anti-PF4/heparin antibodies, higher values were progressively predictive for pathogenic platelet activation. The probability of the development of clinical HIT also increased steeply. In conclusion, platelet-activating anti-PF4/heparin antibodies are relatively common (about 9%) in patients on MCS and are associated with significantly higher thrombotic event rates. Low IgG-specific OD values (< 1.0) in the enzyme-immunoassay indicate low likelihood for the presence of platelet-activating antibodies. These results justify further validation so that anticoagulation during MCS becomes safer and adequate. [source] The management of heparin-induced thrombocytopeniaBRITISH JOURNAL OF HAEMATOLOGY, Issue 3 2006David Keeling Abstract The Haemostasis and Thrombosis Task Force of the British Committee for Standards in Haematology has produced a concise practical guideline to highlight the key issues in the management of heparin-induced thrombocytopenia (HIT) for the practicing physician in the UK. The guideline is evidence-based and levels of evidence are included in the body of the article. All patients who are to receive heparin of any sort should have a platelet count on the day of starting treatment. For patients who have been exposed to heparin in the last 100 d, a baseline platelet count and a platelet count 24 h after starting heparin should be obtained. For all patients receiving unfractionated heparin (UFH), alternate day platelet counts should be performed from days 4 to 14. For surgical and medical patients receiving low-molecular-weight heparin (LMWH) platelet counts should be performed every 2,4 d from days 4 to 14. Obstetric patients receiving treatment doses of LMWH should have platelet counts performed every 2,4 d from days 4 to 14. Obstetric patients receiving prophylactic LMWH are at low risk and do not need routine platelet monitoring. If the platelet count falls by 50% or more, or falls below the laboratory normal range and/or the patient develops new thrombosis or skin allergy between days 4 and 14 of heparin administration HIT should be considered and a clinical assessment made. If the pretest probability of HIT is high, heparin should be stopped and an alternative anticoagulant started at full dosage unless there are significant contraindications while laboratory tests are performed. Platelet activation assays using washed platelets have a higher sensitivity than platelet aggregation assays but are technically demanding and their use should be restricted to laboratories experienced in the technique. Non-expert laboratories should use an antigen-based assay of high sensitivity. Only IgG class antibodies need to be measured. Useful information is gained by reporting the actual optical density, inhibition by high concentrations of heparin, and the cut-off value for a positive test rather than simply reporting the test as positive or negative. In making a diagnosis of HIT the clinician's estimate of the pretest probability of HIT together with the type of assay used and its quantitative result (enzyme-linked immunosorbent assay, ELISA, only) should be used to determine the overall probability of HIT. Clinical decisions should be made following consideration of the risks and benefits of treatment with an alternative anticoagulant. For patients with strongly suspected or confirmed HIT, heparin should be stopped and full-dose anticoagulation with an alternative, such as lepirudin or danaparoid, commenced (in the absence of a significant contraindication). Warfarin should not be used until the platelet count has recovered. When introduced in combination with warfarin, an alternative anticoagulant must be continued until the International Normalised Ratio (INR) is therapeutic for two consecutive days. Platelets should not be given for prophylaxis. Lepirudin, at doses adjusted to achieve an activated partial thromboplastin time (APTT) ratio of 1·5,2·5, reduces the risk of reaching the composite endpoint of limb amputation, death or new thrombosis in patients with HIT and HIT with thrombosis (HITT). The risk of major haemorrhage is directly related to the APTT ratio, lepirudin levels and serum creatinine levels. The patient's renal function needs to be taken into careful consideration before treatment with lepirudin is commenced. Severe anaphylaxis occurs rarely in recipients of lepirudin and is more common in previously exposed patients. Danaparoid in a high-dose regimen is equivalent to lepirudin in the treatment of HIT and HITT. Danaparoid at prophylactic doses is not recommended for the treatment of HIT or HITT. Patients with previous HIT who are antibody negative (usually so after >100 d) who require cardiac surgery should receive intraoperative UFH in preference to other anticoagulants that are less validated for this purpose. Pre- and postoperative anticoagulation should be with an anticoagulant other than UFH or LMWH. Patients with recent or active HIT should have the need for surgery reviewed and delayed until the patient is antibody negative if possible. They should then proceed as above. If deemed appropriate early surgery should be carried out with an alternative anticoagulant. We recommend discussion of these complex cases requiring surgery with an experienced centre. The diagnosis must be clearly recorded in the patient's medical record. [source] | ||||||||||