12 research outputs found

    Increased plasma cardiac troponin I concentration in lambs with myocarditis

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    Background Cardiac troponin I (cTnI) is a blood biomarker of myocardial injury. A human cTnI assay may be useful for measuring cTnI concentrations in lambs with naturally occurring myocarditis. Objective The aims of this study were to evaluate the utility of a commercially available human chemiluminescent microparticle cTnI immunoassay for measuring plasma cTnI concentrations in lambs with naturally occurring myocarditis from infection with foot and mouth disease virus (FMDV), and to determine cTnI expression in cardiac muscle of affected lambs. Methods Ten lambs with myocarditis and 10 clinically healthy lambs (control group) were included. Clinical signs, gross and histologic necropsy findings, and immunoreactivity for cTnI in cardiac tissue were evaluated. Plasma cTnI concentration was determined using the commercial human immunoassay system. Results All lambs with myocarditis died within 1 similar to day of clinical signs. Infection with FMDV was confirmed by PCR analysis. Gross cardiac lesions were evident and histologic examination revealed myocarditis. Immunoreactivity for cTnI was absent in cardiac myocytes that were degenerative or necrotic, but was strong in cardiac myocytes from unaffected areas of the myocardium and in all cardiac myocytes of healthy lambs. The geometric mean plasma concentrations of cTnI for lambs in the myocarditis and control groups were 146.78 similar to mu g/L (95% confidence interval [CI], 61.90348.06) and 0.013 similar to mu g/L (95% CI, 0.0100.017), respectively (t-value 19.27; P similar toBackgroundCardiac troponin I (cTnI) is a blood biomarker of myocardial injury. A human cTnI assay may be useful for measuring cTnI concentrations in lambs with naturally occurring myocarditis.ObjectiveThe aims of this study were to evaluate the utility of a commercially available human chemiluminescent microparticle cTnI immunoassay for measuring plasma cTnI concentrations in lambs with naturally occurring myocarditis from infection with foot and mouth disease virus (FMDV), and to determine cTnI expression in cardiac muscle of affected lambs.MethodsTen lambs with myocarditis and 10 clinically healthy lambs (control group) were included. Clinical signs, gross and histologic necropsy findings, and immunoreactivity for cTnI in cardiac tissue were evaluated. Plasma cTnI concentration was determined using the commercial human immunoassay system.ResultsAll lambs with myocarditis died within 1&nbsp;day of clinical signs. Infection with FMDV was confirmed by PCR analysis. Gross cardiac lesions were evident and histologic examination revealed myocarditis. Immunoreactivity for cTnI was absent in cardiac myocytes that were degenerative or necrotic, but was strong in cardiac myocytes from unaffected areas of the myocardium and in all cardiac myocytes of healthy lambs. The geometric mean plasma concentrations of cTnI for lambs in the myocarditis and control groups were 146.78&nbsp;&mu;g/L (95% confidence interval [CI], 61.90&ndash;348.06) and 0.013&nbsp;&mu;g/L (95% CI, 0.010&ndash;0.017), respectively (t-value 19.27; P&nbsp;&lt;&nbsp;.0001).ConclusionsA commercial human cTnI assay may be used to detect plasma cTnI concentrations in sheep, and cTnI may be used as a blood-based biomarker of myocarditis in this species.</p

    The diagnostic value of two commercially available human cTnI assays in goat kids with myocarditis

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    BackgroundCardiac troponin I (cTnI) is a peripheral blood marker for myocardial damage. Because of the unavailability of goat-specific cTnI assays human cTnI assays may be validated for detection of myocarditis in goat kids

    Hyperferritinemia In The Critically Ill Child With Secondary Hemophagocytic Lymphohistiocytosis/Sepsis/Multiple Organ Dysfunction Syndrome/Macrophage Activation Syndrome: What Is The Treatment?

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    Introduction: Hyperferritinemia is associated with increased mortality in pediatric sepsis, multiple organ dysfunction syndrome (MODS), and critical illness. The International Histiocyte Society has recommended that children with hyperferritinemia and secondary hemophagocytic lymphohistiocytosis (HLH) or macrophage activation syndrome (MAS) should be treated with the same immunosuppressant/cytotoxic therapies used to treat primary HLH. We hypothesized that patients with hyperferritinemia associated secondary HLH/sepsis/MODS/MAS can be successfully treated with a less immunosuppressant approach than is recommended for primary HLH. Methods: We conducted a multi-center cohort study of children in Turkish Pediatric Intensive Care units with hyperferritinemia associated secondary HLH/sepsis/MODS/MAS treated with less immunosuppression (plasma exchange and intravenous immunoglobulin or methyl prednisolone) or with the primary HLH protocol (plasma exchange and dexamethasone or cyclosporine A and/or etoposide). The primary outcome assessed was hospital survival. Results: Twenty-three children with hyperferritinemia and secondary HLH/sepsis/MODS/MAS were enrolled (median ferritin = 6341 mu g/dL, median number of organ failures = 5). Univariate and multivariate analyses demonstrated that use of plasma exchange and methyl prednisolone or intravenous immunoglobulin (n = 17, survival 100%) was associated with improved survival compared to plasma exchange and dexamethasone and/or cyclosporine and/or etoposide (n = 6, survival 50%) (P = 0.002). Conclusions: Children with hyperferritinemia and secondary HLH/sepsis/MODS/MAS can be successfully treated with plasma exchange, intravenous immunoglobulin, and methylprednisone. Randomized trials are required to evaluate if the HLH-94 protocol is helpful or harmful compared to this less immune suppressive and cytotoxic approach in this specific population.Wo

    Critically ill children with pandemic influenza (H1N1) in pediatric intensive care units in Turkey

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    WOS: 000299073000003PubMed ID: 21263368Objectives: To outline the epidemiologic features, clinical presentation, clinical courses, and outcomes in critically ill children with pandemic influenza in pediatric intensive care units. Design: Retrospective, observational, multicenter study. Setting: Thirteen tertiary pediatric intensive care units in Turkey. Patients: Eighty-three children with confirmed infection attributable to pandemic influenza detected by reverse-transcriptase polymerase chain reaction assay between November 1 and December 31, 2009 who were admitted to critical care units. Interventions: None. Measurements and Main Results: During a 2-month period, 532 children were hospitalized with pandemic influenza and 83 (15.6%) needed critical care. For the 83 patients requiring critical care, the median age was 42 (range, 2-204) months, with 24 (28.9%) and 48 (57.8%) of patients younger than 2 and 5 yrs, respectively. Twenty (24.1%) patients had no underlying illness, but 63 (75.9%) children had an underlying chronic illness. Indications for admission to the pediatric intensive care unit were respiratory failure in 66 (79.5%), neurologic deterioration in six (7.2%), and gastrointestinal symptoms in five (6.0%) patients. Acute lung injury was diagnosed in 23 (27.7%), acute respiratory distress syndrome was diagnosed in 34 (41%), and 51 (61.4%) patients were mechanically ventilated. Oseltamivir was used in 80 (96%) patients. The mortality rate for children with pandemic influenza 2009 was 30.1% compared to an overall mortality rate of 13.7% (p = .0016) among pediatric intensive care unit patients without pandemic influenza during the study period. Also, the mortality rate was 31.7% in patients with comorbidities and 25.0% in previously healthy children (p = .567). The cause of death was primary pandemic influenza infection in 16 (64%), nosocomial infection in four (16%), and primary disease progression in five (20%) patients. The odds ratio for respiratory failure was 14.7 (95% confidence interval, 1.85-111.11), and odds ratio for mechanical ventilation was 27.7 (95% confidence interval, 0.003-200). Conclusions: Severe disease and high mortality rates were seen in children with pandemic influenza. Death attributable to pandemic influenza occurred in all age groups of children with or without underlying illness. Multiple organ dysfunction syndrome is associated with increased mortality, and death is frequently secondary to severe lung infection caused by pandemic influenza. (Pediatr Crit Care Med 2012; 13:e11-e17
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