Changes In Acute Phase Research Articles

Multimodal Imaging in Diagnosis of Vogt Koyanagi Harada Disease with Reference to Choroid and Retinal Pigment Epithelium

A 48 year dark skinned North Indian male presented first time to our outpatient with history of bilateral visual decline of 3 weeks duration with associated features of headache, myalgia and rhinitus of 4 weeks duration. A detailed examination confirmed bilateral active anterior granulomatous uveitis with bilateral disc oedema with serous retinal detachment. Multimodal imaging examination was carried out with nideks mirante. Diagnosis in favour of vogt koyanagi harada disease was confirmed. The posterior segment was assessed for various changes in acute and remission phase of vogt koyanagi harada disease with fundus fluorescein angiography, fundus autoflourescence, retroillumination and optical coherence tomography. Thickness and structural change related to central macula thickness, retinal pigment epithelium and choroid were assessed pre and post treatment with additional support of optical coherence tomography and retroillumination. Both these techniques were able to document a greater value change pre and post treatment in these structures. Hence we conclude the need to include these techniques in retinal pigment epithelium and choroidal assessment in vogt koyanagi harada disease.

Longitudinal optogenetic mapping reveals enhanced motor control by the contralesional cortex after traumatic brain injury in mice

Traumatic brain injury (TBI) is a significant cause of human disability, and understanding its spontaneous recovery pattern after injury is critical for potential treatments. However, studies on the function of the contralesional cortex after TBI have mostly focused on acute-phase changes, and long-term dynamic changes in the control of the affected limb by the contralesional cortex are less understood. To unravel long-term adaptations in the contralesional cortex, we developed a mouse model of TBI and used longitudinal optogenetic motor mapping to observe the function of contralesional corticospinal neurons (CSNs) projecting to the unilateral seventh cervical (C7) segment of the spinal cord. We injected a retrograde adeno-associated virus (AAV) expressing channelrhodopsin-2 to optogenetically stimulate and map the functional connections of the motor-sensory cortex. We validated the effectiveness of transcranial optogenetic stimulation for functional mapping and observed a general increase in the control of the affected limb by the contralesional cortex over time. Using retrograde labeling techniques, we showed that TBI does not affect the distribution of C7-CSNs but alters their function, and the labeled CSNs are concentrated in the caudal and rostral forelimb areas. Our findings provide new insights into harnessing contralesional cortical plasticity to improve treatment for affected limbs. This study sheds light on the long-term adaptations in the contralesional cortex after TBI, paving the way for potential clinical applications of optogenetic stimulation to improve motor control and rehabilitation outcomes.

Pathophysiological Aspects of COVID-19-Associated Vasculopathic Diseases.

Since the beginning of coronavirus disease 2019 (COVID-19) pandemic, numerous data reported potential effects on the cardiovascular system due to infection by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), which may lead to COVID-19-associated vasculopathies during the acute phase and measurable vascular changes in the convalescent phase. Infection by SARS-CoV-2 seems to have specific direct and indirect effects on the endothelium, immune and coagulation systems thus promoting endothelial dysfunction, immunothrombosis, and formation of neutrophil extracellular traps although the exact mechanisms still need to be elucidated. This review represents a recent update of pathophysiological pathways of the respective three major mechanisms contributing to COVID-19 vasculopathies and vascular changes and includes clinical implications and significance of outcome data.

Acute phase protein response and changes in lipoprotein particle size in dogs with systemic inflammatory response syndrome

BackgroundImproved methodology to measure acute phase proteins and determination of lipoprotein particle‐size distribution (PSD) could be clinically useful in dogs with systemic inflammatory processes.ObjectivesEvaluate an immunoturbidometric assay for serum amyloid A (SAA) and lipoprotein PSD in dogs with sepsis, nonseptic systemic inflammation, and in healthy controls. Correlate dyslipidemic changes with SAA and C‐reactive protein (CRP) concentrations.AnimalsTwenty‐five dogs with sepsis, 15 dogs with nonseptic systemic inflammation, and 22 healthy controls.MethodsProspective, case‐control study. Variables included SAA, CRP, and electrophoretic subfractionation of high‐ and low‐density lipoproteins (HDL, LDL). Continuous variables were compared using ANOVA or Kruskal‐Wallis tests with linear regression or Spearman's rank correlation used to assess relationships between variables.ResultsMedian SAA and CRP concentrations were greater in dogs with sepsis (SAA 460 mg/L, interquartile range [IQR] 886 mg/L; CRP 133.2 mg/L, IQR 91.6 mg/L) and nonseptic inflammation (SAA 201 mg/L, IQR 436 mg/L; CRP 91.1 mg/L, IQR 88.6 mg/L) compared to healthy dogs (SAA 0.0 mg/L, IQR 0.0 mg/L; CRP 4.9 mg/L, IQR 0.0 mg/L) P < .0001. A cutoff of >677.5 mg/L SAA was 43.2% sensitive and 92.3% specific for sepsis. Low‐density lipoprotein was higher in dogs with sepsis 29.6%, (mean, SD 14.6) compared to 14.4% (mean, SD 5.6) of all lipoproteins in healthy controls (P = .005). High‐density lipoprotein was not associated with CRP but was negatively correlated with SAA (r s −0.47, P < .0001). Subfractions of LDL and HDL differed between groups (all P < .05).Conclusions and Clinical ImportanceMeasurement of SAA using the immunoturbidometric assay evaluated in this study and lipoprotein PSD in dogs with inflammation might help distinguish septic from nonseptic causes of inflammation.

To study thyroid hormone levels (FT3, FT4, and TSH levels) in critically ill children and their correlation with disease severity and clinical outcome in Rajendra Institute of Medical Sciences, Ranchi, Jharkhand.

There are manifold effects on neuro-endocrine and metabolic systems due to critical illness. Abnormalities in thyroid hormone levels in a critically-ill patient with no pre-existing hypothalamo-pituitary-thyroid dysfunction is seen in Euthyroid sick syndrome or Non thyroidal illness syndrome. The understanding of different endocrinal changes in acute phase of critical illness may help us to intervene early and improve by pharmacological intervention. Critically ill children admitted in PICU, RIMS, Ranchi, aged 29 days to 17 years. In our study, it was seen that FT3 and FT4 were low at admission at admission in critically ill children. And among them, the non-survivors had significantly lower values compared to survivors. Among this critically ill patient, more than 70% of patients have shown low free T3 (Type I NTIS) and around 50% of low free T4 levels and free T3 levels (Type II NTIS). We have done this study to assess the thyroid dysfunction in critically ill children admitted in our PICU and its correlation with disease severity and clinical outcome.

Особенности течения гипермобильного синдрома в постковидном периоде и ведение пациентов

Aim: to conduct a comparative analysis of the clinical manifestations and course patterns and needs for medical interventions in two groups of patients with joint hypermobility syndrome (JHS) (after COVID-19 and without it). Patients and Methods: two groups of patients with JHS were observed for 2 months: those who had COVID-19 (n=37) and those without COVID-19 (n=21) aged 18 to 55 years. The inclusion criterion was the absence of injuries, as well as inflammatory and acute-phase changes in blood values recorded in the ambulatory medical record. All complaints were assessed by organs and systems with the identification of the most common ones: clinical manifestations in the post-COVID period, the intensity of the musculoskeletal pain syndrome according to the visual analog scale (VAS), the levels of situational and personal anxiety degree (according to the Spielberger-Hanin test), the exclusion of depression according to the Hospital Anxiety and Depression Scale (HADS), life quality (according to the Russian version of the SF-36 v.2тм questionnaire. Results: the severity of pain in the first group of patients in the categories of "moderate and high pain" was significantly more common versus the group 2 without COVID-19. For the first time, complaints concerning vegetative-vascular dystonia of permanent (heartbeat, tachycardia, spontaneous dyspnea) and paroxysmal (panic attacks) origins were significantly more common in the group of patients who experienced COVID-19. Associations with a higher level of anxiety and a decrease in the life quality were revealed in the group 1 who experienced COVID-19. To relieve musculoskeletal pain, a group of NSAIDs was commonly prescribed in a standard therapeutic dose for 7–10 days. Incomplete pain relief, as well as two- and threefold relapses of musculoskeletal pain were noted in the group 1. The need for prescription of tofisopam anxiolytic 0.05 mg 3 times a day was due to the high and moderate levels of anxiety and permanent and paroxysmal vegetative manifestations in the group experienced COVID-19. The preservation of asthenic syndrome caused the need to prescribe a drug that regulates metabolic processes in the central nervous system: sulbutiamine 200 mg in the morning and at lunch for 4 weeks. After 1 month of treatment with tofisopam and sulbutiamine, there was a significant decrease in the anxiety level, a decrease in the intensity and relief of musculoskeletal pain, as well as an improvement in the life quality. Conclusion: the administration of adjuvant therapy in the form of an anxiolytic (tofisopam) and a drug regulating metabolic processes in the central nervous system (sulbutiamine) to the standard analgesic therapy with NSAIDs in patients who have experienced COVID-19 with severe musculoskeletal pain, vegetative and anxiety disorders leads to a significant reduction or relief of musculoskeletal pain syndromes and an improvement in the life quality. KEYWORDS: joint hypermobility syndrome, COVID-19, joint pain syndrome, post-COVID-19 period. FOR CITATION: Viktorova I.A., Ivanova D.S., Moiseeva M.V. et al. Course patterns and patient management with joint hypermobility syndrome in the post-COVID-19 period. Russian Medical Inquiry. 2022;6(3):133–139 (in Russ.). DOI: 10.32364/2587-6821-2022-6-3-133-139.

Progressive left and right heart dysfunction in coronavirus disease-19: Prospective echocardiographic evaluation.

AimsCardiac dysfunction in coronavirus disease-19 (COVID-19) has been reported during acute phase but serial changes have not been well studied. To determine serial changes in type and severity of echocardiographic left and right heart functions we performed a prospective study.Methods and resultsSuccessive COVID-19 patients at discharge from the hospital from June to December 2020 were enrolled. Clinical details were obtained and echocardiography was performed using Philips IE33X-Matrix. Follow-up evaluation was performed after 3 months. In total, 1789 COVID-19 patients were evaluated. Baseline echocardiography was performed in 1000 eligible patients (men 611, women 389). Mean age was 50.2 ± 15 years, hypertension was in 44.0%, diabetes in 49.4%, and coronary disease in 10.8%. COVID-19 was mild in 47.0%, moderate in 39.5%, and severe in 13.5%. Baseline cardiac parameters were more impaired in severe vs. moderate or mild COVID-19. At 3 months, in 632 patients where baseline and follow-up data were available, decline was observed in select left [left ventricular internal diameter in diastole +0.9 ± 0.2 mm, left atrial volume +7.6 ± 0.1 mL/m2, mitral E/e′ +4.8 ± 0.1, and left ventricular ejection fraction (LVEF) −3.7 ± 0.2%] and right [right ventricular internal diameter in diastole +2.1 ± 0.1 mm, right atrial internal dimension +1.6 ± 0.1 mm, tricuspid Vmax +1.0 ± 0.1 cm, and tricuspid annulus plane systolic excursion (TAPSE) −2.7 ± 0.2 mm] heart variables (P < 0.001). Compared to mild COVID-19, decline was significantly greater in moderate/severe disease, LVEF −1.1 ± 0.3 vs. −3.8 ± 0.3%; mitral E/e′ +3.2 ± 0.1 vs. +4.8 ± 0.1, tricuspid Vmax +0.3 ± 0.1 vs. +1.0 ± 0.1 cm, and TAPSE −0.7 ± 0.2 vs. −2.7 ± 0.2 mm (P < 0.001).ConclusionThis study shows impaired cardiac functions in severe and moderate COVID-19 compared to mild at hospital discharge and progressive decline in left and right heart functions at 3 months. Impairment is significantly greater in patients with moderate to severe disease.

Liver-Dependent Lung Remodeling during Systemic Inflammation Shapes Responses to Secondary Infection.

Systemic duress, such as that elicited by sepsis, burns, or trauma, predisposes patients to secondary pneumonia, demanding better understanding of host pathways influencing this deleterious connection. These pre-existing circumstances are capable of triggering the hepatic acute-phase response (APR), which we previously demonstrated is essential for limiting susceptibility to secondary lung infections. To identify potential mechanisms underlying protection afforded by the lung-liver axis, our studies aimed to evaluate liver-dependent lung reprogramming when a systemic inflammatory challenge precedes pneumonia. Wild-type mice and APR-deficient littermate mice with hepatocyte-specific deletion of STAT3 (hepSTAT3-/-), a transcription factor necessary for full APR initiation, were challenged i.p. with LPS to induce endotoxemia. After 18 h, pneumonia was induced by intratracheal Escherichia coli instillation. Endotoxemia elicited significant transcriptional alterations in the lungs of wild-type and hepSTAT3-/- mice, with nearly 2000 differentially expressed genes between genotypes. The gene signatures revealed exaggerated immune activity in the lungs of hepSTAT3-/- mice, which were compromised in their capacity to launch additional cytokine responses to secondary infection. Proteomics revealed substantial liver-dependent modifications in the airspaces of pneumonic mice, implicating a network of dispatched liver-derived mediators influencing lung homeostasis. These results indicate that after systemic inflammation, liver acute-phase changes dramatically remodel the lungs, resulting in a modified landscape for any stimuli encountered thereafter. Based on the established vulnerability of hepSTAT3-/- mice to secondary lung infections, we believe that intact liver function is critical for maintaining the immunological responsiveness of the lungs.

Influences of gas explosion on acute blast lung injury and time phase changes of pulmonary function in rats under real roadway environment

Objective: The aims of this study were to investigate the effect of gas explosion on rats and to explore the pulmonary function alterations associated with gas explosion-induced acute blast lung injury (ABLI) in real roadway environment. Methods: In April 2018, the large coal mine gas explosion test roadway and explosion test system were used to simulate the real gas explosion roadway environment, fixed the cage and set the explosion parameters. 72 SD rats, male, SPF grade, were randomly divided into nine groups by completely random grouping method according to their body weight: control group, close range group (160 m) , and long range group (240 m) . In each group, there were wound groups (24 h group and 48h group, 8/group, total 48 in six groups) and no wound groups (8/group, total 24 in three groups) . Except for the control group, the other groups were placed in cages at different distances under anesthesia, the experiment of gas explosion was carried out by placing the rats in a position that could force the lungs. The changes of respiratory function of the rats in the non-invasive group were monitored with pulmonary function instrument at 2 h, 24 h, 48 h, 72 h and 168h after the explosion, and were killed under anesthesia 7 days later; the rats in invasive groups were anesthetized and killed at 24 h, 48 h and 168 h, respectively. Gross observation, lung wet-dry ratio and lung histopathology were performed. Results: Compared with the control group, f (respiratory frequency, f) , MV (minute ventilation, MV) , PEF (peak expiratory flow rate, PEF) , PIF (peak inspiratory flow rate, PIF) and EF50 (1/2 tidal volume expiratory flow, EF50) of rats in the close and long range groups decreased significantly after gas explosion 2 h. PAU (respiration pause, PAU) , Te (expiratory time, Te) , Ti (inspiratory time, Ti) and Tr (relaxation time, Tr) were significantly increased (P<0.05) . After 48 h, TV (tidal volume, TV) , Penh (enhanced respiration pause, Penh) , PAU, and PIF of rats in the long range group were significantly increased (P<0.05) . After 72 h, MV in the long range group was significantly decreased (P<0.05) . Compared with the control group, Penh, PAU, Ti and Te were significantly decreased after 168 h in the close and long range groups, with statistical significance (P<0.05) . At the same time, the body weight of rats in different range groups was significantly decreased (P<0.05) . In addition, both HE staining and routine observation of lung tissues of rats in different range groups showed that gas explosion caused pulmonary edema, obviously congested pulmonary capillaries, a large number of inflammatory cells and infiltrated red blood cells. Conclusion: Gas explosion in real roadway environment can cause the change of respiratory function phase and lung tissue damage in rats, suggesting that the model of gas explosion-induced ABLI has been initially established successfully, which would provide a basis for further study on the pathogenesis of ABLI.

Electrical weapons and rhabdomyolysis.

It has been suggested that an application of a conducted electrical weapon (CEW) might cause muscle injury such as rhabdomyolysis and an acute inflammatory response. We explored this hypothesis by testing the effects of electrical weapons on circulating markers of inflammation and muscle damage. In a prospective study, 29 volunteers received a full-trunk 5-s TASER® X26(E) CEW exposure. Venous blood samples were taken before, 5min after, and at 24h following the discharge. We tested for changes in serum levels of C-reactive protein (CRP), alkaline phosphatase (ALP), myoglobin, albumin, globulin, albumin/globulin ratio, aspartate and alanine aminotransferase, creatine kinase, total protein, bilirubin, and lactic acid dehydrogenase. Uncorrected CRP and myoglobin levels were lower in the immediate post exposure period (CRP levels 1.44 ± 1.39 v 1.43 ± 1.32mg/L; p = 0.046 and myoglobin 36.8 ± 11.9 v 36.1 ± 13.9μg/L; p = 0.0019) but these changes were not significant after correction for multiple comparisons. There were no changes in other biomarkers. At 24h, CRP levels had decreased by 30% to 1.01 ± 0.80mg/L (p = 0.001 from baseline). ALP was unchanged immediately after the CEW application but was reduced by 5% from baseline (66.2 ± 16.1 to 62.7 ± 16.1IU/L; p = 0.0003) at 24h. No other biomarkers were different from baseline at 24h. A full-trunk electrical weapon exposure did not lead to clinically significant changes in the acute phase protein levels or changes in measures of muscle cellular injury. We found no biomarker evidence of rhabdomyolysis.

Confiabilidade e validade concorrente da escala de mobilidade hospitalar em pacientes após acidente vascular cerebral

INTRODUÇÃO: A Escala de Mobilidade Hospitalar (EMH) avalia de forma específica a mobilidade de pacientes após AVC no ambiente hospitalar e em estudo prévio foi demonstrada a sua concordância interexaminadores, validade preditiva e a responsividade a mudanças na fase aguda. OBJETIVO: avaliar a validade concorrente da EMH e a sua confiabilidade ao ser aplicada através de entrevista. MATERIAIS E MÉTODOS: Trata-se de um estudo de validação, desenvolvido com pacientes internados em uma Unidade de AVC na cidade de Salvador-Bahia. Para avaliar a validade concorrente da EMH comparamos o seu escore com a pontuação da Escala de Rankin modificada utilizando o teste de Spearman. Ambas escalas foram aplicadas no quinto dia após o AVC pelo mesmo pesquisador, previamente treinado. Para avaliação da confiabilidade da EMH quando aplicada através de entrevista, a escala foi aplicada por dois examinadores em turnos diferentes, no mesmo dia. O primeiro examinador aplicou a escala através da observação do desempenho e o segundo examinador através de entrevista. Utilizamos para esta análise o Coeficiente de Correlação Intraclasse (CCI). RESULTADOS: A pontuação total da EMH apresentou uma correlação positiva muito forte com a ERm (r=0,90) e também foi encontrada uma correlação significativa entre os subitens da EMH e a ERm. Ao comparar a aplicação da EMH através da observação do desempenho e aplicação por entrevista, observamos uma excelente concordância interexaminadores (CCI &gt; 0,90). CONCLUSÃO: A Escala de Mobilidade Hospitalar, projetada especificamente para pacientes após AVC, mostrou um alto grau de validade concorrente e se mostrou confiável quando aplicada através de entrevista.

Review of Inpatient Thrombophilia Testing at a Tertiary Care Center

Abstract Introduction Testing for thrombophilic risk factors is common in patients with thrombosis. However, inpatient hereditary thrombophilia work-ups are prone to false-positive and false-negative results due to concurrent acute phase changes, protein consumption, anticoagulation therapy, and liver disease. A recent ASCP Choosing Wisely guideline recommends against measuring protein C (PC), protein S (PS), or antithrombin III (AT3) to diagnose a hereditary deficiency during an active clotting event. We aimed to review inpatient PC, PS, and AT3 activity assay ordering practices at a tertiary care center. The goal of this study was to determine appropriateness and identify areas for improvement in inpatient thrombophilia ordering practices. Methods A retrospective review of inpatients who underwent thrombophilia testing was performed. Inclusion criteria consisted of adult inpatients with PC, PS, and/or AT3 activity results. Patients for whom AT3 was ordered alone were excluded. The timeframe of testing relative to an acute thrombotic event, anticoagulation therapy, and liver disease was determined via electronic medical record review. Other conditions that can affect PC, PS, or AT3 levels were recorded if noted. Results Over 5 months, 50 inpatients underwent testing for PC, PS, and/or AT3. Testing was performed within 2 weeks of an acute thrombotic event in 92% of patients; 32% received anticoagulation therapy prior to testing and 16% had liver disease. Test results below the reference range were found in the following percentage of patients: 16% PC, 34% PS, and 16% AT3. In total, 23 of 50 (46%) patients had one or more abnormal results; all 23 had potential confounding conditions/drug. Conclusions Inpatient PC, PS, and AT3 testing was frequently performed in clinical settings, which may cause false-positive or false-negative results. This demonstrates the need for increased education and dialogue between the laboratory and clinicians to improve test utilization practices. Potential interventions are currently being analyzed.

NF-κB RelA Is Required for Hepatoprotection during Pneumonia and Sepsis.

Pneumonia and sepsis are distinct but integrally linked public health concerns. The hepatic acute-phase response (APR), which is largely dependent on transcription factors NF-κB RelA and STAT3, is a hallmark of these pathologies and other injurious conditions. Inactivation of the APR can promote liver injury, a frequently observed organ dysfunction during sepsis. However, whether or how the acute-phase changes promote liver tissue resilience during infections is unclear. To determine the hepatoprotective role of the hepatic APR, we utilized mice bearing hepatocyte-specific deletions of either RelA or STAT3. Mice were challenged intratracheally (i.t.), intravenously (i.v.), or intraperitoneally (i.p.) with Escherichia coli, Klebsiella pneumoniae, Streptococcus pneumoniae, lipopolysaccharide (LPS), or alpha-galactosylceramide (αGalCer) to induce pneumonia, sepsis, or NKT cell activation. Liver injury was observed in RelA-null (hepRelAΔ/Δ) mice but not STAT3-null (hepSTAT3Δ/Δ) mice during pneumonia. The absence of RelA resulted in hepatotoxicity across several models of pneumonia, sepsis, and NKT cell activation. Injury was associated with increased levels of activated caspase-3 and -8 and substantial alteration of the hepatic transcriptome. Hepatotoxicity in the absence of RelA could be reversed by neutralization of tumor necrosis factor alpha (TNF-α). These results indicate the requirement of RelA-dependent inducible hepatoprotection during pneumonia and sepsis. Further, the results demonstrate that RelA-dependent gene programs are critical for maintaining liver homeostasis against TNF-α-driven immunotoxicity.

Association between MRI findings and back pain after osteoporotic vertebral fractures: a multicenter prospective cohort study

BACKGROUND CONTEXTOsteoprotic vertebral fractures (OVFs) are common in elderly people. The association between back pain due to OVF with magnetic resonance imaging (MRI) signal change is unclear. In this study we hypothesized that MRI findings would be a predictive factor for back pain measured by visual analogue scale (VAS) at 6 months follow-up. PURPOSEThe aim was to study the MRI findings that predict back pain after OVF and the association between radiological findings and scores of back pain. STUDY DESIGNMulticenter prospective cohort study. PATIENT SAMPLEA total of 153 OVF patients. OUTCOME MEASUREThe outcome measures were VAS back pain and MRI signal change. METHODSThis study was performed from 2012 to 2015. Consecutive patients with less than 2-week-old OVFs at 11 institutions were enrolled prospectively. MRI was performed at enrollment and at 1, 3, and 6 months follow-up. T1- and T2-weighted images (T1WI and T2W1) were obtained at each time point and their association with VAS scores of back pain at 6 months were investigated. Anterior compression ratio, posterior compression ratio, and angular motion of vertebral bodies were also measured on X-rays at each follow-up. This research had no financial support. There are no conflicts of interest. RESULTThe 6 months follow-up was completed by 153 patients. At enrollment, the average VAS score of back pain was 75 mm, and it had improved at the 6-month follow-up to an average score of 20 mm. There was a significant correlation between T1 diffuse low signal change and VAS scores at the 6-month follow-up (p<.01). T2 high signal changes (odds ratio; 4.01, p<.01) and old vertebral fractures (odds ratio; 2.47, p=.04) were independent risk factors for back pain. The correlation between angular motion of vertebrae on X-rays and the VAS score of back pain was significant at all time points. CONCLUSIONThis study demonstrates the radiological factors associated with persistent back pain after an OVF and the association between the VAS score of back pain and radiological findings. In addition, T2 high signal changes in acute phase and old vertebral fractures were independent risk factors for residual back pain.

Influences of ulinastatin on acute lung injury and time phase changes of coagulation parameters in rats with burn-blast combined injuries

Influences of ulinastatin on acute lung injury and time phase changes of coagulation parameters in rats with burn-blast combined injuries

Explaining the decline in coronary heart disease mortality rates in the Slovak Republic between 1993-2008.

ObjectiveBetween the years 1993 and 2008, mortality rates from coronary heart disease (CHD) in the Slovak Republic have decreased by almost one quarter. However, this was a smaller decline than in neighbouring countries. The aim of this modelling study was therefore to quantify the contributions of risk factor changes and the use of evidence-based medical therapies to the CHD mortality decline between 1993 and 2008.MethodsWe identified, obtained and scrutinised the data required for the model. These data detailed trends in the major population cardiovascular risk factors (smoking, blood pressure, total cholesterol, diabetes prevalence, body mass index (BMI) and physical activity levels), and also the uptake of all standard CHD treatments. The main data sources were official statistics (National Health Information Centre and Statistical Office of the Slovak Republic) and national representative studies (AUDIT, SLOVAKS, SLOVASeZ, CINDI, EHES, EHIS). The previously validated IMPACT policy model was then used to combine and integrate these data with effect sizes from published meta-analyses quantifying the effectiveness of specific evidence-based treatments, and population-wide changes in cardiovascular risk factors. Results were expressed as deaths prevented or postponed (DPPs) attributable to risk factor changes or treatments. Uncertainties were explored using sensitivity analyses.ResultsBetween 1993 and 2008 age-adjusted CHD mortality rates in the Slovak Republic (SR) decreased by 23% in men and 26% in women aged 25–74 years. This represented some 1820 fewer CHD deaths in 2008 than expected if mortality rates had not fallen. The IMPACT model explained 91% of this mortality decline. Approximately 50% of the decline was attributable to changes in acute phase and secondary prevention treatments, particularly acute and chronic treatments for heart failure (≈12%), acute coronary syndrome treatments (≈9%) and secondary prevention following AMI and revascularisation (≈8%). Changes in CHD risk factors explained approximately 41% of the total mortality decrease, mainly reflecting reductions in total serum cholesterol. However, other risk factors demonstrated adverse trends and thus generated approximately 740 additional deaths.ConclusionOur analysis suggests that approximately half the CHD mortality fall recently observed in the SR may be attributable to the increased use of evidence-based treatments. However, the adverse trends observed in all the major cardiovascular risk factors (apart from total cholesterol) are deeply worrying. They highlight the need for more energetic population-wide prevention policies such as tobacco control, reducing salt and industrial trans fats content in processed food, clearer food labelling and regulated marketing of processed foods and sugary drinks.

Adverse outcome has a U-shaped relation with acute phase change in insulin sensitivity after ST-Elevation Myocardial Infarction

BackgroundAlthough stress hyperglycemia after myocardial infarction (MI) is consistently associated with increased mortality, recent studies suggest that the addition of upstream markers of glucose metabolism may improve risk identification. Hence, our aim was to evaluate the association between insulin sensitivity changes during MI hospitalization and outcomes. MethodsA prospective cohort of 331 consecutive ST-Elevation MI (STEMI) patients without insulin provision therapy was used for the analyses. Blood samples were collected upon admission (D1) and after 5days (D5) of the inciting event. We measured blood glucose and insulin to estimate insulin sensitivity using the updated Homeostasis Model Assessment (HOMA2S). Patients were assessed for intra-hospital death and major adverse cardiac events (MACE) during follow-up. ResultsHOMA2S was 62%±52% on D1 and 86%±57% on D5 (p<0.001). Total follow-up was a median of 2 (0.9–2.8) years and found a U-shaped relation between the change in HOMA2S from D1 to D5 (ΔHOMA2S) and major adverse cardiac events (MACE) (p=0.017). Fully adjusted cox-regression models showed that patients from T1 and T3 were about 2.5 times more prone to suffer from MACE than those in T2. Net Reclassification Index adding ΔHOMA2S as a categorical variable dichotomized as T2 and T1 or T3 to a model of GRACE risk score with glucose D1 yielded a better predictive model (0.184 [95% CI 0.124–0.264]; p=0.032). ConclusionA U-shaped curve describes the relation between insulin sensitivity change and MACE during acute phase STEMI and, thus indicating that acute dysglycemia must be appreciated in light of a time spectrum and insulin levels.

Serum acute phase response induced by different vaccination protocols against circovirus type 2 and Mycoplasma hyopneumoniae in piglets

The purpose of this study was to compare the acute phase reaction (APR) induced by different vaccination protocols used against Porcine Circovirus (PCV) type-2 and Mycoplasma hyopneumoniae (M.hyo), studying two acute phase proteins (APPs) and changes in rectal temperature (RT). In addition, the possible influence of the time of vaccination and breed were analysed. In the first experiment, 40 commercial crossbred piglets were vaccinated, on the day of weaning, with FLEXcombo® (group A, n=20) or Porcilis PCV® and Stellamune® One (group B, n=20). The second experiment was performed on two farms, on which 40 commercial crossbred piglets or 40 Iberian piglets were vaccinated, 7days post-weaning. On each farm one group (A, n=20) was vaccinated with FLEXcombo® and another group (B, n=20) with Porcilis® PCV-M.hyo. Blood samples were taken before, 24h and 48h after vaccination, and RT were recorded before and 8h after vaccination. Significantly higher increases in group B in RT (P<0.01) and APPs concentrations (P<0.01) were recorded at several sampling times after vaccination compared with group A. The vaccines that produced greater increases in RT also produced higher APPs increases but no influence of the day of vaccination or of the breed were found. Therefore, serum APPs concentrations differed according to the vaccine used, which may be useful, along with RT, for choosing the vaccine or protocol that produces APR of lower magnitude.

Explaining the Decline in Coronary Heart Disease Mortality in the Netherlands between 1997 and 2007.

ObjectiveWe set out to determine what proportion of the mortality decline from 1997 to 2007 in coronary heart disease (CHD) in the Netherlands could be attributed to advances in medical treatment and to improvements in population-wide cardiovascular risk factors.MethodsWe used the IMPACT-SEC model. Nationwide information was obtained on changes between 1997 and 2007 in the use of 42 treatments and in cardiovascular risk factor levels in adults, aged 25 or over. The primary outcome was the number of CHD deaths prevented or postponed.ResultsThe age-standardized CHD mortality fell by 48% from 269 to 141 per 100.000, with remarkably similar relative declines across socioeconomic groups. This resulted in 11,200 fewer CHD deaths in 2007 than expected. The model was able to explain 72% of the mortality decline. Approximately 37% (95% CI: 10%-80%) of the decline was attributable to changes in acute phase and secondary prevention treatments: the largest contributions came from treating patients in the community with heart failure (11%) or chronic angina (9%). Approximately 36% (24%-67%) was attributable to decreases in risk factors: blood pressure (30%), total cholesterol levels (10%), smoking (5%) and physical inactivity (1%). Ten% more deaths could have been prevented if body mass index and diabetes would not have increased. Overall, these findings did not vary across socioeconomic groups, although within socioeconomic groups the contribution of risk factors differed.ConclusionCHD mortality has recently halved in The Netherlands. Equally large contributions have come from the increased use of acute and secondary prevention treatments and from improvements in population risk factors (including primary prevention treatments). Increases in obesity and diabetes represent a major challenge for future prevention policies.

TCT-590 Potent effect of prasugrel on acute phase resolution of intra-stent tissue after percutaneous intervention to acute coronary syndrome

Detailed mechanisms of potent and rapid antiplatelet inhibition with new-generation P2Y12 receptor inhibitor, prasugrel, has not been demonstrated. We aimed to compare the effect of prasugrel and clopidogrel on the acute phase changes of intra-stent tissue (IST) in acute coronary syndrome (ACS)