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Background: Systemic immune-inflammation index (SII) is a novel comprehensive inflammatory marker. Inflammation is associated with impaired lung function. We aimed to explore the possible relationship between SII and lung function to examine the potential of SII in predicting lung function decline. Methods: A cross-sectional survey was conducted using the data of the NHANES from 2007 to 2012. Multiple linear regression models were used to analyze the linear relationship between SII and pulmonary functions. Sensitivity analyses, subgroup analyses, and interaction tests were used to examine the robustness of this relationship across populations. Fitted smooth curves and threshold effect analysis were used to describe the nonlinear relationships. Results: A total of 10,125 patients were included in this study. After adjusting for all covariates, multiple linear regression model analysis showed that high Log2-SII level was significantly associated with decreased FVC(ß, -23.4061; 95% CI, -42.2805- -4.5317), FEV1(ß, -46.7730; 95% CI, -63.3371- -30.2089), FEV1%(ß, -0.7923; 95% CI, -1.1635- -0.4211), FEV1/FVC(ß, -0.6366; 95% CI, -0.8328- -0.4404) and PEF(ß, -121.4468; 95% CI,-164.1939- -78.6998). The negative correlation between Log2-SII and pulmonary function indexes remained stable in trend test and stratified analysis. Inverted U-shaped relationships between Log2-SII and FVC, FEV1, FEV1%, and PEF were observed, while a negative linear correlation existed between FEV1/FVC and Log2-SII. The cutoff values of the nonlinear relationship between Log2-SII and FVC, FEV1, FEV1%, PEF were 8.3736, 8.0688, 8.3745, and 8.5255, respectively. When SII exceeded the critical value, the lung function decreased significantly. Conclusion: This study found a close correlation between SII and pulmonary function indicators. This study investigated the SII threshold when lung functions began to decline in the overall population. SII may become a promising serological indicator for predicting lung function decline. However, prospective studies were needed further to establish the causal relationship between these two factors.
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Mediadores de Inflamación , Inflamación , Pulmón , Encuestas Nutricionales , Valor Predictivo de las Pruebas , Humanos , Masculino , Estudios Transversales , Femenino , Persona de Mediana Edad , Pulmón/fisiopatología , Pulmón/inmunología , Volumen Espiratorio Forzado , Estados Unidos/epidemiología , Adulto , Capacidad Vital , Inflamación/fisiopatología , Inflamación/inmunología , Inflamación/diagnóstico , Inflamación/sangre , Mediadores de Inflamación/sangre , Anciano , Biomarcadores/sangre , Factores de Riesgo , Modelos LinealesRESUMEN
OBJECTIVES: This study aimed to investigate the effects of a 16-week aerobic exercise program on systolic blood pressure, intracellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and oxidized low-density lipoprotein of obese and nonobese elderly women with isolated systolic hypertension. METHODS: Elderly women aged 70-85âyears were recruited and grouped into the normal isolated systolic hypertension ( n â=â12) and obese isolated systolic hypertension groups ( n â=â13). The participants followed an aerobic exercise program, using a wireless heart rate monitor to maintain an appropriate heart rate reserve based on the American College of Sports Medicine exercise guidelines. The two-way repeated measures analysis of variance tested group × time interaction. Pearson's correlation and simple regression assessed the influence of each variable, which showed significant differences. RESULTS: An interaction effect for systolic blood pressure, intracellular cell adhesion molecule-1, and vascular cell adhesion molecule-1 ( P â<â0.05) and a main time effect for oxidized low-density lipoprotein ( P â<â0.05) were observed. A correlation between the rates of change in systolic blood pressure and vascular cell adhesion molecule-1 ( P â<â0.05) with a 42.8% influence ( P â<â0.001) and in intracellular cell adhesion molecule-1 and vascular cell adhesion molecule-1 ( P â<â0.05) with a 21.6% influence ( P â<â0.05) was observed. CONCLUSIONS: These findings collectively showed that the 16-week aerobic exercise program effectively lowered blood pressure in patients with isolated systolic hypertension, particularly in the normal group compared to the obese group. Thus, regular aerobic exercise for 16âweeks or more enhances vascular health, potentially improving the healthy life expectancy of elderly women.
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Presión Sanguínea , Ejercicio Físico , Hipertensión , Obesidad , Molécula 1 de Adhesión Celular Vascular , Humanos , Femenino , Anciano , Hipertensión/fisiopatología , Ejercicio Físico/fisiología , Obesidad/fisiopatología , Obesidad/complicaciones , Presión Sanguínea/fisiología , Anciano de 80 o más Años , Molécula 1 de Adhesión Celular Vascular/sangre , Inflamación/fisiopatología , Lipoproteínas LDL/sangre , Endotelio Vascular/fisiopatología , Molécula 1 de Adhesión Intercelular/sangre , Hipertensión Sistólica AisladaRESUMEN
Cardiorenal syndrome (CRS) describes the maladaptive relationship between heart and kidney dysfunction, with different pathways perpetuating the pathophysiology. Inflammation is one of these mechanisms. It contributes to the final nonhemodynamic pathways of organ dysfunction in the heart-kidney cross-talk. It may be a mediator and amplifier of this pathological communication, playing a vital role in both acute and chronic cardiorenal dysfunction. Current therapeutic strategies are not satisfactory in mitigating the inflammatory pathway in CRS. Hemoadsorption overcomes this limitation, and the soluble mediators of inflammation are potentially amenable to removal by hemoadsorption. This perspective article describes the inflammatory mechanisms in CRS and the rationality of using hemoadsorption in this scenario.
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Síndrome Cardiorrenal , Inflamación , Síndrome Cardiorrenal/fisiopatología , Humanos , Inflamación/fisiopatología , Hemoperfusión/métodosRESUMEN
INTRODUCTION: There has been an increasing amount of research on the consequences of e-cigarette use for respiratory outcomes, which is significant for public health and respiratory medicine. We discuss recent findings and lay out implications for prevention and treatment. AREAS COVERED: Based on literature searches using several databases (PubMed, Web of Science, Google Scholar) for keywords, including synonyms, 'e-cigarettes,' with 'pulmonary function,' 'oxidative stress,' and 'inflammation,' we review studies on acute effects of e-cigarette use for measures of pulmonary function and discuss selected laboratory studies on mechanisms of effect, focusing on processes with known relation to respiratory disease; oxidative stress and inflammation. We discuss available studies that have tested the effectiveness of communication strategies for prevention of e-cigarette use oriented to different audiences, including nonsmoking adolescents and adult smokers. EXPERT OPINION: We conclude that the evidence presents a mixed picture. Evidence is found for adverse consequences of e-cigarette use on measures of lung function and two disease-related biological processes, sometimes but not always less than for cigarette smoking. How to best communicate these results to a complex audience of users, from younger susceptible adolescents to long-term adult smokers interested in quitting, is a question of significant interest and empirically validated communication strategies are greatly needed.
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Sistemas Electrónicos de Liberación de Nicotina , Vapeo , Humanos , Vapeo/efectos adversos , Cese del Hábito de Fumar , Estrés Oxidativo , Pulmón/fisiopatología , Pulmón/efectos de los fármacos , Adolescente , Inflamación/fisiopatología , Enfermedades Respiratorias/fisiopatología , Enfermedades Respiratorias/epidemiología , AdultoRESUMEN
BACKGROUND: Inflammation is an established contributor to the pathophysiology of depression and the prevalence of depression in those with chronic inflammatory disease is two- to four-fold higher than the general population. Yet little is known about the neurobiological changes that confer depression or resilience to depression, that occur when episodes of heightened inflammation are frequent or span many years. METHODS: We used an innovative combination of longitudinal resting state functional magnetic resonance imaging coupled to segmental bronchial provocation with allergen (SBP-Ag) to assess changes in resting state functional connectivity (rsFC) of the salience network (SN) caused by an acute inflammatory exacerbation in twenty-six adults (15 female) with asthma and varying levels of depressive symptoms. Eosinophils measured in bronchoalveolar lavage fluid and blood provided an index of allergic inflammation and the Beck Depression Inventory provided an index of depressive symptoms. RESULTS: We found that in those with the highest symptoms of depression at baseline, SN rsFC declined most from pre- to post-SBP-Ag in the context of a robust eosinophilic response to challenge, but in those with low depressive symptoms SN rsFC was maintained or increased, even in those with the most pronounced SBP-Ag response. CONCLUSIONS: Thus, the maintenance of SN rsFC during inflammation may be a biomarker of resilience to depression, perhaps via more effective orchestration of large-scale brain network dynamics by the SN. These findings advance our understanding of the functional role of the SN during inflammation and inform treatment recommendations for those with comorbid inflammatory disease and depression.
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Asma , Encéfalo , Depresión , Inflamación , Imagen por Resonancia Magnética , Humanos , Femenino , Masculino , Asma/fisiopatología , Asma/psicología , Asma/inmunología , Adulto , Imagen por Resonancia Magnética/métodos , Inflamación/fisiopatología , Inflamación/metabolismo , Depresión/fisiopatología , Depresión/metabolismo , Encéfalo/fisiopatología , Encéfalo/metabolismo , Resiliencia Psicológica , Persona de Mediana Edad , Red Nerviosa/fisiopatología , Red Nerviosa/diagnóstico por imagen , Red Nerviosa/metabolismo , Salud Mental , Pruebas de Provocación Bronquial , Adulto Joven , Eosinófilos/metabolismo , Conectoma/métodos , Alérgenos/inmunologíaRESUMEN
INTRODUCTION: Suicide is a widespread problem, with risk factors still a challenge. The aim was to assess correlations among insomnia, circadian rhythm, and inflammatory markers in individuals who attempted suicide. MATERIALS AND METHODS: Consecutive patients hospitalised following an attempted suicide, were assessed. Psychiatric diagnosis (DSM-5-TR Criteria), lethality of the suicide attempt (Suicide Intent Scale-SIS), and inflammatory parameters NLR (neutrophil-lymphocyte ratio) PLR (platelet-lymphocyte ratio), and SII (systemic inflammation index/neutrophil-to-platelet ratio on lymphocytes), were computed. Depressive and manic symptoms (Beck Depression Inventory-BDI-II, Young Mania Rating Scale- YMRS), circadian rhythms disturbances (Biological Rhythms Interview of Assessment in Neuropsychiatry-BRIAN), insomnia symptoms (Insomnia Severity Index-ISI) were assessed together with socio-demographic, clinical and pharmacological data. RESULTS: The final sample included 52 individuals. Patients who experienced insomnia during the preceding two weeks utilised high lethality methods, reported heightened dysregulation of chronobiological rhythms, heightened severity of depression, and elevated levels of inflammatory markers. High lethality was best predicted by insomnia symptoms (OR = 20.1, CI-95% 4.66-87.25, p = 0.001), by disturbances of circadian rhythms (OR = 6.97, CI-95% 1.82-26.66, p = 0.005), and by NLR indices (OR 4.00, CI-95% 1.14-13.99, p = 0.030). CONCLUSIONS: Sleep disturbances may be a risk factor for suicidal lethality, along with markers of inflammation. It is plausible that insomnia and circadian sleep dysregulation may contribute to inflammation, thereby promoting suicidal risk.
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Biomarcadores , Inflamación , Trastornos del Inicio y del Mantenimiento del Sueño , Intento de Suicidio , Humanos , Femenino , Masculino , Trastornos del Inicio y del Mantenimiento del Sueño/fisiopatología , Trastornos del Inicio y del Mantenimiento del Sueño/sangre , Adulto , Inflamación/sangre , Inflamación/fisiopatología , Persona de Mediana Edad , Biomarcadores/sangre , Trastornos Cronobiológicos/fisiopatología , Trastornos Cronobiológicos/sangre , Ritmo Circadiano/fisiología , Neutrófilos , Factores de Riesgo , Adulto Joven , LinfocitosRESUMEN
BACKGROUND: Cognitive impairment is common in major depressive disorder (MDD) and potentially linked to inflammation-induced alterations in brain function. However, the relationship between inflammation, dynamic brain activity, and cognitive impairment in MDD remains unclear. METHODS: Fifty-seven first-episode, drug-naïve MDD patients and sixty healthy controls underwent fMRI scanning. Dynamic amplitude of low-frequency fluctuations (dALFF) and dynamic functional connectivity (dFC) were measured using the sliding window method. Plasma IL - 6 levels and cognitive function were assessed using enzyme-linked immunosorbent assay (ELISA) and the Repeated Battery for Assessment of Neuropsychological Status (RBANS), respectively. RESULTS: MDD patients exhibited decreased dALFF in the bilateral inferior temporal gyrus (ITG), right inferior frontal gyrus, opercular part (IFGoperc), and bilateral middle occipital gyrus (MOG). Regions of dALFF associated with IL-6 included right ITG (r = -0.400/p = 0.003), left ITG (r = -0.381/p = 0.004), right IFGoperc (r = -0.342/p = 0.011), and right MOG (r = -0.327/p = 0.016). Furthermore, IL-6-related abnormal dALFF (including right ITG: r = 0.309/p = 0.023, left ITG: r = 0.276/p = 0.044) was associated with attention impairment. These associations were absent entirely in MDD patients without suicidal ideation. Additionally, IL-6 levels were correlated with dFC of specific brain regions. LIMITATIONS: Small sample size and cross-sectional study design. CONCLUSIONS: Inflammation-related dALFF was associated with attention impairment in MDD patients, with variations observed among MDD subgroups. These findings contribute to the understanding of the intricate relationship between inflammation, dynamic brain activity and cognitive impairments in MDD.
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Encéfalo , Disfunción Cognitiva , Trastorno Depresivo Mayor , Inflamación , Imagen por Resonancia Magnética , Humanos , Trastorno Depresivo Mayor/fisiopatología , Trastorno Depresivo Mayor/diagnóstico por imagen , Masculino , Femenino , Adulto , Disfunción Cognitiva/fisiopatología , Disfunción Cognitiva/diagnóstico por imagen , Inflamación/fisiopatología , Inflamación/sangre , Encéfalo/fisiopatología , Encéfalo/diagnóstico por imagen , Interleucina-6/sangre , Adulto Joven , Pruebas Neuropsicológicas , Lóbulo Temporal/fisiopatología , Lóbulo Temporal/diagnóstico por imagenRESUMEN
BACKGROUND: Inflammation and immunity play important roles in the formation of coronary collateral circulation (CCC). The pan-immune-inflammation value (PIV) is a novel marker for evaluating systemic inflammation and immunity. The study aimed to investigate the association between the PIV and CCC formation in patients with chronic total occlusion (CTO). METHODS: This retrospective study enrolled 1150 patients who were diagnosed with CTO through coronary angiographic (CAG) examinations from January 2013 to December 2021 in China. The Cohen-Rentrop criteria were used to catagorize CCC formation: good CCC formation (Rentrop grade 2-3) and poor CCC formation group (Rentrop grade 0-1). Based on the tertiles of the PIV, all patients were classified into three groups as follows: P1 group, PIV ≤ 237.56; P2 group, 237.56< PIV ≤ 575.18; and P3 group, PIV > 575.18. RESULTS: A significant relationship between the PIV and the formation of CCC was observed in our study. Utilizing multivariate logistic regression and adjusting for confounding factors, the PIV emerged as an independent risk factor for poor CCC formation. Notably, the restricted cubic splines revealed a dose-response relationship between the PIV and risk of poor CCC formation. In terms of predictive accuracy, the area under the ROC curve (AUC) for PIV in anticipating poor CCC formation was 0.618 (95% CI: 0.584-0.651, P < 0.001). Furthermore, the net reclassification index (NRI) and integrated discrimination index (IDI) for PIV, concerning the prediction of poor CCC formation, were found to be 0.272 (95% CI: 0.142-0.352, P < 0.001) and 0.051 (95% CI: 0.037-0.065, P < 0.001), respectively. It's noteworthy that both the NRI and IDI values were higher for PIV compared to other inflammatory biomarkers, suggesting its superiority in predictive capacity. CONCLUSIONS: PIV was associated with the formation of CCC. Notably, PIV exhibited potential as a predictor for poor CCC formation and showcased superior predictive performance compared to other complete blood count-based inflammatory biomarkers.
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Circulación Colateral , Angiografía Coronaria , Circulación Coronaria , Oclusión Coronaria , Mediadores de Inflamación , Inflamación , Valor Predictivo de las Pruebas , Humanos , Masculino , Persona de Mediana Edad , Oclusión Coronaria/fisiopatología , Oclusión Coronaria/diagnóstico por imagen , Femenino , Estudios Retrospectivos , Enfermedad Crónica , Anciano , Inflamación/diagnóstico , Inflamación/sangre , Inflamación/inmunología , Inflamación/fisiopatología , Mediadores de Inflamación/sangre , Medición de Riesgo , China , Biomarcadores/sangre , Factores de Riesgo , PronósticoRESUMEN
Background and Objectives: This study investigated the impact of nutritional status and foods consumed on inflammation and disease activity in patients with rheumatoid arthritis (RA). Materials and Methods: We designed a cross-sectional observational study, involving 110 patients diagnosed with RA. The patients included were between 18 and 75 years old, diagnosed with rheumatoid arthritis two years ago or earlier, with stable treatment for the last 8 weeks. Data on anthropometric parameters, body mass composition, nutritional status, individual food consumption records, inflammation, disease activity, quality of life, clinical, and laboratory parameters were collected for each study participant. The evaluation parameters of the patients were the simple disease activity index (SDAI), clinical disease activity index (CDAI), systemic immune-inflammation index (SII) and individual food consumption records. A bioimpedance device and measuring tape were used to take body composition and anthropometric measurements of the patients. Results: According to the body mass index, waist circumference and waist-to-height ratio, in our study, we found that 60% of the patients were obese, 80% were at a very high health risk, and approximately 91% were in need of nutritional treatment. There was a significant negative correlation between the dietary intake of total energy, total fat, omega 3, calcium, zinc, cobalamin and the disease activity (SDAI, CDAI). There was a significant negative correlation between polyunsaturated fatty acids, omega 3, carotene, vitamin E, selenium and the SII. Additionally, there was a positive correlation between omega 6 and the SII, SDAI, CDAI (p < 0.05). Conclusions: The results of this study show that the foods consumed in the nutrition of RA patients may have effects on their inflammation and disease activity.
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Artritis Reumatoide , Inflamación , Estado Nutricional , Humanos , Artritis Reumatoide/fisiopatología , Artritis Reumatoide/complicaciones , Persona de Mediana Edad , Femenino , Masculino , Estudios Transversales , Inflamación/fisiopatología , Adulto , Anciano , Índice de Masa Corporal , Adolescente , Calidad de Vida , Índice de Severidad de la EnfermedadRESUMEN
Early in the pandemic, clinicians recognized an overlap between Long COVID symptoms and dysautonomia, suggesting autonomic nervous system (ANS) dysfunction. Our clinical experience at Johns Hopkins with primary dysautonomia suggested heritability of sympathetic dysfunction, manifesting primarily as hyperhidrosis and as other dysautonomia symptoms. Whole exome sequencing revealed mutations in genes regulating electrical signaling in the nervous system, thus providing a genetic basis for the sympathetic overdrive observed. We hypothesize that dysautonomia in Long COVID requires two molecular hits: a genetic vulnerability to prime the ANS and a SARS-CoV-2 infection, as an immune trigger, to further disrupt ANS function resulting in increased sympathetic activity. Indeed, Long COVID patients show signs of chronic inflammation and autoimmunity. We have translated this two-hit concept to the clinic using ion channel inhibitors to target genetic susceptibility and immunomodulators to treat inflammation. This multi-hit hypothesis shows promise for managing Long COVID and merits further study.
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COVID-19 , Síndrome Post Agudo de COVID-19 , Humanos , COVID-19/inmunología , COVID-19/fisiopatología , COVID-19/virología , COVID-19/genética , SARS-CoV-2/inmunología , Transducción de Señal , Predisposición Genética a la Enfermedad , Disautonomías Primarias/fisiopatología , Disautonomías Primarias/inmunología , Inflamación/inmunología , Inflamación/fisiopatologíaRESUMEN
Sepsis stands as a prominent contributor to sickness and death on a global scale. The most current consensus definition characterizes sepsis as a life-threatening organ dysfunction stemming from an imbalanced host response to infection. This definition does not capture the intricate array of immune processes at play in sepsis, marked by simultaneous states of heightened inflammation and immune suppression. This overview delves into the immune-related processes of sepsis, elaborating about mechanisms involved in hyperinflammation and immune suppression. Moreover, we discuss stratification of patients with sepsis based on their immune profiles and how this could impact future sepsis management.
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Interacciones Huésped-Patógeno , Inflamación , Sepsis , Humanos , Sepsis/fisiopatología , Sepsis/complicaciones , Sepsis/inmunología , Inflamación/fisiopatología , Tolerancia InmunológicaRESUMEN
BACKGROUND: Depression and obesity are associated with impaired inhibitory control. Behavioral evidence indicates an exacerbating additive effect when both conditions co-occur. However, the underlying neural mechanisms remain unclear. Moreover, systemic inflammation affects neurocognitive performance in both individuals with depression and obesity. Here, we investigate additive effects of depression and obesity on neural correlates of inhibitory control, and examine inflammation as a connecting pathway. METHODS: We assessed inhibitory control processing in 64 individuals with obesity and varying degrees of depressed mood by probing neural activation and connectivity during an fMRI Stroop task. Additionally, we explored associations of altered neural responses with individual differences in systemic inflammation. Data were collected as part of the BARICO (Bariatric surgery Rijnstate and Radboudumc neuroimaging and Cognition in Obesity) study. RESULTS: Concurrent depression and obesity were linked to increased functional connectivity between the supplementary motor area and precuneus and between the inferior occipital and inferior parietal gyrus. Exploratory analysis revealed that circulating inflammation markers, including plasma leptin, IL-6, IL-8, and CCL-3 correlated with the additive effect of depression and obesity on altered functional connectivity. LIMITATIONS: The observational design limits causal inferences. Future research employing longitudinal or intervention designs is required to validate these findings and elucidate causal pathways. CONCLUSION: These findings suggest increased neural crosstalk underlying impaired inhibitory control in individuals with concurrent obesity and depressed mood. Our results support a model of an additive detrimental effect of concurrent depression and obesity on neurocognitive functioning, with a possible role of inflammation.
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Depresión , Inhibición Psicológica , Imagen por Resonancia Magnética , Obesidad , Humanos , Masculino , Femenino , Obesidad/fisiopatología , Obesidad/complicaciones , Adulto , Depresión/fisiopatología , Persona de Mediana Edad , Inflamación/fisiopatología , Encéfalo/fisiopatología , Encéfalo/diagnóstico por imagen , Test de Stroop , Lóbulo Parietal/fisiopatología , Lóbulo Parietal/diagnóstico por imagenRESUMEN
AIMS: The evidence for joint and independent associations of low muscle mass and low muscle strength with diabetes is limited and mixed. The study aimed to determine the associations of muscle parameters (muscle mass, strength, quality, and sarcopenia) and sarcopenia obesity with diabetes, and the previously unstudied mediating effect of inflammation. MATERIALS AND METHODS: A total of 13,420 adults from the 2023 China National Health Survey (CNHS) and 5,380 adults from the 2011-2014 National Health and Nutrition Examination Survey (NHANES) were included in this study. Muscle mass was determined using bioelectrical impedance analysis (BIA) in the CNHS, and whole-body dual X-ray absorptiometry (DXA) in the NHANES. Muscle strength was assessed using digital hand dynamometer. Multivariate logistic regression models were used to evaluate the associations of muscle parameters and sarcopenia obesity with diabetes. Inflammatory status was assessed using blood cell counts and two systemic inflammation indices (platelet-to-lymphocyte ratio (PLR) and system inflammation response index (SIRI)). Mediation analysis was conducted to examine inflammation's role in these associations. RESULTS: Low muscle mass and strength were independently related to diabetes. Low muscle quality was associated with elevated diabetes risk. Sarcopenia has a stronger association with diabetes compared to low muscle strength alone or mass alone (CNHS, odds ratio (OR) = 1.93, 95 % confidence interval (CI):1.64-2.27; NHANES, OR = 3.80, 95 %CI:2.58-5.58). Participants with sarcopenia obesity exhibit a higher risk of diabetes than those with obesity or sarcopenia alone (CNHS, OR = 2.21, 95 %CI:1.72-2.84; NHANES, OR = 6.06, 95 %CI:3.64-10.08). Associations between muscle parameters and diabetes were partially mediated by inflammation (mediation proportion: 1.99 %-36.64 %, P < 0.05). CONCLUSION: Low muscle mass and muscle strength are independently or jointly associated with diabetes, and inflammation might be a potential mechanism underlying this association. Furthermore, the synergistic effects of sarcopenia and obesity could significantly increase diabetes risk.
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Inflamación , Fuerza Muscular , Músculo Esquelético , Encuestas Nutricionales , Sarcopenia , Humanos , Masculino , Femenino , China/epidemiología , Inflamación/fisiopatología , Inflamación/epidemiología , Persona de Mediana Edad , Sarcopenia/epidemiología , Sarcopenia/fisiopatología , Sarcopenia/patología , Adulto , Fuerza Muscular/fisiología , Estados Unidos/epidemiología , Músculo Esquelético/patología , Músculo Esquelético/fisiopatología , Diabetes Mellitus/epidemiología , Diabetes Mellitus/fisiopatología , Obesidad/epidemiología , Obesidad/fisiopatología , Obesidad/complicaciones , Anciano , Absorciometría de FotónRESUMEN
Heart failure (HF) is a debilitating clinical syndrome affecting 64.3 million patients worldwide. More than 50% of HF cases are attributed to HF with preserved ejection fraction (HFpEF), an entity growing in prevalence and mortality. Although recent breakthroughs reveal the prognostic benefits of sodium-glucose co-transporter 2 inhibitors (SGLT2i) in HFpEF, there is still a lack of effective pharmacological therapy available. This highlights a major gap in medical knowledge that must be addressed. Current evidence attributes HFpEF pathogenesis to an interplay between cardiometabolic comorbidities, inflammation, and renin-angiotensin-aldosterone-system (RAAS) activation, leading to cardiac remodelling and diastolic dysfunction. However, conventional RAAS blockade has demonstrated limited benefits in HFpEF, which emphasises that alternative therapeutic targets should be explored. Presently, there is limited literature examining the use of anti-inflammatory HFpEF therapies despite growing evidence supporting its importance in disease progression. Hence, this review aims to explore current perspectives on HFpEF pathogenesis, including the importance of inflammation-driven cardiac remodelling and the therapeutic potential of anti-inflammatory therapies.
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Antiinflamatorios , Insuficiencia Cardíaca , Inflamación , Volumen Sistólico , Humanos , Insuficiencia Cardíaca/fisiopatología , Insuficiencia Cardíaca/tratamiento farmacológico , Inflamación/tratamiento farmacológico , Inflamación/fisiopatología , Animales , Antiinflamatorios/uso terapéutico , Sistema Renina-Angiotensina/efectos de los fármacos , Sistema Renina-Angiotensina/fisiología , Remodelación Ventricular/efectos de los fármacosRESUMEN
Diabetic macular edema (DME) and neovascular age-related macular degeneration (nAMD) are multifactorial disorders that affect the macula and cause significant vision loss. Although inflammation and neoangiogenesis are hallmarks of DME and nAMD, respectively, they share some biochemical mediators. While inflammation is a trigger for the processes that lead to the development of DME, in nAMD inflammation seems to be the consequence of retinal pigment epithelium and Bruch membrane alterations. These pathophysiologic differences may be the key issue that justifies the difference in treatment strategies. Vascular endothelial growth factor inhibitors have changed the treatment of both diseases, however, many patients with DME fail to achieve the established therapeutic goals. From a clinical perspective, targeting inflammatory pathways with intravitreal corticosteroids has been proven to be effective in patients with DME. On the contrary, the clinical relevance of addressing inflammation in patients with nAMD has not been proven yet. We explore the role and implication of inflammation in the development of nAMD and DME and its therapeutical relevance.
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Retinopatía Diabética , Inflamación , Edema Macular , Degeneración Macular Húmeda , Humanos , Edema Macular/etiología , Edema Macular/tratamiento farmacológico , Edema Macular/fisiopatología , Retinopatía Diabética/fisiopatología , Retinopatía Diabética/tratamiento farmacológico , Inflamación/fisiopatología , Degeneración Macular Húmeda/tratamiento farmacológico , Degeneración Macular Húmeda/fisiopatología , Degeneración Macular Húmeda/diagnóstico , Inhibidores de la Angiogénesis/uso terapéutico , Glucocorticoides/uso terapéutico , Factor A de Crecimiento Endotelial Vascular/antagonistas & inhibidores , Inyecciones IntravítreasRESUMEN
BACKGROUND AND AIM: Obesity is characterized by alterations in fat and muscle mass. Phase angle (PhA) is considered an index of muscle mass, and is related to comorbidities in SO. This work aimed to assess the relationship between PhA, muscle mass, inflammation, and comorbidities in obesity. METHODS AND RESULTS: We included 198 outpatients with obesity (BMI≥30) divided into tertiles according to PhA distribution (<5°, 5°-6°, >7°). Body composition was analyzed using bioimpedance (Tanita MC-780P Multi-Frequency Segmental Body Composition Analyzer). Quantitative variables were compared using the Kruskal-Wallis test and qualitative variables using the chi-square test. A correspondence analysis was built to show the influence of qualitative variables on subjects in each tertile. Patients in the lowest tertile had the lowest skeletal muscle mass and appendicular skeletal muscle mass index (ASMI); the highest inflammatory index (albumin and derived neutrophil-to-lymphocyte ratio, Alb-dNLR); and the highest percentage of individuals with a history of type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), and heart failure (HF). The correspondence analysis showed an association between the lowest tertile and presence of HF with preserved ejection fraction (HFpEF) and CKD. On the logistic regression model, ASMI (OR 0.9, 95%CI 0.85-0.95, p = 0.0004), Alb-dNLR (OR 1.04, 95%CI 1.04-16.4, p = 0.04) and HFpEF and T2DM were significantly associated with the lowest PhA. CONCLUSIONS: Identifying high-risk individuals living with obesity is a priority. These results show that lower PhA is related to inflammation, poorer skeletal muscle mass and consequently, their impact on obesity-related comorbidities and clinical outcomes.
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Comorbilidad , Impedancia Eléctrica , Músculo Esquelético , Obesidad , Sarcopenia , Humanos , Sarcopenia/epidemiología , Sarcopenia/fisiopatología , Sarcopenia/diagnóstico , Femenino , Masculino , Obesidad/epidemiología , Obesidad/fisiopatología , Obesidad/diagnóstico , Persona de Mediana Edad , Anciano , Factores de Riesgo , Músculo Esquelético/fisiopatología , Estudios Transversales , Insuficiencia Renal Crónica/fisiopatología , Insuficiencia Renal Crónica/epidemiología , Insuficiencia Renal Crónica/diagnóstico , Insuficiencia Cardíaca/fisiopatología , Insuficiencia Cardíaca/epidemiología , Insuficiencia Cardíaca/diagnóstico , Valor Predictivo de las Pruebas , Composición Corporal , Medición de Riesgo , Diabetes Mellitus Tipo 2/epidemiología , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/fisiopatología , Adiposidad , Inflamación/epidemiología , Inflamación/fisiopatologíaRESUMEN
Entheses have the challenging task of transferring biomechanical forces between tendon and bone, two tissues that differ greatly in composition and mechanical properties. Consequently, entheses are adapted to withstand these forces through continuous repair mechanisms. Locally specialized cells (mechanosensitive tenocytes) are crucial in the repair, physiologically triggering biochemical processes to maintain hemostasis. When repetitive forces cause "material fatigue," or trauma exceeds the entheses' repair capacity, structural changes occur, and patients become symptomatic. Clinical assessment of enthesopathies mainly depends on subjective reports by the patient and lacks specificity, especially in patients with central sensitization syndromes. Ultrasonography has been increasingly used to improve the diagnosis of enthesopathies. In this article, the literature on how biomechanical forces lead to entheseal inflammation, including factors contributing to differentiation into a "clinical enthesitis" state and the value of ultrasound to diagnose enthesopathies will be reviewed, as well as providing clues to overcome the pitfalls of imaging.
Asunto(s)
Entesopatía , Inflamación , Ultrasonografía , Humanos , Entesopatía/fisiopatología , Entesopatía/diagnóstico por imagen , Inflamación/fisiopatología , Inflamación/diagnóstico por imagen , Fenómenos Biomecánicos , Tendones/fisiopatología , Tendones/diagnóstico por imagenRESUMEN
Preeclampsia (PE) is a multisystemic disorder of pregnancy that not only causes perinatal mortality and morbidity but also has a long-term toll on the maternal and fetal cardiovascular system. Women diagnosed with PE are at greater risk for the subsequent development of hypertension, ischemic heart disease, cardiomyopathy, cerebral edema, seizures, and end-stage renal disease. Although PE is considered heterogeneous, inefficient extravillous trophoblast (EVT) migration leading to deficient spiral artery remodeling and increased uteroplacental vascular resistance is the likely initiation of the disease. The principal pathophysiology is placental hypoxia, causing subsequent oxidative stress, leading to mitochondrial dysfunction, mitophagy, and immunological imbalance. The damage imposed on the placenta in turn results in the "stress response" categorized by the dysfunctional release of vasoactive components including oxidative stressors, proinflammatory factors, and cytokines into the maternal circulation. These bioactive factors have deleterious effects on systemic endothelial cells and coagulation leading to generalized vascular dysfunction and hypercoagulability. A better understanding of these metabolic factors may lead to novel therapeutic approaches to prevent and treat this multisystemic disorder. In this review, we connect the hypoxic-oxidative stress and inflammation involved in the pathophysiology of PE to the resulting persistent cardiovascular complications in patients with preeclampsia.
Asunto(s)
Estrés Oxidativo , Preeclampsia , Humanos , Femenino , Preeclampsia/fisiopatología , Preeclampsia/metabolismo , Embarazo , Salud Materna , Animales , Placenta/metabolismo , Placenta/fisiopatología , Placenta/irrigación sanguínea , Enfermedades Cardiovasculares/fisiopatología , Enfermedades Cardiovasculares/metabolismo , Enfermedades Cardiovasculares/etiología , Inflamación/metabolismo , Inflamación/fisiopatología , Sistema Cardiovascular/metabolismo , Sistema Cardiovascular/fisiopatologíaRESUMEN
BACKGROUND AND AIMS: Sodium-glucose co-transporter 2 (SGLT2) inhibitors have beneficial effects in heart failure (HF), including reverse remodelling, but the mechanisms by which these benefits are conferred are unclear. Inflammation is implicated in the pathophysiology of heart failure (HF) and there are some pre-clinical data suggesting that SGLT2 inhibitors may reduce inflammation. There is however a lack of clinical data. The aim of our study was to investigate whether improvements in cardiac remodelling caused by dapagliflozin in individuals with type 2 diabetes (T2D) and left ventricular hypertrophy (LVH) were associated with its effects on inflammation. METHODS: We measured C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß), interleukin 6 (IL-6), and interleukin 10 (IL-10) and neutrophil-to-lymphocyte ratio (NLR) in plasma samples of 60 patients with T2D and left ventricular hypertrophy (LVH) but without symptomatic HF from the DAPA-LVH trial in which participants were randomised dapagliflozin 10 mg daily or placebo for 12 months and underwent cardiac magnetic resonance imaging (CMR) at baseline and end of treatment. The primary analysis was to investigate the effect of dapagliflozin on inflammation and to assess the relationships between changes in inflammatory markers and LV mass and global longitudinal strain (GLS) and whether the effect of dapagliflozin on LV mass and GLS was modulated by baseline levels of inflammation. RESULTS: Following 12 months of treatment dapagliflozin significantly reduced CRP compared to placebo (mean difference of -1.96; 95% CI -3.68 to -0.24, p = 0.026). There were no significant statistical changes in other inflammatory markers. There were modest correlations between improvements in GLS and reduced inflammation (NLR (r = 0.311), IL-1ß (r = 0.246), TNF-α (r = 0.230)) at 12 months. CONCLUSIONS: Dapagliflozin caused a significant reduction in CRP compared to placebo. There were correlations between reductions in inflammatory markers including IL-1ß and improvements in global longitudinal strain (but not reduced LV mass). Reductions in systemic inflammation might play a contributory role in the cardiovascular benefits of dapagliflozin. TRIAL REGISTRATION: Clinicaltrials.gov NCT02956811 (06/11/2016).