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1.
Drug Alcohol Depend ; 252: 110961, 2023 11 01.
Article in English | MEDLINE | ID: mdl-37748425

ABSTRACT

BACKGROUND: Despite guidelines and recommendations, Wernicke's encephalopathy (WE) treatment lacks evidence, leading to clinical practice variability. AIMS: Given the overall lack of information on thiamine use for WE treatment, we analyzed data from a large, well-characterized multicenter sample of patients with WE, examining thiamine dosages; factors associated with the use of different doses, frequencies, and routes; and the influence of differences in thiamine treatment on the outcome. METHODS: This retrospective study was conducted with data from 443 patients from 21 centers obtained from a nationwide registry of the Spanish Society of Internal Medicine (from 2000 to 2012). Discharge codes and Caine criteria were applied for WE diagnosis, and treatment-related (thiamine dosage, frequency, and route of administration) demographic, clinical, and outcome variables were analyzed. RESULTS: We found marked variability in WE treatment and a low rate of high-dose intravenous thiamine administration. Seventy-eight patients out of 373 (20.9%) received > 300mg/day of thiamine as initial dose. Patients fulfilling the Caine criteria or presenting with the classic WE triad more frequently received parenteral treatment. Delayed diagnosis (after 24h hospitalization), the fulfillment of more than two Caine criteria at diagnosis, mental status alterations, and folic acid deficiency were associated significantly with the lack of complete recovery. Malnutrition, reduced consciousness, folic acid deficiency, and the lack of timely thiamine treatment were risk factors for mortality. CONCLUSIONS: Our results clearly show extreme variability in thiamine dosages and routes used in the management of WE. Measures should be implemented to ensure adherence to current guidelines and to correct potential nutritional deficits in patients with alcohol use disorders or other risk factors for WE.


Subject(s)
Alcoholism , Folic Acid Deficiency , Thiamine Deficiency , Wernicke Encephalopathy , Humans , Wernicke Encephalopathy/diagnosis , Wernicke Encephalopathy/drug therapy , Alcoholism/drug therapy , Retrospective Studies , Folic Acid Deficiency/complications , Folic Acid Deficiency/drug therapy , Thiamine/therapeutic use , Thiamine Deficiency/complications , Thiamine Deficiency/drug therapy
2.
Clin Exp Rheumatol ; 41(6): 1238-1247, 2023 Jun.
Article in English | MEDLINE | ID: mdl-36622095

ABSTRACT

OBJECTIVES: Fibromyalgia is a prevalent disease of unknown aetiology and is difficult to diagnose. Despite the availability of the American College of Rheumatology criteria for diagnosis, it continues to be a challenge in the field of primary health care in terms of identifying individuals with susceptibility to developing the disease. The aim of this study is to design and validate a predictive model of fibromyalgia in subjects with a history of chronic pain. METHODS: This multicentre observational retrospective cohort study was performed on patients aged >18 years, who visited four primary health centres between 2017 and 2020, with a diagnosis of fibromyalgia or arthritis. The Bootstrapping resampling method was used for the validation of the model. RESULTS: A total of 198 subjects with fibromyalgia (93 with osteoarthritis, 20 with other types of arthritis, 4 with rheumatoid arthritis) and 120 without fibromyalgia (116 with osteoarthritis, 23 with other types of arthritis, 7 with rheumatoid arthritis) participated in the study. The predictive factors of the final model were self-reported age at onset of symptoms, first-line family history of neurological diseases, exposure to levels of stress, history of post-traumatic acute emotional stress, and personal history of chronic widespread pain prior to diagnosis, comorbidity, and pharmacological prescription during the year of diagnostic confirmation. The predictive capacity adjusted by Bootstrapping was 0.972 (95% CI: 0.955-0.986). CONCLUSIONS: The proposed model showed an excellent predictive capacity. The risk calculator designed from the predictive model allows health professionals to have a useful tool to identify subjects at risk of developing fibromyalgia.


Subject(s)
Arthritis, Rheumatoid , Chronic Pain , Fibromyalgia , Osteoarthritis , Humans , Fibromyalgia/diagnosis , Fibromyalgia/epidemiology , Fibromyalgia/complications , Retrospective Studies , Chronic Pain/diagnosis , Chronic Pain/epidemiology , Chronic Pain/etiology , Arthritis, Rheumatoid/diagnosis , Arthritis, Rheumatoid/epidemiology , Arthritis, Rheumatoid/complications , Osteoarthritis/complications
3.
Sci Rep ; 11(1): 13733, 2021 07 02.
Article in English | MEDLINE | ID: mdl-34215803

ABSTRACT

To determine the proportion of patients with COVID-19 who were readmitted to the hospital and the most common causes and the factors associated with readmission. Multicenter nationwide cohort study in Spain. Patients included in the study were admitted to 147 hospitals from March 1 to April 30, 2020. Readmission was defined as a new hospital admission during the 30 days after discharge. Emergency department visits after discharge were not considered readmission. During the study period 8392 patients were admitted to hospitals participating in the SEMI-COVID-19 network. 298 patients (4.2%) out of 7137 patients were readmitted after being discharged. 1541 (17.7%) died during the index admission and 35 died during hospital readmission (11.7%, p = 0.007). The median time from discharge to readmission was 7 days (IQR 3-15 days). The most frequent causes of hospital readmission were worsening of previous pneumonia (54%), bacterial infection (13%), venous thromboembolism (5%), and heart failure (5%). Age [odds ratio (OR): 1.02; 95% confident interval (95% CI): 1.01-1.03], age-adjusted Charlson comorbidity index score (OR: 1.13; 95% CI: 1.06-1.21), chronic obstructive pulmonary disease (OR: 1.84; 95% CI: 1.26-2.69), asthma (OR: 1.52; 95% CI: 1.04-2.22), hemoglobin level at admission (OR: 0.92; 95% CI: 0.86-0.99), ground-glass opacification at admission (OR: 0.86; 95% CI:0.76-0.98) and glucocorticoid treatment (OR: 1.29; 95% CI: 1.00-1.66) were independently associated with hospital readmission. The rate of readmission after hospital discharge for COVID-19 was low. Advanced age and comorbidity were associated with increased risk of readmission.


Subject(s)
COVID-19/therapy , Patient Readmission , Age Factors , Aged , Aged, 80 and over , COVID-19/complications , COVID-19/epidemiology , Female , Humans , Male , Middle Aged , Patient Discharge , Retrospective Studies , Risk Factors , SARS-CoV-2/isolation & purification
4.
J Exp Med ; 218(5)2021 05 03.
Article in English | MEDLINE | ID: mdl-33635944

ABSTRACT

Meteorin-like/Meteorin-ß (Metrnl/Metrnß) is a secreted protein produced by skeletal muscle and adipose tissue that exerts metabolic actions that improve glucose metabolism. The role of Metrnß in cardiac disease is completely unknown. Here, we show that Metrnß-null mice exhibit asymmetrical cardiac hypertrophy, fibrosis, and enhanced signs of cardiac dysfunction in response to isoproterenol-induced cardiac hypertrophy and aging. Conversely, adeno-associated virus-mediated specific overexpression of Metrnß in the heart prevents the development of cardiac remodeling. Furthermore, Metrnß inhibits cardiac hypertrophy development in cardiomyocytes in vitro, indicating a direct effect on cardiac cells. Antibody-mediated blockage of Metrnß in cardiomyocyte cell cultures indicated an autocrine action of Metrnß on the heart, in addition to an endocrine action. Moreover, Metrnß is highly produced in the heart, and analysis of circulating Metrnß concentrations in a large cohort of patients reveals that it is a new biomarker of heart failure with an independent prognostic value.


Subject(s)
Cardiomegaly/genetics , Disease Models, Animal , Heart Failure/genetics , Nerve Growth Factors/genetics , Animals , Animals, Newborn , Blood Pressure/genetics , Blood Pressure/physiology , Cardiomegaly/physiopathology , Cardiotonic Agents/metabolism , Cells, Cultured , Echocardiography , Gene Expression Regulation , Heart Failure/physiopathology , Humans , Male , Mice, Inbred C57BL , Mice, Knockout , Muscle, Skeletal/metabolism , Myocytes, Cardiac/cytology , Myocytes, Cardiac/metabolism , Nerve Growth Factors/metabolism , PPAR alpha/genetics , PPAR alpha/metabolism
5.
Ann Med ; 53(1): 103-116, 2021 12.
Article in English | MEDLINE | ID: mdl-33063540

ABSTRACT

BACKGROUND: Hyperglycaemia has emerged as an important risk factor for death in coronavirus disease 2019 (COVID-19). The aim of this study was to evaluate the association between blood glucose (BG) levels and in-hospital mortality in non-critically patients hospitalized with COVID-19. METHODS: This is a retrospective multi-centre study involving patients hospitalized in Spain. Patients were categorized into three groups according to admission BG levels: <140 mg/dL, 140-180 mg/dL and >180 mg/dL. The primary endpoint was all-cause in-hospital mortality. RESULTS: Of the 11,312 patients, only 2128 (18.9%) had diabetes and 2289 (20.4%) died during hospitalization. The in-hospital mortality rates were 15.7% (<140 mg/dL), 33.7% (140-180 mg) and 41.1% (>180 mg/dL), p<.001. The cumulative probability of mortality was significantly higher in patients with hyperglycaemia compared to patients with normoglycaemia (log rank, p<.001), independently of pre-existing diabetes. Hyperglycaemia (after adjusting for age, diabetes, hypertension and other confounding factors) was an independent risk factor of mortality (BG >180 mg/dL: HR 1.50; 95% confidence interval (CI): 1.31-1.73) (BG 140-180 mg/dL; HR 1.48; 95%CI: 1.29-1.70). Hyperglycaemia was also associated with requirement for mechanical ventilation, intensive care unit (ICU) admission and mortality. CONCLUSIONS: Admission hyperglycaemia is a strong predictor of all-cause mortality in non-critically hospitalized COVID-19 patients regardless of prior history of diabetes. KEY MESSAGE Admission hyperglycaemia is a stronger and independent risk factor for mortality in COVID-19. Screening for hyperglycaemia, in patients without diabetes, and early treatment of hyperglycaemia should be mandatory in the management of patients hospitalized with COVID-19. Admission hyperglycaemia should not be overlooked in all patients regardless prior history of diabetes.


Subject(s)
Coronavirus Infections/mortality , Hyperglycemia/complications , Pneumonia, Viral/mortality , Registries , Aged , Aged, 80 and over , Blood Glucose , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/complications , Critical Care/statistics & numerical data , Female , Humans , Hyperglycemia/mortality , Length of Stay , Male , Middle Aged , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Respiration, Artificial/statistics & numerical data , Spain/epidemiology
6.
J Pathol ; 253(2): 198-208, 2021 02.
Article in English | MEDLINE | ID: mdl-33125701

ABSTRACT

Alcoholic cardiomyopathy (ACM) resulting from chronic alcohol misuse is one of the main contributors leading to heart failure and cardiovascular mortality. Fibroblast growth factor 21 (FGF21) is a well-established cardioprotective factor. We aimed to study the role of FGF21 in experimentally induced models and clinical affected patients with cardiac damage due to chronic alcohol consumption. We found that circulating FGF21 levels and cardiac FGF21 and ß-klotho protein levels were increased in subjects with chronic alcohol consumption. As an experimental model of ACM, we fed wild-type and Fgf21 knockout (Fgf21-/- ) mice with a 4% alcohol liquid diet for 4 and 12 weeks. FGF21 circulating levels and FGF21 expression in the myocardium were also increased in wild-type mice after chronic alcohol intake. Fgf21-/- mice develop a higher degree of cardiac hypertrophy, fibrosis, and cardiac dysfunction after chronic alcohol consumption than wild-type mice. Moreover, the myocardium of Fgf21-/- mice showed signs of metabolic deregulation, oxidative stress, and mitochondrial dysfunction after alcohol intake. Finally, human cardiac biopsies from patients with chronic alcohol consumption developing ACM presented a higher degree of oxidative stress which positively correlated with the FGF21 protein levels in the myocardium. We conclude that plasma levels and cardiac myocyte FGF21 expression were induced in response to chronic alcohol consumption. The lack of FGF21 aggravated cardiac damage produced by ACM, in association with enhanced mitochondrial and oxidative stress, thus pointing to FGF21 as a protective agent against development of alcohol-induced cardiomyopathy. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.


Subject(s)
Cardiomegaly/pathology , Cardiomyopathy, Alcoholic/pathology , Fibroblast Growth Factors/metabolism , Heart Failure/pathology , Animals , Cardiomyopathy, Alcoholic/complications , Cardiomyopathy, Alcoholic/drug therapy , Fibroblast Growth Factors/genetics , Heart Failure/etiology , Humans , Male , Mice , Mitochondria/pathology , Myocytes, Cardiac/pathology , Oxidative Stress , Protective Agents/therapeutic use
7.
J Am Coll Cardiol ; 76(25): 2982-3021, 2020 12 22.
Article in English | MEDLINE | ID: mdl-33309175

ABSTRACT

Cardiovascular diseases (CVDs), principally ischemic heart disease (IHD) and stroke, are the leading cause of global mortality and a major contributor to disability. This paper reviews the magnitude of total CVD burden, including 13 underlying causes of cardiovascular death and 9 related risk factors, using estimates from the Global Burden of Disease (GBD) Study 2019. GBD, an ongoing multinational collaboration to provide comparable and consistent estimates of population health over time, used all available population-level data sources on incidence, prevalence, case fatality, mortality, and health risks to produce estimates for 204 countries and territories from 1990 to 2019. Prevalent cases of total CVD nearly doubled from 271 million (95% uncertainty interval [UI]: 257 to 285 million) in 1990 to 523 million (95% UI: 497 to 550 million) in 2019, and the number of CVD deaths steadily increased from 12.1 million (95% UI:11.4 to 12.6 million) in 1990, reaching 18.6 million (95% UI: 17.1 to 19.7 million) in 2019. The global trends for disability-adjusted life years (DALYs) and years of life lost also increased significantly, and years lived with disability doubled from 17.7 million (95% UI: 12.9 to 22.5 million) to 34.4 million (95% UI:24.9 to 43.6 million) over that period. The total number of DALYs due to IHD has risen steadily since 1990, reaching 182 million (95% UI: 170 to 194 million) DALYs, 9.14 million (95% UI: 8.40 to 9.74 million) deaths in the year 2019, and 197 million (95% UI: 178 to 220 million) prevalent cases of IHD in 2019. The total number of DALYs due to stroke has risen steadily since 1990, reaching 143 million (95% UI: 133 to 153 million) DALYs, 6.55 million (95% UI: 6.00 to 7.02 million) deaths in the year 2019, and 101 million (95% UI: 93.2 to 111 million) prevalent cases of stroke in 2019. Cardiovascular diseases remain the leading cause of disease burden in the world. CVD burden continues its decades-long rise for almost all countries outside high-income countries, and alarmingly, the age-standardized rate of CVD has begun to rise in some locations where it was previously declining in high-income countries. There is an urgent need to focus on implementing existing cost-effective policies and interventions if the world is to meet the targets for Sustainable Development Goal 3 and achieve a 30% reduction in premature mortality due to noncommunicable diseases.


Subject(s)
Cardiovascular Diseases/mortality , Cost of Illness , Global Burden of Disease , Global Health , Global Health/statistics & numerical data , Global Health/trends , Health Policy , Heart Disease Risk Factors , Humans , Public Health
8.
Nutrients ; 12(2)2020 Feb 22.
Article in English | MEDLINE | ID: mdl-32098364

ABSTRACT

Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.


Subject(s)
Alcohol Drinking/adverse effects , Cardiomyopathy, Alcoholic/physiopathology , Ethanol/adverse effects , Heart/drug effects , Myocytes, Cardiac/pathology , Alcohol Abstinence , Animals , Cardiomyopathy, Alcoholic/etiology , Cardiomyopathy, Alcoholic/pathology , Cardiomyopathy, Alcoholic/surgery , Disease Models, Animal , Heart/physiopathology , Heart Transplantation/standards , Humans , Myocardial Contraction/drug effects , Myocardium/cytology , Myocardium/pathology , Myocytes, Cardiac/drug effects
9.
J Pathol ; 248(1): 30-40, 2019 05.
Article in English | MEDLINE | ID: mdl-30582148

ABSTRACT

FGF21 is an endocrine factor that contributes to multiple pathophysiological processes, mainly via its action as a metabolic regulator and cardioprotective agent. Recent studies have shown increased circulating FGF21 levels in hypertensive patients and in mouse models of hypertension. However, the relevance of FGF21 in hypertensive heart disease has not been addressed. Hypertension was induced by treating 4-month old WT and Fgf21-/- mice with angiotensin II (AngII) for 1 week, resulting in a similar increase in blood pressure in both genotypes. Plasma FGF21 levels and expression in heart and liver were significantly increased in hypertensive WT mice relative to controls, an effect that was associated with increased expression levels of ß-klotho specifically in the heart. Fgf21-/- mice developed a greater degree of hypertensive heart disease than WT mice, notably characterized by extensive cardiac dysfunction and fibrosis. In vitro and in vivo studies further showed that FGF21 exerted a marked protective effect against cardiac fibrosis. Finally, left ventricle biopsies from human hypertensive heart donors, especially those developing cardiomyopathy, showed a significant increase in FGF21expression compared with normotensive controls, a finding that was associated with significantly enhanced cardiac hypertrophy and fibrosis. We conclude that during hypertension, both systemic and cardiac-produced FGF21 are induced and act on the heart, protecting it from hypertensive heart disease. Thus, FGF21 acts as key factor in the fibrogenesis associated with hypertensive heart disease. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.


Subject(s)
Cardiomegaly/metabolism , Fibroblast Growth Factors/physiology , Hypertension/physiopathology , Myocardium/pathology , Angiotensin II , Animals , Biopsy , Blood Pressure/physiology , Cardiomegaly/etiology , Cardiomegaly/pathology , Cells, Cultured , Disease Models, Animal , Fibroblast Growth Factors/deficiency , Fibroblast Growth Factors/genetics , Fibroblast Growth Factors/metabolism , Fibrosis , Gene Expression Regulation/physiology , Heart Rate/physiology , Heart Ventricles/pathology , Humans , Hypertension/chemically induced , Hypertension/complications , Hypertension/metabolism , Mice, Knockout , Myocardium/metabolism , RNA, Messenger/genetics , Rats, Sprague-Dawley
14.
Adv Protein Chem Struct Biol ; 108: 227-256, 2017.
Article in English | MEDLINE | ID: mdl-28427562

ABSTRACT

Almost 30 years ago, the protein, atrial natriuretic peptide, was identified as a heart-secreted hormone that provides a peripheral signal from the myocardium that communicates to the rest of the organism to modify blood pressure and volume under conditions of heart failure. Since then, additional peripheral factors secreted by the heart, termed cardiokines, have been identified and shown to coordinate this interorgan cross talk. In addition to this interorgan communication, cardiokines also act in an autocrine/paracrine manner to play a role in intercellular communication within the myocardium. This review focuses on the roles of newly emerging cardiokines that are mainly increased in stress-induced cardiac diseases. The potential of these cardiokines as clinical biomarkers for diagnosis and prognosis of cardiac disorders is also discussed.


Subject(s)
Heart Diseases/immunology , Inflammation/immunology , Myocardium/immunology , Activins/analysis , Activins/immunology , Animals , Biomarkers/analysis , Fibroblast Growth Factors/analysis , Fibroblast Growth Factors/immunology , Follistatin/analysis , Follistatin/immunology , Follistatin-Related Proteins/analysis , Follistatin-Related Proteins/immunology , Growth Differentiation Factor 15/analysis , Growth Differentiation Factor 15/immunology , Heart Diseases/complications , Heart Diseases/pathology , Humans , Inflammation/complications , Inflammation/pathology , Interleukin-33/analysis , Interleukin-33/immunology , Myocardium/pathology , Myostatin/analysis , Myostatin/immunology , Paracrine Communication , Stress, Physiological , Transforming Growth Factor beta/analysis , Transforming Growth Factor beta/immunology
15.
Int J Mol Sci ; 17(10)2016 Sep 29.
Article in English | MEDLINE | ID: mdl-27690014

ABSTRACT

High-dose alcohol misuse induces multiple noxious cardiac effects, including myocyte hypertrophy and necrosis, interstitial fibrosis, decreased ventricular contraction and ventricle enlargement. These effects produce diastolic and systolic ventricular dysfunction leading to congestive heart failure, arrhythmias and an increased death rate. There are multiple, dose-dependent, synchronic and synergistic mechanisms of alcohol-induced cardiac damage. Ethanol alters membrane permeability and composition, interferes with receptors and intracellular transients, induces oxidative, metabolic and energy damage, decreases protein synthesis, excitation-contraction coupling and increases cell apoptosis. In addition, ethanol decreases myocyte protective and repair mechanisms and their regeneration. Although there are diverse different strategies to directly target alcohol-induced heart damage, they are partially effective, and can only be used as support medication in a multidisciplinary approach. Alcohol abstinence is the preferred goal, but control drinking is useful in alcohol-addicted subjects not able to abstain. Correction of nutrition, ionic and vitamin deficiencies and control of alcohol-related systemic organ damage are compulsory. Recently, several growth factors (myostatin, IGF-1, leptin, ghrelin, miRNA, and ROCK inhibitors) and new cardiomyokines such as FGF21 have been described to regulate cardiac plasticity and decrease cardiac damage, improving cardiac repair mechanisms, and they are promising agents in this field. New potential therapeutic targets aim to control oxidative damage, myocyte hypertrophy, interstitial fibrosis and persistent apoptosis In addition, stem-cell therapy may improve myocyte regeneration. However, these strategies are not yet approved for clinical use.

16.
Rev Esp Salud Publica ; 90: e1-7, 2016 Aug 18.
Article in English, Spanish | MEDLINE | ID: mdl-27535808

ABSTRACT

BACKGROUND: Chronic Fatigue Syndrome (CFS) is a complex and multifactorial disease. Stressful situations experienced could be related to the presentation of the disease. Few studies have determined which factors could trigger CFS. The main objective of this study was to explore the stressful situations which can be associated with CFS presentation. METHODS: Retrospective observational case-control study with CFS diagnosed patients according to the Fukuda's criteria. Controls were matched to cases by sex, age and educational level with a 1:1 ratio. Participants aged between 18 and 75 years from the province of Lleida. Information was obtained through personal questionnaires. The measure of association was the odds ratio. RESULTS: In total, 77 cases and 77 controls were included. Association found between stressful life events and presentation of disease were pregnancy ORa=31.7 (CI95%:2.2-456.7), spousal abuse ORa= 10.2 (CI95%:1.2-88.4) and mobbing ORa=6.9 (CI95%:1.3-36.9), eating disorders=7.5 (CI95%:1.3-42.1), car accident ORa=5.5 (CI95%:1.7-17 9), economic problems ORa=5.1 (CI95%:2.1-12.6) and changes in sleep habits ORa=2.8 (CI95%:1.1-7.5). CONCLUSIONS: Stressful life events as pregnancy, spousal abuse, mobbing, eating disorders, car accident, economic problems and changes in sleep habits felt by those affected must be taken into consideration when compiling background information related to the onset of Chronic Fatigue Syndrome. Adequate identification of these stressful life events in risk people could contribute to early diagnosis of Chronic Fatigue Syndrome.


OBJETIVO: El síndrome de fatiga crónica (SFC) es una enfermedad compleja y multifactorial. Situaciones estresantes vividas podrían relacionarse con la presentación de la enfermedad. Son pocos los estudios que han determinado estos factores desencadenantes de la presentación del SFC. El objetivo principal del presente estudio fue explorar cuáles pueden ser las Situaciones estresantes asociadas al desencadenamiento del síndrome de fatiga crónica. METODOS: Estudio observacional retrospectivo de casos y controles con pacientes diagnosticados de SFC según los criterios de Fukuda. Los controles se emparejaron con los casos según sexo, edad y nivel de estudios con una razón 1:1. Ambos tenían edades comprendidas entre los 18 y los 75 años y eran residentes en la provincia de Lleida. Se aplicó una tabla de acontecimientos vitales estresantes (AVE). La información se obtuvo mediante encuestas personales. Se realizó regresión logística binaria calculando la odds ratio como medida de asociación. RESULTADOS: Se incluyeron 77 casos y 77 controles. Se evidenció asociación entre acontecimientos vitales estresantes y presentación de la patología, como embarazo con ORa=31,7 (IC95%: 2,2-456,7), maltrato por parte de la pareja ORa=10,2 (IC95%:1,2-88,4), mobbing ORa=6,9 (IC95%:1,3-36,9), trastornos de la alimentación ORa=7,5 (IC95%:1,3-42,1), accidente de tráfico ORa=5,5 (IC95%:1,7-17,9), problemas económicos ORa=5,1 (IC95%:2,1-12,6) y cambios de hábitos de sueño ORa=2,8 (IC95%:1,1-7,5). CONCLUSIONES: Acontecimientos vitales estresantes como el embarazo, el maltrato por parte de la pareja, mobbing, trastornos de alimentación, accidente de tráfico, problemas económicos y cambios de hábitos de sueño percibidos por los afectados, deben tenerse en cuenta al explorar la información relacionada con el desencadenamiento del síndrome de fatiga crónica. Su hallazgo en personas de riesgo podría contribuir a un diagnóstico precoz del síndrome de fatiga crónica.


Subject(s)
Fatigue Syndrome, Chronic/psychology , Stress, Psychological/complications , Adolescent , Adult , Aged , Case-Control Studies , Female , Humans , Logistic Models , Male , Middle Aged , Retrospective Studies , Risk Factors , Spain , Stress, Psychological/diagnosis , Surveys and Questionnaires , Young Adult
17.
Alcohol Alcohol ; 51(4): 457-64, 2016 Jul.
Article in English | MEDLINE | ID: mdl-26818195

ABSTRACT

AIM: To determine the detection rates, clinical features, and risk factors for lack of registration of alcohol use in medical patients admitted in European hospitals. METHODS: A point-prevalence, cross-sectional, multicenter survey involving 2100 medical inpatients from 43 hospitals from 8 European countries. Patients were screened for current alcohol use, using standardized questionnaires. Alcohol use recording in medical records was assessed. RESULTS: Of the 2100, more than a half reported alcohol use. Significant differences were shown in the prevalence of drinking and the recording rates of alcohol use among the hospitals and countries involved. Overall, 346 patients (16%) fulfilled criteria for alcohol use disorder. Alcohol use was registered in 909 (43%) of medical records, with quantification in 143 (7%). Multivariate analysis showed that women (OR 1.49), older age patients (OR 1.23), patients from the Northern European countries (OR 4.79) and from hospitals with high local alcohol prevalence (OR 1.59) were more likely to have lack of alcohol use registration in their medical files. CONCLUSIONS: A considerable proportion of medical patients admitted in European hospitals fulfill criteria for alcohol use disorders. These patients are frequently overlooked during hospitalization and not appropriately registered in medical records. Women, older patients, and inpatients from European areas with high local alcohol use prevalence are at higher risk associated with a non-recording of alcohol use.


Subject(s)
Alcohol Drinking/epidemiology , Hospitals/statistics & numerical data , Adolescent , Adult , Age Factors , Aged , Aged, 80 and over , Cross-Sectional Studies , Europe/epidemiology , Female , Humans , Male , Medical Records/statistics & numerical data , Middle Aged , Prevalence , Risk Factors , Sex Factors , Young Adult
18.
Rev. esp. salud pública ; 90: 0-0, 2016. tab, ilus
Article in Spanish | IBECS | ID: ibc-155974

ABSTRACT

Fundamentos: El síndrome de fatiga crónica (SFC) es una enfermedad compleja y multifactorial. Situaciones estresantes vividas podrían relacionarse con la presentación de la enfermedad. Son pocos los estudios que han determinado estos factores desencadenantes de la presentación del SFC. El objetivo principal del presente estudio fue explorar cuáles pueden ser las Situaciones estresantes asociadas al desencadenamiento del síndrome de fatiga crónica. Métodos: Estudio observacional retrospectivo de casos y controles con pacientes diagnosticados de SFC según los criterios de Fukuda. Los controles se emparejaron con los casos según sexo, edad y nivel de estudios con una razón 1:1. Ambos tenían edades comprendidas entre los 18 y los 75 años y eran residentes en la provincia de Lleida. Se aplicó una tabla de acontecimientos vitales estresantes (AVE). La información se obtuvo mediante encuestas personales. Se realizó regresión logística binaria calculando la odds ratio como medida de asociación. Resultados: Se incluyeron 77 casos y 77 controles. Se evidenció asociación entre acontecimientos vitales estresantes y presentación de la patología, como embarazo con ORa=31,7 (IC95%: 2,2-456,7), maltrato por parte de la pareja ORa=10,2 (IC95%:1,2-88,4), mobbing ORa=6,9 (IC95%:1,3-36,9), trastornos de la alimentación ORa=7,5 (IC95%:1,3-42,1), accidente de tráfico ORa=5,5 (IC95%:1,7-17,9), problemas económicos ORa=5,1 (IC95%:2,1-12,6) y cambios de hábitos de sueño ORa=2,8 (IC95%:1,1-7,5). Conclusiones: Acontecimientos vitales estresantes como el embarazo, el maltrato por parte de la pareja, mobbing, trastornos de alimentación, accidente de tráfico, problemas económicos y cambios de hábitos de sueño percibidos por los afectados, deben tenerse en cuenta al explorar la información relacionada con el desencadenamiento del síndrome de fatiga crónica. Su hallazgo en personas de riesgo podría contribuir a un diagnóstico precoz del síndrome de fatiga crónica (AU)


Background: Chronic Fatigue Syndrome (CFS) is a complex and multifactorial disease. Stressful situations experienced could be related to the presentation of the disease. Few studies have determined which factors could trigger CFS. The main objective of this study was to explore the stressful situations which can be associated with CFS presentation. Methods: Retrospective observational case-control study with CFS diagnosed patients according to the Fukuda’s criteria. Controls were matched to cases by sex, age and educational level with a 1:1 ratio. Participants aged between 18 and 75 years from the province of Lleida. Information was obtained through personal questionnaires. The measure of association was the odds ratio. Results: In total, 77 cases and 77 controls were included. Association found between stressful life events and presentation of disease were pregnancy ORa=31.7 (CI95%:2.2-456.7), spouse abuse ORa=10.2 (CI95%:1.2-88.4) and mobbing ORa=6.9 (CI95%:1.3-36.9), eating disorders=7.5 (CI95%:1.3-42.1), car accident ORa=5.5 (CI95%:1.7-17 9), economic problems ORa=5.1 (CI95%:2.1-12.6) and changes in sleep habits ORa=2.8 (CI95%:1.1-7.5). Conclusions: Stressful life events as pregnancy, spousal abuse, mobbing, eating disorders, car accident, economic problems and changes in sleep habits felt by those affected must be taken into consideration when compiling background information related to the onset of Chronic Fatigue Syndrome. Adequate identification of these stressful life events in risk people could contribute to early diagnosis of Chronic Fatigue Syndrome (AU)


Subject(s)
Humans , Stress, Psychological/complications , Fatigue Syndrome, Chronic/etiology , Early Diagnosis , Logistic Models , Depression/epidemiology , Sleep Wake Disorders/epidemiology , Feeding and Eating Disorders/epidemiology
19.
Nat Rev Cardiol ; 12(10): 576-87, 2015 Oct.
Article in English | MEDLINE | ID: mdl-26099843

ABSTRACT

The heart and vascular system are susceptible to the harmful effects of alcohol. Alcohol is an active toxin that undergoes widespread diffusion throughout the body, causing multiple synchronous and synergistic effects. Alcohol consumption decreases myocardial contractility and induces arrhythmias and dilated cardiomyopathy, resulting in progressive cardiovascular dysfunction and structural damage. Alcohol, whether at binge doses or a high cumulative lifetime consumption-both of which should be discouraged-is clearly deleterious for the cardiovascular system, increasing the incidence of total and cardiovascular mortality, coronary and peripheral artery disease, heart failure, stroke, hypertension, dyslipidaemia, and diabetes mellitus. However, epidemiological, case-control studies and meta-analyses have shown a U-type bimodal relationship so that low-to-moderate alcohol consumption (particularly of wine or beer) is associated with a decrease in cardiovascular events and mortality, compared with abstention. Potential confounding influences-alcohol-dose quantification, tobacco use, diet, exercise, lifestyle, cancer risk, accidents, and dependence-can affect the results of studies of both low-dose and high-dose alcohol consumption. Mendelian methodological approaches have led to doubts regarding the beneficial cardiovascular effects of alcohol, and the overall balance of beneficial and detrimental effects should be considered when making individual and population-wide recommendations, as reductions in alcohol consumption should provide overall health benefits.


Subject(s)
Alcohol Drinking , Cardiovascular Diseases/chemically induced , Cardiovascular Diseases/prevention & control , Alcohol Drinking/adverse effects , Humans , Life Style , Public Health , Risk Factors
20.
J Hypertens ; 33(4): 851-8; discussion 859, 2015 Apr.
Article in English | MEDLINE | ID: mdl-25915890

ABSTRACT

OBJECTIVE: The physiopathological mechanisms implicated in hypertensive heart disease are multi-factorial, including myocyte hypertrophy, apoptosis and myocardial remodelling. In this process, some hormonal and local growth factors have a regulatory influence. The aim of this study was to evaluate the potential role of myostatin and insulin-like growth factor-1 (IGF-1) myocardial expression in the development of hypertensive-induced cardiac damage. METHODS: Samples of human myocardium tissue from organ donors were prospectively collected and classified according to the presence of hypertension, alcohol consumption, other causes of myocardial damage and the presence of structural cardiomyopathy (CMP). Myocardial samples were studied by immunohistochemistry and myostatin, and IGF-1 myocardial expression was evaluated in all the different groups of donors. Hypertensive donors were compared to other groups. RESULTS: A total of 66 heart samples from human donors were collected: 33 donors had no previous or present history of hypertension and 33 donors presented defined hypertension. Donors with hypertension presented higher myocyte cell and nuclear hypertrophy and showed similar myostatin myocardial expression as controls, but lower IGF-1 myocardial expression. Myostatin expression was significantly higher in hypertensive donors with CMP compared to non-hypertensive healthy donors. The presence of CMP of diverse origin (alcoholic, valve and coronary) also significantly increased myostatin myocardial expression. CONCLUSION: The presence of hypertension significantly decreases IGF-1 myocardial expression. Myostatin myocardial expression increases in the presence of structural CMP either of hypertensive or other origin. These effects open the possibility of modulating hypertensive-induced cardiac damage.


Subject(s)
Heart Diseases/metabolism , Hypertension/metabolism , Insulin-Like Growth Factor I/metabolism , Myocardium/metabolism , Myostatin/metabolism , Adult , Aged , Alcoholism/metabolism , Apoptosis , Case-Control Studies , Female , Gene Expression , Heart Diseases/etiology , Humans , Hypertension/complications , Male , Middle Aged , Prospective Studies , Tissue Donors
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