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Background: Critically ill patients are at high risk of Intensive Care Unit (ICU) Acquired weakness, which negatively impacts clinical outcomes. Traditional muscle mass and nutritional status assessments are often impractical in the ICU. Ultrasound offers a promising, non-invasive alternative. This study evaluates the relationship between ultrasound-based muscle assessments, patients' nutritional support, and clinical outcomes in the ICU., Methods: A prospective cohort study was conducted in three ICUs of a tertiary center. Daily nutritional intake, ultrasound measurements of the quadriceps muscle (rectus femoris cross-sectional area - RFCSA - and quadriceps muscle layer thickness - QMLT), and clinical data were collected on days 1, 3, and 7 of ICU., Results: A total of 128 patients were included in the analysis, with a mean age of 65.4 (±18.1) years and a median ICU stay of 6 (4-10) days. QMLT decreased by 5 % and 13 %, and RFCSA decreased by 10 % and 27 % on days 3 and 7, respectively. A significant correlation was found between lower caloric and protein intake and greater muscle mass loss within the initial 3 days of ICU admission. Multivariate logistic regression indicated that QMLT reduction significantly contributed to 28-day mortality (adjusted OR 1.088, 95 % CI: 1.018-1.113, p = 0.015). Lower daily caloric and protein intake was depicted in non-surviving patients (p < 0.001)., Conclusions: Our study demonstrates that critically ill patients experience significant muscle mass loss within the first 72 h of ICU. QMLT reduction significantly impacts 28-day mortality, with an 8.8 % increase in the odds of death per 0.1 cm reduction., Competing Interests: Declaration of competing interest The authors do not declare conflicts of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Objective: To elucidate the impact of lymphopenia on critical COVID-19 patient outcomes., Methods: We conducted a multicenter prospective cohort study across five hospitals in Portugal and Brazil from 2020 to 2021. The study included adult patients admitted to the intensive care unit with SARS-CoV-2 pneumonia. Patients were categorized into two groups based on their lymphocyte counts within 48 hours of intensive care unit admission: the Lymphopenia Group (lymphocyte serum count < 1 × 109/L) and the Nonlymphopenia Group. Multivariate logistic regression, propensity score matching, Kaplan‒Meier survival curve analysis and Cox proportional hazards regression analysis were used., Results: A total of 912 patients were enrolled, with 191 (20.9%) in the Nonlymphopenia Group and 721 (79.1%) in the Lymphopenia Group. Lymphopenia patients displayed significantly elevated disease severity indices, including Sequential Organ Failure Assessment and Simplified Acute Physiology Score 3 scores, at intensive care unit admission (p = 0.001 and p < 0.001, respectively). Additionally, they presented heightened requirements for vasopressor support (p = 0.045) and prolonged intensive care unit and in-hospital stays (both p < 0.001). Multivariate logistic regression analysis after propensity score matching revealed a significant contribution of lymphopenia to mortality, with an odds ratio of 1,621 (95%CI: 1,275 - 2,048; p < 0.001). Interaction models revealed an increase of 8% in mortality for each decade of longevity in patients with concomitant lymphopenia. In the subanalysis utilizing three-group stratification, the Severe Lymphopenia Group had the highest mortality rate, not only in direct comparisons but also in Kaplan‒Meier survival analysis (log-rank test p = 0.0048)., Conclusion: Lymphopenia in COVID-19 patients is associated with increased disease severity and an increased risk of mortality, underscoring the need for prompt support for critically ill high-risk patients. These findings offer important insights into improving patient care strategies for COVID-19 patients.

Summary: Riedel's thyroiditis is the rarest form of thyroiditis, occasionally resulting in rapid thyroid enlargement and potential tracheal obstruction. Here, we detail the case of an 81-year-old woman with a medical history including Hodgkin lymphoma, Hashimoto's thyroiditis, and multinodular goiter. She presented to the emergency room with stridor, cervical swelling, and breathing difficulties for over 2 days. CT scans revealed substantial thyroid enlargement causing significant glottal and tracheal compression, to a minimum tracheal diameter of 7 mm. Due to the severity of the compressive symptoms, orotracheal intubation and mechanical ventilation were deemed necessary. Surprisingly, despite the initial suspicion of malignancy given the rapid growth in the elderly, subsequent cytological and histological evaluations indicated a benign form of invasive fibrous thyroiditis - Riedel's thyroiditis. Although surgical intervention was advised, the patient declined and opted for endobronchial treatment with a prosthetic stent and subsequent treatment with systemic glucocorticoids. Following successful treatment, she was discharged within a week and resumed normal activities without respiratory distress. This case is noteworthy for its rapid benign mass growth, rare emergent presentation, and the patient's advanced age., Learning Points: The rapid enlargement of the thyroid gland in elderly patients poses a diagnostic challenge, stemming from the higher occurrence of aggressive thyroid carcinomas. Despite the clinical presentation, a comprehensive diagnostic workup, including fine-needle aspiration and core-needle biopsy, is crucial for accurately distinguishing between benign and malignant causes of thyroid nodule enlargement. This case report illustrates diverse treatment options for Riedel's thyroiditis, and the importance of individualized treatment plans based on the degree of airway obstruction, patient preferences, and response to initial interventions. Clinicians should contemplate the inclusion of glucocorticoids in the therapeutic regimen for Riedel's thyroiditis, particularly in cases where surgical intervention is not feasible or declined by the patient.

Severe acute respiratory infections, such as community-acquired pneumonia, hospital-acquired pneumonia, and ventilator-associated pneumonia, constitute frequent and lethal pulmonary infections in the intensive care unit (ICU). Despite optimal management with early appropriate empiric antimicrobial therapy and adequate supportive care, mortality remains high, in part attributable to the aging, growing number of comorbidities, and rising rates of multidrug resistance pathogens. Biomarkers have the potential to offer additional information that may further improve the management and outcome of pulmonary infections. Available pathogen-specific biomarkers, for example, Streptococcus pneumoniae urinary antigen test and galactomannan, can be helpful in the microbiologic diagnosis of pulmonary infection in ICU patients, improving the timing and appropriateness of empiric antimicrobial therapy since these tests have a short turnaround time in comparison to classic microbiology. On the other hand, host-response biomarkers, for example, C-reactive protein and procalcitonin, used in conjunction with the clinical data, may be useful in the diagnosis and prediction of pulmonary infections, monitoring the response to treatment, and guiding duration of antimicrobial therapy. The assessment of serial measurements overtime, kinetics of biomarkers, is more informative than a single value. The appropriate utilization of accurate pathogen-specific and host-response biomarkers may benefit clinical decision-making at the bedside and optimize antimicrobial stewardship., (© 2024. The Author(s).)

Introduction: Graves' disease (GD) is associated with primary hyperthyroidism, leading to weight loss before treatment. During the treatment, weight gain is frequently observed, often surpassing the initial weight loss. This study aimed to analyze weight fluctuations in GD patients, focusing on the subset of overweight and obese (OAO) individuals, considering the significant metabolic implications and heightened cardiovascular risk of these weight changes., Methods: A retrospective cohort study included 122 GD patients with biochemical primary hyperthyroidism and at least 12 months of clinical follow-up after treatment for analysis. The OAO cohort comprised individuals with a body mass index (BMI) ≥25 kg/m². Data on laboratory, demographic, and weight variables were collected longitudinally., Results: During the hyperthyroidism state, 34.4% (n=42) of patients presented with weight loss, a phenomenon linked to lower serum thyroid-stimulating hormone levels at diagnosis (p=0.010) and an extended need for anti-thyroid drug treatment (p<0.001). Following treatment, around 60% (n=73) of individuals encountered weight gain, exhibiting a higher prevalence among women (p<0.001) and those undergoing definitive treatment modalities (p=0.024). Notably, 26.2% (n=32) experienced excessive weight gain, which was correlated with higher premorbid BMI and diminished weight loss induced by hyperthyroidism (p<0.001). Within the OAO cohort, 66.7% (n=26) observed an increase in weight post-treatment, and in 28.2% (n=11), excessive weight gain was reported. Weight gain and excessive weight gain were noted in patients with higher initial BMIs., Conclusions: This study highlights that post-treatment weight gain is common, emphasizing the need for careful weight management in GD. In OAO GD patients, the association between initial BMI and increased weight underscores potential cardiovascular risks, warranting vigilant monitoring and early intervention., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Guia Lopes et al.)

The SARS-CoV-2 infection is a cause of hypoxemic acute respiratory failure, leading to frequent intensive care unit (ICU) admission. Due to invasive organ support and immunosuppressive therapies, these patients are prone to nosocomial infections. Our aim was to assess the value of daily measurements of C-reactive protein (CRP) and Procalcitonin (PCT) in the early identification of ICU-acquired infections in COVID-19 patients., Methods: We undertook a prospective observational cohort study (12 months). All adult mechanically ventilated patients admitted for ≥72 h to ICU with COVID-19 pneumonia were divided into an infected group ( n = 35) and a non-infected group ( n = 83). Day 0 was considered as the day of the diagnosis of infection (infected group) and Day 10 was that of ICU stay (non-infected group). The kinetics of CRP and PCT were assessed from Day -10 to Day 10 and evaluated using a general linear model, univariate, repeated-measures analysis., Results: 118 patients (mean age 63 years, 74% males) were eligible for the analysis. The groups did not differ in patient age, gender, CRP and PCT serum levels at ICU admission. However, the infected group encompassed patients with a higher severity (SOFA score at ICU admission, p = 0.009) and a higher 28-day mortality ( p < 0.001). Before D0, CRP kinetics showed a significant increase in infected patients, whereas in noninfected it remained almost unchanged ( p < 0.001), while PCT kinetics did not appear to retain diagnostic value to predict superinfection in COVID-19 patients ( p = 0.593)., Conclusion: COVID-19 patients who developed ICU-acquired infections exhibited different biomarker kinetics before the diagnosis of those infections. Daily CRP monitoring and the recognition of the CRP kinetics could be useful in the prediction of ICU-acquired infections.

Purpose Graves' disease (GD) is an autoimmune disorder caused by the presence of antibodies to the thyroid stimulating hormone (TSH) receptor (TRAbs), usually presenting with clinical signs of hyperthyroidism. Previous evidence suggests that higher serum levels of thyroid peroxidase antibodies (TPOAbs) may lead to more sustained remission of hyperthyroidism after treatment with antithyroid drugs (AT). However, doubts about the influence of TPOAbs in Graves' disease outcomes still remain. Methods A retrospective, unicenter cohort study was performed. All patients with GD (TRAbs > 1.58U/L), biochemical primary hyperthyroidism (TSH < 0.4 µUI/mL), and TPOAbs measurement at diagnosis, treated with AT between January 2008 and January 2021, were included for analysis. Results One hundred and forty-two patients (113 women) with a mean age of 52 ± 15 years old were included. They were followed up for 65.4 ± 43.8 months. TPOAbs positivity was present in 71.10% (n=101) of those patients. Patients were treated with AT for a median of 18 (IQR (12; 24)) months. Remission occurred in 47.2% of patients. Patients with remission presented with lower TRAbs and free thyroxine (FT4) levels at the diagnosis. (p-value <0.001, p-value 0.003, respectively). No association was found in the median TPOAbs serum levels of patients who remitted and those who maintained biochemical hyperthyroidism after the first course of AT. Relapse of hyperthyroidism occurred in 54 patients (57.4%). No difference was found in TPOAbs serum levels regarding the patient's relapse. Moreover, a time-based analysis revealed no differences in the relapse rate after 18 months of AT therapy between patients with and without TPOAbs positivity at the diagnosis (p-value 0.176). It was found a weak positive correlation (r=0.295; p-value <0.05) between TRAbs and TPOAbs titters at the moment of Graves' diagnosis. Conclusion In this study, a correlation between TRAbs measurements and TPOAbs titter was described, although no significant association was found between the presence of TPOAbs and the outcomes of patients with GD treated with AT. These results do not support the use of TPOAbs as a useful biomarker to predict remission or relapse of hyperthyroidism in GD patients., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Guia Lopes et al.)

Purpose : COVID-19 presents complex pathophysiology, and evidence collected points towards an intricate interaction between viral-dependent and individual immunological mechanisms. Identifying phenotypes through clinical and biological markers may provide a better understanding of the subjacent mechanisms and an early patient-tailored characterization of illness severity. Methods: A multicenter prospective cohort study was performed in 5 hospitals in Portugal and Brazil for one year between 2020-2021. All adult patients with an Intensive Care Unit admission with SARS-CoV-2 pneumonia were eligible. COVID-19 was diagnosed using clinical and radiologic criteria with a SARS-CoV-2 positive RT-PCR test. A two-step hierarchical cluster analysis was made using several class-defining variables. Results: 814 patients were included. The cluster analysis revealed a three-class model, allowing for the definition of three distinct COVID-19 phenotypes: 407 patients in phenotype A, 244 patients in phenotype B, and 163 patients in phenotype C. Patients included in phenotype A were significantly older, with higher baseline inflammatory biomarkers profile, and a significantly higher requirement of organ support and mortality rate. Phenotypes B and C demonstrated some overlapping clinical characteristics but different outcomes. Phenotype C patients presented a lower mortality rate, with consistently lower C-reactive protein, but higher procalcitonin and interleukin-6 serum levels, describing an immunological profile significantly different from phenotype B. Conclusions: Severe COVID-19 patients exhibit three different clinical phenotypes with distinct profiles and outcomes. Their identification could have an impact on patients' care, justifying different therapy responses and inconsistencies identified across different randomized control trial results.

Objective: To analyze and compare COVID-19 patient characteristics, clinical management and outcomes between the peak and plateau periods of the first pandemic wave in Portugal., Methods: This was a multicentric ambispective cohort study including consecutive severe COVID-19 patients between March and August 2020 from 16 Portuguese intensive care units. The peak and plateau periods, respectively, weeks 10 - 16 and 17 - 34, were defined., Results: Five hundred forty-one adult patients with a median age of 65 [57 - 74] years, mostly male (71.2%), were included. There were no significant differences in median age (p = 0.3), Simplified Acute Physiology Score II (40 versus 39; p = 0.8), partial arterial oxygen pressure/fraction of inspired oxygen ratio (139 versus 136; p = 0.6), antibiotic therapy (57% versus 64%; p = 0.2) at admission, or 28-day mortality (24.4% versus 22.8%; p = 0.7) between the peak and plateau periods. During the peak period, patients had fewer comorbidities (1 [0 - 3] versus 2 [0 - 5]; p = 0.002) and presented a higher use of vasopressors (47% versus 36%; p < 0.001) and invasive mechanical ventilation (58.1 versus 49.2%; p < 0.001) at admission, prone positioning (45% versus 36%; p = 0.04), and hydroxychloroquine (59% versus 10%; p < 0.001) and lopinavir/ritonavir (41% versus 10%; p < 0.001) prescriptions. However, a greater use of high-flow nasal cannulas (5% versus 16%, p < 0.001) on admission, remdesivir (0.3% versus 15%; p < 0.001) and corticosteroid (29% versus 52%, p < 0.001) therapy, and a shorter ICU length of stay (12 days versus 8, p < 0.001) were observed during the plateau., Conclusion: There were significant changes in patient comorbidities, intensive care unit therapies and length of stay between the peak and plateau periods of the first COVID-19 wave.

Background: Coronavirus disease 2019 (COVID-19) can be associated with life-threatening organ dysfunction due to septic shock, frequently requiring intensive care unit (ICU) admission, respiratory and vasopressor support. Therefore, clear clinical criteria are pivotal for early recognition of patients more likely to need prompt organ support. Although most patients with severe COVID-19 meet the Sepsis-3.0 criteria for septic shock, it has been increasingly recognized that hyperlactatemia is frequently absent, possibly leading to an underestimation of illness severity and mortality risk., Aim: To identify the proportion of severe COVID-19 patients with vasopressor support requirements, with and without hyperlactatemia, and describe their clinical outcomes and mortality., Methods: We performed a single-center prospective cohort study. All adult patients admitted to the ICU with COVID-19 were included in the analysis and were further divided into three groups: Sepsis group, without both criteria; Vasoplegic Shock group, with persistent hypotension and vasopressor support without hyperlactatemia; and Septic Shock 3.0 group, with both criteria. COVID-19 was diagnosed using clinical and radiologic criteria with a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive RT-PCR test., Results: 118 patients (mean age 63 years, 87% males) were included in the analysis ( n = 51 Sepsis group, n = 26 Vasoplegic Shock group, and n = 41 Septic Shock 3.0 group). SOFA score at ICU admission and ICU length of stay were different between the groups ( P < 0.001). Mortality was significantly higher in the Vasoplegic Shock and Septic Shock 3.0 groups when compared with the Sepsis group ( P < 0.001) without a significant difference between the former two groups ( P = 0.713). The log rank tests of Kaplan-Meier survival curves were also different ( P = 0.007). Ventilator-free days and vasopressor-free days were different between the Sepsis vs Vasoplegic Shock and Septic Shock 3.0 groups (both P < 0.001), and similar in the last two groups ( P = 0.128 and P = 0.133, respectively). Logistic regression identified the maximum dose of vasopressor therapy used (AOR 1.046; 95%CI: 1.012-1.082, P = 0.008) and serum lactate level (AOR 1.542; 95%CI: 1.055-2.255, P = 0.02) as the major explanatory variables of mortality rates ( R 2 0.79)., Conclusion: In severe COVID-19 patients, the Sepsis 3.0 criteria of septic shock may exclude approximately one third of patients with a similarly high risk of a poor outcome and mortality rate, which should be equally addressed., Competing Interests: Conflict-of-interest statement: The authors declare that they have no conflict-of-interest to disclose., (©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.)

Due to the large number of patients with severe coronavirus disease 2019 (COVID-19), many were treated outside the traditional walls of the intensive care unit (ICU), and in many cases, by personnel who were not trained in critical care. The clinical characteristics and the relative impact of caring for severe COVID-19 patients outside the ICU is unknown. This was a multinational, multicentre, prospective cohort study embedded in the International Severe Acute Respiratory and Emerging Infection Consortium World Health Organization COVID-19 platform. Severe COVID-19 patients were identified as those admitted to an ICU and/or those treated with one of the following treatments: invasive or noninvasive mechanical ventilation, high-flow nasal cannula, inotropes or vasopressors. A logistic generalised additive model was used to compare clinical outcomes among patients admitted or not to the ICU. A total of 40 440 patients from 43 countries and six continents were included in this analysis. Severe COVID-19 patients were frequently male (62.9%), older adults (median (interquartile range (IQR), 67 (55-78) years), and with at least one comorbidity (63.2%). The overall median (IQR) length of hospital stay was 10 (5-19) days and was longer in patients admitted to an ICU than in those who were cared for outside the ICU (12 (6-23) days versus 8 (4-15) days, p<0.0001). The 28-day fatality ratio was lower in ICU-admitted patients (30.7% (5797 out of 18 831) versus 39.0% (7532 out of 19 295), p<0.0001). Patients admitted to an ICU had a significantly lower probability of death than those who were not (adjusted OR 0.70, 95% CI 0.65-0.75; p<0.0001). Patients with severe COVID-19 admitted to an ICU had significantly lower 28-day fatality ratio than those cared for outside an ICU., Competing Interests: Conflict of interest: L.F. Reyes has nothing to disclose. Conflict of interest: S. Murthy declares receiving salary support from the Health Research Foundation and Innovative Medicines Canada Chair in Pandemic Preparedness Research. Conflict of interest: E. Garcia-Gallo has nothing to disclose. Conflict of interest: M. Irvine has nothing to disclose. Conflict of interest: L. Merson has nothing to disclose. Conflict of interest: I. Martin-Loeches declares consulting fees for Gilead outside of the submitted work. Conflict of interest: J. Rello has nothing to disclose. Conflict of interest: F.S. Taccone has nothing to disclose. Conflict of interest: R.A. Fowler has nothing to disclose. Conflict of interest: A.B. Docherty has nothing to disclose. Conflict of interest: C. Kartsonaki has nothing to disclose. Conflict of interest: I. Aragao has nothing to disclose. Conflict of interest: P.W. Barrett has nothing to disclose. Conflict of interest: A. Beane has nothing to disclose. Conflict of interest: A. Burrell has nothing to disclose. Conflict of interest: M.P. Cheng has nothing to disclose. Conflict of interest: M.D. Christian has nothing to disclose. Conflict of interest: J.P. Cidade has nothing to disclose. Conflict of interest: B.W. Citarella has nothing to disclose. Conflict of interest: C.A. Donnelly has nothing to disclose. Conflict of interest: S.M. Fernandes has nothing to disclose. Conflict of interest: C. French has nothing to disclose. Conflict of interest: R. Haniffa has nothing to disclose. Conflict of interest: E.M. Harrison has nothing to disclose. Conflict of interest: A.Y.W. Ho declares grant funding from Medical Research Council UK, Scottish Funding Council – Grand Challenges Research Fund and the Wellcome Trust, outside this submitted work. Conflict of interest: M. Joseph has nothing to disclose. Conflict of interest: I. Khan has nothing to disclose. Conflict of interest: M.E. Kho has nothing to disclose. Conflict of interest: A.B. Kildal has nothing to disclose. Conflict of interest: D. Kutsogiannis declares personal fees for a lecture from Tabuk Pharmaceuticals and the Saudi Critical Care Society. Conflict of interest: F. Lamontagne has nothing to disclose. Conflict of interest: T.C. Lee declares research salary support from les Fonds de recherche du Québec – Santé. Conflict of interest: G.L. Bassi has nothing to disclose. Conflict of interest: J.W. Lopez Revilla has nothing to disclose. Conflict of interest: C. Marquis has nothing to disclose. Conflict of interest: J. Millar has nothing to disclose. Conflict of interest: R. Neto has nothing to disclose. Conflict of interest: A. Nichol declares a grant from the Health Research Board of Ireland to support data collection in Ireland (CTN-2014-012). Conflict of interest: R. Parke has nothing to disclose. Conflict of interest: R. Pereira has nothing to disclose. Conflict of interest: S. Poli has nothing to disclose. Conflict of interest: P. Povoa declares personal fees (for lectures and advisory boards) from MSD, Technophage, Sanofi and Gilead. Conflict of interest: K. Ramanathan has nothing to disclose. Conflict of interest: O. Rewa declares consulting fees from Baxter Inc. Conflict of interest: J. Riera has nothing to disclose. Conflict of interest: S. Shrapnel participated as an investigator for an observational study analysing intensive care unit patients with COVID-19 (for the Critical Care Consortium including ECMOCARD) funded by The Prince Charles Hospital Foundation during the conduct of this study. S. Shrapnel reports in kind support from the Australian Research Council Centre of Excellence for Engineered Quantum Systems (CE170100009). Conflict of interest: M.J. Silva has nothing to disclose. Conflict of interest: A. Udy has nothing to disclose. Conflict of interest: T. Uyeki has nothing to disclose. Conflict of interest: S.A. Webb has nothing to disclose. Conflict of interest: E-J. Wils has nothing to disclose. Conflict of interest: A. Rojek has nothing to disclose. Conflict of interest: P.L. Olliaro has nothing to disclose., (Copyright ©The authors 2022.)

Background: COVID-19 is a new form of acute respiratory failure leading to multiorgan failure and ICU admission. Gathered evidence suggests that a 3-fold rise in D-dimer concentrations may be linked to poor prognosis and higher mortality., Purpose: To describe D-dimer admission profile in severe ICU COVID19 patients and its predictive role in outcomes and mortality., Methods: Si ngle-center retrospective cohort study. All adult patients admitted to ICU with COVID19 were divided into 3 groups: (1) Lower-values group (D-dimer levels < 3-fold normal range value [NRV] [500ng/mL]), Intermediate-values group (D-dimer ≥3-fold and <10-fold NRV) and Higher-value group (≥10-fold NRV)., Results: 118 patients (mean age 63 years, 73% males) were included (N = 73 Lower-values group, N = 31 Intermediate-values group; N = 11 Higher-values group). Mortality was not different between groups (p = 0.51). Kaplan-Meier survival curves revealed no differences (p = 0.52) between groups, nor it was verified even when gender, age, ICU length of stay, and SOFA score were considered as covariables., Conclusions: In severe COVID19 patients, the D-dimer profile does not retain a predictive value regarding patients' survivability and should not be used as a surrogate of disease severity.

Background: The non-alcoholic fatty liver disease is the hepatic counterpart of the metabolic syndrome. ZSF1 rats are a metabolic syndrome animal model in which liver changes have not been described yet., Aim: The characterization of liver histological and innate immunity changes in ZSF1 rats., Methods: Five groups of rats were included (n = 7 each group): healthy Wistar-Kyoto control rats (Ctrl), hypertensive ZSF1 lean (Ln), ZSF1 obese rats with a normal diet (Ob), ZSF1 obese rates with a high-fat diet (Ob-HFD), and ZSF1 obese rats with low-intensity exercise training (Ob-Ex). The animals were sacrificed at 20 weeks of age, their livers were collected for: a) measurements of the area of steatosis, fibrosis and inflammation (histomorphological analysis); and b) innate immunity (toll-like receptor [TLR] 2, TLR4, peroxisome proliferator-activated receptor γ [PPARγ], toll interacting protein [TOLLIP]) and inflammatory marker (tumor necrosis factor-alpha [TNFα], interleukin 1 [IL-1]) expression analysis by real-time PCR., Results: Ob, Ob-HFD and Ob-Ex were significantly heavier than Ln and Ctrl animals. Ob, Ob-HFD and Ob-Ex animals had impaired glucose tolerance and insulin resistance. ZSF1 Ob, Ob-HFD and Ob-Ex presented a higher degree of steatosis (3,5x; p < 0.05) than Ctrl or ZSF1 Ln rats. Steatohepatitis and fibrosis were not observed in any of the groups. No differences in expression were observed between Ctrl, Ln and Ob animals (except for the significantly higher expression of TOLLIP observed in the Ob vs Ln comparison). Ob-HFD and Ob-Ex rats showed increased expression of PPARγ and TOLLIP as compared to other groups. However, both groups also showed increased expression of TLR2 and TLR4. Nevertheless, this did not translate into a differential expression of TNFα or IL-1 in any of the groups., Conclusion: The ZSF1 model is associated with liver steatosis but not with steatohepatitis or a significantly increased expression of innate immunity or inflammation markers.

Background and Aim: The human colonic mucosa is populated by a wide range of microorganisms, usually in a symbiotic relation with the host. Sometimes this balance is lost and a state of dysbiosis arises, exposing the colon to different metabolic and inflammatory stimuli (according to the microbiota's changing profile). Recent findings lead to hypothesize that this unbalance may create a subclinical pro-inflammatory state that increases DNA mutations and, therefore, colorectal carcinogenesis. In this article we aim to systematically review the scientific evidence regarding colonic microbiota and its role in colorectal carcinogenesis., Methods: Systematic review of PubMed searching results for original articles studying microbiota and colorectal cancer until November 2014., Results: Thirty-one original articles studied the role of colon microbiota in colorectal carcinoma including both human and animal studies. Different and heterogeneous methods were used and different bacteria were considered. Nevertheless, some bacteria are consistently augmented (such as Fusobacteria, Alistipes, Porphyromonadaceae, Coriobacteridae, Staphylococcaceae, Akkermansia spp. and Methanobacteriales), while other are constantly diminished in colorectal cancer (such as Bifidobacterium, Lactobacillus, Ruminococcus, Faecalibacterium spp., Roseburia, and Treponema). Moreover, bacteria metabolites amino acids are increased and butyrate is decreased throughout colonic carcinogenesis., Conclusion: Conclusive evidence shows that colorectal carcinogenesis is associated with microbial dysbiosis. This information may be used to create new prophylactic, diagnostic and therapeutic strategies for colorectal cancer.

Introduction: Metabolic syndrome is an emerging problem in developed countries and presents itself as a potential threat worldwide. The role of diabetes, dyslipidaemia and hepatic steatosis as pivotal components of the metabolic syndrome is well known. However, their common persistent chronic inflammation and its potential cause still elude. This systematic review aims to present evidence of the mechanisms that link the intestinal microbioma, innate immunity and metabolic syndrome., Methods: A comprehensive research was made using PubMed database and 35 articles were selected., Results: We found that metabolic syndrome is associated to increased levels of innate immunity receptors, namely, Toll-like receptors, both in intestine and systemically and its polymorphisms may change the risk of metabolic syndrome development. Microbioma dysbiosis is also present in metabolic syndrome, with lower prevalence of Bacteroidetes and increased prevalence of Firmicutes populations. The data suggest that the link between intestinal microbiota and Toll-like receptors can negatively endanger the metabolic homeostasis., Conclusion: Current evidence suggests that innate immunity and intestinal microbiota may be the hidden link in the metabolic syndrome development mechanisms. In the near future, this can be the key in the development of new prophylactic and therapeutic strategies to treat metabolic syndrome patients.