Emilton Lima Junior

Background/Objectives: Psoriasis and atopic dermatitis have been conceived as opposite immunological poles, yet molecular overlap and clinically recognised coexistence challenge this dichotomy. We sought to adjudicate among three architectures: overlap with no discriminating systemic signature, a shared inflammatory and metabolic continuum with additive coexistence, and distinct phenotypes with synergy. Methods: Cross-sectional analysis of a selected UK Biobank subsample of 160,782 participants, classified by International Classification of Diseases, 10th revision codes L40 and L20 as control, isolated atopic dermatitis (n = 12,859), isolated psoriasis (n = 15,146) and coexistence (n = 1068). Haematological indices, a biochemical and metabolomic panel including glycoprotein acetyls, and circulating inflammatory proteins were evaluated through converging evidence from ordinal effect sizes, equivalence testing at a margin equivalent to an area under the receiver operating characteristic curve of 0.574, quantile regression with interaction terms, permutational multivariate analysis of variance, supervised classification and mixture modelling. Results: Effect sizes were negligible for 46 of 48 contrasts against a comorbidity-free comparator, and 38 of 48 met formal equivalence. None of the 16 interaction terms survived false discovery rate control. Multivariate separation was detectable but explained 0.6% of dispersion, classification reached an area under the curve of 0.57, and latent classes bore no correspondence to clinical diagnosis. When cardiometabolic exclusions were applied symmetrically to all four groups, every contrast met equivalence, and the ordering of the dominant factor did not persist. Polygenic risk scores confirmed that the coded groups carry the expected genetic architecture. Conclusions: Within the systemic biomarkers evaluated these conditions are not discriminable, and coexistence is not an emergent phenotype.

Background/Objectives: Psoriasis and atopic dermatitis have historically been conceived as opposite immunological poles (Th17 versus Th2), yet molecular overlap and increasing clinical coexistence challenge this dichotomy. We aimed to adjudicate, using a multivariate approach, among three nosological architectures: a shared inflammatory–metabolic spectrum with additive coexistence (H1), distinct phenotypes with synergy (H2) and predominant overlap (H0). Methods: Cross-sectional analysis of a selected UK Biobank subsample (160,785 participants), classified by L20/L40 codes as control, isolated atopic dermatitis (n = 12,859), isolated psoriasis (n = 15,146) and coexistence (n = 1,068). Haemato-inflammatory indices, a biochemical–metabolomic panel (including GlycA) and Olink inflammatory proteins were evaluated using Cliff's delta, quantile regression with an interaction term, MANOVA/PERMANOVA, supervised classifiers, Gaussian mixture modelling, dominant-factor ordination with the Jonckheere–Terpstra test and equivalence testing (TOST; margin |δ| = 0.147). Restricted and broad control definitions were adopted. Results: Effect sizes were largely negligible (46/48 contrasts with |δ| < 0.147 under the restricted control; 38/48 formally equivalent). No psoriasis × atopic dermatitis interaction survived false-discovery-rate control (0/16), and the global multivariate interaction, although significant, was trivial (Pillai's trace = 0.0005). The dominant inflammatory factor was monotonically ordered (control < atopic dermatitis < psoriasis ≈ coexistence; Jonckheere |z| = 8.6; p < 0.001). Multivariate separation was detectable yet negligible (PERMANOVA R² = 0.6%; multiclass AUC 0.53), and latent classes did not coincide with clinical labels (adjusted Rand index = 0.004). Conclusions: The evidence favours a shared inflammatory–metabolic spectrum with approximately additive coexistence, superimposed on predominant between-group indistinguishability. Coexistence lies at the severe extreme of a common axis rather than constituting a third, emergent phenotype.

Introduction: Hepatocellular Carcinoma (HCC) is a primary liver neoplasm and the fastest-growing cause of cancer-related deaths, and the third leading cause globally. The risk of HCC varies with liver fibrosis, increasing significantly in cirrhotic patients. This study aimed to identify, systematically analyze, and summarize the best available evidence on the cutoff value in kPa for diagnostic yield of ultrasound liver elastography compared to MRI, CT, or liver biopsy. Material and methods: A systematic review of studies which analyses elastography and MRI for HCC. A systematic search of the relevant literature was conducted in the PubMed, EMBASE, Cochrane Library, Web of Science, Scopus and LILACS databases, for articles published up to April, 30 2024, relating studies comparing kPa results from ultrasound hepatic elastography (TE, SWE, and 2D-SWE) to MRI for HCC detection were included. Results: Out of the 1,723 studies reviewed, 11 met the established quality criteria. Among these, only the study by Imai et al. (2015) adhered to the PICO framework, demonstrating high sensitivity and specificity in diagnosing hepatocellular carcinoma (HCC) using shear wave elastography (ROC-AUC 0.963; sensitivity and specificity of 83.3% for SWE ≥ 6.5 kPa) when compared to MRI. Conclusion: SWE shows potential as a low-cost, accessible, non-invasive diagnostic tool for early HCC detection, especially in resource-limited settings. However, further high-quality studies are needed to conduct a meta-analysis and establish a standardized kPa threshold for diagnosing HCC.

Background: Kombucha is the fastest growing product in the beverage market and one of the world’s most popular low-alcohol fermented beverages, and can be characterized as a bittersweet probiotic drink, produced from the fermentation of black tea or sweetened green tea, with a symbiotic culture of acetic acid bacteria and yeast with bacteria. Objective: To verify the effects of Kombucha on blood glucose, dyslipidemia and body weight, through a Systematic Review (SR) and meta-analysis in rats with diabetes. Methods: The research question and developments were based on the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA). Two reviewers independently applied the eligibility criteria, according to the SYRCLE risk of bias tool and extracted data from the PubMed, SCOPUS, Web of Science, LILACS, Cochrane Central Register of Controlled Trials databases. A random effects model was used for the meta-analysis, to assess an effect size measure and heterogeneity, I2 and Cochran’s Q test calculator. Results: A total of 2357 articles were found and, after evaluation, as a result of duplicate databases and exclusion criteria, 5 studies were included in the RS, and from these, 2 were included in the meta-analysis. These results of this SR referred to the reduction of blood glucose and lipid levels, such as LDL cholesterol, Col-T, TG, and the increase in HDL cholesterol levels, as well as the positive effect on body weight control. The results of the metanalysis showed that kombucha significantly increases HDL-c levels (Effect Size = 1.73; 95% CI 0.37; 3.08). Conclusion: Kombucha in diabetic rats leads to increased HDL-c levels. Further studies are recommended to investigate the use of it as an adjuvant treatment of DM.

Background/Objectives: The guideline targets for blood pressure (BP), hemoglobin A1c (HbA1c), and low-density lipoprotein cholesterol (LDL-C) are frequently unmet, and physicians often misjudge control. This study aimed to characterize the real-world control of BP, HbA1c, and LDL-C in patients with type 2 diabetes (T2D) and hypertension, herein called cardiometabolic multimorbidity (CMM), and to compare guideline-based versus physician-perceived disease control. Methods: We conducted SNAPSHOT–Brazil, a nationwide, multicenter, cross-sectional study to gather real-world data on patients with CMM. The ESC guidelines defined the cardiovascular (CV) risk and control targets. Results: We included 451 patients with hypertension and T2D (median age 65 years; 60% female; 54% White). Most patients (98%) were on pharmacotherapy and reported high adherence (according to the Hill–Bone Medication Adherence Scale). A very high CV risk predominated (78%); 22% of the patients were at a high risk. The guideline-defined control was achieved in 27% for BP, 34% for HbA1c, 13% for LDL-C, and 6% for both BP and LDL-C; only 3% met all three targets simultaneously. The physicians accurately stratified the CV risk in 49% of patients, while 50% had their CV risk underestimated. They systematically overestimated control in 29% of cases for BP, 35% for LDL-C, and 25% for both. The sensitivity ranged from 0.88 to 0.98; the positive predictive values ranged from 0.19 to 0.48, and the positive likelihood ratios ranged from 2.16 to 3.65. Conclusions: The SNAPSHOT–Brazil study revealed a low attainment of BP, HbA1c, and LDL-C targets, despite the widespread pharmacotherapy and the high self-reported adherence. The physicians consistently overestimated disease control and underestimated the CV risk.

Background Arterial remodeling leading to increased arterial stiffness involves mechanisms such as oxidative stress, reactive oxygen species production, neuroendocrine alterations, and genetic predisposition. These processes are also involved in the pathophysiology of COVID-19. However, the relationship between arterial stiffness, hemodynamic parameters, and clinical-functional outcomes in post-COVID-19 patients has not yet been adequately investigated. Objectives To investigate arterial stiffness, central and peripheral hemodynamic parameters, functional performance, quality of life, fatigue, dyspnea, and sleep quality in post-COVID-19 patients. Methods This cross-sectional study was conducted with individuals in the post-COVID-19 group (PCG) and matched individuals in the control group (n = 32). Arterial stiffness was assessed using pulse wave velocity (PWV) and the augmentation index corrected to a heart rate of 75 bpm (AIx@75). Functional performance was evaluated using the five-times sit-to-stand test, handgrip strength, quality of life (assessed with the 12-Item Short Form Survey), fatigue (assessed with the Brazilian version of the Fatigue Severity Scale), dyspnea (assessed with the modified Medical Research Council scale), and sleep quality. Results The PCG showed higher PWV values (Δ = 0.80 m/s; 95%CI, 0.08 to 1.52; p = 0.03) and AIx@75 (Δ = 8.34; 95%CI, 2.02 to 14.66; p = 0.01) as well as higher levels of central and peripheral blood pressure. Worse functional performance was observed (Δ = 4.39 s; 95%CI, 2.70 to 6.08; p < 0.01), along with poorer quality of life in the physical component (Δ = −9.35; 95%CI, −12.45 to −6.25; p < 0.01). Fatigue, dyspnea, and sleep quality outcomes were also significantly worse in the PCG. In the adjusted analysis, PWV was independently associated with age and systolic blood pressure, but not with post-COVID-19 status. Conclusion Post-COVID-19 patients exhibit greater arterial stiffness, hemodynamic alterations, and poorer clinical-functional performance. However, arterial stiffness appears to be predominantly determined by hemodynamic factors and aging rather than by post-COVID-19 status independently, suggesting that the observed functional impairment results from multifactorial mechanisms.

Resumo Fundamento O remodelamento arterial que culmina no aumento da rigidez arterial envolve mecanismos como estresse oxidativo, produção de espécies reativas de oxigênio, alterações neuroendócrinas e predisposição genética. Esses processos também estão presentes na fisiopatologia da covid-19. Entretanto, a relação entre rigidez arterial, parâmetros hemodinâmicos e desfechos clínico-funcionais em pacientes pós-covid-19 ainda não foi adequadamente investigada. Objetivos Investigar a rigidez arterial, os parâmetros hemodinâmicos centrais e periféricos, o desempenho funcional, a qualidade de vida, a fadiga, a dispneia e a qualidade do sono em pacientes pós-covid-19. Métodos Estudo transversal conduzido com indivíduos do grupo pós-covid-19 (GpC) e indivíduos pareados do grupo controle (n = 32). A rigidez arterial foi avaliada por meio da velocidade da onda de pulso (VOP) e do índice de aumentação corrigido para frequência cardíaca de 75 bpm (AIx@75). Foram avaliados o desempenho funcional pelo teste de sentar e levantar cinco vezes, a força de preensão manual, a qualidade de vida (avaliada pelo 12-Item Short Form Survey), a fadiga (avaliada pela Fatigue Severity Scale – versão brasileira), a dispneia (avaliada pela escala modificada do Medical Research Council) e a qualidade do sono. Resultados O GpC apresentou valores mais elevados de VOP (Δ = 0,80 m/s; intervalo de confiança de 95% [IC95%], 0,08 a 1,52; p = 0,03) e AIx@75 (Δ = 8,34; IC95%, 2,02 a 14,66; p = 0,01), além de níveis mais elevados de pressão arterial central e periférica. Observou-se pior desempenho funcional (Δ = 4,39 s; IC95%, 2,70 a 6,08; p < 0,01) e pior qualidade de vida no componente físico (Δ = −9,35; IC95%, −12,45 a −6,25; p < 0,01). Fadiga, dispneia e qualidade do sono também apresentaram resultados significativamente piores no GpC. Na análise ajustada, a VOP associou-se independentemente à idade e à pressão arterial sistólica, mas não à condição pós-covid-19. Conclusão Pacientes pós-covid-19 apresentam maior rigidez arterial, alterações hemodinâmicas e pior desempenho clínico-funcional. Contudo, a rigidez arterial parece ser predominantemente determinada por fatores hemodinâmicos e pelo envelhecimento, e não pela condição pós-covid-19 de forma independente, sugerindo que o comprometimento funcional observado decorra de mecanismos multifatoriais.