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Background: The effective use of combination antiretroviral therapy (ART) has significantly improved the life expectancy of people living with the human immunodeficiency virus (HIV). However, complications have shifted from opportunistic infections to issues such as drug toxicity and resistance, as well as an increase in premature cardiovascular diseases (CVD). These conditions are attributed to chronic immune activation and persistent inflammation caused by HIV, along with lipid abnormalities and insulin resistance. Objective: The objective of the study was to predict cardiovascular risk at 5 and 10 years in people living with HIV with combination ART using three algorithmic models. Methods: This study included 186 HIV-seropositive patients under treatment. The variables analyzed included anthropometric measurements, family history of hypertension and CVDs, years of infection, years of treatment, and treatment scheme. We used three well-established algorithmic models for assessing cardiovascular risk: Framingham (10-year period), Data Collection on Adverse Events of Anti-HIV Drugs Study (D: A: D) reduced, and full (5-year period). Results: Approximately 65% of the study participants were undergoing a treatment regimen comprising two nucleoside reverse transcriptase inhibitors (NRTIs) combined with a non-NRTIs. The mean body mass index analysis indicated that 28.5% of the participants were overweight and 17.7% obese. In addition, 53.8% of the patients exhibited hypertriglyceridemia, and 54.8% met the diagnostic criteria for metabolic syndrome. The D: A: D reduced and full models identified significant risk factors for individuals over 30 years of age, highlighting notable associations with cholesterol levels, triglyceride levels, and smoking status. In contrast, the Framingham model did not demonstrate significant risk associations. (Rev Invest Clin. 2024;76(6):274-85).
As a first-line chemotherapy agent for colorectal cancer (CRC), oxaliplatin suffers from limited efficacy due to acquired resistance. This study investigated whether geniposide can overcome oxaliplatin resistance in preclinical models and elucidated the underlying molecular mechanisms. We employed MTT, colony formation, flow cytometry, wound healing, and Transwell assays to evaluate viability, proliferation, apoptosis, migration, and invasion in oxaliplatin-resistant CRC cells (SW480/R, LoVo/R) treated with geniposide and/or oxaliplatin. Xenograft models bearing SW480/R or LoVo/R tumors were established to assess in vivo efficacy. Immunofluorescence analysis quantified Ki67-positive proliferating cells, while Western blot measured apoptosis markers (Bax, Bcl-2) and PI3K/AKT/mTOR pathway activity. Geniposide-oxaliplatin combination therapy significantly inhibited proliferation, migration, and invasion while inducing apoptosis in resistant CRC cells beyond monotherapy effects. In vivo, geniposide restored oxaliplatin sensitivity, substantially reducing tumor growth and Ki67 proliferation index. Mechanistically, geniposide suppressed phosphorylation of AKT and mTOR in both cellular and xenograft models, with maximal inhibition observed in combination groups. Geniposide reverses oxaliplatin resistance in CRC through PI3K/AKT pathway inhibition, demonstrating that geniposide-oxaliplatin combination therapy represents a promising therapeutic strategy for oxaliplatin-resistant CRC. .
Autosomal dominant polycystic kidney disease (ADPKD) is the leading monogenic cause of end-stage kidney disease (ESKD). Because disease-modifying therapy is costly and can cause adverse effects, identifying patients most likely to benefit is essential. We developed and internally validated a model to predict ESKD by age 80 in class 1 ADPKD, hypothesizing that combining baseline eGFR with an exponential estimate of kidney growth would improve forecasting. We retrospectively analyzed 142 adults with class 1 ADPKD followed at a tertiary center in Mexico City (2012-2023). Total kidney volume (TKV) was measured by the ellipsoid method and eGFR by CKD-EPI 2021. Data were split 50/50 into derivation and validation sets. Future eGFR was modeled using baseline eGFR plus an exponential TKV growth surrogate; ESKD risk (eGFR <15ml/min/1.73m2) was derived from the standard normal cumulative distribution. Performance was compared with the Mayo Clinic Predictive Model (MCPM) and a Cox model. In validation, the model achieved adjusted R2=0.858 (vs. 0.830 for MCPM). ESKD prediction showed excellent discrimination (C-index=0.94) and calibration, comparable to Cox (C-index=0.95). This approach supports individualized lifetime ESKD risk prediction in class 1 ADPKD to guide targeted therapy and resource allocation.
Accurate segmentation of blood vessels in glioma pathological images is crucial for understanding tumor vasculature and progression, yet remains challenging due to complex vessel morphology and image variations. This study aimed to develop and evaluate a novel approach using a finetuned masked autoencoder self-attention mechanism (MedSAM) framework for interactive segmentation of glioma blood vessels in pathological images called GliomaVascularSAM. We utilized a dataset of 2632 image patches derived from multiple glioma datasets. These patches were obtained from tissue samples of 879 patients from The Cancer Genome Atlas and 179 patients from three hospitals. The performance of GliomaVascularSAM was compared with convolutional neural network-based models (including nnU-Net, Pathology-nnU-Net, and nnSAM) and SAM-based segmentation methods. Model performance was evaluated using the dice similarity coefficient, sensitivity, and positive predictive value. The proposed GliomaVascularSAM outperformed traditional-based models, achieving a dice similarity coefficient of 0.784, sensitivity of 0.767, and positive predictive value of 0.820. Compared with the nnU-Net model (dice similarity coefficient: 0.652), our approach yielded a 13.2% improvement. GliomaVascularSAM significantly enhanced the accuracy and interactivity of glioma blood vessel segmentation in pathological images. This approach can assist clinicians in the precise analysis of glioma vasculature, thereby contributing to improved diagnosis and management of patients with glioma.
Background: In severe aplastic anemia (AA) sibling haploidentical hematopoietic stem cell transplantation (haplo-HSCT) from the peripheral blood (PB) is an alternative when an HLA-identical donor is unavailable. Objective: To document the results of haplo-HSCT in high-risk severe AA. Methods: Twelve patients with severe AA who failed medical therapy and received a haploidentical PB unmanipulated HSCT from a sibling at an academic medical center were analyzed. Overall (OS) and event-free survival (EFS) were determined by Kaplan-Meier analyses. Results: The median between AA diagnosis and haplo-HSCT was 6.5 months (2-19). Median of age was 25.5 (range, 4-54) years; 9 (75%) recipients were males, and all suffered multiple treatment failures. Anti-thymocyte globulin-based conditioning regimens were given to 6 (50%) patients. Five (41.7%) HSCT were ambulatory. Infections developed in all patients and graft failure in 9 (75%). 2-year OS was 52% and EFS 25%. High transfusion burden, treatment failure, and donors > 30 years had no effect on OS (p = 0.518, p = 0.984, p = 0.321) or EFS (p = 0.113, p = 0.692, p = 0.199). Patient's age > 40 was not significant for survival (p = 0.395). Three of five evaluable patients developed acute graft-versus-host disease that progressed to chronic disease. Conclusions: Delayed PB haplo-HSCT for severe AA offered poor outcomes. Rapid referral for HSCT is critically required. (Rev Invest Clin. 2025;77(1):26-33).
The efficacy and safety of thrombolytics within the first 4.5h of ischemic stroke symptom onset are well documented; however, evidence beyond this timeframe remains contentious. To assess the efficacy and safety of delayed thrombolysis (4.5-24-h window) for ischemic stroke. We conducted a systematic search to identify studies comparing thrombolytics to placebo or standard care in ischemic stroke patients treated within 4.5-24h of symptom onset. The primary outcome was functional independence at 90 days, with additional efficacy outcomes exploring recanalization and reperfusion at 24h, as well as safety outcomes of 90-day mortality and symptomatic intracranial hemorrhage. The statistical analysis was performed using R studio. We included five randomized controlled trials with 1398 patients. The mean age was 70.2 years, 61% were male, and the median NIHSS score was 10.2. Compared with controls, thrombolysis improved functional independence at 90 days (OR 1.32; 95% CI: 1.06-1.63; p=0.01; I2=0%), although it increased the risk of symptomatic intracranial hemorrhage (OR 2.5; 95% CI: 1.10-5.71; p=0.02; I2=0%). No significant difference in mortality at 90 days was observed (OR 1.15; 95% CI: 0.84-1.57; p=0.39; I2=0%). In ischemic stroke, thrombolytics administered within 4.5-24h improve functional independence at 90 days, also increasing the risk of symptomatic intracranial hemorrhage. At this point, careful and individualized patient selection, including advanced imaging, is mandatory for thrombolysis beyond the conventional 4.5-h treatment window.
The 5th edition of the World Health Organization Classification of Hematolymphoid Tumors recently defined immune deficiency/dysregulation (IDD)-associated-lymphoid-proliferations in HIV settings, where information is scarce, often gone under or misdiagnosed. To describe the clinical picture, histopathology, and outcomes of IDD-associated-lymphoidproliferations Epstein-Barr virus+ (EBV) in people living with HIV without organ transplantation, antiretroviral therapy (ART) treated. HIV+ patients diagnosed with IDD-associated-lymphoid-proliferations seen at an academic medical center in Mexico from 2016 to 2019 were included. Immunohistochemical studies, in situ hybridization, and polymerase chain reaction analysis for EBV and LMP1 gene deletions were performed and correlated with clinical data. We included 27 patients, all men who have sex with men, median age 36 years (interquartile range [IQR] 22-54). The median baseline CD4+ T cells were 113/mL (IQR 89-243), the CD4+/CD8+ ratio was 0.15 (IQR: 0.09-0.22), and the HIV viral load was 184,280 copies/mL (IQR: 76,000-515,707). Twenty patients (74.07%) had IDD-associated-lymphoid-proliferations hyperplasia plasma cell type EBV+, 3 (11.1%) had hyperplasia mononucleosis-like type (IM-type), 1 patient (3.70%) had florid follicular hyperplasia, 3 (11.1%) IDD-associated-lymphoid-proliferations polymorphic type, and there were 22 cases (81.4%) of synchronic Kaposi Sarcoma. Two patients were diagnosed with Hodgkin lymphoma following a second positron emission tomography-computed tomography scan-guided biopsy. The median follow-up was 228 weeks (IQR 50-269); 6 patients died (22.2%) of causes unrelated to IDD-associated-lymphoid-proliferations related. IDD-associated-lymphoid-proliferations EBV+ occured in severely immunosuppressed HIV+ patients, a high percentage of whom had concomitant Kaposi sarcoma. The prognosis was good in patients treated only with ART.
Between 1949 and 1964, advancements in chemistry and medicine, along with societal demands, made fertility regulation possible. Most of the chemical work occurred outside traditional centers, and it was at Syntex S.A. in Mexico City that the pioneering work of George Rosenkranz, Carl Djerassi, and Luis Miramontes achieved a breakthrough, resulting in the synthesis of norethindrone (19-nor-17α-ethynyl testosterone) on October 15, 1951. This compound was a potent and orally active progestogen, establishing the basis for modern contraception. Meanwhile, Syntex's simultaneous success in synthesizing cortisone from diosgenin (a compound found in Mexican yams) demonstrated how an industrial laboratory in a developing scientific country could compete with and outperform better-funded international rivals. Meanwhile, across the border, research on contraceptive steroids gained momentum. Frank B. Colton (G.D. Searle) synthesized norethynodrel in the United States, which became the first FDA-approved oral contraceptive in 1960. However, history would restore its balance. In fact, norethindrone and its derivatives from Syntex were soon available worldwide, becoming the most widely used progestins in oral contraceptives. This review examines the interactions between scientific and social history, clarifying the roles of key figures and situating Mexico's contributions within a broader global context of reproductive autonomy.
Background: COVID-19 is a disease that had a great impact in the world, generating lifestyle changes; among these are changes in sleep quality, with the elderly being one of the most affected age groups. Objective: To identify sleep alterations in Mexican people older than 60 years post COVID-19 pandemic. Methods: We performed a descriptive study on subjects older than 60 years from the aging cohort of the National Institute of Respiratory Diseases. Demographic data, sleep questionnaires (Pittsburgh), and quality of life (SF-12) were assessed pre-pandemic. During the period from June 2021 to August 2022, the questionnaires were repeated post-pandemic through telephone. Qualitative variables were analyzed with frequencies and percentages, whereas quantitative variables were analyzed with means and standard deviations. The groups were compared using the X2 test and Student's t-test. Results: We analyzed 279 subjects who completed two questionnaires. An alteration in sleep quality variables was observed post-COVID, including a decrease in sleep hours (7.33 h versus 7.17 h, p = 0.03), and a trend to a longer time to fall asleep (23 m vs 27 m, p = 0.06). In the questionnaire on toxicology, we found higher alcohol consumption (18% vs. 27%, p = 0.01) and vitamin ingestion (34% vs. 46%, p = 0.003). Subjects also described more nighttime awakenings, with more than 3 times per week (25% vs. 44%, p < 0.0001), generating a worse auto perception of healthy well-being (88.3 vs. 82.02 p < 0.0001). Conclusions: The COVID-19 pandemic affected sleep quality in different aspects, and it increased the consumption of alcohol and vitamins. (Rev Invest Clin. 2024;76(6):239-42).
Healthcare workers (HCWs) are at risk of body fluids' exposure. The objective of this study was to study the incidence of occupational body fluid exposures in HCW at a tertiary hospital and largest coronavirus disease 2019 (COVID-19) center in Mexico. Data on sociodemographics, exposure factors, and vaccination status were collected from questionnaires of HCWs self-reporting exposures (January 2013-December 2022). Hepatitis B and C virus (HBV and HCV) and human immunodeficiency virus (HIV) serology data were retrieved from the laboratory platform. Descriptive statistics and variable associations were analyzed. Four hundred and eighty-two exposures occurred, 311 in women (64.5%). Exposure incidence was 19.09/1000 person-years; 80% were percutaneous; and 20% were splashes. Median age of exposed HCWs was 21 years (standard deviation = 9.65). Nurses were the most exposed (n = 172, 35.6%), mainly in patients room (n = 223, 46%). About 40.5% of HCW had protective antibody titers to HBV surface antigen (anti-HBs). Self-reported vaccination status and protective anti-HBs titers had poor concordance (kappa = 0.02). One hundred and ninety-seven HCW required HIV post-exposure prophylaxis (40.8%) with no seroconversions. Exposures were highest in 2020 (78 cases, p = 0.001 vs. all years). A high proportion of HCW lacked protective anti-HBs titers. Increased occupational exposures during the COVID-19 pandemic underline the need for standard precautions, HBV immunization, staff training, and post-exposure protocols to enhance pandemics preparedness.
Super-enhancers (SEs) play a key role in cell fate determination by regulating the transcription of cell-specific target genes and may contribute to the pathogenesis of neurodegenerative diseases. Targeted inhibition of the activity of SEs or knockout of SEs fragments may represent a novel therapeutic strategy for neurodegenerative diseases. This article mainly outlines the discovery, structure, and identification methods of SEs; lists the current SE database platforms; summarizes the main regulatory mechanisms of SEs and strategies to acquire disease-specific SEs; and reviews recent research advances on SEs in neurodegenerative diseases. These findings provide new insights into the molecular mechanisms and development of treatment for neurodegenerative diseases.
Asthma is a common chronic respiratory disease characterized by persistent airway inflammation. This study investigated the role of cinnamic acid (CA) in an in vitro model of asthma and its mechanisms. Human small airway epithelial cells (HSAECs) were stimulated with platelet-activating factor (PAF), then exposed to CA (20, 50, or 100μM). Cell viability and apoptosis were assessed using CCK-8 assay and flow cytometry. Inflammatory cytokine levels were measured by ELISA. Barrier function was evaluated via lucifer yellow permeability assay. Western blotting and RT-qPCR were used to measure levels of TGF-β1 pathway-related factors. To investigate whether CA acts through TGF-β1 inhibition, PAF-treated cells were co-incubated with CA and TGF-β1. CA treatment significantly reduced PAF-induced apoptosis in HSAECs. It also attenuated the PAF-induced upregulation of TNF-α, IL-1β, and IL-6 levels as well as the downregulation of PGE2 levels. CA improved epithelial barrier function by reducing permeability. CA downregulated TGF-β1 and Smad4 levels and inhibited Smad2 and Smad3 phosphorylation. Exogenous activation of TGF-β1 abolished the protective effects of CA against apoptosis, inflammation, and barrier integrity. Our findings demonstrate that CA inhibits apoptosis, inflammation, and barrier dysfunction in asthmatic airway cells by inhibiting the TGF-β1/Smad pathway.
Vitamin B12 deficiency is a reversible cause of hematologic and neurologic morbidity, but its etiologic spectrum in Latin American referral centers remains poorly defined. We retrospectively studied consecutive adults with vitamin B12 deficiency evaluated in hematology and oncology clinics at a Mexican tertiary referral center from January 2013 to July 2023. Etiologies were classified as pernicious anemia, non-surgical malabsorption, post-surgical malabsorption, reduced intake, drug-related causes, or unknown, and pernicious anemia was compared with all other etiologies. Among 270 patients (median age 64 years; 52% female), pernicious anemia was the most frequent etiology (52.6%), followed by non-surgical malabsorption (28.1%) and post-surgical states (7.7%). Compared with other causes, pernicious anemia was associated with more comorbidities, lower hemoglobin, lower platelet counts, lower vitamin B12 levels, higher mean corpuscular volume, higher mean corpuscular hemoglobin, and higher indirect bilirubin. Weight loss, gastrointestinal symptoms, and neurologic alterations were common in both groups. In this tertiary Mexican cohort, pernicious anemia was the leading identified cause of vitamin B12 deficiency and showed greater hematologic and biochemical severity. Importantly, patients with non-pernicious etiologies had a median MCV within the normocytic range, supporting systematic etiologic evaluation and avoiding overreliance on macrocytosis alone.
Polycystic ovary syndrome (PCOS) is a multifactorial endocrine and metabolic disorder in women of reproductive age characterized by hormonal imbalances, menstrual irregularities, and changes in ovarian morphology. Excess body fat plays a significant role in the clinical development of PCOS. The complex relationship between adiposity and PCOS involves disruptions in hormonal balance and inflammatory processes, which both contribute to the clinical and phenotypic manifestations of the syndrome. Insulin resistance is a significant factor linking adiposity and PCOS. Moreover, reduced fertility is associated with adiposity in PCOS, with obesity exacerbating anovulation. Recent studies have raised questions about the role of androgen exposure during fetal life, including genetic factors related to PCOS identified in genome-wide association studies and Mendelian randomization studies. Managing PCOS should concentrate on addressing adiposity as a crucial target, positively impacting the syndrome, particularly regarding reproductive and fertility outcomes. This review aims to understand how metabolic conditions such as obesity and insulin resistance are linked to PCOS and how early prenatal androgen exposure is involved in its etiology. Particular attention is given to its role in developmental programming, fat distribution, and fat type, as well as how these factors contribute to the onset of metabolic disturbances in adulthood.
Several models have been developed to assess bleeding risk in patients with venous thromboembolism, such as HAS-BLED, but their external validity has not been adequately assessed. The objective of the study was to evaluate the discriminative ability and calibration of the HAS-BLED scale for predicting 1-month bleeding risk in patient's anticoagulated for venous thromboembolism. External validation study of a prediction model based on a retrospective cohort of patients with venous thromboembolism treated between November 2019 and January 2022. Calibration of the HAS-BLED scale was evaluated using the Hosmer-Lemeshow test and the ratio of observed to expect events within each risk category. Discriminatory ability was assessed using the area under the curve (AUC) of a receiver operating characteristic curve. We included 735 patients (median age 64 years, female sex 55.2%), pulmonary embolism was diagnosed in most patients (60.7%), and 4.9% presented bleeding events. Regarding calibration, the HAS-BLED scale systematically underestimates the risk both in the general population (ROE 3.76, p < 0.001) and in cancer patients (ROE 4.16). The Hosmer-Lemeshow test rejected the hypothesis of adequate calibration (p < 0.001). Discriminatory ability was limited both in the general population (AUC = 0.57, 95% confidence interval [CI]: 0.48-0.66) and in the subgroup with active cancer (AUC = 0.53, 95% CI: 0.36-0.69). The HAS-BLED scale in patients with venous thromboembolism underestimates the risk of bleeding at 1 month and has a low ability to discriminate high-risk patients. Cautious interpretation of the scale is recommended until additional evidence is available.
The aim of this study is to evaluate the correlation between psoriasis and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD). This provides an important reference for formulating guidelines for the management of psoriasis comorbidities and improving the long-term prognosis of patients. A systematic search was conducted across four databases: PubMed, Web of Science, Embase, and the Cochrane Library, covering the period from their inception to November 2025. A meta-analysis employing random-effects model (DerSimonian-Laird method) was conducted to assess the association between MASLD in psoriatic and non-psoriatic patients. Subgroup analyses were performed for psoriatic arthritis (PsA) and patients with moderate-to-severe psoriasis. This review included 13 studies comprising 6 case-control studies, 3 cohort studies, and 4 cross-sectional studies. Meta-analysis results indicated that individuals with psoriasis exhibited an increased risk of MASLD compared to those without psoriasis (OR=2.16, 95% CI: 1.65-2.83). Further subgroup analysis revealed that patients with moderate to severe psoriasis exhibited a heightened risk of MASLD compared to those with mild psoriasis (OR=2.81, 95% CI: 1.62-4.86). Additionally, the risk of MASLD among patients with PsA was not statistically significant (OR=1.48, 95% CI: 0.69-3.19). There is an association between psoriasis and MASLD, and patients with moderate to severe psoriasis have a higher risk of MASLD. Current evidence does not show a clear association between PsA and MASLD, but this conclusion is limited by the small number of included studies and requires further validation. This study provides a reference basis for formulating guidelines for the management of comorbidities in psoriasis, but it should be interpreted with caution due to the inherent limitations of observational studies.
Background: Clinical practice has advanced toward a combined diagnostic approach that involves clinical criteria and biological markers for Alzheimer's disease (AD) and other dementias. Objective: To establish the level of diagnostic agreement between an initial clinical diagnosis and cerebrospinal fluid (CSF) and [18F]-fluorodeoxyglucose (FDG)-positron emission tomography (PET) biomarkers in a cohort of patients from a memory clinic. Methods: This is a observational, retrospective, cohort study conducted at an outpatient memory clinic. Between July 2018 and September 2023, data from adults' ≥ 55 years with a mild cognitive impairment or dementia diagnosis without etiological diagnosis were obtained, complemented with the evaluation of biomarkers in CSF and [18F] FDG-PET biomarker assessment were included. Kappa coefficients (κ) were used to establish the level of agreement between CSF and [18F] FDG-PET results. Results: Seventy-seven patients had an available [18F] FDG-PET scan, and 25 (32.5%) had both biomarkers. We observed a fair-to-moderate diagnostic agreement between patients' initial and their final diagnosis in the presence of CSF (κ = 0.233, 95% confidence interval [CI]: -0.099-0.566) and [18F] FDG-PET (κ = 0.451, 95% CI: 0.277-0.625, p < 0.001) results. The Kappa value for diagnostic concordance between [18F] FDG-PET and CSF to differentiate between AD and other dementias was 0.733 (95% CI: 0.425-1.000, p < 0.005). Conclusion: This study demonstrates good agreement between the CSF and FDG-PET biomarkers to differentiate AD from other dementias. (Rev Invest Clin. 2024;76(5):230-7).
Background: Osmotic demyelination syndrome is a rare neurological disorder caused by damage to the myelin sheath of oligodendrocytes, typically due to a rapid increase in serum osmolarity. Objective: The objective of the study was to investigate the factors associated with the development of pontine or extrapontine myelinolysis. Methods: A retrospective, observational study which included patients with magnetic resonance imaging-confirmed diagnosis of pontine and extrapontine myelinolysis from 1990 to 2024 at a referral hospital in Mexico City. Results: Fourteen patients were included; the median age was 49 years, and 35.7% were men. Regarding comorbidities, diabetes was the most frequent (35.7%), followed by liver cirrhosis, malnutrition, and chronic alcoholism. Significantly, hyponatremia was found in 11 patients (78.5%), being severe in 42.8% of the patients. Other frequent biochemical abnormalities were hypokalemia (42.8%) and hypomagnesemia in 5 (35.7%). Sodium overcorrection occurred in 50% of patients, and the 90-day mortality rate was 28.5%. Conclusions: Electrolyte disturbances, particularly hyponatremia, were common in this population, along with the comorbidities traditionally associated with this condition. Although neurological sequelae and mortality have decreased over time, they remain present in 64% and 28.5% of patients, respectively. (Rev Invest Clin. 2025;77(1):1-5).
Background: Smoking remains a significant issue that increases the prevalence of multiple sclerosis (MS) and its progression to secondary progressive forms. Objectives: The goal is to identify the relationship between smoking and disease progression in MS patients who have undergone autologous hematopoietic stem cell transplantation (auto-HSCT) at the Centro de Hematología y Medicina Interna, Clínica Ruiz, Puebla, Mexico. Methods: This retrospective study involved MS patients treated with auto-HSCT, followed for 12 months. The response to transplantation was measured using the difference in Expanded Disability Status Scale (EDSS) scores before and 12 months after the transplant. A difference of -0.5 or greater indicated a good response, while a difference below 0.5 indicated a poor response. Results: The study included 419 patients, with a median age of 47 years (IQR: 40-53). The majority were non-smokers (315) compared to smokers/ex-smokers (104). In patients with PMSS, EDSS stabilization at 12 months was observed in both smokers/ex-smokers (median 6, interquartile range (IQR) = 1 vs. 6, IQR = 1, p = 0.466) and non-smokers (median 6, IQR = 1 vs. 6, IQR = 1.5, p = 0.001), although non-smokers showed a statistically significant difference. Conclusion: Smoking may negatively impact MS progression, especially in its progressive forms. (Rev Invest Clin. 2024;76(5):223-9).
MiR-155 plays a role in inflammatory pathways and cardiovascular diseases, though its relationship with inflammation, atherosclerosis, and outcomes in ST-elevation myocardial infarction (STEMI) is not well established. To investigate associations between miR-155 levels, inflammation, atherosclerotic burden, and major adverse cardiovascular events (MACE) in STEMI patients. Sixty-nine STEMI patients and 16 healthy controls were recruited from a specialized university-affiliated cardiovascular center. MiR-155 expression and serum interleukin (IL)-1β, IL-6, and tumor necrosis factor levels were measured. Patients were grouped into tertiles based on miR-155 expression. Clinical data, atherosclerotic burden (through cardiac catheterization), and in-hospital MACE were recorded. MiR-155 levels were significantly lower in STEMI patients compared to controls (median 54.2, vs. 152.8 arbitrary units; p = 0.003). Higher miR-155 tertiles were associated with a greater prevalence of three-vessel occlusion (34% vs. 13% vs. 4%; p = 0.007) and increased incidence of pulmonary edema (13% vs. 0% vs. 0%; p = 0.030). No significant correlation was found between miR-155 and inflammatory or myocardial markers. Dysregulated miR-155 expression in STEMI patients may influence disease severity and MACE risk, independent of inflammation or myocardial damage markers.