Scielo RSS <![CDATA[Revista de investigación clínica]]> http://www.scielo.org.mx/rss.php?pid=0034-837620220002&lang=es vol. 74 num. 2 lang. es <![CDATA[SciELO Logo]]> http://www.scielo.org.mx/img/en/fbpelogp.gif http://www.scielo.org.mx <![CDATA[Triglyceride-Rich Lipoproteins: Their Role in Atherosclerosis]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0034-83762022000200061&lng=es&nrm=iso&tlng=es ABSTRACT The term “triglyceride-rich lipoproteins” (TRLs) includes chylomicrons and their remnants, very low-density lipoproteins (VLDL), and intermediate-density lipoproteins (IDL). In this manuscript, the mechanisms by which atherogenic TRLs contribute to the formation of atheroma plaques are reviewed. Cholesterol from TRLs that can be retained in the subendothelial space (i.e., remnants, IDLs, and small VLDLs) contributes to the genesis of atherosclerosis. Triglycerides of atherogenic TRLs induce inflammation of the arterial wall. Mechanisms that explain the involvement of TRLs in atherosclerosis are the generation of pro-atherogenic changes in high-density lipoproteins and low-density lipoproteins, accumulation of TRLs in plasma, and their passage to the subendothelial space where they cause endothelial dysfunction and inflammation of the vascular wall. Furthermore, plasma accumulation of TRLs causes hyperviscosity and a procoagulant state. Finally, this manuscript summarizes the controversial aspects of the clinical approach and the treatment of cases with dyslipidemia explained by atherogenic TRLs. <![CDATA[Result Turnaround Time of RT-PCR for SARS-CoV-2 is the Main Cause of COVID-19 Diagnostic Delay: A Country-Wide Observational Study of Mexico and Colombia]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0034-83762022000200071&lng=es&nrm=iso&tlng=es ABSTRACT Background: Delay in COVID-19 diagnosis due to late real-time reverse transcription-polymerase chain reaction reporting has been described to be an important cause of suboptimal COVID-19 surveillance and outbreak containment. Objective: The objective of the study was to determine the duration of diagnostic delay due to test turnaround time and its association with marginalization status. Methods: In this observational study using national open data of Mexico and Colombia, we quantified the delay in COVID-19 diagnosis that occurred in both countries. We considered two periods that contributed to the delay in diagnosis: the time from symptom onset until testing (delay-one) and test turnaround time (delay-two). Marginalization status was determined according to country-specific scores. Results: Among 3,696,773 patients from Mexico and Colombia, delay-two was generally longer than delay-one. Median delay-one was 3 days and delay-two 7 days in Colombia, while in Mexico, they were 3 days and 4 days, respectively. In Colombia, worse marginalization status prolonged delay-two. In Mexico, a lower number and percentage of rapid tests were performed in areas with worse marginalization. Conclusion: Diagnostic delay was mostly due to test turnaround time. Marginalization status was an important barrier to diagnostic test access. <![CDATA[Epistasis Between Two Gene Variants of Leptin and Vascular Endothelial Growth Factor Genes in the Development of Primary Knee Osteoarthritis]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0034-83762022000200081&lng=es&nrm=iso&tlng=es ABSTRACT Background: The association of leptin (LEP) and vascular endothelial growth factor A (VEGFA) genes with the susceptibility to knee osteoarthritis (OA) has been analyzed; however, the epistasis between them has not been investigated. Objective: The objective of the study was to analyze the association of LEP and VEGFA variants and their interaction with primary knee OA in a Mexican Mestizo population. Methods: A case-control study was developed. Cases were ≥40 years, BMI ≤27 kg/m2, with primary knee OA and radiologic Grade ≥2. Controls were participants with no knee OA and a radiologic Grade &lt;2. The rs2167270 of LEP and rs2010963 of VEGFA were genotyped. Genotypic association was tested under codominant, dominant, and recessive models. Uni- and multi-variate analyses were developed through non-conditional logistic regression. The multifactor dimensionality reduction algorithm was developed to detect epistasis. Results: Participants comprised 103 cases and 179 controls. Allelic and genotypic distributions did not show differences between the groups. Notwithstanding, a statistically significant interaction was observed between the LEP and VEGFA genes (p = 0.02) with a testing accuracy of 0.5199 and cross-validation consistency of 10/10. This interaction model confers an increased risk to knee OA (OR [95% CI] = 1.8 [1.1-2.9]). Conclusion: Interaction between LEP and VEGFA is related with genetic susceptibility to developing primary knee OA. <![CDATA[Factors Associated with Development of Acute Kidney Injury After Liver Transplantation]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0034-83762022000200090&lng=es&nrm=iso&tlng=es ABSTRACT Background: Early post-liver transplant (LT) acute kidney injury (AKI) has been associated with worse short-term and long-term outcomes, but the incidence and risk factors in our population are unknown. Methods: We designed a prospective, single-center, longitudinal cohort study to determine the incidence of AKI during the immediate postoperative period of LT, and to identify the risk factors associated with AKI after LT. Pre-operative and intraoperative variables were analyzed to determine if there was any correlation with the development of post-operative AKI. Results: Eighty-six patients were included in the final analysis; from them, 45 (52%) developed AKI in the following 30 days after LT. The presence of hepatic encephalopathy prior to LT was the factor most strongly associated with the development of AKI (Relative Risk 3.67, 95% Confidence Interval 1.08-8.95). Other factors associated with AKI development were male gender and a higher serum lactate during surgery. Conclusion: AKI was a frequent complication that significantly worsened the prognosis of LT recipients and was associated with an increased 30-day mortality rate. The presence of hepatic encephalopathy strongly predicted the development of severe AKI. <![CDATA[The Prognostic Value of C-Reactive Protein/Albumin Ratio in Acute Pulmonary Embolism]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0034-83762022000200097&lng=es&nrm=iso&tlng=es ABSTRACT Background: Serum C-reactive protein (CRP) to albumin ratio (CAR) has been defined as an inflammation-based prognostic marker. We evaluated the association and prognostic value of CRP/albumin ratio in patients with pulmonary embolism (PE). Methods: A total of 256 patients with acute PE who were hospitalized between March 2016 and December 2020 were retrospectively reviewed. PE severity index (PESI) was calculated. Serum levels of CRP and albumin that were obtained at the time of admission were used for calculation. CAR was evaluated for correlation with PESI, and thus, foresee the risk of death due to PE. Results: There were 186 patients eligible for inclusion. 54 patients were in intermediate, 34 patients were in high risk and 98 patients were in very high-risk group according to PESI score. In the correlation analysis, we observed moderate positive correlations between CRP/albumin ratio, troponin and PESI score (r = 0.584, p &lt; 0.0001; r = 521, p &lt; 0.0001, respectively). Regression analysis revealed that only CRP/albumin ratio and PESI score were independent risk factors associated with 6-month mortality of acute PE patients. The AUC for CRP/albumin ratio was 0.643, 0.751, and 0.763 for 30-day, 90-day, and 6-month mortality, respectively (95% CI: 0.550-0.737, 0.672-0.830, 0.687-0.838]. A cut-off value of 5.33 for CRP/albumin ratio was associated with 65.3% sensitivity and 65.6% specificity in predicting 6-month mortality. Conclusion: The CRP/albumin ratio, an inexpensive and easily measurable laboratory variable, may be a useful prognostic marker of PE, especially when other causes that alter serum levels are excluded from the study. <![CDATA[Admission Monocyte/HDL Ratio Predicts Adverse Cardiac Remodeling After St-Elevation Myocardial Infarction]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0034-83762022000200104&lng=es&nrm=iso&tlng=es ABSTRACT Background: Inflammation plays a critical role in cardiac remodeling after myocardial infarction (MI). Monocyte to high-density lipoprotein-cholesterol (HDL-C) ratio (MHR) has emerged as a potential indicator of inflammation. Objectives: The study aimed to investigate the prognostic role of MHR at the time of hospital admission in late cardiac remodeling and subsequent 1-year mortality in an academic training and research hospital. Methods: This prospective multicenter study included 231 patients with acute ST-elevation MI. Left ventricular (LV) functions and volumes were assessed by cardiac magnetic resonance (CMR) imaging at 2 weeks and 6 months post-MI. The definition of adverse cardiac remodeling (AR) was based on the increase of LV end-diastolic volume by ≥ 12% at 6 months post-MI. All patients were followed for survival for 1 year after the second CMR imaging measurements. Results: At 6 months post-MI, 20 patients (23.8%) exhibited AR. The median MHR was higher in the AR group compared to the group without AR (2.2 vs. 1.5, p &lt; 0.001). A positive correlation was found between MHR and infarct size in the groups with and without AR. High MHR was an independent predictor of AR (OR: 3.21, p = 0.002). The cut-off value of MHR in predicting AR was found to be &gt;1.6 with 92.7% sensitivity and 70.1% specificity (AUC ± SE: 0.839 ± 0.03, p &lt; 0.001). Mortality risk was 5.62-fold higher in the group with MHR of &gt;1.6 (HR: 5.62, p &lt; 0.001). Conclusions: These results indicate that admission MHR is a useful tool to predict patients with AR who are at risk of progression to heart failure and mortality after MI. <![CDATA[Association between <em>APOE</em>-ε<sup>4</sup> Carrier Status and Qualitative Neuroimaging Characteristics in Older Adults with Mild Cognitive Impairment]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0034-83762022000200113&lng=es&nrm=iso&tlng=es ABSTRACT Background: The pathogenesis of mild cognitive impairment (MCI) is multifactorial and includes the presence of genetic variants such as the ε4 allele of the apolipoprotein E gene (APOE-ε4). Association between the APOE-ε4 carrier status and deleterious structural and functional changes on magnetic resonance imaging (MRI) has been previously described in individuals with Alzheimer's disease. However, the central nervous system changes may possibly develop in earlier stages of cognitive impairment, as reflected in MCI. Objective: The objective of the study was to determine the association between APOE-ε4 carrier status and qualitative changes on MRI (medial temporal and parietal atrophy), as well as the detection of white matter hyperintensities (WMH) in older adults with MCI, in the memory clinic of a tertiary care hospital in Mexico City. Methods: A cross-sectional study of 72 adults aged 60 years or above who underwent an exhaustive clinical, neuroimaging, and neuropsychological evaluation. Multivariate logistic regression models were constructed to determine the association between APOE-ε4 carrier status and qualitative/quantitative changes on MRI. Results: Mean age was 75.2 years (± 7.2) and 64% were female. Twenty-one participants were cognitively normal and 51 had MCI. Almost 56% were APOE-ε4 carriers and were associated with medial-temporal atrophy according to the Scheltens scale (odds ratio [OR]: 20.0, 95% confidence intervals [CI]: 3.03-131.7), parietal atrophy according to the Koedam's score (OR: 6.3; 95% CI 1.03-39.53), and WMH according to the Fazekas scale (OR: 11.7, 95% CI: 1.26-108.2), even after adjusting for age, educational level, and cardiovascular risk factors. Conclusion: The APOE-ε4 carrier status was associated with medial temporal and parietal atrophy, as well as WMH. Our findings support the hypothesis suggesting the contribution of this genotype to neurodegeneration and cerebral vascular pathology.