ATR1 A1166C (rs5186), FII G20210A (rs1799963), FV G1691A (rs6025), FXIII 97G > T (rs11466016) and MTHFR A1298C (rs1801131) polymorphisms and the risk of ST-elevation myocardial infarction in young Mexican individuals.

BACKGROUND: Previous studies had identified genetic variants associated with Myocardial Infarction, but results are inconclusive. We examined the association between FII G20210A (rs1799963), FV G1691A (rs6025), FXIII 97G > T (rs11466016), ATR1 A1166C (rs5186) and MTHFR A1298C (rs1801131) polymorphisms and ST elevation Myocardial Infarction in young Mexican individuals. METHODS: We included a total of 350 patients with Myocardial Infarction <45 years old and 350 controls matched by age and gender. The polymorphisms were analyzed by PCR-RFLP using specific restriction enzymes. DNA fragments were separated by electrophoresis in 2% gel of agarose and visualized using SYBR green. RESULTS: The A1166C (p = 0.004) but not FXIII 97G > T (p = 0.19), G20210A (p = 0.32), G1691A (p = No significant) and A1298C (p = 0.21) polymorphisms were associated with increased risk for ST elevation Myocardial Infarction. Moreover, dyslipidemia, hypertension, smoking and family history of atherothrombotic disease were associated. CONCLUSIONS: We found that A1166C represented increased risk for ST elevation Myocardial Infarction. However, G20210A, G1691A, 97G > T, and A1298C were not associated. In addition, we had determined that Glu298Asp, PLA1/A2, TAFI Thr325Ile, ACE I/D, AGT M235T and PAI-1 4G/5G polymorphisms represented increased risk in the same group of patients. However, MTHFR C677T, AGT T174M, FV G1691A, TSP-1 N700S, MTHFR C677T and TAFI 174 M polymorphisms were no associated. Our results suggest that in young patients with ST Myocardial Infarction, those polymorphisms could contribute to premature endothelial dysfunction, atherothrombosis, vasoconstriction, increased platelet aggregation, muscle cell migration and proliferation. Further studies are required to try to better assess gene-gene and gene-modifiable factors interaction.

Soluble Endoglin and Uterine Artery Flow Doppler Ultrasonography as Markers of Progression to Preeclampsia in Women with Gestational Hypertension.

INTRODUCTION: Gestational hypertension (GH) pregnancies are at a high risk of developing adverse outcomes, including progression to preeclampsia. Prediction of GH-related adverse outcomes is challenging because there are no available clinical tests that may predict their occurrence. OBJECTIVE: The aim of the study was to determine the clinical usefulness of the soluble endoglin (sEng) and parameters of uterine artery flow (UtAF) measured by Doppler ultrasonography as markers of progression to preeclampsia in women with GH. SETTING: Mexico City, Mexico. MATERIAL AND METHODS: We included 77 singleton pregnant women with GH in a nested case-control study. Cases were women who progressed to preeclampsia (n = 36), and controls were those who did not (n = 41). Serum sEng and UtAF measurements were performed at enrollment. The main outcomes measured were progression to preeclampsia and occurrence of preterm delivery (PD) <37 and <34 weeks of gestation, small for gestational age infant (SGA), and fetal growth restriction (FGR). RESULTS: Women with sEng values in the highest tertile had higher risk of progression to preeclampsia, preterm delivery <34 weeks of gestation, and fetal growth restriction, odds ratios (ORs) ≥3.7. Patients with abnormal UtAF Dopp-ler-pulsatility index had higher risk of progression to preeclampsia, preterm delivery <34 weeks of gestation, small for gestational age infant, and fetal growth restriction (ORs ≥3.3). The presence of notch was associated with higher risk of progression to preeclampsia, preterm delivery <37 and <34 weeks of gestation, SGA infant, and fetal growth restriction (ORs ≥2.9). However, logistic regression analysis revealed that only serum sEng was a significant and independent risk factor for progression of GH to preeclampsia, preterm delivery <34 weeks of gestation, and fetal growth restriction (ORs ≥3.1). CONCLUSIONS: In GH pregnancies, UtAF Doppler ultrasonography is associated with increased risk of adverse outcomes and progression to preeclampsia. However, serum sEng concentration appears to be a better predictor to assess the risk of adverse maternal and perinatal outcomes and progression to preeclampsia.

Interleukin-6 in Amniotic Fluid: A Reliable Marker for Adverse Outcomes in Women in Preterm Labor and Intact Membranes.

INTRODUCTION: Amniotic fluid (AF) interleukin-6 (IL-6) concentration has been associated to preterm delivery and perinatal morbidity and mortality in women with preterm labor and intact membranes. Nevertheless, the clinical significance of this biomarker of intra-amniotic inflammation (IAI) is still unclear due in part to the paucity of large studies. METHODS: AF IL-6 concentrations were determined in 452 consecutive women with preterm labor and intact membranes, categorized into 3 groups: 302 without IAI (IL-6 of <2.6 ng/mL), 64 with mild IAI (IL-6 of 2.6-11.2 ng/mL), and 86 with severe IAI (IL-6 of ≥11.3 ng/mL). RESULTS: The severe IAI group had a short pregnancy duration from amniocentesis to delivery (median 3 days) than in without IAI group (median 45 days); meanwhile, the mild IAI group had a latency that was intermediate to the severe and without IAI groups (median 9.5 days). As compared to women without IAI, women with mild and severe IAI had higher rates of preterm delivery at both <34 and <37 weeks of gestation and perinatal morbidity and mortality. Furthermore, the risk of various individual adverse outcomes (short latency from amniocentesis to delivery [at ≤3 days, ≤7 days, and ≤14 days], preterm delivery at both <34 and <37 weeks of gestation, histologic chorioamnionitis, respiratory distress syndrome, and congenital sepsis) was higher in women with severe IAI (OR ≥ 2.8), compared with women without IAI. CONCLUSIONS: AF IL-6 concentrations appear to be suitable marker to assess the degree of IAI and are associated with increased risk of adverse outcomes.

[Polimorfismos asociados a disfunción endotelial y a un estado protrombótico en jóvenes mexicanos con infarto cerebral].

OBJECTIVE: To examine the contribution the polymorphisms G20210A, G1691A and G10976A in the coagulation factors FII, FV, FVII, respectively; Glu298Asp and C677T in eNOS and 5,10 MTHFR in young Mexican population with cerebral infarction (CI). METHODS: 224 patients ≤ 45 years of age with CI and 224 controls matched by age and gender were recruited from 2006 and 2014. The polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: We identified a significant difference in the genotype distribution of Glu298Asp (p = 0.001) and C677T (p = 0.01) polymorphisms between CI patients and control groups. The genotype distribution in the FII G20210A, FV G1691A and FVII G10976A polymorphisms were similar. There were independent factors for ischemic stroke: Glu298Asp and C677T polymorphisms, smoking; hypertension, and familial history of thrombotic disease. CONCLUSIONS: The Glu298Asp and C677T, but not FII G20210A, FV G1691A and FVII G10976A polymorphisms were associated with CI. Our results suggest that endothelial dysfunction and the synergist interaction with other factors such as smoking and hypertension contribute to CI in young individuals.

OBJETIVO: Examinar la contribución de los polimorfismos G20210A, G1691A y G10976A en los factores de coagulación FII, FV y FVII respectivamente; Glu298Asp y C677T en la óxido nítrico sintasa endotelial y 5,10 metilentetrahidrofolato reductasa, en población joven mexicana con infarto cerebral (IC). MÉTODO: Se incluyeron 224 pacientes ≤ 45 años de edad con diagnóstico de IC y 224 controles pareados por edad y sexo, de 2006 a 2014. Los polimorfismos fueron determinados por la técnica de reacción en cadena de la polimerasa-polimorfismos de longitud de fragmentos de restricción. RESULTADOS: Identificamos una diferencia significativa en la distribución genotípica de los polimorfismos Glu298Asp (p = 0.001) y C677T (p = 0.01) entre el grupo de pacientes con IC y el control. La distribución genotípica de los polimorfismos FII G20210A, FV G1691A y FVII G10976A fue similar entre ambos grupos. Se identificaron como factores independientes de IC los polimorfismos Glu298Asp y C677T, el tabaquismo, la hipertensión y el antecedente de familiar de enfermedad trombótica. CONCLUSIONES: Los polimorfismos Glu298Asp y C677T, pero no FII G20210A, FV G1691A y FVII G10976A, se asociaron con IC. Nuestros resultados sugieren que la disfunción endotelial en interacción sinérgica con otros factores de riesgo, como tabaquismo e hipertensión, contribuye al IC en individuos jóvenes.

GLU298ASP and 4G/5G Polymorphisms and the Risk of Ischemic Stroke in Young Individuals.

BACKGROUND: Polymorphisms in the endothelial nitric oxide synthase (eNOS) and in the plasminogen activator inhibitor -1 (PAI-1) genes have been implicated in stroke pathogenesis but results are still controversial. The aim of this study was to examine the possible contribution of Glu298Asp in the eNOS and 4G/5G in the PAI-1polymorphisms with ischemic stroke in a young Mexican population. MATERIALS AND METHODS: In a case-control study, conducted between January 2006 and June 2010, 204 patients ≤45 years of age with ischemic stroke and 204 controls matched by age and gender, were recruited. The Glu298Asp and 4G/5G polymorphisms were determined in all participants by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: There was a significant difference in the Glu298Asp genotype distribution (P=0.001) and allele frequency between the two groups (P=0.001). The 4G/5G genotype distribution (P=0.40) and the allele frequency was similar between groups; (P=0.13). There were independent factors for ischemic stroke: Asp carriage (GluAsp+AspAsp) (P=0.02); smoking (P=0.01); hypertension (P=0.03), and familial history of atherothrombotic disease (P=0.04). CONCLUSIONS: The Asp allele from the Gu298Asp gene represents an independent risk factor for ischemic stroke in a young Mexican population. In contrast, the 4G/5G was not associated with an increased risk for this disease in the same group of patients, as previously has been demonstrated in other populations.

[Atypical preeclampsia: case report]. / Preeclampsia atípica. Reporte de un caso.

BACKGROUND: Preeclampsia that occurs at < 20 weeks of gestation is rare and has been usually reported with molar or hydropic degeneration of the placenta and antiphospholipid syndrome. CASE REPORT: To describe the clinical presentation of atypical preeclampsia of a patient of 37 years old at her first gestation who developed this entity at 18.5 weeks of gestation. She had history of pre-existing hypertension and infertility. This pregnancy was obtained through in vitro fertility. She reported a severe headache and was admitted to our hospital secondary to elevated blood pressure of 160/110 mm Hg. The laboratory evaluation revealed platelet count 51,000, alanine aminotransferase of 331 UI/L, aspartate aminotransferase of 285 UI/L, lactate dehydrogenase 421 UI/L and urinalysis with +2 proteinuria, soluble fms-like tyrosine kinase-1/placental growth factor ratio 895.5. The diagnosis of chronic hypertension and superimposed preeclampsia and incomplete HELLP syndrome was supported. After termination of pregnancy, the patient improved rapidly. She was discharged home on postoperative day 7 with a blood pressure of 120/70 mm Hg with normal laboratory. CONCLUSIONS: Clinicians should consider the diagnosis of preeclampsia and HELLP syndrome before 20 weeks of gestation in women presenting with clinical or laboratory abnormalities consistent with this disease.

[Progression of gestational hypertension to preeclampsia]. / Evolución de hipertensión gestacional a preeclampsia.

BACKGROUND: 15 to 25% of patients with gestational hypertension progress to preeclampsia. OBJECTIVE: To determine the number of patients with gestational hypertension who developed preeclampsia. MATERIALS AND METHODS: Observational prospective comparative and longitudinal study realized between november 2010 to december 2012. We included pregnant patients diagnosed with mild gestational hypertension who were followed during pregnancy to observe the progression to preeclampsia. We compared the clinical features of each group among those who developed and not the disease. RESULTS: We included a total of 146 patients, of whom 36 (25%, IC 95% 17.7-31.7%) progress to preeclampsia. In this group 3 (8%) developed mild preeclampsia and 33 (92%) severe preeclampsia, of which 8 (24%) account HELLP syndrome. The remaining 110 patients (75%), did not develop preeclampsia. From 12 (8%) patients with gestational age < to 28 weeks, 7 (58%) developed preeclampsia, 46 (31%) patients between 28-33 weeks, 12 (26%) evolved into preeclampsia, 39 (27%) patients between 34-36 weeks, 11 (28%) progressed to preeclampsia and finally 49 (34%) with pregnancy > 37 weeks, 6 (12%) developed to preeclampsia. When comparing these groups we found that a lower gestational age was more frequent the progression to preeclampsia (p < 0.004). The onset of gestational hypertension before 28 weeks was significantly associated with the progression of preeclampsia (OR 5.1 IC 95% 1.5-17.2). The weight of infants and gestational age was lower in children of women who developed the disease in comparison that those who did not (p < 0.001). There were no significance differences between both groups in relation with body mass index, maternal age, parity and antecedent of preeclampsia. CONCLUSIONS: The progression of gestational hypertension into preeclampsia appreciated in one of each four patients. The progression of gestational hypertension in preeclampsia was more common in preterm pregnancy. Most of the patients developed the severe form of the disease.

Antimicrobial Resistance and Antibiotic Consumption in a Secondary Care Hospital in Mexico.

BACKGROUND: Antimicrobial resistance is a global health problem, due to morbidity, mortality, and healthcare costs. The misuse of antimicrobials is the main cause of antimicrobial resistance. The aim of this study was to report antimicrobial resistance and antibiotic consumption in a secondary care hospital in Mexico. METHODS: Within a cross-sectional study, antimicrobial resistance data on ESKAPE pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) and antibiotic consumption from 2020 to 2022 were collected. Antimicrobial resistance was reported based on percentages of resistance and consumption was analyzed using the defined daily dose (DDD)/100 bed days and the AWaRe (Access, Surveillance, Reservation) antibiotic group. RESULTS: Antibiotic consumption in 2020, 2021 and 2022 was 330, 175 and 175 DDD/100 beds day, respectively. The rate of ceftriaxone resistance in E. coli (n = 526) and K. pneumoniae (n = 80) was 76% and 69%, respectively, the rate of carbapenem resistance in A. baumannii (n = 168) and P. aeruginosa (n = 108) was 92% and 52%, respectively; the rate of oxacillin resistance in S. aureus (n = 208) was 27%; and the rate of vancomycin resistance in E. faecium (n = 68) was 47%. CONCLUSION: The reported results are congruent with global estimates of antibiotic resistance and consumption, providing an overview that could generate actions for antimicrobial optimization at the local and regional levels.

Platelet glycoprotein IIIA PIA1/A2 polymorphism in young patients with ST elevation myocardial infarction and idiopathic ischemic stroke.

It has been identified that platelet glycoprotein IIIa PIA1/A2 polymorphism plays an important role in atherothrombotic disease such as myocardial infarction and stroke, but results remain controversial. Here, we investigated whether the PIA2 allele is associated with ST myocardial infarction or idiopathic ischemic stroke in young individuals in two independent studies. In a case-control study 275 patients with ST elevation myocardial infarction ≤45 years of age and 278 controls were recruited. In a second study, 200 patients with idiopathic ischemic stroke ≤45 years of age and 200 controls were enrolled. In both studies cases and controls were matched by age and gender. The PIA1/A2 polymorphism was determined in all participants by a polymerase chain reaction-restriction fragment length polymorphism assay. There was a significant difference in the PIA1/A2 genotype distribution (P = 0.001) and allele frequency (P = 0.001), between ST elevation myocardial infarction and control groups, but not in the PIA1/A2 genotype distribution (P = 0.61) and allele frequency (P = 0.80), between idiopathic ischemic stroke. The allele PIA2 represented an independent risk for ST elevation myocardial infarction but not for idiopathic ischemic stroke. Hypertension, smoking, and family history of atherothrombotic disease were also associated with ST elevation myocardial infarction and idiopathic ischemic stroke. Our results suggest that PA2 allele represents a risk factor for ST elevation myocardial infarction in young Mexican individuals but not for idiopathic ischemic stroke.

[Anti-Müllerian hormone serum levels in women with and without uterine fibroids]. / Concentraciones en suero de hormona antimülleriana en mujeres con y sin miomatosis uterina.

BACKGROUND: The etiology of uterine leiomyomatosis is multifactorial and it is unknown if a relation between anti-Müllerian hormone (hormona anti-mülleriana) and uterine leiomyomatosis exists. OBJECTIVE: To determine the differences of hormona anti-mülleriana levels in women with and without uterine leiomyomatosis. METHODS: 60 women were studied (30 with and 30 without uterine leiomyomatosis). The diagnosis was confirmed by histopathology. Both groups were paired by age and in all them serum levels of hormona antimülleriana were measured using ELISA, also estradiol and progesterone serum levels were determined. hormona anti-mülleriana-RII immunohistochemistry was done in healthy myometrium and in leiomyomas. RESULTS: The mean age between the groups didn't show statistical difference (41.8 +/- 5.6 years vs. 41.4 +/- 5.7 years). Also no differences were found in weight, height and body mass index. Serum levels of hormona antimülleriana were lower in those with leiomyomatosis [0.21 (0-10.4) ng/ml vs. 1.83 (0-6.38) ng/ml, p < 0.005]. No statistical differences were found in estradiol and progesterone serum levels between the groups. The hormona antimülleriana receptor was no expressed neither in the healthy myometrium nor in the leiomyomas. CONCLUSIONS: Women with leiomyomatosis had lower hormona antimülleriana levels. More studies are needed to determine if a relation exists between hormona antimülleriana and uterine leiomyomas.

Polymorphisms in the Renin-Angiotensin System and eNOS Glu298Asp Genes Are Associated with Increased Risk for Essential Hypertension in a Mexican Population.

Background: Essential hypertension is the result of modifiable and genetic factors, and it is associated with increased risk for atherothrombosis. Some polymorphisms are associated with hypertensive disease. The objective was to analyze the association between eNOS Glu298Asp, MTHR C677T, AGT M235T, AGT T174M, and A1166C and ACE I/D polymorphisms with essential hypertension in the Mexican population. Materials and Methods: In the present study, 224 patients with essential hypertension and 208 subjects without hypertension were included. The Glu298Asp, C677T, M235T, T174M, A1166C, and I/D polymorphisms were determined by the PCR-RFLP technique. Results: We found statistical differences in age, gender, BMI, systolic and diastolic blood pressure, and total cholesterol between control and cases. However, we found no significant differences in HbA1c and triglycerides between both groups. We observed statistical significant differences in the genotype distribution of Glu298Asp (P = 0.001), I/D (P = 0.02), and M235T (P = 0.004) polymorphisms between both groups. In contrast, there were no differences related to distribution of genotypes of MTHFR C677T (P = 0.12), M174T (P = 0.46), and A1166C (P = 0.85) between cases and control groups. Conclusions: We identified that Glu298Asp, I/D, and M234T polymorphisms represented an increased risk for essential hypertension and those genetic variants could contribute to the presence of endothelial dysfunction and vasopressor effect, hyperplasia, and hypertrophy of smooth muscle cells, which had an impact for hypertension. In contrast, we found no association between C677C, M174T, and A1166C polymorphisms and hypertensive disease. We suggested that those genetic variants could be identified in individuals with high risk to avoid hypertension and thrombotic disease.

Genetic Variants Associated with High Susceptibility of Premature Ischemic Stroke.

Background: Several polymorphisms had been associated with an increased risk of ischemic stroke, but results are inconclusive. The aim of this study was to examine the association between AGTR1 A1166C and TSP-1 N700S polymorphisms and ischemic stroke in a young Mexican population. Methods: In a case-control study, 250 patients ≤ 45 years of age with ischemic stroke and 250 controls matched by age and gender were included. The polymorphisms were determined in all participants by polymerase chain reaction. Results: There were statistical differences in genotype distribution (p = 0.01) and allele frequency (p = 0.001) of AGTR1 A1166C polymorphism. In contrast, there was a similar genotype distribution (p = 0.96) and allele frequency (p = 0.76) of the TSP1 N700S genetic variant between groups. Hypertension (p = 0.03), smoking (p = 0.02), and family history of atherothrombotic disease (p = 0.04) were associated with stroke, but not diabetes (p = 0.30) and dyslipidemia (p = 0.08). Conclusions: This is the first study in Mexican population to explore several genetic variants in young patients with ischemic stroke. Our results suggest that polymorphisms in the renin-angiotensin-aldosterone system could contribute to premature hypertension, endothelial dysfunction, atherothrombosis, vasoconstriction, smooth muscle cell migration, and proliferation. In contrast, polymorphisms in the coagulation factors are not associated with ischemic stroke. Environmental factors such as diabetes and dyslipidemia could be less important in the pathogenesis of ischemic stroke at a young age. We suggest that those polymorphisms should be determined in individuals with a family history of thrombosis to avoid the stroke development. Therefore, genotype-environmental combination could determine several possible phenotypes at different moments in life.

[Prognostic scale for in-hospital mortality in patients with COVID-19 viral pneumonia]. / Escala pronóstica para mortalidad intrahospitalaria en pacientes con neumonía viral COVID-19.

Background: The COVID-19 pandemic represented a challenge in medical care. A tool would be very useful to establish the prognosis of in-hospital death that is reliable and can be applied to the Mexican population entitled to the IMSS. Objective: To propose a prognostic scale to stratify patients with viral pneumonia COVID-19 in the emergency services. Material and methods: A nested case-control study was conducted in a cohort of patients who were consecutively admitted to the emergency department with viral pneumonia COVID-19. The cases were those patients who died, and the controls were those who were discharged due to health improvement. An association analysis was performed between the variables with significant differences between groups. Subsequently, the association was adjusted using a multivariate logistic regression model, from which the prognostic scale was developed. Results: A total of 70 subjects with COVID-19 were included, 34 cases and 36 controls. Chronic diseases, smoking, severe pulmonary involvement diagnosed by tomography, leukocytosis, and pulse oximetry less than 80% with were associated with in-hospital mortality; Odds Ratio (OR) of >1.1. Vaccination was a protective factor (OR = 0.04, CI95%: 0.01-0.16). A score greater than 3 points on the prognostic scale predicts in-hospital mortality with a specificity of 0.86 and a sensitivity of 0.73. Conclusions: The proposed prognostic scale can be a useful tool in the classification of patients with COVID-19 viral pneumonia in the emergency room services of secondary care level Hospitals.

Introducción: la pandemia por COVID-19 representó un reto en la atención médica. Sería de gran utilidad una herramienta para establecer el pronóstico de muerte intrahospitalaria que sea confiable y pueda aplicarse a la población mexicana derechohabiente del Instituto Mexicano del Seguro Social. Objetivo: proponer una escala pronóstica para estratificar a los pacientes con neumonía viral por COVID-19 en los servicios de urgencias de los hospitales de segundo nivel. Material y métodos: se realizó un estudio de casos y controles anidado en una cohorte de pacientes adultos que fueron admitidos consecutivamente en el servicio de Urgencias con diagnóstico de neumonía viral por COVID-19. Los casos fueron aquellos pacientes que fallecieron y los controles aquellos que fueron egresados de la unidad por mejoría. Se realizó un análisis de asociación ente las variables con diferencias significativas entre ambos grupos, se ajustó la asociación mediante un modelo de regresión logística multivariada a partir del cual se elaboró la escala pronóstica. Resultados: se incluyeron en total 70 personas con COVID-19, 34 casos y 36 controles. Se asociaron a la mortalidad intrahospitalaria: las enfermedades crónicas, el tabaquismo, la afectación pulmonar severa diagnosticada por tomografía, la leucocitosis y la oximetría de pulso menor a 80% con una razón de Momios (RM) de > 1.1. La vacunación fue un factor protector (RM: 0.29, IC95%: 0.11-0.80). Un puntaje mayor a 3 puntos en la escala pronóstica predice la mortalidad intrahospitalaria (sensibilidad: 0.73, especificidad: 0.86). Conclusiones: la escala pronóstica propuesta puede ser una herramienta útil en la clasificación de los pacientes con neumonía viral por COVID-19 en los servicios de urgencias de los hospitales de segundo nivel de atención.

Risk Factors for Severe-Critical COVID-19 in Pregnant Women.

Risk factors associated with severe-critical COVID-19 (coronavirus disease 2019) are based on findings in the general population. Pregnant women are at increased risk of severe-critical infection, and few reports are based on these women. A multicentric case-control study was conducted at the Mexican Institute of Social Security, State of Mexico, during the COVID-19 pandemic. We included pregnant women who were consecutively admitted to respiratory care units and were followed until 30 days after the resolution of pregnancy. A total of 758 pregnant women with a positive RT-PCR test for SARS-CoV-2 were enrolled from June 2020 to July 2021. We defined groups using the World Health Organization Severity Classification; cases were pregnant women with severe-critical COVID-19 (n = 123), and controls were subjects with non-severe COVID-19 (n = 635). Data was gathered from clinical files. A multivariate logistic regression analysis was used to adjust odds ratios and their 95% confidence intervals of factors associated with severe-critical COVID-19. Risk factors associated with severe-critical COVID-19 in pregnancy were non-vaccination (OR 10.18), blood type other than O (OR 6.29), maternal age > 35 years (OR 5.76), history of chronic hypertension (OR 5.12), gestational age at infection ≥ 31 weeks (OR 3.28), and multiparity (OR 2.80).

Platelet glycoprotein IIIA PIA2 polymorphism is associated with ST elevation acute myocardial infarction in young Mexican population.

Platelet membrane glycoprotein IIb/IIIa plays an important role in adhesion and platelet aggregation. Polymorphisms of genes in platelet activation and fibrinolysis have been associated with myocardial infarction (MI), however this has not been confirmed by others, and results are still controversial. The aim of this study was to determine the frequency distribution and association of polymorphism in the platelet glycoprotein GPIIIa PLA/A2 and the possible interaction with the 4G/5G in the plasminogen activator inhibitor genes with ST elevation acute myocardial infarction (STEAMI) in young Mexican subjects. A total of 254 unrelated patients with first STEAMI ≤45 years of age, who were admitted to a cardiovascular intense care unit and 254 healthy controls matched by age and gender were recruited from January 2006 and May 2011. The PIA1/A2 and 4G/5G polymorphism were determined in all participants by a PCR restriction based restriction endonuclease digestion. There was a difference in the PIA2 allele distribution between both groups (P = 0.001). Also, we found an increased percent of 4G allele in the group of patients compared to control group (P = 0.001). There was an increased risk for STEAMI in carries with the allele PIA2 and 4G (OR = 4.3, CI 95 % 1.7-6.5). The modifiable risk factors such: smoking, hypertension, family history of cardiovascular disease, and dyslipidemia were associated with myocardial infarction. This is the first study to evaluate the role of gene polymorphism in both the thrombotic and fibrinolytic pathways in young Mexican individuals with STEAMI and suggest a synergistic effect between PIA2 and 4G allele.

Clinical usefulness of angiogenic factors in women with chronic kidney disease and suspected superimposed preeclampsia.

BACKGROUND: Preeclampsia is a condition often superimposed to CKD. OBJECTIVE: The purpose of this study was to evaluate the clinical characteristics and outcomes of pregnant women with chronic kidney disease (CKD) with suspected superimposed preeclampsia, stratified according to the degree of their angiogenic imbalance, as assessed by the soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio. METHODS: Using a cross-sectional design, we studied 171 pregnancies in patients with CKD and with suspected superimposed preeclampsia, admitted to a teaching hospital. Patients were divided into three groups based on their degree of angiogenic imbalance, evaluated by the sFlt-1/PlGF ratio: no angiogenic imbalance (sFlt-1/PlGF ratio≤ 38), mild angiogenic imbalance (sFlt-1/PlGF ratio> 38 to < 85), and severe angiogenic imbalance (sFlt-1/PlGF ratio≥ 85). Superimposed preeclampsia and preeclampsia-related adverse outcomes were defined according to The American College of Obstetricians and Gynecology criteria.  Measurements of sFlt-1 and PlGF were performed on single serum samples using the Elecsys sFlt-1 and PlGF assays (Roche Diagnostics). Serum soluble endoglin (sEng) levels were also determined (ELISA R&D Systems, Minneapolis, MN). Glomerular filtration rate (GFR) was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula, whenever possible on pre-prengancy data. RESULTS: Patients with severe angiogenic imbalance had higher rates of confirmed superimposed preeclampsia and preeclampsia-related adverse maternal and perinatal outcomes (p < 0.001) when compared to patients with no or mild angiogenic imbalance. A significant trend towards higher serum sEng levels was observed as the degree of angiogenic imbalance increased. Interestingly, the rate of progression to superimposed preeclampsia increased progressively as the degree of angiogenic imbalance increased (no 11.8%, mild 60.0%, and severe 100%). CONCLUSION: In women with CKD and suspected superimposed preeclampsia, severe angiogenic imbalance was associated with confirmed superimposed preeclampsia or progression to superimposed preeclampsia. Patients with no angiogenic imbalance displayed lower rates of progression to superimposed preeclampsia, whereas outcomes were intermediate, supporting a systematic use of sFlt-1/PlGF ratio, and other biomarkers in the clinical management of CKD pregnacies.

Circulating angiogenic factors are associated with progression to preeclampsia and the occurrence of adverse outcomes in women with gestational hypertension.

OBJECTIVE: Gestational hypertension is characterized by an imbalance in angiogenic factors. The goal of the current study was to evaluate whether circulating concentrations of proangiogenic and antiangiogenic factors are associated with the risk of progression to preeclampsia and development of adverse outcomes in women with gestational hypertension. METHODS: We studied 496 women with gestational hypertension. Patients were divided into three groups based on their degree of angiogenic imbalance, evaluated by the soluble fms-like tyrosine kinase-1/placental growth factor ratio: no angiogenic imbalance (≤38), mild angiogenic imbalance (>38-<85), and severe angiogenic imbalance (≥85) or stratified into tertiles according to soluble endoglin (sEng) levels. RESULTS: The concentrations of all angiogenic factors were significantly different in patients with gestational hypertension than in healthy pregnancy. A significant trend towards higher serum sEng levels was observed as the degree of angiogenic imbalance increased. Patients with severe angiogenic imbalance had higher rates of adverse maternal and perinatal outcomes and progression to preeclampsia (P < 0.001) when compared with patients with no or mild angiogenic imbalance. The risk of combined adverse maternal outcomes and specific adverse outcomes (hemolysis, elevated liver enzymes, low platelet count syndrome, preterm delivery, small-for-gestational-age infant, perinatal death, and progression to preeclampsia within 7, 14, 28, and 56 days) was higher in patients with severe angiogenic imbalance or sEng values in the highest tertile (odds ratio ≥5.6 and ≥2.0, respectively), compared with no angiogenic imbalance or the lowest tertile. CONCLUSION: In women with gestational hypertension at the time of initial evaluation, circulating concentrations of the soluble fms-like tyrosine kinase-1/placental growth factor ratio and sEng appear to be suitable markers to assess the risk of adverse maternal and perinatal outcomes and progression to preeclampsia.

The C677T polymorphism of the methylenetetrahydrofolate reductase gene is associated with idiopathic ischemic stroke in the young Mexican-Mestizo population.

BACKGROUND AND PURPOSE: Previous studies have demonstrated that a common polymorphism in the gene encoding 5,10-methylenetetrahydrofolate reductase (MTHFR) is associated with an increased risk for stroke. However, this relation remains controversial. Our aim was to investigate the possible association between the C677T polymorphism in the MTHFR gene and idiopathic ischemic stroke in the young Mexican-Mestizo population. METHODS: One hundred seventy-eight patients <45 years with idiopathic ischemic stroke and 183 controls were tested for the C677T polymorphism in the MTHFR gene. Causes of primary thrombophilia as well as classical risk factors for atherothrombotic disease were also evaluated. RESULTS: There was a significant difference in the genotype distribution between patients and controls (p = 0.01), but the allele frequency was similar in both groups (p = 0.09). The univariate analysis identified the T allele as a risk factor for ischemic stroke (TT and CT carriers), as compared with homozygous for C allele (p = 0.01). Hypertension and smoking prevalences were significantly higher in the group of patients. Also the T allele was significantly associated with large-vessel ischemic stroke. The postoral methionine load homocysteine levels were higher in patients with ischemic stroke versus controls (p < 0.001). There was a low prevalence of primary thrombophilia markers. CONCLUSIONS: The T allele from the C677T polymorphism of the MTHFR gene represents an independent risk factor for idiopathic ischemic stroke at young age in the Mexican-Mestizo population. Also, hypertension and smoking were independent risk factors in our study population. Primary thrombophilic risk factors were not associated with ischemic stroke in our population.

COVID-19 during pregnancy: a narrative. / Enfermedad por COVID-19 durante el embarazo: una narrativa.

Coronavirus disease 2019 (COVID-19) was first identified in December 2019, in Wuhan, China, and it is a serious public health emergency, particularly to vulnerable populations. Pregnant women and their fetuses represent high-risk population during outbreaks of infectious diseases. They have very high risk of infection, due to changes in their immune system. Limited data are available on COVID-19 during pregnancy. Therefore, we searched articles published between December 2019 and May 30, 2020, in three databases: PubMed, Embase and Web of Science, using MeSH words COVID-19, SARS-CoV-2 and 2019-nCoV. 39 articles were included, and they revealed that clinical symptoms of COVID-19 in pregnant women are not different from those of general population, and they can turn into atypical pneumonia. Only one maternal death was reported. Fetal distress, prematurity, and respiratory distress syndrome are frequent in newborns; one intrauterine death and one perinatal death were reported. The most frequent sign found was fever (77-86%). The main maternal perinatal complications were prematurity (47%) and pneumonia (40%); serious illness was rare (4.4%) and similar to the reported in the general population (5%); the most frequent route of interruption was cesarean section in 89% of the cases. Maternal-fetal transmission is not ruled out, since 8.5% (4/47) of the included cases had positive SARS-CoV-2 tests. More research is needed on the subject and management protocols in pregnancy with intentional search for transmission to the newborn.

Identificada por primera vez en diciembre de 2019 en Wuhan, China, la enfermedad por coronavirus 2019 (COVID-19) es una grave emergencia de salud pública, en especial para poblaciones vulnerables. Las mujeres embarazadas y sus fetos son población de alto riesgo. Su frecuencia de contagio es muy alta y tienen mayor riesgo debido a los cambios en el sistema inmunológico. Se dispone de datos limitados sobre COVID-19 durante el embarazo. Por lo tanto, se buscaron los artículos publicados de diciembre de 2019 al 30 de mayo de 2020 en PubMed, Embase y Web of Science; se utilizaron los términos MeSH COVID-19, SARS-CoV-2, 2019-nCoV. Se incluyeron 39 artículos que revelaron que los síntomas clínicos son similares a los de la población general y pueden complicarse con neumonía atípica. Solo una muerte materna fue reportada. El sufrimiento fetal, la prematurez y el síndrome de dificultad respiratoria son frecuentes en los recién nacidos; una muerte intrauterina y una muerte perinatal fueron reportadas. El signo más encontrado fue la fiebre (77-86%). Las principales complicaciones materno-perinatales fueron la prematurez (47%) y la neumonía (40%); mientras que la enfermedad grave fue poco frecuente (4.4%) y similar a la reportada en población general (5%); la vía de interrupción más frecuente fue la cesárea en el 89% de los casos. La transmisión materno-fetal no se descarta, pues el 8.5% (4/47) de los casos incluidos tuvo prueba positiva a SARS-CoV-2. Se requieren más investigaciones en el tema y protocolos de manejo en el embarazo con búsqueda intencionada de transmisión al recién nacido.

Usefulness of the sFlt-1/PlGF (Soluble fms-Like Tyrosine Kinase-1/Placental Growth Factor) Ratio in Diagnosis or Misdiagnosis in Women With Clinical Diagnosis of Preeclampsia.

Preeclampsia is characterized by angiogenic imbalance (AI), sFlt-1 (soluble fms-like tyrosine kinase-1)/PlGF (placental growth factor) is useful for its diagnosis and prediction of adverse outcomes, but the relationship among the degrees of AI as assessed by this ratio with the correct diagnosis, clinical characteristics, and outcomes in women with clinical diagnosis of preeclampsia are unclear. We studied 810 women with clinical diagnosis of preeclampsia. Patients were divided into 3 groups based on their degree of AI, evaluated by the sFlt-1/PlGF ratio: no AI (≤38), mild AI (>38-<85), and severe AI (≥85). Patients with no AI were more likely to have comorbidities and false significant proteinuria compared with patients with mild and severe AI (P<0.001). The rates of preterm delivery, delivery within 14 days, and small-for-gestational-age infant were higher among patients with severe AI than in patients with no and mild AI (P<0.001) and in patients with mild AI that in those with no AI (P≤0.01). The occurrence of any adverse maternal outcome (HELLP syndrome, elevated liver enzymes, thrombocytopenia, placental abruption, acute kidney injury) was only present in patients with severe AI. Interestingly, the frequency of misdiagnosis of preeclampsia was progressively lower as the degrees of AI increased (no AI: 100%, mild AI: 88.2%, and severe AI: 15.6%). We concluded that in women with clinical diagnosis of preeclampsia, severe AI is characterized by high frequency of true preeclampsia and preeclampsia-related adverse outcomes, in contrast, no and mild AI, are characterized by unnecessary early deliveries, often due to misdiagnosis.