Mortality trends and risk of dying from liver cancer in Mexico, 2000-2013.

INTRODUCTION: Liver cancer (LC) is a public health problem in the world, since is the second leading cause of death and Mexico is no exception, in 2013 the LC ranked fourth of mortality among malignancies. MATERIAL AND METHODS: The records of mortality associated to LC for the period 2000-2013 were obtained from National Institute of Statistics and Geography. National mortality rates were calculated by state and by socioeconomic region. The strength of association of the states of residency and educational level with mortality from LC was determined. RESULTS: In 2000-2013, the crude death rate per 100,000 people increased from 4.2 to 4.9. Individuals with no schooling or incomplete elementary school the relative risk (RR) of dying from LC was the highest (RR 8.61, 95% CI 8.35-8.89), while in individuals with senior in high school or equivalent the RR decreased (RR 0.74, 95% CI 0.71-0.77). Chihuahua had the highest risk of dying [RR 30.3, 95% CI 19.6-46.8 (2000) and RR 22.3, 95% CI 15.1-33 (2013)]. Region 2 had the highest mortality rate. CONCLUSIONS: In Mexico in the study period, the crude death rate increased from LC. Individuals with no schooling or with incomplete elementary school the RR of dying from LC was the highest. Chihuahua had the highest mortality rate and the highest risk of dying. Region 2 had the highest mortality rate. ANTECEDENTES: El cáncer de hígado es un problema de salud pública en el mundo, ya que es la segunda causa de muerte, y México no es la excepción; en 2013, dicho cáncer ocupó el cuarto lugar en mortalidad entre las neoplasias malignas. MÉTODO: Se obtuvieron los registros de mortalidad asociada al cáncer de hígado correspondientes al periodo 2000-2013 del Instituto Nacional de Estadística y Geografía. Se calcularon las tasas de mortalidad nacional, por Estados y por región socioeconómica. Se determinó la fuerza de la asociación de los Estados donde residían los individuos y el nivel de estudios con la mortalidad por cáncer de hígado. RESULTADOS: En 2000-2013, la tasa cruda de mortalidad por 100,000 individuos se incrementó de 4.2 a 4.9. En individuos sin escolaridad o con primaria incompleta, el riesgo relativo (RR) de morir por cáncer de hígado fue el mayor (RR: 8.61; intervalo de confianza del 95% [IC95%]: 8.35-8.89), mientras que en aquellos con preparatoria disminuyó (RR: 0.74; IC95%: 0.71-0.77). El Estado que tuvo el mayor riesgo de morir fue Chihuahua (RR: 30.3, IC95%: 19.6-46.8 en 2000 y RR: 22.3, IC95%: 15.1-33 en 2013). La región socioeconómica con la mayor tasa de mortalidad fue la región 2. CONCLUSIONES: En México, en el periodo de estudio, la tasa cruda de mortalidad por cáncer de hígado se incrementó. En individuos sin escolaridad o con primaria incompleta, el RR de morir por cáncer de hígado fue el mayor. El Estado que tuvo la mayor tasa de mortalidad y el mayor riesgo de morir fue Chihuahua. La región socioeconómica con la mayor tasa de mortalidad fue la región 2.

Preeclampsia is associated with lower production of vascular endothelial growth factor by peripheral blood mononuclear cells.

BACKGROUND: Recent studies show that vascular endothelial growth factor (VEGF) downregulation is implicated in preeclampsia (PE) pathophysiology. This study assessed the relationship between PE and VEGF levels produced by peripheral blood mononuclear cells (PBMCs) and their serum levels. METHODS: A cross-sectional design was performed in 36 patients who had hypertensive disorders during pregnancy. We also used a longitudinal design with 12 pregnant women with risk factors for PE development and/or abnormal uterine arteries by Doppler study. VEGF and soluble fms-like tyrosine kinase-1 (sFlt-1) levels were measured for all patients in both designs. RESULTS: sFlt-1 serum was higher in preeclamptic patients (n = 26), whereas VEGF produced by stimulated PBMCs was lower than in healthy pregnant women and VEGF levels produced by stimulated PBMCs were even lower (p <0.003) in severe PE (n = 16). The receiver-operating characteristic curve analysis allowed establishing a cut-off value to identify patients with PE. VEGF production by PBMCs was 339.87 pg/mL. In addition, a robust linear regression model was performed to adjust the variance in VEGF levels. The patients' age decreased VEGF levels and was adjusted by weeks of gestation (WG) in our model. In the longitudinal study, 7/12 patients developed PE. VEGF produced by PBMCs cells was significantly lower in PE at 24-26 WG. CONCLUSIONS: VEGF production by PBMCs is inhibited during PE, creating a downregulation of the microenvironment; this deficiency may contribute to the pathogenesis of disease.