Pancreas fat content, insulin homeostasis and circulating endothelial microparticles in male essential hypertensive patients.

The pancreas fat content has been poorly investigated in essential hypertension. The authors aim to relate pancreas and liver fat content with parameters measuring insulin resistance, beta-cell function and also with markers of endothelial dysfunction and platelet or endothelial cell destruction. The authors studied a group of 40 male hypertensive patients with well-controlled blood pressure, maintaining a stable weight, and having not changed their medication during the last year. Pancreas fat content was correlated with HOMA-IR (r = .616, p < .001), HOMA-S (r = -.439, p < .005), beta cell function parameter (r = .457, p < .005), and QUICKI (r = .412, p < .01), whereas liver fat was not patients in the highest quartile of pancreas fat content had more circulating endothelial microparticles than patients in the other quartiles (median 129 [94.3-200] vs. 60.9 [49.4-88.8], p = .002). However, patients in the highest quartile of the pancreas fat content distribution did not differ from the lowest in hyperemic response after ischemia nor circulating platelet microparticles count. Liver fat content was not related to any of the parameters studied. In a multivariate stepwise binary logistic regression analysis (Wald Method) circulating endothelial microparticles remain significantly associated with pancreas fat content after adjusting for confounding factors, such as tobacco, diabetes mellitus, hypercholesterolemia, or metabolic syndrome. Our results reflect that in essential hypertension, pancreas fat content is superior to liver fat to study beta-cell functionality and insulin resistance. Moreover, the authors described for the first time that pancreas fat content is related to endothelial cell destruction. Further studies are needed to confirm this point.

Clusters of inflammation in COVID-19: descriptive analysis and prognosis on more than 15,000 patients from the Spanish SEMI-COVID-19 Registry.

Uncontrolled inflammation following COVID-19 infection is an important characteristic of the most seriously ill patients. The present study aims to describe the clusters of inflammation in COVID-19 and to analyze their prognostic role. This is a retrospective observational study including 15,691 patients with a high degree of inflammation. They were included in the Spanish SEMI-COVID-19 registry from March 1, 2020 to May 1, 2021. The primary outcome was in-hospital mortality. Hierarchical cluster analysis identified 7 clusters. C1 is characterized by lymphopenia, C2 by elevated ferritin, and C3 by elevated LDH. C4 is characterized by lymphopenia plus elevated CRP and LDH and frequently also ferritin. C5 is defined by elevated CRP, and C6 by elevated ferritin and D-dimer, and frequently also elevated CRP and LDH. Finally, C7 is characterized by an elevated D-dimer. The clusters with the highest in-hospital mortality were C4, C6, and C7 (17.4% vs. 18% vs. 15.6% vs. 36.8% vs. 17.5% vs. 39.3% vs. 26.4%). Inflammation clusters were found as independent factors for in-hospital mortality. In detail and, having cluster C1 as reference, the model revealed a worse prognosis for all other clusters: C2 (OR = 1.30, p = 0.001), C3 (OR = 1.14, p = 0.178), C4 (OR = 2.28, p < 0.001), C5 (OR = 1.07, p = 0.479), C6 (OR = 2.29, p < 0.001), and C7 (OR = 1.28, p = 0.001). We identified 7 groups based on the presence of lymphopenia, elevated CRP, LDH, ferritin, and D-dimer at the time of hospital admission for COVID-19. Clusters C4 (lymphopenia + LDH + CRP), C6 (ferritin + D-dimer), and C7 (D-dimer) had the worst prognosis in terms of in-hospital mortality.

Abnormal levels of antioxidant defenses in a large sample of patients with hypertensive disorders of pregnancy.

Increased levels of oxidative stress have been demonstrated in Preeclampsia in previous studies, but this finding has not been established in other hypertensive disorders in pregnancy (HDP). We measured different markers of lipid peroxidation and antioxidant defenses by spectrophotometry or enzymoimmunoanalysis in 339 pregnant women: 85 with gestational hypertension (GH), 88 chronic hypertension (CH), 104 Preeclampsia and 62 healthy pregnant control women (PCW). Lower activity of superoxide dismutase and higher levels of catalase were found in GH, CH and preeclampsia compared with PCW (964.4±116.5, 970.0±120.4, 971.2±137.5 and 1063.4±133.7 U g(-1) Hb, P<0.001; and 313.0±71.7, 292.2±45.3, 297.1±47.2, 215.5±26.2 U mg(-1) Hb, P<0.0001; respectively). Regarding the glutathione REDOX cycle, we found the following in GH, CH and preeclampsia compared with PCW: a decrease in its reduced form (2.6±0.6, 2.7±0.8, 2.7±0.9, 3.3±1.3 µmol l(-1), P<0.003), a parallel increase in the oxidized form (185.6±68.9, 194.7±75.0, 184.3±78.3, 85.1±27.5 µmol l(-1), P<0.0001) and an increment in glutathione peroxidase (85.9±22.0, 86.4±20.9, 82.1±23.5 and 77.2±19.7 U g(-1) Hb, P<0.04) and glutathione reductase (6384.3±1261.9, 6724.6±1154.1, 6287.9±1399.9 and 6044.4±1208.4 mU g(-1) Hb, P<0.01, respectively). Nitrites/nitrates were higher in patients with preeclampsia than in PCW (31.50±15.08, 26.80±8.39 µmol l(-1), P<0.002). Although malondialdehyde and oxidized-LDL levels were similar among groups, free fatty acids were increased in every HDP (GH 514.6±194.6, CH 501.3±197.4, preeclampsia 555.2±230.1 µmol l(-1)) compared with PCW (351.4±146.1 µmol l(-1)), P<0.0001. Our results show an oxidation/reduction imbalance with an increase in oxidative stress coupled with a decreased capacity of antioxidant systems, not only in preeclampsia but also in every HDP.