Effect of Hypomagnesemia On The Prognosis of Patients With Sepsis in ICU: A Retrospective Cohort Study

Objective Existing studies have shown that the incidence of hypomagnesemia may be as high as 60%. However, the correlation between hypomagnesia and sepsis mortality remains elusive. The current study evaluated the effect of hypomagnesemia on the prognosis of patients with sepsis in ICU. Methods It was a retrospective cohort study based on an online database named MIMIC III. A total of 1448 sepsis patients with serum magnesium were admitted to the database, among which 645 patients were screened out. Results At 28 days, 99 patients (30.84%) in the hypomagnesemia group and 123 patients (38.0%) (P = 0.06) in the non-hypomagnesemia group died. There was no correlation between hypomagnesemia and 28-day mortality in patients with sepsis (HR = 1.07; P = 0.87, 95% CI). However, the duration of mechanical ventilation (P < 0.01), the duration of vasoactive drug use (P < 0.01), the length of ICU stay (P < 0.01), and the length of hospital stay (P < 0.01) of patients in the hypomagnesemia group were higher than those in the non-hypomagnesemia group. In the subgroup analysis, the time of no vasopressor (P < 0.01) and the time of no mechanical ventilation (P < 0.01) in the magnesium supplementation group were significantly longer than those in the non-magnesium supplementation group. More importantly, the 14-day mortality (30.8% vs 48.9%, P < 0.01) and 28-day mortality (33.8% vs 48.9%, P = 0.03) in patients with magnesium supplementation were lower than patients without magnesium supplementation. Conclusions For sepsis patients in ICU, although hypomagnesemia had no significant correlation with 28-day mortality, it still prolonged the duration of mechanical ventilation and vasoactive drug use, and increased the length of ICU stay and hospital stay. Even for patients with normal serum magnesium levels, optimizing serum magnesium levels may improve the prognosis of patients with sepsis.

Functional and neurometabolic asymmetry in SHR and WKY rats following vasoactive treatments

A lateralized distribution of neuropeptidase activities in the frontal cortex of normotensive and hypertensive rats has been described depending on the use of some vasoactive drugs and linked to certain mood disorders. Asymmetrical neuroperipheral connections involving neuropeptidases from the left or right hemisphere and aminopeptidases from the heart or plasma have been suggested to play a role in this asymmetry. We hypothesize that such asymmetries could be extended to the connection between the brain and physiologic parameters and metabolic factors from plasma and urine. To assess this hypothesis, we analyzed the possible correlation between neuropeptidases from the left and right frontal cortex with peripheral parameters in normotensive (Wistar Kyoto [WKY]) rats and hypertensive rats (spontaneously hypertensive rats [SHR]) untreated or treated with vasoactive drugs such as captopril, propranolol and L-nitro-arginine methyl ester. Neuropeptidase activities from the frontal cortex were analyzed fluorometrically using arylamide derivatives as substrates. Physiological parameters and metabolic factors from plasma and urine were determined using routine laboratory techniques. Vasoactive drug treatments differentially modified the asymmetrical neuroperipheral pattern by changing the predominance of the correlations between peripheral parameters and central neuropeptidase activities of the left and right frontal cortex. The response pattern also differed between SHR and WKY rats. These results support an asymmetric integrative function of the organism and suggest the possibility of a different neurometabolic response coupled to particular mood disorders, depending on the selected vasoactive drug.