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Background
Pro‐protein convertase subtilisin/kexin 9 (PCSK9) is a proenzyme primarily known to regulate low‐density lipoprotein receptor re‐uptake on hepatocytes. Whether PCSK9 can concurrently trigger inflammation or not remains unclear. Here, we investigated the potential association between circulating levels of PCSK9 and mortality in patients with severe sepsis or septic shock.
Methods
Plasma PCSK9 levels at days 1, 2 and 7 were measured in 958 patients with severe sepsis or septic shock previously enrolled in the Albumin Italian Outcome Sepsis (ALBIOS) trial. Correlations between levels of PCSK9 and pentraxin 3 (PTX3), a biomarker of disease severity, were evaluated with ranked Spearman’s coefficients. Cox proportional hazards models were used to assess the association of PCSK9 levels at day 1 with 28‐ and 90‐day mortality.
Results
Median plasma PCSK9 levels were 278 [182–452] ng mL−1 on day 1. PCSK9 correlated positively with PTX3 at the three time‐points, and patients with septic shock within the first quartile of PCSK9 showed higher levels of PTX3. Similar mortality rates were observed in patients with severe sepsis across PCSK9 quartiles. Patients with septic shock with lower PCSK9 levels on day 1 (within the first quartile) showed the highest 28‐ and 90‐day mortality rate as compared to other quartiles.
Conclusion
In our sub‐analysis of the ALBIOS trial, we found that patients with septic shock presenting with lower plasma PCSK9 levels experienced higher mortality rate. Further studies are warranted to better evaluate the pathophysiological role of PCSK9 in sepsis.
The concentrations of harmful products in the circuit were negligible and were lower using the new-generation absorbers. Using Amsorb Plus, the temperatures in the canisters were lower than with the other two absorbers.
Our analysis provided an overview of 5 biological meshes currently available on the market. The different types of meshes showed a marked statistical variability in the clinical outcomes. Hence, nearly all comparisons between different meshes in the two clinical end-points did not reach statistical significance. One exception was represented by the finding that cross-linked meshes had a significantly lower recurrence rate at 12 months than non-cross-linked meshes.
Increased intra-abdominal pressure (IAP) may occur in critically ill patients. The easiest method to estimate IAP at the bedside is the bladder pressure measurement. A standard procedure (same volume infused, pressure transducers, and patient's position) should be used to obtain comparable and reproducible data among different patients and during different stages and time of the disease. The increase in IAP leads to two major pathological conditions: 1) the intraabdominal hypertension (IAP above 16 cmH2O) and 2) the abdominal compartment syndrome (IAP above 30 cmH2O). Increased IAP negatively affects pulmonary, cardiovascular, renal, gastrointestinal and central nervous system function. Most of critically ill patients have an intraabdominal hypertension, while few of them (less than 5%) present clinical characteristics of abdominal compartment syndrome. IAP is different among different categories of patients. The highest mean values during intensive care unit stay have been reported in respiratory and cardiologic patients among medical categories and in neurologic patients among surgical patients. IAP seems to be correlated with severity scores but its relation to mortality is uncertain. Routine measurements of IAP by means of bladder pressure are not associated with an increased rate of urinary tract infections. Future trials are warranted to better evaluate the role of routine IAP measurements on clinical management of critically ill patients
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