5 research outputs found
Infected pancreatic necrosis: outcomes and clinical predictors of mortality. A post hoc analysis of the MANCTRA-1 international study
: The identification of high-risk patients in the early stages of infected pancreatic necrosis (IPN) is critical, because it could help the clinicians to adopt more effective management strategies. We conducted a post hoc analysis of the MANCTRA-1 international study to assess the association between clinical risk factors and mortality among adult patients with IPN. Univariable and multivariable logistic regression models were used to identify prognostic factors of mortality. We identified 247 consecutive patients with IPN hospitalised between January 2019 and December 2020. History of uncontrolled arterial hypertension (pâ=â0.032; 95% CI 1.135-15.882; aOR 4.245), qSOFA (pâ=â0.005; 95% CI 1.359-5.879; aOR 2.828), renal failure (pâ=â0.022; 95% CI 1.138-5.442; aOR 2.489), and haemodynamic failure (pâ=â0.018; 95% CI 1.184-5.978; aOR 2.661), were identified as independent predictors of mortality in IPN patients. Cholangitis (pâ=â0.003; 95% CI 1.598-9.930; aOR 3.983), abdominal compartment syndrome (pâ=â0.032; 95% CI 1.090-6.967; aOR 2.735), and gastrointestinal/intra-abdominal bleeding (pâ=â0.009; 95% CI 1.286-5.712; aOR 2.710) were independently associated with the risk of mortality. Upfront open surgical necrosectomy was strongly associated with the risk of mortality (pâ<â0.001; 95% CI 1.912-7.442; aOR 3.772), whereas endoscopic drainage of pancreatic necrosis (pâ=â0.018; 95% CI 0.138-0.834; aOR 0.339) and enteral nutrition (pâ=â0.003; 95% CI 0.143-0.716; aOR 0.320) were found as protective factors. Organ failure, acute cholangitis, and upfront open surgical necrosectomy were the most significant predictors of mortality. Our study confirmed that, even in a subgroup of particularly ill patients such as those with IPN, upfront open surgery should be avoided as much as possible. Study protocol registered in ClinicalTrials.Gov (I.D. Number NCT04747990)
Proteomic Profile of Human Aortic Stenosis: Insights into the Degenerative Process
Degenerative aortic stenosis is the most common worldwide
cause
of valve replacement. While it shares certain risk factors with coronary
artery disease, it is not delayed or reversed by reducing exposure
to risk factors (e.g., therapies that lower lipids). Therefore, it
is necessary to better understand its pathophysiology for preventive
measures to be taken. In this work, aortic valve samples were collected
from 20 patients that underwent aortic valve replacement (55% males,
mean age of 74 years) and 20 normal control valves were obtained from
necropsies (40% males, mean age of 69 years). The proteome of the
samples was analyzed by quantitative differential electrophoresis
(2D-DIGE) and mass spectrometry, and 35 protein species were clearly
increased in aortic valves, including apolipoprotein AI, alpha-1-antitrypsin,
serum albumin, lumican, alfa-1-glycoprotein, vimentin, superoxide
dismutase CuâZn, serum amyloid P-component, glutathione S-transferase-P,
fatty acid-binding protein, transthyretin, and fibrinogen gamma. By
contrast, 8 protein species were decreased (transgelin, haptoglobin,
glutathione peroxidase 3, HSP27, and calreticulin). All of the proteins
identified play a significant role in cardiovascular processes, such
as fibrosis, homeostasis, and coagulation. The significant changes
observed in the abundance of key cardiovascular proteins strongly
suggest that they can be involved in the pathogenesis of degenerative
aortic stenosis. Further studies are warranted to better understand
this process before we can attempt to modulate it
Proteomic Profile of Human Aortic Stenosis: Insights into the Degenerative Process
Degenerative aortic stenosis is the most common worldwide
cause
of valve replacement. While it shares certain risk factors with coronary
artery disease, it is not delayed or reversed by reducing exposure
to risk factors (e.g., therapies that lower lipids). Therefore, it
is necessary to better understand its pathophysiology for preventive
measures to be taken. In this work, aortic valve samples were collected
from 20 patients that underwent aortic valve replacement (55% males,
mean age of 74 years) and 20 normal control valves were obtained from
necropsies (40% males, mean age of 69 years). The proteome of the
samples was analyzed by quantitative differential electrophoresis
(2D-DIGE) and mass spectrometry, and 35 protein species were clearly
increased in aortic valves, including apolipoprotein AI, alpha-1-antitrypsin,
serum albumin, lumican, alfa-1-glycoprotein, vimentin, superoxide
dismutase CuâZn, serum amyloid P-component, glutathione S-transferase-P,
fatty acid-binding protein, transthyretin, and fibrinogen gamma. By
contrast, 8 protein species were decreased (transgelin, haptoglobin,
glutathione peroxidase 3, HSP27, and calreticulin). All of the proteins
identified play a significant role in cardiovascular processes, such
as fibrosis, homeostasis, and coagulation. The significant changes
observed in the abundance of key cardiovascular proteins strongly
suggest that they can be involved in the pathogenesis of degenerative
aortic stenosis. Further studies are warranted to better understand
this process before we can attempt to modulate it
Proteomic Profile of Human Aortic Stenosis: Insights into the Degenerative Process
Degenerative aortic stenosis is the most common worldwide
cause
of valve replacement. While it shares certain risk factors with coronary
artery disease, it is not delayed or reversed by reducing exposure
to risk factors (e.g., therapies that lower lipids). Therefore, it
is necessary to better understand its pathophysiology for preventive
measures to be taken. In this work, aortic valve samples were collected
from 20 patients that underwent aortic valve replacement (55% males,
mean age of 74 years) and 20 normal control valves were obtained from
necropsies (40% males, mean age of 69 years). The proteome of the
samples was analyzed by quantitative differential electrophoresis
(2D-DIGE) and mass spectrometry, and 35 protein species were clearly
increased in aortic valves, including apolipoprotein AI, alpha-1-antitrypsin,
serum albumin, lumican, alfa-1-glycoprotein, vimentin, superoxide
dismutase CuâZn, serum amyloid P-component, glutathione S-transferase-P,
fatty acid-binding protein, transthyretin, and fibrinogen gamma. By
contrast, 8 protein species were decreased (transgelin, haptoglobin,
glutathione peroxidase 3, HSP27, and calreticulin). All of the proteins
identified play a significant role in cardiovascular processes, such
as fibrosis, homeostasis, and coagulation. The significant changes
observed in the abundance of key cardiovascular proteins strongly
suggest that they can be involved in the pathogenesis of degenerative
aortic stenosis. Further studies are warranted to better understand
this process before we can attempt to modulate it