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Background: Prolonged donor hepatectomy time may be implicated in early and late complications of liver transplantation., Aim: To evaluate the impact of donor hepatectomy time on outcomes of liver transplant recipients, mainly early allograft dysfunction., Methods: This multicenter retrospective study included brain-dead donors and adult liver graft recipients. Donor-recipient matching was obtained through a crossover list. Clinical and laboratory data were recorded for both donors and recipients. Donor hepatectomy, cold ischemia, and warm ischemia times were recorded. Primary outcome was early allograft dysfunction. Secondary outcomes included need for retransplantation, length of intensive care unit and hospital stay, and patient and graft survival at 12 months., Results: From January 2019 to December 2021, a total of 243 patients underwent a liver transplant from a brain-dead donor. Of these, 57 (25%) developed early allograft dysfunction. The median donor hepatectomy time was 29 (23-40) min. Patients with early allograft dysfunction had a median hepatectomy time of 25 (22-38) min, whereas those without it had a median time of 30 (24-40) min ( P = 0.126)., Conclusion: Donor hepatectomy time was not associated with early allograft dysfunction, graft survival, or patient survival following liver transplantation., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Background: Diabetes mellitus (DM) is not associated with increased mortality in critically ill patients, a phenomenon known as the "diabetes paradox". However, DM is a risk factor for increased mortality in patients with COVID-19. This study aims to investigate the association of DM and stress-induced hyperglycemia at intensive care unit (ICU) with mortality in this population., Methods: This is a retrospective study. Electronic medical records from patients admitted from March 2020 to September 2020 were reviewed. Primary outcome was mortality. Secondary outcomes were ICU and hospital mortality and stay, and need for mechanical ventilation and renal replacement therapy., Results: 187 patients were included. Overall mortality was 43.2%, higher in patients with DM (55.7% vs. 34%; p = 0.007), even after adjustment for age, hypertension, and disease severity. When patients were separated into groups, named normoglycemia (without DM and glycemia ≤140 mg/dL), stress-induced hyperglycemia (without DM and glycemia >140 mg/dL), and DM (previous diagnosis or HbA1c ≥ 6.5%), the mortality rate was 25.8%, 37.3%, and 55.7%, respectively (p = 0.021). Mortality was higher in patients with higher glycemic variability. No statistical difference related to secondary outcomes was observed., Conclusions: DM, hyperglycemia, and glycemic variability associated with increased mortality in critically ill patients with severe COVID-19, but did not increase the rates of other clinical outcomes. More than stress-induced hyperglycemia, DM was associated with mortality., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors. Published by Elsevier Ltd.)

Background: Previous studies have demonstrated a beneficial effect of early use of corticosteroids in patients with COVID-19. This study aimed to compare hospitalized patients with COVID-19 who received short-course corticosteroid treatment with those who received prolonged-course corticosteroid treatment to determine whether prolonged use of corticosteroids improves clinical outcomes, including mortality., Methods: This is a retrospective cohort study including adult patients with positive testing for Sars-CoV-2 hospitalized for more than 10 days. Data were obtained from electronic medical records. Patients were divided into two groups, according to the duration of treatment with corticosteroids: a short-course (10 days) and a prolonged-course (longer than 10 days) group. Inverse probability treatment weighting (IPTW) analysis was used to evaluate whether prolonged use of corticosteroids improved outcomes. The primary outcome was in-hospital mortality. Secondary outcomes were hospital infection and the association of different doses of corticosteroids with hospital mortality. Restricted cubic splines were used to assess the nonlinear association between mortality and dose and duration of corticosteroids use., Results: We enrolled 1,539 patients with COVID-19. Among them, 1127 received corticosteroids for more than 10 days (prolonged-course group). The in-hospital mortality was higher in patients that received prolonged course corticosteroids (39.5% vs. 26%, p < 0.001). The IPTW revealed that prolonged use of corticosteroids significantly increased mortality [relative risk (RR) = 1.52, 95% confidence interval (95% CI): 1.24-1.89]. In comparison to short course treatment, the cubic spline analysis showed an inverted U-shaped curve for mortality, with the highest risk associated with the prolonged use at 30 days (RR = 1.50, 95% CI 1.21-1.78)., Conclusions: Prolonged course of treatment with corticosteroids in hospitalized patients with COVID-19 was associated with higher mortality., (© 2023. The Author(s).)

Although advanced age, male sex, and some comorbidities impact the clinical course of COVID-19, these factors only partially explain the inter-individual variability in disease severity. Some studies have shown that genetic polymorphisms contribute to COVID-19 severity; however, the results are inconclusive. Thus, we investigated the association between polymorphisms in ACE1 , ACE2 , DPP9 , IFIH1 , IFNAR2 , IFNL4 , TLR3 , TMPRSS2 , and TYK2 and the clinical course of COVID-19. A total of 694 patients with COVID-19 were categorized as: (1) ward inpatients (moderate symptoms) or patients admitted at the intensive care unit (ICU; severe symptoms); and (2) survivors or non-survivors. In females, the rs1990760/ IFIH1 T/T genotype was associated with risk of ICU admission and death. Moreover, the rs1799752/ ACE1 Ins and rs12329760/ TMPRSS2 T alleles were associated with risk of ICU admission. In non-white patients, the rs2236757/ IFNAR2 A/A genotype was associated with risk of ICU admission, while the rs1799752/ ACE1 Ins/Ins genotype, rs2236757/ IFNAR2 A/A genotype, and rs12329760/ TMPRSS2 T allele were associated with risk of death. Moreover, some of the analyzed polymorphisms interact in the risk of worse COVID-19 outcomes. In conclusion, this study shows an association of rs1799752/ ACE1 , rs1990760/ IFIH1 , rs2236757/ IFNAR2 , rs12329760/ TMPRSS2 , and rs2304256/ TYK2 polymorphisms with worse COVID-19 outcomes, especially among female and non-white patients.

Since the global coronavirus disease 2019 (COVID-19) pandemic began, findings indicate that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) might induce autoimmune disorders. Thrombotic thrombocytopenic purpura (TTP) is a devastating disease if not emergently treated. It presents with severe thrombocytopenia, microangiopathic hemolytic anemia, and neurologic findings with or without renal insufficiency. The antibody-mediated reduced activity of the disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) induces the accumulation of ultrahigh-molecular-weight multimers of von Willebrand factor, leading to platelet aggregation and thrombosis. TTP can be an unusual presentation of COVID-19 disease mediated by the virus-induced immune response. We report a case of a healthy young patient presenting with the classic TTP pentad a few days after a diagnosis of COVID-19 confirmed by a positive SARS-CoV-2 RT-PCR test. The patient was initially treated with high-dose methylprednisolone and fresh frozen plasma until she was transferred to a tertiary care facility and plasma exchange was available. She evolved with a malignant ischemic vascular accident and was declared brain-dead 24 hours after the first plasma exchange section., Competing Interests: The authors declare that there are no conflicts of interest regarding the publication of this paper., (Copyright © 2022 Mariana Codevila Buere Pereira et al.)

Background: Critically ill patients have a higher incidence of pulmonary embolism (PE) than non-critically ill patients, yet no diagnostic algorithm has been validated in this population, leading to the overuse of pulmonary artery computed tomographic angiogram (CTA). This study aimed to comparatively evaluate the diagnostic accuracy of point-of-care ultrasound (POCUS) combined with laboratory data versus CTA in predicting PE in critically ill patients., Methods: A prospective diagnostic accuracy study. Critically ill patients with suspected acute PE undergoing CTA were prospectively enrolled. Demographic and clinical data were collected from electronic medical records. Blood samples were collected, and the Wells and revised Geneva scores were calculated. Standardized multiorgan POCUS and CTA were performed. The discriminatory power of multiorgan POCUS combined with biochemical markers was tested using ROC curves, and multivariate analysis was performed., Results: A total of 88 patients were included, and 37 (42%) had PE. Multivariate analysis showed a relative risk (RR) of PE of 2.79 (95% CI, 1.61-4.84) for the presence of right ventricular (RV) dysfunction, of 2.54 (95% CI, 0.89-7.20) for D-dimer levels >1000 ng/mL, and of 1.69 (95% CI, 1.12-2.63) for the absence of an alternative diagnosis to PE on lung POCUS or chest radiograph. The combination with the highest diagnostic accuracy for PE included the following variables: 1- POCUS transthoracic echocardiography with evidence of RV dysfunction; 2- lung POCUS or chest radiograph without an alternative diagnosis to PE; and 3- plasma D-dimer levels >1000 ng/mL. Combining these three findings resulted in an area under the curve of 0.85 (95% CI, 0.77-0.94), with 50% sensitivity and 96% specificity., Conclusions: Multiorgan POCUS combined with laboratory data has acceptable diagnostic accuracy for PE compared with CTA. The combined use of these methods might reduce CTA overuse in critically ill patients., Competing Interests: The authors have declared that no competing interests exist.

Aims: We hypothesized that critically ill patients with SARS-CoV-2 infection and insulin resistance would present a reduced Heat Shock Response (HSR), which is a pathway involved in proteostasis and anti-inflammation, subsequently leading to worse outcomes and higher inflammation. In this work we aimed: (i) to measure the concentration of extracellular HSP72 (eHSP72) in patients with severe COVID-19 and in comparison with noninfected patients; (ii) to compare the HSR between critically ill patients with COVID-19 (with and without diabetes); and (iii) to compare the HSR in these patients with noninfected individuals., Methods: Sixty critically ill adults with acute respiratory failure with SARS-CoV-2, with or without diabetes, were selected. Noninfected subjects were included for comparison (healthy, n = 19 and patients with diabetes, n = 22). Blood samples were collected to measure metabolism (glucose and HbA1c); oxidative stress (lypoperoxidation and carbonyls); cytokine profile (IL-10 and TNF); eHSP72; and the HSR (in vitro)., Results: Patients with severe COVID-19 presented higher plasma eHSP72 compared with healthy individuals and noninfected patients with diabetes. Despite the high level of plasma cytokines, no differences were found between critically ill patients with COVID-19 with or without diabetes. Critically ill patients, when compared to noninfected, presented a blunted HSR. Oxidative stress markers followed the same pattern. No differences in the HSR (extracellular/intracellular level) were found between critically ill patients, with or without diabetes., Conclusions: We demonstrated that patients with severe COVID-19 have elevated plasma eHSP72 and that their HSR is blunted, regardless of the presence of diabetes. These results might explain the uncontrolled inflammation and also provide insights on the increased risk in developing type 2 diabetes after SARS-CoV-2 infection.

Competing Interests: The authors declare no conflict of interest regarding this work.

Objectives: Copeptin, an equimolar indicator of serum antidiuretic hormone levels, has been associated with higher mortality in critically ill patients and with the development of diabetes in the general population. The aim of the present study was to investigate the association of copeptin levels with glycemic parameters in critically ill patients and to compare the time-course of copeptin in survivors and non-survivors., Design: Prospective cohort study., Patients: From June to October 2019, critically ill patients were prospectively enrolled and followed for 90 days., Measurements: Plasma copeptin levels were determined at intensive care unit (ICU) admission (copeptin T1), 24 h (copeptin T2), and 48 h (copeptin T3) after study entry. Blood glucose and glycated hemoglobin levels were measured. ICU, in-hospital, and 90-day mortality, and length of stay in the ICU and hospital were evaluated., Results: 104 patients were included. No significant correlation was detected between copeptin levels and blood glucose (r = -0.17, p = 0.09), HbA1c (r = 0.01, p = 0.9), glycemic gap (r = -0.16, p = 0.11), and stress hyperglycemia ratio (r = -0.14, p = 0.16). Copeptin T3 levels were significantly higher in survivors than in non-survivors at hospital discharge (561 [370-856] vs 300 [231-693] pg/mL, p = 0.015) and at 90 days (571 [380-884] vs 300 [232-698] pg/mL, p = 0.03)., Conclusions: No significant correlations were found between copeptin levels and glycemic parameters, suggesting that copeptin is not a relevant factor in the induction of hyperglycemia during critical illness. Copeptin levels at ICU day 3 were higher in survivors than in non-survivors., Competing Interests: The authors have declared that no competing interests exist.

Objective: To evaluate serum uteroglobin-related protein 1 expression early after smoke inhalation injuries and its association with the severity of inhalation injury in burned patients., Methods: Smoke or chemical inhalation injury is associated with morbidity and mortality. The consequences of inhalation result from an inflammatory response. Uteroglobin-related protein 1 is an anti-inflammatory protein and may improve lung inflammation. We hypothesized that uteroglobin-related protein 1 levels could reflect disease severity and predict outcome in patients with inhalation injury. Sixteen patients diagnosed with acute respiratory distress syndrome secondary to smoke inhalation injury were prospectively included in the study. Plasma was collected upon intensive care unit admission and within 24 hours of the inhalation injury. Bronchoscopies were carried out in all patients to assess the severity of inhalation injury within 72 hours. Uteroglobin-related protein 1 plasma levels were determined in duplicate with enzyme-linked immunosorbent assay., Results: The mean age was 23 ± 5 years, and the inhalation injury distribution was as follows: three of grade 1, four of grade 2, and nine of grade 3. The level of uteroglobin-related protein 1 was related to inhalation severity (grade 1: 0.389 ± 0.053 arbitrary units versus grade 2: 0.474 ± 0.0423 arbitrary units versus grade 3: 0.580 ± 0.094 arbitrary units; p = 0.007)., Conclusion: Plasma levels of uteroglobin-related protein 1 are associated with the degree of lung inhalation injury.

Objective: To contribute to updating the recommendations for brain-dead potential organ donor management., Methods: A group of 27 experts, including intensivists, transplant coordinators, transplant surgeons, and epidemiologists, answered questions related to the following topics were divided into mechanical ventilation, hemodynamics, endocrine-metabolic management, infection, body temperature, blood transfusion, and checklists use. The outcomes considered were cardiac arrests, number of organs removed or transplanted as well as function / survival of transplanted organs. The quality of evidence of the recommendations was assessed using the Grading of Recommendations Assessment, Development, and Evaluation system to classify the recommendations., Results: A total of 19 recommendations were drawn from the expert panel. Of these, 7 were classified as strong, 11 as weak and 1 was considered a good clinical practice., Conclusion: Despite the agreement among panel members on most recommendations, the grade of recommendation was mostly weak.

Objective: To contribute to updating the recommendations for brain-dead potential organ donor management., Method: A group of 27 experts, including intensivists, transplant coordinators, transplant surgeons, and epidemiologists, joined a task force formed by the General Coordination Office of the National Transplant System/Brazilian Ministry of Health (CGSNT-MS), the Brazilian Association of Intensive Care Medicine (AMIB), the Brazilian Association of Organ Transplantation (ABTO), and the Brazilian Research in Intensive Care Network (BRICNet). The questions were developed within the scope of the 2011 Brazilian Guidelines for Management of Adult Potential Multiple-Organ Deceased Donors. The topics were divided into mechanical ventilation, hemodynamic support, endocrine-metabolic management, infection, body temperature, blood transfusion, and use of checklists. The outcomes considered for decision-making were cardiac arrest, number of organs recovered or transplanted per donor, and graft function/survival. Rapid systematic reviews were conducted, and the quality of evidence of the recommendations was assessed using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system. Two expert panels were held in November 2016 and February 2017 to classify the recommendations. A systematic review update was performed in June 2020, and the recommendations were reviewed through a Delphi process with the panelists between June and July 2020., Results: A total of 19 recommendations were drawn from the expert panel. Of these, 7 were classified as strong (lung-protective ventilation strategy, vasopressors and combining arginine vasopressin to control blood pressure, antidiuretic hormones to control polyuria, serum potassium and magnesium control, and antibiotic use), 11 as weak (alveolar recruitment maneuvers, low-dose dopamine, low-dose corticosteroids, thyroid hormones, glycemic and serum sodium control, nutritional support, body temperature control or hypothermia, red blood cell transfusion, and goal-directed protocols), and 1 was considered a good clinical practice (volemic expansion)., Conclusion: Despite the agreement among panel members on most recommendations, the grade of recommendation was mostly weak. The observed lack of robust evidence on the topic highlights the importance of the present guideline to improve the management of brain-dead potential organ donors.

Carbonic anhydrase inhibitors, such as acetazolamide, are widely used in the treatment of open-angle glaucoma. Severe metabolic acidosis is a rare complication of acetazolamide use, and life-threatening acidosis occurs most commonly in elderly patients, in patients with advanced renal failure, and in patients with diabetes. We describe an unusual case of an elderly patient with diabetic nephropathy and chronic renal failure who presented to the emergency department with severe metabolic acidosis and coma after exposure to high doses of acetazolamide in the postoperative period of ophthalmic surgery. As symptoms of acetazolamide intoxication and uremia are similar, high suspicion is required to detect excessive plasma drug concentrations and intoxication in patients presenting with concomitant uremia. Clinical symptoms are potentially reversible with prompt diagnosis and treatment, including supportive treatment, bicarbonate therapy, and renal replacement therapy. Hemodialysis is particularly helpful in the management of acetazolamide overdose as the medication is dialyzable., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2020 Juliana Maria Kerber et al.)

The aim of the present study was to investigate the association of multiple glycemic parameters at intensive care unit (ICU) admission with outcomes in critically ill patients. Critically ill adults admitted to ICU were included prospectively in the study and followed for 180 days until hospital discharge or death. Patients were assessed for glycemic gap, hypoglycemia, hyperglycemia, glycemic variability, and stress hyperglycemia ratio (SHR). A total of 542 patients were enrolled (30% with preexisting diabetes). Patients with glycemic gap >80 mg/dL had increased need for renal replacement therapy (RRT; 37.7% vs. 23.7%, p = 0.025) and shock incidence (54.7% vs. 37.4%, p = 0.014). Hypoglycemia was associated with increased mortality (54.8% vs. 35.8%, p = 0.004), need for RRT (45.1% vs. 22.3%, p < 0.001), mechanical ventilation (MV; 72.6% vs. 57.5%, p = 0.024), and shock incidence (62.9% vs. 35.8%, p < 0.001). Hyperglycemia increased mortality (44.3% vs. 34.9%, p = 0.031). Glycemic variability >40 mg/dL was associated with increased need for RRT (28.3% vs. 14.4%, p = 0.002) and shock incidence (41.4% vs.31.2%, p = 0.039). In this mixed sample of critically ill subjects, including patients with and without preexisting diabetes, glycemic gap, glycemic variability, and SHR were associated with worse outcomes, but not with mortality. Hypoglycemia and hyperglycemia were independently associated with increased mortality.

Objective: To examine the association between donor plasma cytokine levels and the development of primary graft dysfunction of organs transplanted from deceased donors., Methods: Seventeen deceased donors and the respective 47 transplant recipients were prospectively included in the study. Recipients were divided into two groups: group 1, patients who developed primary graft dysfunction; and group 2, patients who did not develop primary graft dysfunction. Donor plasma levels of TNF, IL-6, IL-1β, and IFN-γ assessed by ELISA were compared between groups., Results: Sixty-nine organs were retrieved, and 48 transplants were performed. Donor plasma cytokine levels did not differ between groups (in pg/mL): TNF, group 1: 10.8 (4.3 - 30.8) versus group 2: 8.7 (4.1 - 33.1), p = 0.63; IL-6, group 1: 1617.8 (106.7 - 5361.7) versus group 2: 922.9 (161.7 - 5361.7), p = 0.56; IL-1β, group 1: 0.1 (0.1 - 126.1) versus group 2: 0.1 (0.1 - 243.6), p = 0.60; and IFN-γ, group 1: 0.03 (0.02 - 0.2) versus group 2: 0.03 (0.02 - 0.1), p = 0.93). Similar findings were obtained when kidney transplants were analyzed separately., Conclusion: In this sample of transplant recipients, deceased donor plasma cytokines TNF, IL-6, IL-1β, and IFN-γ were not associated with the development of primary graft dysfunction.

Brain death (BD) is associated with a systemic inflammation leading to worse graft outcomes. This study aimed to compare plasma cytokine values between brain-dead and critically ill patients, including septic and non-septic controls, and evaluate cytokine release kinetics in BD. Sixteen brain-dead and 32 control patients (16 with and 16 without sepsis) were included. Plasma cytokines were measured by magnetic bead assay after the first clinical exam consistent with BD and every 6 hours thereafter, and at the time of study entry in the control group. The values for IL-8 and IFN-γ were higher in brain-dead and septic patients than in non-septic patients [IL-8: 80.3 (18.7-169.6) vs. 68.2 (22.4-359.4) vs. 16.4 (9.2-42.7) pg/mL; P = 0.006; IFN-γ: 2.8 (1.6-6.1) vs. 3.4 (1.2-9.0) vs. 0.5 (0.5-1.8) pg/mL; P = 0.012]. TNF showed a clear tendency to increase in brain-dead patients [2.7 (1.0-4.8) vs. 1.0 (1.0-5.6) vs. 1.0 (1.0-1.0) pg/mL; P = 0.051], and IL-6 values were higher in brain-dead patients than in non-septic controls [174.5 (104.9-692.5) vs. 13.2 (7.3-38.6) pg/mL; P = 0.002]. These differences remained even after excluding brain-dead patients who also had sepsis ( n = 3). IL-1β and IL-10 values increased from baseline to time point 2 (∼6 hours later) [IL-1β: 5.39 (1.93-16.89) vs. 7.11 (1.93-29.13) pg/mL; P = 0.012; IL-10: 8.78 (3.62-16.49) vs. 15.73 (5.49-23.98) pg/mL; P = 0.009]. BD-induced and sepsis-induced plasma cytokine values were similarly high, and both were higher than the observed in non-septic critically ill patients.

Objectives: Imaging studies are expected to produce reliable information regarding the size and fat content of the pancreas. However, the available studies have produced inconclusive results. The aim of this study was to perform a systematic review and meta-analysis of imaging studies assessing pancreas size and fat content in patients with type 1 diabetes (T1DM) and type 2 diabetes (T2DM)., Methods: Medline and Embase databases were performed. Studies evaluating pancreatic size (diameter, area or volume) and/or fat content by ultrasound, computed tomography, or magnetic resonance imaging in patients with T1DM and/or T2DM as compared to healthy controls were selected. Seventeen studies including 3,403 subjects (284 T1DM patients, 1,139 T2DM patients, and 1,980 control subjects) were selected for meta-analyses. Pancreas diameter, area, volume, density, and fat percentage were evaluated., Results: Pancreatic volume was reduced in T1DM and T2DM vs. controls (T1DM vs. controls: -38.72 cm3, 95%CI: -52.25 to -25.19, I2 = 70.2%, p for heterogeneity = 0.018; and T2DM vs. controls: -12.18 cm3, 95%CI: -19.1 to -5.25, I2 = 79.3%, p for heterogeneity = 0.001). Fat content was higher in T2DM vs. controls (+2.73%, 95%CI 0.55 to 4.91, I2 = 82.0%, p for heterogeneity<0.001)., Conclusions: Individuals with T1DM and T2DM have reduced pancreas size in comparison with control subjects. Patients with T2DM have increased pancreatic fat content.

Pancreatic beta cell failure is the central event leading to diabetes. Beta cells share many phenotypic traits with neurons, and proper beta cell function relies on the activation of several neuron-like transcription programs. Regulation of gene expression by alternative splicing plays a pivotal role in brain, where it affects neuronal development, function, and disease. The role of alternative splicing in beta cells remains unclear, but recent data indicate that splicing alterations modulated by both inflammation and susceptibility genes for diabetes contribute to beta cell dysfunction and death. Here we used RNA sequencing to compare the expression of splicing-regulatory RNA-binding proteins in human islets, brain, and other human tissues, and we identified a cluster of splicing regulators that are expressed in both beta cells and brain. Four of them, namely Elavl4, Nova2, Rbox1, and Rbfox2, were selected for subsequent functional studies in insulin-producing rat INS-1E, human EndoC-βH1 cells, and in primary rat beta cells. Silencing of Elavl4 and Nova2 increased beta cell apoptosis, whereas silencing of Rbfox1 and Rbfox2 increased insulin content and secretion. Interestingly, Rbfox1 silencing modulates the splicing of the actin-remodeling protein gelsolin, increasing gelsolin expression and leading to faster glucose-induced actin depolymerization and increased insulin release. Taken together, these findings indicate that beta cells share common splicing regulators and programs with neurons. These splicing regulators play key roles in insulin release and beta cell survival, and their dysfunction may contribute to the loss of functional beta cell mass in diabetes., (© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.)

Cardiac arrest is a high mortality event and the associated brain ischemia frequently causes severe neurological damage and persistent vegetative state. Therapeutic hypothermia is an important tool for the treatment of post-anoxic coma after cardiopulmonary resuscitation. It has been shown to reduce mortality and to improve neurological outcomes after cardiac arrest. Nevertheless, hypothermia is underused in critical care units. This manuscript aims to review the hypothermia mechanism of action in cardiac arrest survivors and to propose a simple protocol, feasible to be implemented in any critical care unit.

Background and Objectives: Organ transplantation has long been considered the treatment of choice for many end-stage organ diseases. As soon as transplantation turned to be a viable therapy, organ shortage became the major limitation for the procedures. Nowadays, there is an increasing imbalance between organ supply and demand. Apparently, the most promising way to increase organ supply is optimizing the care for the brain death organ donor. The objective of this manuscript was to review the pathophysiological aspects and therapeutic strategies for the optimized care of the potential organ donor., Contents: Brain death causes a massive catecholamine release, inducing a variety of deleterious effects that can threat organ perfusion. Studies have documented a sudden decrease in cortisol, insulin, thyroid and pituitary hormones. In this scenario of hemodynamic and metabolic instability, a special attention to the multiple organ donor support is required., Conclusions: An extensive knowledge of the complex brain death pathophysiology is extremely important for the implementation of rational aggressive management protocols of the potential organ donor, aiming to increase the number of harvested organs and the number of organs harvested per donor.

Background and Objectives: Since organ transplantation has become the treatment of choice for several end-stage diseases, organ shortage is the most important barrier for the procedures and waiting lists are increasing out of proportion. The objective of this study was to review the best practices concerning family referral and how these issues and others aspects of the donation process can influence consent rates., Contents: Despite the growing number of live donors, the brain death donor continuous to be the major source of organs for transplantation and the only source of extra-renal organs. Many problems have been identified in the donation process, including non-identification of the brain death donor, inadequate care of the donors and family refusal to donation. Increasing the consent rate for donation seems to be a good alternative to reduce organ shortage., Conclusions: Family decision to donate organs is influenced by several aspects. Highly trained professionals in family referral can affect consent rates.

Background and Objectives: Cardiac arrest is a state of severe cerebral perfusion deficit. Patients recovering from a cardiopulmonary resuscitation are at great risk of subsequent death or incapacitating neurologic injury, including persistent vegetative state. The early definition of prognosis for these patients has ethical and economic implications. The main purpose of this manuscript was to review the prognostic value of serum Neuron-Specific Enolase (NSE) in predicting outcomes in patients early after a cardiac arrest., Contents: Severe neurologic disability is the most feared complication after a cardiac arrest. Many studies are trying to find prognostic markers that can be associated with outcomes in patients surviving a cardiac arrest. Biochemical markers of neuronal injury seem to be promising in this scenario. Therefore, NSE levels have been studied in patients after a cardiac arrest and high enzyme levels suggest more extensive brain damage and are associated with unfavorable clinical outcomes., Conclusions: Outcome after a cardiac arrest is mostly determined by the degree of hypoxic brain damage and early determinations of serum NSE level can be a valuable ancillary method for assessing outcome in these patients.

Introduction: Outcome after cardiac arrest is mostly determined by the degree of hypoxic brain damage. Patients recovering from cardiopulmonary resuscitation are at great risk of subsequent death or severe neurological damage, including persistent vegetative state. The early definition of prognosis for these patients has ethical and economic implications. The main purpose of this study was to investigate the prognostic value of serum neuron-specific enolase (NSE) in predicting outcomes in patients early after in-hospital cardiac arrest., Methods: Forty-five patients resuscitated from in-hospital cardiac arrest were prospectively studied from June 2003 to January 2005. Blood samples were collected, at any time between 12 and 36 hours after the arrest, for NSE measurement. Outcome was evaluated 6 months later with the Glasgow outcome scale (GOS). Patients were divided into two groups: group 1 (unfavorable outcome) included GOS 1 and 2 patients; group 2 (favorable outcome) included GOS 3, 4 and 5 patients. The Mann-Whitney U test, Student's t test and Fisher's exact test were used to compare the groups., Results: The Glasgow coma scale scores were 6.1 +/- 3 in group 1 and 12.1 +/- 3 in group 2 (means +/- SD; p < 0.001). The mean time to NSE sampling was 20.2 +/- 8.3 hours in group 1 and 28.4 +/- 8.7 hours in group 2 (p = 0.013). Two patients were excluded from the analysis because of sample hemolysis. At 6 months, favorable outcome was observed in nine patients (19.6%). Thirty patients (69.8%) died and four (9.3%) remained in a persistent vegetative state. The 34 patients (81.4%) in group 1 had significantly higher NSE levels (median 44.24 ng/ml, range 8.1 to 370) than those in group 2 (25.26 ng/ml, range 9.28 to 55.41; p = 0.034)., Conclusion: Early determination of serum NSE levels is a valuable ancillary method for assessing outcome after in-hospital cardiac arrest.