Nonpreferential but Detrimental Accumulation of Macrophages With Clonal Hematopoiesis-Driver Mutations in Cardiovascular Tissues-Brief Report.

BACKGROUND: Clonal hematopoiesis of indeterminate potential (CHIP) is an acquired genetic risk factor for both leukemia and cardiovascular disease. It results in proinflammatory myeloid cells in the bone marrow and blood; however, how these cells behave in the cardiovascular tissue remains unclear. Our study aimed at investigating whether CHIP-mutated macrophages accumulate preferentially in cardiovascular tissues and examining the transcriptome of tissue macrophages from DNMT3A (DNA methyltransferase 3 alpha) or TET2 (Tet methylcytosine dioxygenase 2) mutation carriers. METHODS: We recruited patients undergoing carotid endarterectomy or heart surgeries to screen for CHIP mutation carriers using targeted genomic sequencing. Myeloid and lymphoid cells were isolated from blood and cardiovascular tissue collected during surgeries using flow cytometry. DNA and RNA extracted from these sorted cells were subjected to variant allele frequency measurement using droplet digital polymerase chain reaction and transcriptomic profiling using bulk RNA sequencing, respectively. RESULTS: Using droplet digital polymerase chain reaction, we detected similar variant allele frequency of CHIP in monocytes from blood and macrophages from atheromas and heart tissues, even among heart macrophages with and without CCR2 (C-C motif chemokine receptor 2) expression. Bulk RNA sequencing revealed a proinflammatory gene profile of myeloid cells from DNMT3A or TET2 mutation carriers compared with those from noncarriers. CONCLUSIONS: Quantitatively, CHIP-mutated myeloid cells did not preferentially accumulate in cardiovascular tissues, but qualitatively, they expressed a more disease-prone phenotype.

Liver metastases of colorectal adenocarcinoma with intrahepatic biliary spread pattern: clinical manifestation and importance of immunohistochemical analysis.

Liver metastases of colorectal carcinoma (LMCC) with macroscopic intrabiliary ductal involvement are a rare entity that can clinically and radiologically mimic a cholangiocarcinoma. However, a thorough anatomopathologic and immunohistochemical study of biliary ductal involvement is required because of its distinctive clinical features and relatively indolent biological behavior, reflecting a better prognosis and long-term survival. We present the case of a patient who debuted with LMCC with intrahepatic biliary ductal involvement, whose definitive diagnosis was established by immunohistochemical analysis, showing a characteristic CK7 - /CK20 + pattern.

A comparative gene expression matrix in Apoe-deficient mice identifies unique and atherosclerotic disease stage-specific gene regulation patterns in monocytes and macrophages.

BACKGROUND AND AIMS: Atherosclerosis is a systemic and chronic inflammatory disease propagated by monocytes and macrophages. Yet, our knowledge on how transcriptome of these cells evolves in time and space is limited. We aimed at characterizing gene expression changes in site-specific macrophages and in circulating monocytes during the course of atherosclerosis. METHODS: We utilized apolipoprotein E-deficient mice undergoing one- and six-month high cholesterol diet to model early and advanced atherosclerosis. Aortic macrophages, peritoneal macrophages, and circulating monocytes from each mouse were subjected to bulk RNA-sequencing (RNA-seq). We constructed a comparative directory that profiles lesion- and disease stage-specific transcriptomic regulation of the three cell types in atherosclerosis. Lastly, the regulation of one gene, Gpnmb, whose expression positively correlated with atheroma growth, was validated using single-cell RNA-seq (scRNA-seq) of atheroma plaque from murine and human. RESULTS: The convergence of gene regulation between the three investigated cell types was surprisingly low. Overall 3245 differentially expressed genes were involved in the biological modulation of aortic macrophages, among which less than 1% were commonly regulated by the remote monocytes/macrophages. Aortic macrophages regulated gene expression most actively during atheroma initiation. Through complementary interrogation of murine and human scRNA-seq datasets, we showcased the practicality of our directory, using the selected gene, Gpnmb, whose expression in aortic macrophages, and a subset of foamy macrophages in particular, strongly correlated with disease advancement during atherosclerosis initiation and progression. CONCLUSIONS: Our study provides a unique toolset to explore gene regulation of macrophage-related biological processes in and outside the atheromatous plaque at early and advanced disease stages.

Two stage hepatectomy (TSH) versus ALPPS for initially unresectable colorectal liver metastases: A systematic review and meta-analysis.

BACKGROUND: Although numerous comparisons between conventional Two Stage Hepatectomy (TSH) and Associating Liver Partition and Portal Vein Ligation for staged hepatectomy (ALPPS) have been reported, the heterogeneity of malignancies previously compared represents an important source of selection bias. This systematic review and meta-analysis aimed to compare perioperative and oncological outcomes between TSH and ALPPS to treat patients with initially unresectable colorectal liver metastases (CRLM). METHODS: Main electronic databases were searched using medical subject headings for CRLM surgically treated with TSH or ALPPS. Patients treated for primary or secondary liver malignancies other than CRLM were excluded. RESULTS: A total of 335 patients from 5 studies were included. Postoperative major complications were higher in the ALPPS group (relative risk [RR] 1.46, 95% confidence interval [CI] 1.04-2.06, I2 = 0%), while no differences were observed in terms of perioperative mortality (RR 1.53, 95% CI 0.64-3.62, I2 = 0%). ALPPS was associated with higher completion of hepatectomy rates (RR 1.32, 95% CI 1.09-1.61, I2 = 85%), as well as R0 resection rates (RR 1.61, 95% CI 1.13-2.30, I2 = 40%). Nevertheless, no significant differences were achieved between groups in terms of overall survival (OS) (RR 0.93, 95% CI 0.68-1.27, I2 = 52%) and disease-free survival (DFS) (RR 1.08, 95% CI 0.47-2.49, I2 = 54%), respectively. CONCLUSION: ALPPS and TSH to treat CRLM seem to have comparable operative risks in terms of mortality rates. No definitive conclusions regarding OS and DFS can be drawn from the results.

Outcomes of Enhanced Recovery After Surgery Protocols Versus Conventional Management in Patients Undergoing Bariatric Surgery.

Background: Enhanced recovery after surgery (ERAS) pathways focus on decreasing surgical stress and promoting return to normal function for patients undergoing surgical procedures. The aim of our study was to evaluate the impact of an ERAS protocol on outcomes of patients undergoing primary sleeve gastrectomy and Roux-en-Y gastric bypass. Outcomes included hospital length of stay (LOS), and management of postoperative pain and postoperative nausea and vomiting (PONV) measured by pain medications and antiemetic use, respectively. Incidence of 90-day emergency department (ED) visits, readmissions, and complications were also analyzed. Methods: A retrospective review was performed from October 1, 2016 to October 31, 2018 of patients enrolled in the ERAS versus the conventional pathway. Patient baseline characteristics, pain and nausea scores, LOS, and postoperative outcome variables were collected. Results: Non-ERAS (n = 193) and ERAS (n = 173) groups had similar patient characteristics. Fewer ERAS patients required postoperative opioids and antiemetics (P < .01), with a significant difference in postoperative nausea control in favor of ERAS patients (P < .05). There was a decreasing trend in median LOS (2 versus 1, P = .28), 90-day postoperative readmissions (10.4% versus 8.1%, P = .47), and major adverse events (5.2% versus 1.7%, P = .07) after ERAS implementation. The ED visits and postoperative need for intravenous fluid for dehydration were significantly lower in the ERAS group (P = .01). Conclusion: Implementation of ERAS pathway for bariatric surgery was associated with less opioid usage, PONV, ED visits, and postoperative need for intravenous fluids, without increasing LOS, 90-day readmission or rates of adverse effects.

Chronic exposure to polluted urban air aggravates myocardial infarction by impaired cardiac mitochondrial function and dynamics.

Air pollution exposure positively correlates with increased cardiovascular morbidity and mortality rates, mainly due to myocardial infarction (MI). Herein, we aimed to study the metabolic mechanisms underlying this association, focusing on the evaluation of cardiac mitochondrial function and dynamics, together with its impact over MI progression. An initial time course study was performed in BALB/c mice breathing filtered air (FA) or urban air (UA) in whole-body exposure chambers located in Buenos Aires City downtown for up to 16 weeks (n = 8 per group and time point). After 12 weeks, lung inflammatory cell recruitment was evident in UA-exposed mice. Interestingly, impaired redox metabolism, characterized by decreased lung SOD activity and increased GSSG levels and NOX activity, precede local inflammation in this group. At this selected time point, additional mice were exposed to FA or UA (n = 12 per group) and alveolar macrophage PM uptake and nitric oxide (NO) production was observed in UA-exposed mice, together with increased pro-inflammatory cytokine levels (TNF-α and IL-6) in BAL and plasma. Consequently, impaired heart tissue oxygen metabolism and altered mitochondrial ultrastructure and function were observed in UA-exposed mice after 12 weeks, characterized by decreased active state respiration and ATP production rates, and enhanced mitochondrial H2O2 production. Moreover, disturbed cardiac mitochondrial dynamics was detected in this group. This scenario led to a significant increase in the area of infarcted tissue following myocardial ischemia reperfusion injury in vivo, from 43 ± 3% of the area at risk in mice breathing FA to 66 ± 4% in UA-exposed mice (n = 6 per group, p < 0.01), together with a sustained increase in LVEDP during myocardial reperfusion. Taken together, our data unravel cardiac mitochondrial mechanisms that contribute to the understanding of the adverse health effects of urban air pollution exposure, and ultimately highlight the importance of considering environmental factors in the development of cardiovascular diseases.

Oxidative metabolism in the cardiorespiratory system after an acute exposure to nickel-doped nanoparticles in mice.

There is an increasing concern over the harmful effects that metallic nanoparticles (NP) may produce on human health. Due to their redox properties, nickel (Ni) and Ni-containing NP are particularly relevant. Hence, the aim of this study was to establish the toxicological mechanisms in the cardiorespiratory oxidative metabolism initiated by an acute exposure to Ni-doped-NP. Mice were intranasally instilled with silica NP containing Ni (II) (Ni-NP) (1 mg Ni (II)/kg body weight) or empty NP as control, and 1 h after exposure lung, plasma, and heart samples were obtained to assess the redox metabolism. Results showed that, NP were mainly retained in the lungs triggering a significantly increased tissue O2 consumption rate, leading to Ni-NP-increased reactive oxygen species production by NOX activity, and mitochondrial H2O2 production rate. In addition, an oxidant redox status due to an altered antioxidant system showed by lung GSH/GSSG ratio decreased, and SOD activity increased, resulting in an increased phospholipid oxidation. Activation of circulating polymorphonuclear leukocytes, along with GSH/GSSG ratio decreased, and phospholipid oxidation were found in the Ni-NP-group plasma samples. Consequently, in distant organs such as heart, Ni-NP inhalation alters the tissue redox status. Our results showed that the O2 metabolism analysis is a critical area of study following Ni-NP inhalation. Therefore, this work provides novel data linking the redox metabolisms alterations elicited by exposure to Ni (II) adsorbed to NP and cardiorespiratory toxicity.

Prognostic models for stage I-III esophageal cancer: a comparison between existing calculators.

BACKGROUND: Determining the best approach for esophageal cancer and predicting accurate prognosis are critical. Multiple studies evaluated characteristics associated with overall survival, and several prediction models have been developed. This study aimed to evaluate existing models and perform external validation of selected models. METHODS: A retrospective investigation of a multi-site institutional enterprise for patients with a diagnosis of esophageal cancer between 2013-2014 was performed. Selected survival prediction models included the Roswell Park Comprehensive Cancer Center (RPCCC) calculator, Oregon Health & Science University (OHSU) calculator, and two nomograms published by Shapiro et al. and Sun et al. One-year overall survival, level of agreement, and performance for each model were evaluated. RESULTS: A total of 104 patients were included and used to assess the prediction models. One-year overall survival was 0.76. Different calculators tended to rank patients similarly; however, they did not agree on predicted overall survival. The least disparity in correlation was observed between OHSU and Shapiro calculators. Shapiro's model achieved the highest performance [area under the curve (AUC) =0.63]. CONCLUSIONS: Selected models showed fair results in estimating individual overall survival, although none achieved a high performance. While these tools may support the decision-making process for esophageal cancer patients, their implementation in clinical practice requires improved refinement to optimize their clinical utility.

CaMKII activation in early diabetic hearts induces altered sarcoplasmic reticulum-mitochondria signaling.

Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca2+ leak and arrhythmias due to increased activity of the Ca2+/calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondrial structure, and mitochondrial metabolisms. To address this knowledge gap we measured SR-mitochondrial proximity, intracellular Ca2+, and mitochondrial metabolism in wild type (WT) and AC3-I transgenic mice, with myocardial-targeted CaMKII inhibition, fed with control diet (CD) or with FRD. Confocal images showed significantly increased spontaneous Ca2+ release events in FRD vs. CD WT cardiomyocytes. [3H]-Ryanodine binding assay revealed higher [3H]Ry binding in FRD than CD WT hearts. O2 consumption at State 4 and hydrogen peroxide (H2O2) production rate were increased, while respiratory control rate (RCR) and Ca2+ retention capacity (CRC) were decreased in FRD vs. CD WT isolated mitochondria. Transmission Electron Microscopy (TEM) images showed increased proximity at the SR-mitochondria microdomains, associated with increased tethering proteins, Mfn2, Grp75, and VDAC in FRD vs. CD WT. Mitochondria diameter was decrease and roundness and density were increased in FRD vs. CD WT specimens. The fission protein, Drp1 was significantly increased while the fusion protein, Opa1 was unchanged in FRD vs. CD WT hearts. These differences were prevented in AC3-I mice. We conclude that SR-mitochondria microdomains are subject to CaMKII-dependent remodeling, involving SR-Ca2+ leak and mitochondria fission, in prediabetic mice induced by FRD. We speculate that CaMKII hyperactivity induces SR-Ca2+ leak by RyR2 activation which in turn increases mitochondria Ca2+ content due to the enhanced SR-mitochondria tethering, decreasing CRC.

Complete Mesocolic Excision and D3 Lymphadenectomy versus Conventional Colectomy for Colon Cancer: A Systematic Review and Meta-Analysis.

BACKGROUNDS: Previous systematic reviews suggest that the implementation of 'complete mesocolon excision' (CME) for colon tumors entails better specimen quality but with limited long-term outcomes. We performed a meta-analysis to compare the pathological, perioperative, and oncological results of CME with conventional surgery (CS) in primary colon cancer. METHODS: Embase, MEDLINE and CENTRAL databases were searched using Medical Subject Headings for CME and D3 lymphadenectomy. The systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. RESULTS: A total of 18,989 patients from 27 studies were included. Postoperative complications were higher in the CME group (relative risk [RR] 1.13, 95% confidence interval [CI] 1.04-1.22, I2 = 0%), while no differences were observed in terms of anastomotic leak (I2 = 0%) or perioperative mortality (I2 = 49%). CME was associated with a higher number of lymph nodes harvested (I2 = 95%), distance to high tie (I2 = 65%), bowel length (I2 = 0%), and mesentery area (I2 = 95%). CME also had positive effects on 3- and 5-year overall survival (RR 1.09, 95% CI 1.04-1.15, I2 = 88%; and RR 1.05, 95% CI 1.02-1.08, I2 = 62%, respectively) and 3-year disease-free survival (RR 1.10, 95% CI 1.04-1.17, I2 = 22%), as well as decreased local (RR 0.35, 95% CI 0.24-0.51, I2 = 51%) and distant recurrences (RR 0.71, 95% CI 0.60-0.85, I2 = 34%). CONCLUSIONS: Limited evidence suggests that CME improves oncological outcomes with a higher postoperative adverse events rate but no increase in anastomotic leak rate or perioperative mortality, compared with CS.

Energy management and mitochondrial dynamics in cerebral cortex during endotoxemia.

Mitochondria play an essential role in inflammatory processes such as sepsis or endotoxemia, contributing to organ-cellular redox metabolism, emerging as the energy hub of the cell, and as an important center of action of second messengers. In this work, we aimed to elucidate the energy state, redox balance, and mitochondrial remodeling status in cerebral cortex in an experimental model of endotoxemia. Female Sprague-Dawley rats were subjected to a single dose of LPS (ip 8 mg kg-1 body weight) for 6 h. State 3 O2 consumption was observed increased, ATP production and P/O ratio were observed decreased, probably indicating an inefficient oxidative phosphorylation process. O2- production and both systemic and tissue NO markers were observed increased in treated animals. The existence of nitrated proteins suggests an alteration in the local redox balance and possible harmful effects over energetic processes. Increases in PGC-1α and mtTFA expression, and in OPA-1 expression, suggest an increase in de novo formation of mitochondria and fusion of pre-existing mitochondria. The observed elongation of mitochondria correlates with the occurrence of mild mitochondrial dysfunction and increased levels of systemic NO. Our work presents novel results that contribute to unravel the mechanism by which the triad endotoxemia-redox homeostasis-energy management interact in the cerebral cortex, leading to propose a relevant mechanism for future developing therapeutics with the aim of preserving this organ from inflammatory and oxidative damage.

Mitochondrial Dynamics and VMP1-Related Selective Mitophagy in Experimental Acute Pancreatitis.

Mitophagy and zymophagy are selective autophagy pathways early induced in acute pancreatitis that may explain the mild, auto limited, and more frequent clinical presentation of this disease. Adequate mitochondrial bioenergetics is necessary for cellular restoration mechanisms that are triggered during the mild disease. However, mitochondria and zymogen contents are direct targets of damage in acute pancreatitis. Cellular survival depends on the recovering possibility of mitochondrial function and efficient clearance of damaged mitochondria. This work aimed to analyze mitochondrial dynamics and function during selective autophagy in pancreatic acinar cells during mild experimental pancreatitis in rats. Also, using a cell model under the hyperstimulation of the G-coupled receptor for CCK (CCK-R), we aimed to investigate the mechanisms involved in these processes in the context of zymophagy. We found that during acute pancreatitis, mitochondrial O2 consumption and ATP production significantly decreased early after induction of acute pancreatitis, with a consequent decrease in the ATP/O ratio. Mitochondrial dysfunction was accompanied by changes in mitochondrial dynamics evidenced by optic atrophy 1 (OPA-1) and dynamin-related protein 1 (DRP-1) differential expression and ultrastructural features of mitochondrial fission, mitochondrial elongation, and mitophagy during the acute phase of experimental mild pancreatitis in rats. Mitophagy was also evaluated by confocal assay after transfection with the pMITO-RFP-GFP plasmid that specifically labels autophagic degradation of mitochondria and the expression and redistribution of the ubiquitin ligase Parkin1. Moreover, we report for the first time that vacuole membrane protein-1 (VMP1) is involved and required in the mitophagy process during acute pancreatitis, observable not only by repositioning around specific mitochondrial populations, but also by detection of mitochondria in autophagosomes specifically isolated with anti-VMP1 antibodies as well. Also, VMP1 downregulation avoided mitochondrial degradation confirming that VMP1 expression is required for mitophagy during acute pancreatitis. In conclusion, we identified a novel DRP1-Parkin1-VMP1 selective autophagy pathway, which mediates the selective degradation of damaged mitochondria by mitophagy in acute pancreatitis. The understanding of the molecular mechanisms involved to restore mitochondrial function, such as mitochondrial dynamics and mitophagy, could be relevant in the development of novel therapeutic strategies in acute pancreatitis.

Urban air pollution induces alterations in redox metabolism and mitochondrial dysfunction in mice brain cortex.

Previous reports indicate that the central nervous system (CNS) is a target of air pollution, causing tissue damage and functional alterations. Oxidative stress and neuroinflammation have been pointed out as possible mechanisms mediating these effects. The aim of this work was to study the chronic effects of urban air pollution on mice brain cortex, focusing on oxidative stress markers, and mitochondrial function. Male 8-week-old BALB/c mice were exposed to filtered air (FA, control) or urban air (UA) inside whole-body exposure chambers, located in a highly polluted area of Buenos Aires city, for up to 4 weeks. Glutathione levels, assessed as GSH/GSSG ratio, were decreased after 1 and 2 weeks of exposure to UA (45% and 25% respectively vs. FA; p < 0.05). A 38% increase in lipid peroxidation was found after 1 week of UA exposure (p < 0.05). Regarding protein oxidation, carbonyl content was significantly increased at week 2 in UA-exposed mice, compared to FA-group, and an even higher increment was found after 4 weeks of exposure (week 2: 40% p < 0.05, week 4: 54% p < 0.001). NADPH oxidase (NOX) and glutathione peroxidase (GPx) activities were augmented at all the studied time points, while superoxide dismutase (Cu,Zn-SOD cytosolic isoform) and glutathione reductase (GR) activities were increased only after 4 weeks of UA exposure (p < 0.05). The increased NOX activity was accompanied with higher expression levels of NOX2 regulatory subunit p47phox, and NOX4 (p < 0.05). Also, UA mice showed impaired mitochondrial function due to a 50% reduction in O2 consumption in active state respiration (p < 0.05), a 29% decrease in mitochondrial inner membrane potential (p < 0.05), a 65% decrease in ATP production rate (p < 0.01) and a 30% increase in H2O2 production (p < 0.01). Moreover, respiratory complexes I-III and II-III activities were decreased in UA group (30% and 36% respectively vs. FA; p < 0.05). UA exposed mice showed alterations in mitochondrial function, increased oxidant production evidenced by NOX activation, macromolecules damage and the onset of the enzymatic antioxidant system. These data indicate that oxidative stress and impaired mitochondrial function may play a key role in CNS damage mechanisms triggered by air pollution.

Alterations in oxygen metabolism are associated to lung toxicity triggered by silver nanoparticles exposure.

Along with the AgNP applications development, the concern about their possible toxicity has increasingly gained attention. As the respiratory system is one of the main exposure routes, the aim of this study was to evaluate the harmful effects developed in the lung after an acute AgNP exposure. In vivo studies using Balb/c mice intranasally instilled with 0.1 mg AgNP/kg b.w, were performed. 99mTc-AgNP showed the lung as the main organ of deposition, where, in turn, AgNP may exert barrier injury observed by increased protein content and total cell count in BAL samples. In vivo acute exposure showed altered lung tissue O2 consumption due to increased mitochondrial active respiration and NOX activity. Both O2 consumption processes release ROS triggering the antioxidant system as observed by the increased SOD, catalase and GPx activities and a decreased GSH/GSSG ratio. In addition, increased protein oxidation was observed after AgNP exposure. In A549 cells, exposure to 2.5 µg/mL AgNP during 1 h resulted in augment NOX activity, decreased mitochondrial ATP associated respiration and higher H2O2 production rate. Lung 3D tissue model showed AgNP-initiated barrier alterations as TEER values decreased and morphological alterations. Taken together, these results show that AgNP exposure alters O2 metabolism leading to alterations in oxygen metabolism lung toxicity. AgNP-triggered oxidative damage may be responsible for the impaired lung function observed due to alveolar epithelial injury.

Prognostic Significance of Complete Pathologic Response Obtained with Chemotherapy Versus Chemoradiotherapy in Gastric Cancer.

BACKGROUND: Few studies have compared the survival advantage of complete pathologic response (cPR) achieved through neoadjuvant chemotherapy (nCT) versus neoadjuvant chemoradiotherapy (nCRT) in gastric adenocarcinoma. Our study utilizes a large national cancer database to address this question. PATIENTS AND METHODS: This is a retrospective review of patients with clinical stage I to III gastric adenocarcinoma from 2004 to 2013 who received nCT or nCRT. Patients who achieved cPR were selected. Associations were evaluated using Mann-Whitney U and Fisher's exact tests. Survival information was summarized using standard Kaplan-Meier methods, where estimates of the median and 5-year survival rates were estimated with 95% confidence intervals. RESULTS: A total of 413 patients who had cPR were identified. Eighty-four patients received nCT and 329 patients received nCRT. Patients in the nCRT group had higher clinical stage (88.4% vs. 75.0%) and more proximal location of tumors (95.4% vs. 45.2%). The nCT group (n = 84) had a 94% 5-year survival rate, while the nCRT group's (n = 329) rate was 60% (p < 0.001). On Cox regression modeling using a propensity-weighted approach, nCT treatment was an independent predictor of improved overall survival (nCRT vs. nCT; HR 10.44, p < 0.001). CONCLUSIONS: The use of nCT leads to a significant increase in overall survival in patients when compared with nCRT for those who achieved cPR in gastric adenocarcinoma. While this study is limited in identifying the cause for this difference in overall survival, this important finding nonetheless requires further investigation and should be considered in the development of future gastric cancer trials.

Linfografía como opción diagnóstica y terapéutica en la fuga quilosa posoperatoria de cáncer colorrectal.

La fuga quilosa es una complicación muy poco frecuente tras la cirugía colorrectal. Se presenta el caso de un paciente de 70 años con neoplasia de recto medio intervenido de forma electiva tras un ciclo largo de neoadyuvancia mediante una resección anterior de recto por laparoscopia. El cuarto día de posoperatorio presentó un drenaje pélvico de aspecto quiloso y el día 13 se confirmó la fuga quilosa en la linfografía. Posteriormente el débito se redujo de forma rápida. La linfografía no solo es un método diagnóstico, sino que en el 35-70% de los casos puede también ser terapéutica.Chylous leakage is an extremely rare complication after colorectal surgery. We report the case of a 70 year-old male with a mid-rectal cancer who underwent a laparoscopic anterior resection of the rectum after long course neoadjuvant therapy. On postoperative day 4 the patient presented with chylous pelvic drainage, and a chylous leakage was proved by lymphography on postoperative day 13. Hereinafter, the drainage was drastically reduced. The lymphography is not only a diagnostic technique, but it can be also a therapeutic method in up to 35-70% of the cases.

Prospective Analysis Regarding Health-Related Quality of Life (HR-QOL) between Morbid Obese Patients Following Bariatric Surgery Versus on a Waiting List.

BACKGROUND: Major impairment of health-related quality of life (HRQoL) is one of the main reasons why obese patients request surgical treatment. OBJECTIVE: To prospectively analyze the impact of HRQoL between obese patients who underwent surgery and those who were wait-listed. METHODS: Between April 2017 and March 2018, 70 surgical and 69 wait-listed patients were interviewed twice, at baseline and at the 12-month follow-up. Quality of life was measured by the SF-12v2 and the Impact of Weight on Quality of Life-Lite (IWQoL-Lite) questionnaires. Sociodemographic-, clinical-, and surgical-related variables were collected. RESULTS: One hundred thirty-nine patients were analyzed, showing similar baseline characteristics but differences in HRQoL. Performing more qualified work improved scores on some aspects of the SF-12 survey. In contrast, women scored worse on the self-esteem domain, and men scored worse on the mental health domain. By group, at the 12-month follow-up, statistically significant differences were found among all aspects of the questionnaires between both groups (P < 0.001) and between baseline and postoperative 12-month follow-up in the surgical group (P < 0.001). Furthermore, scores were lower in all domains in the evolution of wait-listed patients, with statistically significant differences among the Bodily Pain, Emotional Role, Mental Health, and Mental Component Summary Domains (P < 0.05). CONCLUSION: HRQoL is a multimodal concept that allows the identification of factors impacting obese patients' quality of life. It promotes the benefit of surgery against waiting list delays, which can take up to 4 years in our hospital. Therefore, HRQoL is an important pillar to justify more resources for reducing unacceptable surgical delays.