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Introduction: Bariatric/metabolic surgery (BMS) is the most effective treatment of morbid obesity, while Enhanced Recovery After Surgery (ERAS) after BMS represents a multimodal perioperative protocol designed to achieve early recovery for patients with peculiar characteristics. The aim of the current narrative review is to summarize and discuss the current role, the application, and the future developments of ERAS protocols in the field of BMS. Methods: A literature search for studies published up to June 30, 2022, with no restrictions on language or publication period, was performed on Medline and Embase, using the keywords "ERAS" OR "enhanced recovery after surgery" AND "bariatric surgery" OR "metabolic surgery". Postoperative length of hospital stay LOS, overall and major morbidity and mortality, readmission rates, postoperative nausea or vomit PONV, opioids and antiemetics use, hospital costs, ERAS in specific health care settings, barriers to ERAS and further developments were analyzed. Results/Conclusions: The results were presented with a narrative review, using tabulation to summarize the results of meta-analyses and RCTs: 6 articles reporting guidelines, 5 metaanalyses, 9 randomized controlled trials, and 48 observational studies. ERAS protocols are feasible and safe in the setting of BMS, and associated to reduced LOS, PONV and postoperative pain, reduced opioid and antiemetic use and reduced costs. Postoperative mortality and readmission rates are similar between patients receiving standard care and those with ERAS protocols. Furthermore, increase of ERAS application may be useful in health care systems dealing with epidemic infectious diseases and implemented by technological advancements.
Assuntos
Cirurgia Bariátrica , Obesidade Mórbida , Humanos , Náusea e Vômito Pós-Operatórios , Resultado do Tratamento , Cirurgia Bariátrica/métodos , Obesidade Mórbida/cirurgia , Tempo de Internação , Complicações Pós-OperatóriasRESUMO
Background: Adipose tissue (AT) wasting in cancer is an early catabolic event with negative impact on outcomes. Circulating miRNAs may promote body weight loss and cachexia. We measured circulating miRNAs linked to AT alterations and compared their levels between i) gastrointestinal (GI) cancer patients and controls, ii) cachectic and non-cachectic cancer patients, and iii) according to adiposity level and its distribution. Methods: Patients with GI cancer and subjects with benign diseases as controls were considered. Cachexia was assessed and adiposity evaluated by CT-scan for subcutaneous AT area (SAT), visceral AT area and the total AT area (TAT). MiRNAs involved were measured in plasma by RT-qPCR. Results: 37 naïve GI cancer patients and 14 controls were enrolled. Patients with cachexia presented with lower SAT compared to non-cachectic (p < 0.05). In cancer patients, we found higher levels of miR-26a, miR-128, miR-155 and miR-181a vs. controls (p < 0.05). Cancer patients with BMI < 25 kg/m2 showed higher levels of miR-26a vs. those with BMI ≥ 25 (p = 0.035). MiR-26a and miR-181a were higher in cachectic and non-cachectic vs. controls (p < 0.05). Differences between cachectic and controls were confirmed for miR-155 (p < 0.001) but not between non-cachectic vs. control (p = 0.072). MiR-155 was higher in cachectic patients with low TAT vs. those without cachexia and high TAT (p = 0.036). Conclusion: Our data confirm a modulation of specific and different miRNAs involved in AT metabolism in cancer and cachexia. MiR-155 levels were higher in patients presenting with cachexia and low adiposity with implications in the pathogenic mechanisms and clinical consequences of GI cancer patients.
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BACKGROUND: Adipose tissue metabolism may be impaired in patients with cancer. In particular, increased lipolysis was described in cancer-promoting adipose tissue atrophy. For this reason, we assessed the expression of the lipolysis-associated genes and proteins in subcutaneous adipose tissue (SAT) of gastrointestinal (GI) cancer patients compared to controls to verify their involvement in cancer, among different types of GI cancers, and in cachexia. METHODS: We considered patients with GI cancer (gastric, pancreatic, and colorectal) at their first diagnosis, with/without cachexia, and controls with benign diseases. We collected SAT and total RNA was extracted and ATGL, HSL, PPARα, and MCP1 were analyzed by qRT-PCR. Western blot was performed to evaluate CGI-58, PLIN1 and PLIN5. RESULTS: We found higher expression of ATGL and HSL in GI cancer patients with respect to controls (p ≤ 0.008) and a trend of increase for PPARα (p = 0.055). We found an upregulation of ATGL in GI cancer patients with cachexia (p = 0.033) and without cachexia (p = 0.017) vs controls. HSL was higher in patients with cachexia (p = 0.020) and without cachexia (p = 0.021), compared to controls. ATGL was upregulated in gastric cancer vs controls (p = 0.014) and higher HSL was found in gastric (p = 0.008) and in pancreatic cancer (p = 0.033) vs controls. At the protein level, we found higher CGI-58 in cancer vs controls (p = 0.019) and in cachectic vs controls (p = 0.029), as well as in gastric cancer vs controls (p = 0.027). CONCLUSION: In our cohort of GI cancer patients, we found a modulation in the expression of genes and proteins involved in lipolysis, and differences were interestingly detected according to cancer type.