The postcholecystectomy syndrome in morbid obesity.
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ABSTRACT:
SUBMITTER: Ng C
PROVIDER: S-EPMC7340458 | biostudies-literature | 2020 Jul
REPOSITORIES: biostudies-literature
Publications
The postcholecystectomy syndrome in morbid obesity.
Ng Cindy C Ejimakor Michelle M Goldson Tove M TM Forjuoh Samuel N SN
Proceedings (Baylor University. Medical Center) 20200427 3
Choledocholithiasis has been found in about 5% to 20% of the approximately 20 million Americans with cholelithiasis who have undergone cholecystectomy. We report a case of a 64-year-old woman who developed gallstones after undergoing a cholecystectomy >40 years earlier. The potential of retained gallstones, incomplete gallbladder removal, or regeneration of gallstones in the gallbladder remnant or cystic duct remnant after a long time following cholecystectomy is discussed. ...[more]
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Project description:Purpose:Postcholecystectomy syndrome (PCS) is characterized by abdominal symptoms following gallbladder removal. However, there is no consensus for the definition or treatment for PCS. The purpose of this study was to define PCS among various symptoms after laparoscopic cholecystectomy, and to identify risk factors affecting PCS. Methods:This study was conducted at Dongguk University Ilsan Hospital and Chung-Ang University Hospital (2012-2013). Outcomes were assessed using European Organization for Research and Treatment of Cancer QLQ-C30 questionnaire. Symptom cluster for determining PCS was made by factor analysis. Cluster analysis evaluating risk factors of PCS was made by Ward methods and Dentogram. Results:Factor analysis revealed three distinct symptom clusters, those are 'insomnia and financial difficulties (eigenvalue, 1.707; Cronbach ?, 0.190),' 'appetite loss and constipation (eigenvalue, 1.413; Cronbach ?, 0.480),' and 'right upper quadrant (RUQ) pain and diarrhea (eigenvalue, 1.245; Cronbach ?, 0.315).' Among these symptom clusters, the cluster of 'RUQ pain and diarrhea' was determined as PCS. However, we could not find any risk factors between high symptomatic group and low symptomatic group. Conclusion:PCS could consist of RUQ pain and diarrhea. Well-designed prospective trials are needed to determine risk factors of PCS.
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Project description:Background and objectiveThere is compelling evidence that obstructive sleep apnoea (OSA) can affect metabolic syndrome (MetS) and cardiovascular risk, but the intermediate mechanisms through which it occurs have not been well defined. We explored the impact of OSA in morbidly obese patients with MetS on adipokines, pro-inflammatory markers, endothelial dysfunction, and atherosclerosis markers.MethodsWe included 52 morbidly obese patients in an observational study matched for age, gender and central obesity in 3 groups (OSA-MetS, Non-OSA-MetS, and Non OSA-non-MetS). Anthropometrical, blood pressure, and fasting blood measurements were obtained the morning after an overnight polysomnography. VEGF, soluble CD40 ligand (sCD40L), TNF-?, IL-6, leptin, adiponectin, and chemerin were determined in serum by ELISA. OSA was defined as apnea/ hypopnea index ? 15 and MetS by NCEP-ATP III.ResultsCases and control subjects did not differ in age, BMI, waist circumference, and gender (43 ± 10 years, 46 ± 5 kg/m(2), 128 ± 10 cm, 71% females). The cases had severe OSA with 47 (32-66) events/h, time spent < 90% SpO2 7% (5%-31%). All groups presented similar serum cytokines, adipokines, VEGF, and sCD40L levels.ConclusionsIn a morbidly obese population with established MetS, the presence of OSA did not determine any differences in the studied mediators when matched by central obesity. Morbidly obese NonOSA-NonMetS had a similar inflammatory, adipokine VEGF, and sCD40L profile as those with established MetS, with or without OSA. Obesity itself could overwhelm the effect of sleep apnea and MetS in the studied biomarkers.CitationSalord N; Gasa M; Mayos M; Fortuna-Gutierrez AM; Montserrat JM; Sánchez-de-la-Torre M; Barceló A; Barbé F; Vilarrasa N; Monasterio C. Impact of OSA on biological markers in morbid obesity and metabolic syndrome.
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Project description:Morbid obesity is characterized by chronic, low-grade inflammation, which is associated with 'inflamm-aging'. The presence of metabolic syndrome (MetS) might accelerate this phenomenon of metaflammation. In this study, we assessed the effects of morbid obesity and MetS on the composition of a broad spectrum of immune cells present within the circulation. A total of 117 morbidly obese patients (MOP) without MetS (MetS-), 127 MOP with MetS (MetS+) and 55 lean controls (LC) were included in this study. Absolute numbers of T cell, B cell, NK cell and monocyte subsets were assessed within peripheral blood using flow cytometry. Both absolute cell numbers and proportion of cells were evaluated correcting for covariates age, body mass index and cytomegalovirus serostatus. Although the absolute number of circulating CD4+ T cells was increased in the MetS+ group, the CD4+ T cell composition was not influenced by MetS. The CD8+ T cell and B cell compartment contained more differentiated cells in the MOP, but was not affected by MetS. Even though the absolute numbers of NK cells and monocytes were increased in the MOP as compared to LC, there was no difference in proportions of NK and monocyte subsets between the three study groups. In conclusion, although absolute numbers of CD4+ and CD8+ T cells, B cells, NK cells and monocytes are increased in MOP, obesity-induced effects of the composition of the immune system are confined to a more differentiated phenotype of CD8+ T cells and B cells. These results were not affected by MetS.
| S-EPMC8330422 | biostudies-literature
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Project description:DNA Methyltransferase 3A (DNMT3A) is an important facilitator of differentiation of both embryonic and hematopoietic stem cells. Heterozygous germline mutations in DNMT3A lead to Tatton-Brown-Rahman Syndrome (TBRS), characterized by obesity and excessive height. While DNMT3A is known to impact feeding behavior via the hypothalamus, here we investigated a role in adipocyte progenitors utilizing heterozygous knockout mice that recapitulate cardinal TBRS phenotypes. These mice become morbidly obese due to adipocyte enlargement and tissue expansion. Adipose tissue in these mice exhibited defects in preadipocyte maturation and precocious activation of inflammatory gene networks, including interleukin-6 signaling. Adipocyte progenitor cell lines lacking DNMT3A exhibited aberrant differentiation. Furthermore, mice in which Dnmt3a was specifically ablated in adipocyte progenitors showed enlarged fat depots and increased progenitor numbers, partly recapitulating the TBRS obesity phenotypes. Loss of DNMT3A led to constitutive DNA hypomethylation, such that the DNA methylation landscape of young adipocyte progenitors resemble that of older wild-type mice. Together, our results demonstrate that DNMT3A coordinates both the central and local control of energy storage required to maintain normal weight and prevent inflammatory obesity.
2022-05-10 | GSE164892 | GEO
Project description:Background There is a paucity of outcome data on patients who are morbidly obese (MO) undergoing transcatheter aortic valve replacement. We aimed to determine their periprocedural and midterm outcomes and investigate the impact of obesity phenotype. Methods and Results Consecutive patients who are MO (body mass index, ≥40 kg/m2, or ≥35 kg/m2 with obesity-related comorbidities; n=910) with severe aortic stenosis who underwent transcatheter aortic valve replacement in 18 tertiary hospitals were compared with a nonobese cohort (body mass index, 18.5-29.9 kg/m2, n=2264). Propensity-score matching resulted in 770 pairs. Pre-transcatheter aortic valve replacement computed tomography scans were centrally analyzed to assess adipose tissue distribution; epicardial, abdominal visceral and subcutaneous fat. Major vascular complications were more common (6.6% versus 4.3%; P=0.043) and device success was less frequent (84.4% versus 88.1%; P=0.038) in the MO group. Freedom from all-cause and cardiovascular mortality were similar at 2 years (79.4 versus 80.6%, P=0.731; and 88.7 versus 87.4%, P=0.699; MO and nonobese, respectively). Multivariable analysis identified baseline glomerular filtration rate and nontransfemoral access as independent predictors of 2-year mortality in the MO group. An adverse MO phenotype with an abdominal visceral adipose tissue:subcutaneous adipose tissue ratio ≥1 (VAT:SAT) was associated with increased 2-year all-cause (hazard ratio [HR], 3.06; 95% CI, 1.20-7.77; P=0.019) and cardiovascular (hazard ratio, 4.11; 95% CI, 1.06-15.90; P=0.041) mortality, and readmissions (HR, 1.81; 95% CI, 1.07-3.07; P=0.027). After multivariable analysis, a (VAT:SAT) ratio ≥1 remained a strong predictor of 2-year mortality (hazard ratio, 2.78; P=0.035). Conclusions Transcatheter aortic valve replacement in patients who are MO has similar short- and midterm outcomes to nonobese patients, despite higher major vascular complications and lower device success. An abdominal VAT:SAT ratio ≥1 identifies an obesity phenotype at higher risk of adverse clinical outcomes.
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