The Role of Ultrasound in the Diagnosis of Hepatic Steatosis in Morbidly Obese Patients

Background: Hepatic steatosis is prevalent in obese patients. Although it requires histology for diagnosis, ultrasound may indicate its presence. We evaluated the importance of ultrasound in the diagnosis of steatosis in morbidly obese patients, and considered its clinical relevance for patients with BMI of 35-40 kg/m² without co-morbidities. Methods: 187 morbidly obese patients submitted to bariatric surgery were prospectively studied. All patients had ultrasound before the operation, and hepatic biopsies during the operation, which were compared. Results: The prevalence of steatosis histologically was 91.4%. The sensitivity and specificity of ultrasound in diagnosing steatosis was 49.1% and 75%, respectively,with a positive predictive value of 95.4%. Conclusion: The biopsies found a very high prevalence of steatosis in the studied population. The ultrasound results yielded a high positive predictive value (95.4%), suggesting its use as a diagnostic tool for this co-morbidity in morbidly obese patients.The low sensitivity of the method could be related to the lack of objective criteria for the ultrasound diagnosis of steatosis, and probably, technical problems in performing ultrasound in such patients. We believe that in patients with a BMI of 35-40 kg/m² without other comorbidities, the ultrasound finding of steatosis could be of value as an indication for bariatric surgery.     

Histological Behavior of Hepatic Steatosis in Morbidly Obese Patients after Weight Loss Induced by Bariatric Surgery

Background: Hepatic steatosis has a high prevalence among morbidly obese patients. Its relation to steatohepatitis and cirrhosis has been extensively studied among these patients. The aim of this study was to evaluate the behavior of hepatic steatosis with weight loss 1 year after bariatric surgery. Methods: This study is a historical cohort that compared liver biopsies obtained from morbidly obese patients during the bariatric operation, with percutaneous biopsies taken from the same patient 1 year after surgery. The results were compared with weight loss, patients' profile (gender, age, body mass index (BMI) and waist/hip ratio), and with the presence of co-morbidities such as diabetes, hypertension, and dyslipidemia. Results: 90 patients who had liver biopsies taken at the operation and postoperative period for bariatric surgery were included. The prevalence of hepatic steatosis was 87.6%. The average percent of excess weight loss was 81.4%. On the second biopsy, 16 patients (17.8%) of the total had the same degree of steatosis, 25 (27.8%) improved their steatosis pattern and 49 (54.4%) had normal hepatic tissue. There was no statistical difference regarding age, BMI, waist/hip ratio, and co-morbidities (P>0.05), but there was a difference in gender (P=0.044). Conclusion: Significant improvement in the hepatic histology of steatosis was observed after weight loss induced by bariatric surgery in most patients. There was no patient with a worsening in the histology.     

Rapid Weight Loss Is Associated with Preoperative Hypovolemia in Morbidly Obese Patients

Background

In morbidly obese patients (MO), adequate levels of venous return (VR) and left ventricular filling pressures (LVFP) are crucial in order to augment perioperative safety. Rapid weight loss (RWL) preparation with very low calorie diet is commonly used aiming to facilitate bariatric surgery. However, the impact of RWL on VR and LVFP is poorly studied.

Methods

In this prospective, controlled, single-center study, we hypothesized that RWL-prepared MO prior to bariatric surgery can be hypovolemic (i.e., low VR) and compared MO to lean controls with conventional overnight fasting. Twenty-eight morbidly obese patients were scheduled consecutively for bariatric surgery and 19 lean individuals (control group, CG) for elective general surgery. Preoperative assessment of VR, LVFP, and biventricular heart function was performed by a transthoracic echocardiography (TTE) protocol to all patients in the awake state. Assessment of VR and LVFP was made by inferior vena cava maximal diameter (IVCmax) and inferior vena cava collapsibility index- (IVCCI) derived right atrial pressure estimations.

Results

A majority of MO (71.4 %) were hypovolemic vs. 15.8 % of lean controls (p?<?0.001, odds ratio?=?13.3). IVCmax was shorter in MO than in CG (p?<?0.001). IVCCI was higher in MO (62.1?±?23 %) vs. controls (42.6?±?20.8; p?<?0.001). Even left atrium anterior–posterior diameter was shorter in MO compared to CG.

Conclusions

Preoperative RWL may induce hypovolemia in morbidly obese patients. Hypovolemia in MO was more common vs. lean controls. TTE is a rapid and feasible tool for assessment of preload even in morbid obesity.     

Lipoprotein Lipase Expression in Livers of Morbidly Obese Patients Could be Responsible for Liver Steatosis

Background  Most patients with morbid obesity develop non-alcoholic fatty liver disease (NAFLD). The origins of lipid deposition in the liver and the effects of bariatric surgery in the obese with NAFLD are controversial. Methods  We analyzed lipids and lipoprotein lipase (LPL) in both plasma and liver biopsies performed before and 12–18 months after Roux-en-Y gastric bypass surgery in 26 patients. Results  In the livers of morbidly obese patients, the levels of LPL messenger RNA (mRNA) were higher (4.5-fold) before surgery than afterwards than control livers. In these patients, LPL activity was also significantly higher (91 ± 7 mU/g) than in controls (51 ± 3 mU/g, p = 0.0026) and correlated with the severity of the liver damage. All hepatic lipids were significantly increased in obese patients; however, after bariatric surgery, these lipids, with the exception of NEFA, tended to recover to normal levels. Conclusions  The liver of obese patients presented higher LPL activity than controls, and unlike the controls, this enzyme could be synthesized in the liver because it also present LPL mRNA. The presence of the LPL activity could enable the liver to capture circulating triacylglycerides, thus favoring the typical steatosis observed in these patients.     

Supplemental Postoperative Oxygen and Tissue Oxygen Tension in Morbidly Obese Patients

Background  

Subcutaneous tissue oxygen tension (PsqO₂) is a major predictor for wound healing and the occurrence of wound infections. Perioperative subcutaneous wound and tissue oxygen tension is significantly reduced in morbidly obese patients. Even during intraoperative supplemental oxygen administration, PsqO₂ remains low. Tissue hypoxia is pronounced during surgery and might explain the substantial increase in infection risk in obese patients. It remains unknown whether long-term supplemental postoperative oxygen augments tissue oxygen tension. Consequently, we tested the hypothesis that 80% inspired oxygen administration during 12–18 postoperative hours significantly increases PsqO₂ compared to 30% inspired oxygen fraction.     

Cellularity and Adipogenic Profile of the Abdominal Subcutaneous Adipose Tissue From Obese Adolescents: Association With Insulin Resistance and Hepatic Steatosis

OBJECTIVE

We explored whether the distribution of adipose cell size, the estimated total number of adipose cells, and the expression of adipogenic genes in subcutaneous adipose tissue are linked to the phenotype of high visceral and low subcutaneous fat depots in obese adolescents.

RESEARCH DESIGN AND METHODS

A total of 38 adolescents with similar degrees of obesity agreed to have a subcutaneous periumbilical adipose tissue biopsy, in addition to metabolic (oral glucose tolerance test and hyperinsulinemic euglycemic clamp) and imaging studies (MRI, DEXA, ¹H-NMR). Subcutaneous periumbilical adipose cell-size distribution and the estimated total number of subcutaneous adipose cells were obtained from tissue biopsy samples fixed in osmium tetroxide and analyzed by Beckman Coulter Multisizer. The adipogenic capacity was measured by Affymetrix GeneChip and quantitative RT-PCR.

RESULTS

Subjects were divided into two groups: high versus low ratio of visceral to visceral + subcutaneous fat (VAT/[VAT+SAT]). The cell-size distribution curves were significantly different between the high and low VAT/(VAT+SAT) groups, even after adjusting for age, sex, and ethnicity (MANOVA P = 0.035). Surprisingly, the fraction of large adipocytes was significantly lower (P < 0.01) in the group with high VAT/(VAT+SAT), along with the estimated total number of large adipose cells (P < 0.05), while the mean diameter was increased (P < 0.01). From the microarray analyses emerged a lower expression of lipogenesis/adipogenesis markers (sterol regulatory element binding protein-1, acetyl-CoA carboxylase, fatty acid synthase) in the group with high VAT/(VAT+SAT), which was confirmed by RT-PCR.

CONCLUSIONS

A reduced lipo-/adipogenic capacity, fraction, and estimated number of large subcutaneous adipocytes may contribute to the abnormal distribution of abdominal fat and hepatic steatosis, as well as to insulin resistance in obese adolescents.White adipose tissue (WAT) plays a critical role in obesity-related metabolic dysfunctions. Danforth (1) and Shulman (2) raised the hypothesis that inadequate subcutaneous fat stores result in lipid overflow into visceral fat and other nonadipose tissues, which was elegantly explored by Ravussin and Smith (3). Sethi and Vidal-Puig proposed that impaired subcutaneous WAT expandability might cause obesity-associated insulin resistance (4). In adults, increased fat cell size, a marker of impaired adipogenesis, was reported to be related to insulin resistance and predicts the development of type 2 diabetes (5). Recent studies by McLaughlin et al. (6) reported in adults that an increase in the proportion of small adipocytes, but not increased fat cell size, and an impaired expression of markers for adipogenesis are related to insulin resistance. Little is known about adipocyte size and adipogenic capacity during adolescence, a time when the expansion of WAT results from combined adipocyte hypertrophy and hyperplasia. In contrast, adult adipocytes exhibit a remarkably constant turnover (7). Recently, we described a group of obese adolescents presenting with a reduced subcutaneous abdominal fat depot, increased visceral fat, hepatic steatosis, and marked insulin resistance (8). Building on these findings, we asked the following question: is the adipogenic capacity of the abdominal subcutaneous fat depot in obese adolescents associated with a decreased proportion of large adipose cells and reduced expression of genes regulating adipocyte differentiation? We hypothesized that, in some obese adolescents, the lack of expandability of the subcutaneous abdominal fat might be linked to adipocyte size, its adipogenic expression, and the fat accumulation in liver and muscle. To test this hypothesis, we used metabolic and imaging techniques, together with direct measurements of adipocyte size and gene expression, in two groups of obese adolescents with marked differences in the proportion of visceral to subcutaneous abdominal fat.     

Expression of Cytokine Signaling Genes in Morbidly Obese Patients with Non-Alcoholic Steatohepatitis and Hepatic Fibrosis

Background  White adipose tissue (WAT) from visceral adiposity plays an important role in the pathogenesis of non-alcoholic steatohepatitis (NASH). Development of NASH and its progression to fibrosis is partially due to cytokines and adipokines produced by WAT. The aim of this study was to assess the association of hepatic fibrosis and NASH by evaluating the intrinsic differences in the inflammatory cytokine signaling in the visceral adipose tissue obtained from morbidly obese patients. Methods  We used targeted microarrays representing human genes involved in the inflammatory and fibrogenic reactions to profile visceral adipose samples of 15 well-matched NASH patients with and without fibrosis. Additionally, visceral adipose samples were subjected to real-time polymerase chain reaction profiling of 84 inflammations related genes. Results  Eight genes (CCL2, CCL4, CCL18, CCR1, IL10RB, IL15RA, and LTB) were differentially expressed in NASH with fibrosis. Additionally, an overlapping but distinct list of the differentially expressed genes were found in NASH with type II diabetes (DM; IL8, BLR1, IL2RA, CD40LG, IL1RN, IL15RA, and CCL4) as compared to NASH without DM. Conclusions  Inflammatory cytokines are differentially expressed in the adipose tissue of NASH with fibrosis, as well in NASH with DM. These findings point at the interaction of adipose inflammatory cytokines, DM, hepatic fibrosis in NASH, and its progression to cirrhosis and end-stage liver disease. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Laparoscopic Adjustable Gastric Banding Reduces Subcutaneous Adipose Tissue and Blood Inflammation in Nondiabetic Morbidly Obese Individuals

Background

Significant and sustained excess weight loss (EWL) appears to reduce the risk of obesity-related comorbidities (insulin resistance, hyperlipidemia, and inflammation), but this has been primarily shown in adult diabetic obese patients. We evaluated whether the EWL obtained 3 years after laparoscopic adjustable gastric banding (LAGB) improves the metabolic phenotype in nondiabetic morbidly obese (NDMO) individuals from south Italy.

Methods

Serum and subcutaneous adipose tissue (SAT) samples from 20 obese individuals (median BMI?=?41.5 kg/m²) before (T0) and after LAGB (T1) and from 10 controls (median BMI?=?22.8 kg/m²) were taken. Serum leptin, adiponectin, C reactive protein (CRP), and main analyte levels were evaluated by routine methods or immunoassay. In SAT, adipocyte size was measured by hematoxylin/eosin staining, cluster of differentiation 68 (CD68) macrophage infiltration marker by immunohistochemistry, and adiponectin, adiponectin receptors 1 and 2, and interleukin 6 (IL6) messenger RNAs by qRT-PCR.

Results

The average EWL was 66.7 %, and CRP, triglycerides, hepatic markers, leptin levels, homeostasis model assessment, and the leptin/adiponectin ratio were lower (p?p?p?R ²?=?0.905) of EWL (dependent variable) was explained by CD68, adiponectinemia, triglyceridemia, CRP, and total protein levels.

Conclusions

The EWL obtained 3 years after LAGB resulted in an improvement of lipid metabolism and a reduction of inflammation in NDMO patients, thereby decreasing the risk of obesity-associated diseases.     

Induction of Pneumoperitoneum in Morbidly Obese Patients

Background: Induction of pneumoperitoneum can be a difficult, time-consuming, and occasionally hazardous task in a morbidly obese patient. Methods: We have induced pneumoperitoneum in 600 consecutive morbidly obese patients using a 120 mm Veress needle inserted <1 mm beneath the left costal margin, between the mid-clavicular and anterior axillary lines. Absolute muscular relaxation was necessary. Results: A distinct "pop" was felt on entering the peritoneal cavity. The expected intraperitoneal pressure was 7-14 mmHg. A pressure >20 mmHg indicated that the Veress needle was in the abdominal wall. CO2 infusion began at a flow of <1 L/min. "Shaking" the Veress needle to-and-fro improved flow to 1-2 L/min. Complete filling of the abdomen occurred at 4.0 L or more at a pressure limit of 15 mmHg. Increasing the pressure limit to 17 mmHg did not change the rate or final volume of CO₂ infusion. After initial trocar placement, the Veress needle was observed. Frequently it was in the omentum and there was CO₂ beneath the omentum. There was one visceral injury in the 600 patients - a puncture wound to the muscularis, but not the lumen, of the transverse colon. It was repaired laparoscopically with a single stitch. There have been no episodes of perforation of a hollow viscus, no unusual bleeding from the abdominal wall or viscera, and no injuries to the liver or spleen. Conclusion: Percutaneous induction of a pneumoperitoneum with the Veress needle in the left upper quadrant is a safe and effective technique in morbidly obese patients.     

Visceral Adipose Tissue Is Associated With Bone Microarchitecture in the Framingham Osteoporosis Study

Obesity has been traditionally considered to protect the skeleton against osteoporosis and fracture. Recently, body fat, specifically visceral adipose tissue (VAT), has been associated with lower bone mineral density (BMD) and increased risk for some types of fractures. We studied VAT and bone microarchitecture in 710 participants (58% women, age 61.3 ± 7.7 years) from the Framingham Offspring cohort to determine whether cortical and trabecular BMD and microarchitecture differ according to the amount of VAT. VAT was measured from CT imaging of the abdomen. Cortical and trabecular BMD and microarchitecture were measured at the distal tibia and radius using high‐resolution peripheral quantitative computed tomography (HR‐pQCT). We focused on 10 bone parameters: cortical BMD (Ct.BMD), cortical tissue mineral density (Ct.TMD), cortical porosity (Ct.Po), cortical thickness (Ct.Th), cortical bone area fraction (Ct.A/Tt.A), trabecular density (Tb.BMD), trabecular number (Tb.N), trabecular thickness (Tb.Th), total area (Tt.Ar), and failure load (FL) from micro–finite element analysis. We assessed the association between sex‐specific quartiles of VAT and BMD, microarchitecture, and strength in all participants and stratified by sex. All analyses were adjusted for age, sex, and in women, menopausal status, then repeated adjusting for body mass index (BMI) or weight. At the radius and tibia, Ct.Th, Ct.A/Tt.A, Tb.BMD, Tb.N, and FL were positively associated with VAT (all p‐trend <0.05), but no other associations were statistically significant except for higher levels of cortical porosity with higher VAT in the radius. Most of these associations were only observed in women, and were no longer significant when adjusting for BMI or weight. Higher amounts of VAT are associated with greater BMD and better microstructure of the peripheral skeleton despite some suggestions of significant deleterious changes in cortical measures in the non–weight bearing radius. Associations were no longer significant after adjustment for BMI or weight, suggesting that the effects of VAT may not have a substantial effect on the skeleton independent of BMI or weight. © 2016 American Society for Bone and Mineral Research.     

Bariatric Surgery Prior to Total Hip Arthroplasty Is Cost-Effective in Morbidly Obese Patients

BackgroundThe cost-effectiveness of bariatric surgery to achieve weight loss prior to total hip arthroplasty (THA), and decrease the complications and costs associated with THA in the morbidly obese, is unknown. This study evaluated the cost-effectiveness of bariatric surgery prior to THA for morbidly obese patients with end-stage hip osteoarthritis (OA).MethodsA state-transition Markov model was constructed to compare the cost-utility of 2 treatment protocols for patients with morbid obesity and end-stage hip OA: (1) immediate THA and (2) bariatric surgery 2 years prior to THA (combined protocol). The analysis was performed from both a payer and a societal perspective using direct and indirect costs over a 40-year time horizon. Utilities, associated costs, and probabilities for health state transitions were derived from the literature. One-way, 2-way and probabilistic sensitivity analyses were performed to validate the robustness of the base case results, using the standard willingness-to-pay threshold of $100,000/quality-adjusted life years.ResultsFrom the societal perspective, the combined protocol was more effective (13.16 vs 12.26) with less cost ($91,717 vs $92,684) and thus was the dominant strategy over immediate THA. These results were stable across broad ranges for independent model variables. Monte Carlo simulation with 100,000 samples demonstrated that bariatric surgery prior to THA was the preferred cost-effective strategy over 95% of the time from both a societal and payer perspective.ConclusionIn the morbidly obese patient with end-stage hip OA, bariatric surgery prior to THA is a cost-effective strategy for improving quality of life and decreasing societal and payer costs.Level of EvidenceII     

Effect of Weight Loss in the Morbidly Obese Patient with Severe Disability

An impairment can result in disability which can result in handicap. In Canada, disabilities have been based on 17 activities of daily living (ADL), nine of which may be due to massive obesity. Severe disability (SD) is inability to perform three or more of these ADL. During 1985, all patients with SD who underwent weight loss surgery were surveyed. Of 120 morbidly obese patients, 44 fulfilled the SD criteria. Effect of weight loss was observed over 5 years in 42 SD patients (initial mean body mass index 47.8, final 27.8), two being lost to follow-up. Disability became moderate (unable to do one or two of the ADL) in three, mild (difficult but able to perform) in 17, and disappeared in 22 patients. Two who regained lost weight redeveloped SD.     

Risks and Benefits of Gastric Bypass in Morbidly Obese Patients With Severe Venous Stasis Disease

OBJECTIVE: To determine the risks and benefits of gastric bypass-induced weight loss on severe venous stasis disease in morbid obesity. SUMMARY BACKGROUND DATA: Severe obesity is associated with a risk of lower extremity venous stasis disease, pretibial ulceration, cellulitis, and bronze edema. METHODS: The GBP database was queried for venous stasis disease including pretibial venous stasis ulcers, bronze edema, and cellulitis. RESULTS: Of 1,976 patients undergoing GBP, 64 (45% female) met the criteria. Mean age was 44 +/- 10 years. Thirty-seven patients had pretibial venous stasis ulcers, 4 had bronze edema, 23 had both, and 17 had recurrent cellulitis. All had 2 to 4+ pitting pretibial edema. Mean preoperative body mass index (BMI) was 61 +/- 12 kg/m(2) and weight was 179 +/- 39 kg (270 +/- 51% ideal body weight), significantly greater than in patients who underwent GBP without venous stasis disease. Two patients had a pulmonary embolus and four had Greenfield filters in the remote past. Additional comorbidities included obesity hypoventilation syndrome, sleep apnea syndrome, hypertension, gastroesophageal reflux, degenerative joint disease symptoms, type 2 diabetes mellitus, pseudotumor cerebri, and urinary incontinence. Comorbidities were significantly more frequent in the patients with venous stasis disease than for those without. At 3.9 +/- 4 years after surgery, patients lost 55 +/- 21 % of excess weight, 62 +/- 33 kg, reaching 40 +/- 9 kg/m(2) BMI or 176 +/- 41% ideal body weight. Venous stasis ulcers resolved in all but three patients. Complications included anastomotic leaks with peritonitis and death, fatal pulmonary embolism, fatal respiratory arrest, wound infections or seromas, staple line disruptions, marginal ulcerations treated with acid suppression, stomal stenoses treated with endoscopic dilatation, late small bowel obstructions, and incisional hernias. There were six other late deaths. CONCLUSIONS: Severe venous stasis disease was associated with a significantly greater weight, BMI, male sex, age, comorbidity, and surgical risk (pulmonary embolus, leak, death, incisional hernia) than in other patients who underwent GBP. Surgically induced weight loss corrected the venous stasis disease in almost all patients as well as their other obesity-related problems.     

Impact of the Ratio of Visceral to Subcutaneous Adipose Tissue in Donor Nephrectomy Patients

Objective

It was reported that a metabolic syndrome affected the remaining renal function after living donor nephrectomy. However, the measurement of waist circumference is unclear because it cannot distinguish between visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT). We investigate the clinical correlation between body adipose tissue and renal function recovery after living donor nephrectomy.