Influence of Pre-operative HbA1c on Bariatric Surgery Outcomes-the Sunderland (UK) Experience.

PURPOSE: UK guidelines recommend an HbA1c < 8.5% prior to elective surgery. Optimisation of pre-operative glycaemic control can be often difficult. Aim to correlate the effect of pre-operative HbA1c on the peri-operative complication rates and whether elective bariatric surgery should be delayed in poorly controlled diabetics. MATERIAL AND METHODS: Retrospective data of consecutive patients who underwent laparoscopic Roux-en-Y gastric bypass, one-anastomosis gastric bypass and laparoscopic sleeve gastrectomy during January 2014 and April 2018. Patients were categorised into group 1, non-diabetics with an HbA1c < 6.5%; group 2, well-controlled diabetics with HbA1c between 6.5 and 8.4%; and group 3, poorly controlled diabetics with HbA1c ≥ 8.5%. Primary outcome was peri-operative complication rates. RESULTS: Group 1 (n = 978), 81.8% female, median (i.q.r.) age 44.0 (34-52) years, median (i.q.r.) BMI 42.0 (38.7-46.7); group 2 (n = 350), 66.3% female, age 51.0 (45-59) years, BMI 41.8 (37.5-46.5); and group 3 (n = 90), 60% female, age 52.0 (45-56) years and BMI 41.4(36.9-44.8). Early complication rates in each group were low, 1.0% vs 1.7% vs 1.1% (p = 0.592). Mean length of stay was 2 days across the groups (p > 0.05). There was no difference in 30-day re-admission rates between groups 2.8%, 2.9% and 3.3% (p = 0.983). At 6 months and 1 year, there was sustained and equal reduction in HbA1c in all groups (p < 0.05). CONCLUSION: Patients undergoing metabolic surgery for poorly controlled diabetes achieve non-inferior peri-operative outcomes. Hence, delaying metabolic surgery in an attempt to optimise diabetic control is not justifiable.

How to Diagnose Nonalcoholic Fatty Liver Disease.

Patients with nonalcoholic fatty liver disease (NAFLD) are asymptomatic and present with either unexplained abnormal liver blood tests or a bright liver on ultrasonography. Some patients will have normal liver blood tests raising the issue of whether patients with risk factors for NAFLD (diabetes and/or metabolic syndrome [MS]) should be screened for its presence with biomarkers, such as the fatty liver index (FLI). The diagnosis of NAFLD requires the exclusion of other causes of chronic liver disease and steatosis, especially heavy alcohol consumption and viral hepatitis particularly HCV genotype 3. Diagnostic work-up should include evaluation of family and personal history of components of the MS and assessment of liver tests, fasting blood glucose, triglycerides and HDL levels. A drug history is important due to a number being associated with steatosis. To confirm the diagnosis of NAFLD and quantify steatosis, ultrasound (US) and MRI-based techniques are available but none are in routine use outside clinical trials. Standard US is no more accurate than biomarkers such as FLI. The accurate staging of NAFLD requires liver biopsy; however, this is clearly impractical for such a prevalent disease. Accordingly, a number of imaging and blood-based biomarker tests have been evaluated. While none have proved reliable for the diagnosis of nonalcoholic steatohepatitis, several have proved accurate in diagnosing the presence of stage 3 or 4 fibrosis, including the NAFLD fibrosis score, fibrosis-4 and the enhanced liver fibrosis test. Of the imaging techniques, elastography has received the most attention and is being used in routine clinical practice. US acoustic radiation force impulse imaging, and MR-based elastography have recently been described but none are sufficiently accurate to replace liver biopsy for clinical trials as yet or are cost effective for use in routine clinical settings.

Monitoring of Liver Function Tests after Roux-en-Y Gastric Bypass: An Examination of Evidence Base.

There is no consensus on the monitoring of liver function tests after Roux-en-Y gastric bypass (RYGB). Since the main objective of such monitoring would be to diagnose early those who will eventually develop liver failure after RYGB, we performed a systematic review on this topic. An extensive search of literature revealed only 10 such cases in 6 published articles. It would hence appear that liver failure is a rare problem after RYGB. Routine lifelong monitoring of liver function tests is therefore unnecessary for otherwise asymptomatic individuals. Such monitoring should hence be reserved for high-risk groups, such as patients with liver cirrhosis, those undergoing extended limb/distal RYGB, patients with new illnesses, those abusing alcohol, those on hepatotoxic drugs and those presenting with a surgical complication.

Copper Deficiency after Gastric Bypass for Morbid Obesity: a Systematic Review.

A large number of patients undergoing bariatric surgery are deficient in copper, and Roux-en-Y gastric bypass can further aggravate it. Delays in diagnosis and treatment of copper deficiency can leave patients with residual neurological disability. This has led to recommendation from the British Obesity and Metabolic Surgery Society that copper levels should be monitored annually after gastric bypass. This review concludes that copper deficiency in adequately supplemented patients is rare and can be adequately treated if a related haematological or neurological disorder is diagnosed. The cost of routine monitoring may therefore not be justified for adequately supplemented, asymptomatic patients who have undergone Roux-en-Y gastric bypass. The screening may however be necessary for high-risk patient groups to prevent severe complications and permanent disability.

Bariatric Surgery in Type 1 Diabetes Mellitus: A Systematic Review.

Bariatric surgery is recognised as an effective treatment strategy for obese patients with type 2 diabetes mellitus. An increasing number of patients with type 1 diabetes mellitus also suffer with obesity and obesity-associated comorbidities but the role of bariatric and metabolic surgery in this group of patients is unclear. This systematic review investigates published English language scientific literature to understand the results of bariatric surgery in obese patients with type 1 diabetes mellitus. We found that these patients can experience significant weight loss and comorbidity resolution with bariatric surgery. Though most patients also see a decline in total insulin requirement, glycaemic control remains difficult. Most of the patients reported in literature have undergone gastric bypass but data is insufficient to recommend any particular procedure.

Genes and nonalcoholic fatty liver disease.

Whereas most individuals with nonalcoholic fatty liver disease (NAFLD) will have steatosis, only a minority will ever develop progressive disease. Family studies and interethnic variations in susceptibility suggest that genetic factors may be important in determining disease risk. Although no genetic associations with advanced NAFLD have been replicated in large studies, preliminary data suggest that polymorphisms in the genes encoding microsomal triglyceride transfer protein, superoxide dismutase 2, the CD14 endotoxin receptor, tumor necrosis factor-alpha, transforming growth factor-beta, and angiotensinogen may be associated with steatohepatitis and/or fibrosis. With the advent of high-throughput gene analyses and the reduced cost of whole genome-wide scans, it seems likely that genes contributing to inherited susceptibility to this common disease will be identified in the near future.

Non-alcoholic fatty liver disease: the mist gradually clears.

Non-alcoholic fatty liver disease (NAFLD) is now the commonest liver disorder in the developed world affecting up to a third of individuals. It is closely associated with features of the metabolic syndrome, particularly obesity and diabetes. It can progress to cirrhosis, hepatocellular carcinoma and liver failure and is an increasing indication for transplantation. Dietary and genetic factors determine susceptibility to NAFLD and its progression. NAFLD may also be involved in the pathogenesis of cardiovascular disease. Most patients present with incidentally found abnormal liver blood tests. Diagnosis is usually one of exclusion. Liver biopsy is required for disease staging, but new imaging modalities and biomarkers are emerging which may eventually fulfil this role. There is, as yet no firm evidence-based treatment for NAFLD. Therapy is currently directed at treating components of the metabolic syndrome which may also be beneficial for the liver. The recent elucidation of the mechanisms leading to progressive disease suggests a variety of novel targets worthy of testing in animal models of NAFLD and subsequently in pilot studies in humans.

Genetics of alcoholic liver disease and nonalcoholic fatty liver disease.

Although the vast majority of heavy drinkers and individuals with obesity, insulin resistance, and the metabolic syndrome have steatosis, only a minority ever develop steatohepatitis, fibrosis, and cirrhosis. Genetic and environmental risk factors for advanced alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) seem likely to include factors that influence the severity of steatosis and oxidative stress, the cytokine milieu, the magnitude of the immune response, and/or the severity of liver fibrosis. For ALD, the dose and pattern of alcohol intake, coffee intake, and dietary and other lifestyle factors leading to obesity are the most important environmental determinants of disease risk. For NAFLD, dietary saturated fat and antioxidant intake, small bowel bacterial overgrowth, and obstructive sleep apnea syndrome may play a role. Family studies and interethnic variations in susceptibility suggest that genetic factors are important in determining disease risk. For ALD, functional polymorphisms in the ADH and ALDH alcohol metabolizing genes play a role in determining susceptibility in Oriental populations. No genetic associations with advanced NAFLD have been replicated in large studies. Preliminary data suggest that polymorphisms in the genes encoding microsomal triglyceride transfer protein, superoxide dismutase 2, the CD14 endotoxin receptor, tumor necrosis factor alpha, transforming growth factor beta, and angiotensinogen may be associated with steatohepatitis or hepatic fibrosis or both.