Mistakes in NAFLD and how to avoid them
Management of NAFLD requires a multidisciplinary approach.
Nonalcoholic fatty liver disease (NAFLD) is defined as the accumulation of excess fat (triglyceride) in the liver in the absence of excessive alcohol consumption. Disease severity ranges from simple steatosis (nonalcoholic fatty liver [NAFL]) to nonalcoholic steatohepatitis (NASH), fibrosis, or cirrhosis, with the potential to develop hepatocellular carcinoma (HCC) or require liver transplantation.NAFLD is believed to affect up to 25% of the Western population,1 and is fast becoming the leading reason for liver transplantation worldwide.2 It affects up to 70% of those who are obese,3 and is strongly linked to the metabolic syndrome. Management of NAFLD therefore requires a multidisciplinary approach, not only to identify those patients at risk of progressive liver disease, but also to improve long-term liver and cardiovascular morbidity and mortality. Here, we highlight some of the mistakes commonly made by medical practitioners when managing NAFLD, and give an evidence-based (where possible) or experience-based approach to management of the condition.
Thank you from UEG E-learning!
We wouldn’t be able to provide high-quality, valued content if not for our contributors.
This month has seen UEG E-learning reach a wonderful landmark, with 3,000 learners actively taking a UEG online course. Added to this are the thousands of pageviews attracted by our Mistakes in… series—more than 38,000 so far this year alone! Given UEG’s aim to enhance the education of young professionals in the field, we’re delighted that our content is being so well used.Of course, we wouldn’t be in the position to provide such high-quality, valued content were it not for our contributors. Now, therefore, seems an appropriate time to say a big thank you to all our authors for their time, expertise and enthusiasm. Here, you’ll find a few UEG E-learning facts, figures and thoughts that demonstrate just how far the project has come in the past few years (since January 2014). At the end of this blog, you’ll find a list of the UEG E-learning content that’s currently available and the names of all our fantastic contributors. If you haven’t had a chance to look at our content then I recommend looking at the list and visiting the UEG Education website. Thank you, once more, to all our contributors—we truly appreciate your generosity and investment in UEG E-learning and look forward to working with you again in the future! Download the infographic
Mistakes in medical management of IBD and how to avoid them
The subtleties and challenges of contemporary IBD management.
The prevalence of inflammatory bowel disease (IBD) is ~0.5%–1% and rising.1 In many healthcare systems, the frequency of IBD is too rare for it to be managed solely by primary care practitioners, but still common enough to fall within the caseload of general gastroenterologists. Whilst the disease may run a relatively quiescent course, some patients face years of severe, disabling symptoms. The relatively unpredictable prognosis of IBD, combined with the ability of its extraintestinal manifestations to impact multiple organ systems, requires a nimble and individual approach to patient management. Indeed, the treating clinician must liaise closely with colleagues in other disciplines, including nursing, surgery, radiology, histopathology and numerous other medical specialties.Advances in our understanding of IBD pathogenesis and in diagnostic modalities, therapeutic options and surgical techniques for Crohn’s disease and ulcerative colitis have fundamentally altered the landscape of IBD management in the past two decades. The challenge for physicians treating IBD is to leverage these changes to improve patient outcomes, avoiding the many potential pitfalls. Here, we discuss some of the pitfalls that may await the treating clinican, drawing upon evidence when possible and on our clinical experience. If some of these pitfalls seem contradictory, this is deliberately so, to highlight the subtleties and challenges of contemporary IBD management. Many of the pitfalls may also seem somewhat obvious when taken in isolation, and yet we believe them to be relatively common, raising important questions around how we can configure and manage our services to avoid those problems that we all still encounter in practice.
Mistakes in cases on call and how to avoid them
Evaluating and managing GI cases on call is a difficult task.
It is a difficult task and a great responsibility to evaluate and manage patients with acute - and potentially life-threatening - clinical presentations. It is even more complex to achieve high standards of care for cases on call. Indeed, on-call gastroenterologists, hepatologists and endoscopists are faced with a wide and protean range of gastrointestinal, liver and pancreatic emergencies.The decision-making process for cases on call is mainly based on information received over the phone, on medical knowledge and clinical experience, and on the resources available. As the degree of confidence in any information given on call may vary, it is of tremendous importance to note, and to document, with precise timing, what has been communicated by, proposed to, and eventually decided with, multiple caregivers (i.e. nurses, emergency physicians, intensive care physicians, surgeons, radiologists etc.) Here, we discuss 10 mistakes that are often seen when managing GI cases on call. Most of the proposals are based on medical evidence, but others are formed from our own clinical experience.
Mistakes in endoscopic resection and how to avoid them
Endoscopic resection is an advanced technique used to remove superficial lesions.
Endoscopic resection is a widespread, advanced endoscopic technique that can be used to remove superficial lesions in the gastrointestinal tract. Lesions present in all parts of the gastrointestinal tract, such as the oesophagus, stomach, duodenum, small intestine and, above all, colon, can be removed by endoscopic resection. Lesion detection and characterization, the use of appropriate resection devices and methods, and the management of malignant polyps are all important parts of a multistep process that requires training, experience, expertise and a multidisciplinary approach.The diagnostic and therapeutic mistakes discussed here are based on our endoscopic experience. We present the most important mistakes that are often seen in endoscopic resection in our practice and have major consequences for the patient. We propose, from our experience, a simple approach to avoid these mistakes.
Mistakes in GORD diagnosis and how to avoid them
Conditions to be aware of to avoid making an erroneous diagnosis of GORD
According to the Montreal definition, “[gastro-oesophageal reflux disease (GORD)] is a condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications.”1 GORD has a negative effect on quality of life and is frequently encountered in clinical practice, with an estimated prevalence of around 24% in Europe.2 In the US, GORD-related healthcare costs account for $9 billion per year.3 A variety of symptoms are associated with GORD—heartburn and regurgitation are typical symptoms, while chest pain, cough and sore throat are considered atypical symptoms—but none is pathognomonic.In case of a typical presentation of GORD in a young patient, and in the absence of alarm signs (e.g. bleeding, dysphagia, weight loss), it is common practice to treat the GORD without investigation. In other cases, upper gastrointestinal endoscopy is usually the first-line examination, more to rule out mucosal complications than to make a positive diagnosis of GORD. Although the presence of erosive oesophagitis is specific to GORD, most patients in whom GORD is suspected based on their clinical presentation have normal endoscopy findings. In this situation, ambulatory reflux monitoring (either pH or pH-impedance monitoring) may be required to identify reflux episodes, to link them with symptom occurrence and then to confirm the clinical diagnosis of GORD. Another common clinical presentation is a patient with symptoms suggestive of GORD that persist despite proton pump inhibitor (PPI) therapy. Indeed 20–60% of patients with GORD-suggestive symptoms are not satisfied with PPI therapy.4,5 After evaluating a patient’s compliance with their treatment, complementary examinations are indicated to determine if resistance to treatment is secondary to persistent GORD, to reflux hypersensitivity or to an erroneous diagnosis of GORD.
Here, we report 10 conditions that clinicians should be aware of to avoid making an erroneous diagnosis of GORD. The discussion draws on a combination of published data and clinical experience.
Enhance your knowledge of constipation.
Mistakes in CT for the acute abdomen and how to avoid them
There are many pitfalls to be aware of when requesting/interpreting abdominal CT scans
Abdominal CT (computed tomography) is among the most common imaging tests performed for the investigation of acute abdominal pathology. There are many pitfalls that clinicians and radiologists should be aware of when requesting these studies and interpreting the findings.This article covers ten mistakes frequently made with abdominal CT, focusing on gastrointestinal tract and hepatobiliary pathology. These mistakes and their discussions are based on the available literature where possible and thereafter on our clinical experience.
Malignant liver lesions
Enhance your knowledge of malignant liver lesions.
EPC Training Course
The translational interactive hands-on-training on epithelial ion transport in the GI tract takes place in Budapest on June 27-28.
Alcohol, GI cancer and microbiota
To what extent might alcohol consumption drive or modify the relationship between gut microbiota and GI cancer?
In the ‘European Code Against Cancer', the International Agency for Research on Cancer (IARC) identify 12 ways to reduce the risk of developing cancer, one of which has to do with alcohol consumption.1 Indeed, the Code advises “If you drink alcohol of any type, limit your intake. Not drinking alcohol is better for cancer prevention.” This recommendation is perhaps not surprising given that alcohol has been identified as a cause of at least seven types of cancer, most of which are gastrointestinal (i.e. cancer of the mouth, pharynx, oesophagus, liver, colon and rectum).1Working with clinical microbiology and microbiome analysis on a daily basis, I’m interested in the use of gut microbiota profiling for predicting human health and disease, including relationships between microbes and cancer. Dysbiosis and predominance of particular gut microbiota communities are thought to be involved in the development of, for example, colorectal cancer (CRC).2–4 But to what extent might alcohol consumption drive or modify such relationships? There may be several answers to this question, and, as exemplified by a recent study, they may not be black and white…5 In their study, Tsuruya et al. investigated the ecophysiological consequences of alcoholism on human gut microbiota.5 Detailing and corroborating the findings of others,6 they found that the gut microbiota of alcoholics were depleted in dominant obligate anaerobes (e.g. Ruminococcus) and enriched in aerotolerant (facultative anaerobic) groups, including Streptococcus and other minor species. That the distribution is skewed towards facultative anaerobes in alcoholics reflects—at least in part—the influence of oxidative stress due to ethanol-induced formation of reactive oxygen species by, for example, gut mucosal cells. The team go on to explain how the different major groups of bacteria metabolize ethanol under different ecological circumstances, which includes the production of acetaldehyde (the carcinogenic metabolite derived from alcohol that is thought to be critical to the development of ethanol-related CRC). While I strongly encourage you to acknowledge the complexity of these intricate relationships, what I find particularly intriguing is the extent to which it is possible to predict gut ecology (e.g. the level of oxidative stress) by microbiota profiling, since this could impact the way we manage and prevent cancers such as CRC. Strong epidemiological data suggest there is a dose–response relationship between alcohol consumption and the risk of CRC.7–10 And when it comes to alcohol (ab)use and the risk of developing and dying from CRC, it might be useful to look not only at the gut bacteria that are present and what they do, but also at those bacteria that are absent. For instance, the diet of individuals who consume excessive amounts of alcohol might favour gut microbiota changes that increase susceptibility to cancer development. Some bacteria produce short-chain fatty acids (SCFAs), which are most likely protective against the development of CRC.4,11 Such bacteria are established in the gut typically in relation to a diet rich in fibre. If the overall diet of alcoholics promotes (e.g. via malnutrition) a reduction in bacteria producing SCFAs, this could indirectly lead to an increased CRC risk. The possible opportunities here are manifold, but I will end by mentioning what I consider the two most important ones. First, microbiota profiling can be used as a noninvasive diagnostic/prognostic marker for various aspects of health and disease; stool analysis might in the future enable us to tell if a patient is an alcoholic, what type of food they eat (if you include profiling of eukaryotic cells in stool as well), and what the likelihood of, for example, CRC is in this patient. Second, microbiota manipulation—through diet, antibiotics, or gut microbiota transplantation—may be used with a view to reducing morbidity and mortality from cancer, not only CRC, but possibly also other types of cancer. References
- International Agency for Research on Cancer. European Code Against Cancer (https://cancer-code-europe.iarc.fr/index.php/en/) [accessed March 21, 2017].
- Gagnière J, Raisch J, Veziant J, et al. Gut microbiota imbalance and colorectal cancer. World J Gastroenterol 2016; 22: 501–518.
- Dulal S and Keku TO. Gut microbiome and colorectal adenomas. Cancer J 2014; 20: 225–231.
- Vipperla K and O’Keefe SJ. Diet, microbiota, and dysbiosis: a ‘recipe’ for colorectal cancer. Food Funct 2016; 7: 1731–1740.
- Tsuruya A, Kuwahara A, Saito Y, et al. Ecophysiological consequences of alcoholism on human gut microbiota: implications for ethanol-related pathogenesis of colon cancer. Sci Rep 2016; 6: 27923.
- Mutlu EA, Gillevet PM, Rangwala H, et al. Colonic microbiome is altered in alcoholism. Am J Physiol Gastrointest Liver Physiol 2012; 302: G966–978.
- Bailie L, Loughrey MB and Coleman HG. Lifestyle risk factors for serrated colorectal polyps: a systematic review and meta-analysis. Gastroenterology 2017; 152: 92–104.
- Wang YM, Zhou QY, Zhu JZ, et al. Systematic review with meta-analyses: alcohol consumption and risk of colorectal serrated polyp. Dig Dis Sci 2015; 60: 1889–1902.
- Bagnardi V, Rota M, Botteri E, et al. Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis. Br J Cancer 2015; 112: 580–593.
- Cai S, Li Y, Ding Y, et al. Alcohol drinking and the risk of colorectal cancer death: a meta-analysis. Eur J Cancer Prev 2014; 23: 532-539.
- Bultman SJ. Interplay between diet, gut microbiota, epigenetic events, and colorectal cancer. Mol Nutr Food Res 2017; 61.
ESGAR & EPC Pancreas workshop
This multidisciplinary course takes place on September 21 - 22, 2017 in Stockholm – register now!
Mistakes in the use of PPIs and how to avoid them
PPIs are frequently prescribed—being knowledgeable about them is fundamental.
Proton pump inhibitors (PPIs) inhibit gastric acid secretion by blocking the gastric hydrogen potassium ATPase (H-K-ATPase). When omeprazole, the first PPI, became available in 1988, it soon appeared to be more effective than H2 antagonists, and PPIs rapidly became one of the most prescribed drug classes worldwide.1PPIs have proven highly efficient for the management of gastro-oesophageal reflux disease (GORD), gastroduodenal ulcers and in the treatment of Helicobacter pylori infections. PPIs are, however, also commonly prescribed for chronic complaints of dyspepsia and upper abdominal discomfort, for which there is no proof that gastric acid is an underlying pathophysiological factor. Lately, the safety of long-term PPI use has been the subject of debate, because chronic use of PPIs has been linked to several complications, such as vitamin and mineral malabsorption, pneumonia, gastrointestinal infections and dementia.2 For anyone working in gastroenterology, having knowledge of one of the most prescribed drugs in this field is fundamental. As such, we address nine frequently made mistakes when it comes to the use of PPIs, and also hope to disprove some of the misconceptions about PPI use.
Mistakes in alcoholic liver disease and how to avoid them
ALD is multifaceted—its management poses many difficulties and pitfalls.
Alcohol consumption is the most prevalent aetiology for liver cirrhosis in Europe and the third leading risk factor for overall mortality.1,2 In fact, alcoholic liver cirrhosis accounts for almost half a million deaths a year worldwide, corresponding to 50% of all cases of cirrhosis, according to the World Health Organization (WHO).3 Alcoholic liver disease (ALD) is multifaceted, with several cofactors influencing its progression. Patients abusing alcohol can simultaneously have viral hepatitis B or C, or a genetic disease, such as alpha-1 antitrypsin deficiency or haemochromatosis.Alcohol consumption is usually assessed in pure grams per day and has a direct relationship with liver damage. Daily alcohol consumption of >30 g for men and >20 g for women is considered the cut-off volume at which there is a risk of developing alcohol-related liver disease.4 Besides volume, the pattern of consumption is also a significant factor, with heavy episodic drinking (HED) defined as an intake of 60 g or more of pure alcohol on at least one occasion in the past 30 days. Regarding HED, there is scarce information on the threshold to be applied to this pattern of drinking.5 Although the relationship between alcohol consumption and ALD is well defined, it must be acknowledged that severe disease only develops in a fraction of those who consume excessive amounts of alcohol. Nonetheless, the disease course is very much influenced by the pattern of drinking, with periods of abstinence or heavy drinking clearly altering its progression.5 ALD can present in different stages, ranging from steatosis to more severe disease, such as the clinical syndrome of alcoholic hepatitis, or decompensated liver cirrhosis, which is sometimes complicated by liver cancer. In the setting of alcoholic hepatitis, several scores, such as the Maddrey discriminant function, Glasgow alcoholic hepatitis score (GASH) and ABIC, may be used to evaluate disease severity, predict short-term survival, and decide on the need for specific treatment. Later on, the Lille score, which includes the reduction in serum bilirubin levels at day 7, evaluates the response to prednisolone after one week, in order to decide whether to continue or stop treatment.5 Despite being a frequent disease, the different aspects of ALD mean that its management still poses many difficulties and pitfalls. In this article we discuss frequent mistakes in ALD, based on the current guidelines and some paradigmatic real-life cases.
Mistakes in EoE and how to avoid them
EoE is the second-most frequent cause of chronic oesophagitis.
Eosinophilic oesophagitis (EoE) is a chronic immune-mediated inflammatory condition that is confined to the oesophagus. Clinically, EoE is characterized by symptoms of oesophageal dysfunction; histologically, by eosinophil-predominant inflammation.1,2 At present, EoE is the second-most frequent cause of chronic oesophagitis (gastro-oesophageal reflux disease [GORD] is the primary cause) and the foremost cause of dysphagia and food impaction in young adults and children.The first descriptions of EoE date back to the early 1990s,3,4 but at that time the condition was largely underappreciated and treated as GORD. Recognition of EoE grew with the rapid increase of paediatric and adult patients diagnosed since 2003, but so did confusion surrounding diagnostic criteria and treatment. The first consensus guidelines for the diagnosis and management of EoE were published in 2007 and were instrumental in bringing EoE to light as a distinct new condition.5 Since 2007, the diagnostic criteria for EoE have constantly and rapidly changed. New evidence for therapeutic agents has mounted, especially during the past 5 years. Here, we discuss the critical pitfalls that frequently occur in daily practice when dealing with EoE patients. The discussion is evidence based and in line with the recommendations included in the updated guidelines for diagnosis and management of EoE in children and adults.6
Mistakes in liver function test abnormalities and how to avoid them
Liver function tests (LFTs) are routinely used to screen for liver disease, but the assessment of LFTs can be challenging. The LFT itself must be clearly understood and the results interpreted in light of the specific clinical setting.
Liver function tests (LFTs) are routinely used to screen for liver disease. A correct interpretation of LFT abnormalities may suggest the cause, severity, and prognosis of an underlying disease. Once the diagnosis has been established, sequential LFT assessment can be used to assess treatment efficacy.Abnormal LFTs are frequently encountered in clinical practice, since elevation of at least one LFT occurs in more than 20% of the population.1 Many patients with abnormal LFTs, however, do not suffer from structural liver disease, since these tests can be influenced by factors unrelated to significant liver damage or liver function loss. During normal pregnancy, for example, serum albumin levels fall due to plasma volume expansion, and alkaline phosphatase (ALP) levels rise due to placental influx. Patients who have elevated transaminase levels may not suffer from liver disease, but rather from cardiac or skeletal muscle damage. Conversely, patients who suffer from advanced liver disease, such as chronic hepatitis or compensated liver cirrhosis, may have normal LFTs.
In short, the assessment of LFTs can represent a challenge for physicians. The observations above demonstrate the need for a firm understanding of the individual LFT, and the ability to interpret the results in the light of a specific clinical setting. Such an understanding is not merely a goal on its own, but may serve as a template to avoid mistakes in interpreting LFT abnormalities. In the following sections, we discuss several mistakes frequently made in the interpretation of LFTs and how to avoid them. Most of the discussion is evidence based, but where evidence is lacking the discussion is based on extensive clinical experience.
Jointly organised by ESDO and ESGE
Early-bird registration for this UEG supported event is open until March 30, 2017.