Mistakes in decompensated liver cirrhosis and how to avoid them

Protecting against future decompensation episodes is key

Patients with early stages of chronic liver disease and even those with compensated cirrhosis can present without any clinical symptoms, which means that liver disease and ongoing liver damage can remain unidentified for many years. However, morbidity and mortality drastically increase once the stage of ‘decompensated cirrhosis’ has been reached.1,2 Decompensated cirrhosis describes the development of clinically overt signs of portal hypertension and/or impairment of hepatic function (e.g. variceal bleeding, ascites or overt hepatic encephalopathy). The first hepatic decompensation event significantly increases the risk that further complications of liver cirrhosis and decompensation episodes will occur.2 Moreover, individuals who have advanced stages of liver cirrhosis are four times more susceptible to infection, which is, in turn, the most frequent trigger of hepatic decompensation.3,4 

Optimal management is required to sufficiently treat patients who have decompensated liver cirrhosis, to protect them from future decompensation episodes and prevent further deterioration of hepatic function. However, decompensated liver cirrhosis is a highly complex disease and there are many pitfalls that may occur with regard to comorbidities, management of acute complications and appropriate medication. 
In this article, we cover some of the mistakes frequently made when managing decompensated liver cirrhosis and ways to prevent them. The discussion is based on the available evidence and our personal clinical experience.  

Mistakes in chronic hepatitis B management and how to avoid them

All patients require long-term monitoring. 

Hepatitis B virus (HBV) infection is the most common chronic viral infection in the world. Despite the availability of a preventative vaccine, more than 250 million people worldwide are chronically infected with HBV. The complications of chronic HBV infection—cirrhosis and hepatocellular cancer (HCC)—account for more than 850,000 deaths per year.1 HBV is transmitted haematogenously and sexually, with the majority of HBV infections being transmitted vertically (or perinatally) in high prevalence regions.2 HBV infection acquired at birth or in early childhood results in chronicity in >95% of cases, whereas only 5–10% of those who are infected in adulthood will progress to chronic infection. 

Treatment options for chronic hepatitis B (CHB) are mostly non-curative. Although antiviral therapy can provide adequate viral suppression, cases of functional cure (or hepatitis B surface antigen [HBsAg] loss) are limited and therefore long-term therapy is required. CHB is a dynamic disease, which means that all patients with CHB require long-term monitoring to inform treatment and management decisions. The treatment paradigm in CHB is undergoing rapid change—a number of novel agents are entering the clinical trial pipeline with the therapeutic goal of HBsAg loss or functional cure. It will be important to optimise patient management in advance of these clinical trials, and maintaining viral suppression will be an important prerequisite for many of them. In addition, viral suppression is mandated in a number of patient groups, especially those with advanced disease and cirrhosis, to prevent the complications of CHB.
Here we highlight some of the mistakes frequently made by clinicians when managing CHB and provide an evidence and experience-based approach to its management. 

Mistakes in the management of ECF and how to avoid them

Gl fistulae can be one of the most challenging complications of intestinal disease to manage

Gastrointestinal fistulae can be one of the most challenging complications of intestinal disease to manage. These abnormal tracts connect the epithelialised gut surface to either another part of the gut, another organ or tissue, or to the skin (table 1). This connection can cause enteric contents to bypass important absorptive surfaces, resulting in insidious malnutrition or overt diarrhoea, infection within other organs or the exquisitely embarrassing occurrence of having faeculant material in a woman’s vagina or on a person’s skin. Understandably, this can have a major impact on a person’s quality of life and psychological wellbeing and hamper overall prognosis in terms of general health and wellbeing. Through careful multidisciplinary management of the situation much can be done to address the fears and expectations of patients: careful stoma management, medical therapies to control output, nutritional support and consideration of the central role that surgery plays in resolving a fistula.  

Enterocutaneous and enteroatmospheric fistulae both connect the gut to the skin, but the difference between them is whether there is skin around the fistula opening (enterocutaneous) or the fistula opens onto a laparostomy wound (enteroatmospheric). Most enterocutaneous fistulae develop following surgical intervention; however, fistulae can occur spontaneously. Spontaneous fistulae typically arise with mucosal inflammation such as that occurring with Crohn’s disease, but they can also appear in patients with neoplasia, following radiation treatment, or in the presence of foreign bodies or infections (e.g. tuberculosis or actinomycosis). 
Here, we focus on the errors that can be made when managing enterocutaneous fistulae, based on our clinical experience and the available evidence. 

Mistakes in refractory coeliac disease and how to avoid them

Assessing adherence to a GFD and the initial coeliac disease diagnosis are important

Refractory coeliac disease (RCD) is characterized by the persistence or recurrence of symptoms and signs of malabsorption associated with villous atrophy in patients with coeliac disease who have adhered to a strict gluten-free diet (GFD) for more than 12 months.1–3 Serology is usually negative or, in a small percentage of cases, positive at a low titre.4 Splenic hypofunction, a risk factor for RCD, can be indicated by Howell–Jolly bodies and pitted red cells in a peripheral blood smear. A reduced spleen size visible on ultrasound examination also provides direct evidence of hyposplenism.5 

RCD is subdivided into two main clinical subsets—primary and secondary. Patients with primary RCD show no improvement on a GFD, whereas those with secondary RCD experience symptom relapse after a variable period of wellbeing.1–3 RCD can be also classified as type 1 and type 2 (table 1). RCD type 1 and 2 have a similar incidence (0.04% to 1.5%) and age at diagnosis (generally after the age of 50 years);6 however, they differ significantly in terms of complications, prognosis and treatment options, making correct diagnosis essential.7–13  
The diagnostic approach to RCD includes assessment of dietary adherence to a GFD and revision of the initial coeliac disease diagnosis. Re-evaluation of duodenal histopathology is mandatory, with immunohistochemical characterization aimed at identifying aberrant intraepithelial lymphocytes (IELs) and TCRℽ chain clonality (regarded as pre- or low-grade lymphoma). Videocapsule endoscopy (VCE) is necessary to determine the extent of the lesions, whereas double balloon enteroscopy (DBE) can be useful for obtaining biopsy samples from distal lesions previously identified by imaging (i.e. entero-MR and entero-CT).8,9 A practical algorithm summarizing the diagnostic process for RCD type 1 and 2 is shown in figure 1.
In this article, we discuss the mistakes most frequently made in patients who have suspected RCD, based on the available evidence and our clinical experience in the field. 
Figure 1 | Diagnosis of refractory coeliac disease. A practical algorithm that we developed to summarize the diagnostic process for refractory coeliac disease (RCD) type 1 and 2 compared with slow responding coeliac disease, nonresponsive coeliac disease and other nongluten-dependent enteropathies. EGDS, esophagogastroduodenal endoscopy; GFD, gluten-free diet; TCRℽ, T-cell receptor ℽ. 

Mistakes in the management of carbohydrate intolerance and how to avoid them 

Carbohydrates not absorbed in the small intestine are fermented by colonic bacteria to organic acids and gases1 (e.g. carbon dioxide, hydrogen and methane), part of which is absorbed in the colon, the other part remaining in the lumen.2,3 Large interindividual differences have been demonstrated for the production of such acids and gas.4,5 Carbohydrate malabsorption can be diagnosed by using the hydrogen breath test, because the gases produced after administration of a provocative dose of carbohydrate are unique products of bacterial carbohydrate fermentation.6,7 

Fermentation products are thought to cause symptoms of bloating, abdominal pain, diarrhoea and nausea;8 however, the role of the intestine in the pathogenesis of such symptoms is unclear in both adults and children.9–11 Indeed, an important discrepancy between the degree of malabsorption and symptom severity has been established.12,13 
Here, we discuss mistakes that are made when managing patients who have bloating, abdominal pain, diarrhoea and nausea, in whom carbohydrate malabsorption or intolerance have been diagnosed or are thought to contribute to the condition. The discussion focuses on lactose malabsorption, because of its well-known pathophysiology and high prevalence; however, similar mechanisms apply for intolerances to other poorly-absorbed fermentable, oligosaccharides, disaccharides, monosaccharides and polyols (sugar alcohols) (FODMAPs) and related artificial sweeteners. As treatment focuses on symptom relief, evaluation of complaints that are presumably related to carbohydrate ingestion has to place emphasis on symptom assessment.14 

Mistakes in enteral stenting and how to avoid them

Indications include stenosis (oesophageal and colonic) and gastric outlet obstruction

Gastrointestinal stent placement was introduced at the end of the nineteenth century when it was performed in patients who had a malignant oesophageal obstruction.1 Nowadays, gastrointestinal stents are placed for multiple indications, such as oesophageal stenosis (Figure 1), gastric outlet obstruction (Figure 2) and colonic stenosis (Figure 3). 

Palliation of dysphagia caused by a malignant tumour is the most common indication for stent placement in the oesophagus. However, benign oesophageal strictures are occasionally also treated by stenting because circular ulceration can result in the formation of additional oesophageal strictures and dysphagia.2 Other oesophageal indications include perforations, fistulas, and anastomotic leaks or strictures that can arise after oesophagectomy or bariatric surgery.3 Stent placement in the distal stomach or duodenum is frequently performed for palliation of malignant gastric outlet obstruction. In Western countries, gastric outlet obstruction is most frequently caused by pancreatic cancer, whereas in Asia it occurs more often in patients who have gastric cancer.4–6 Regarding colonic stent placement, it is important to realize that 8–13% of colorectal cancer patients present with acute intestinal obstruction, which in the past was always treated with emergency surgery.7 As multiple studies demonstrated high mortality and morbidity rates after such emergency surgery, colonic stent placement was introduced as a bridge to elective tumour resection.8–11 Finally, for nonoperable patients who have an ileus caused by colonic cancer, stents are also used for palliation. 
Although similar-looking stents are used in the oesophagus, distal stomach/duodenum and colon, it should be emphasized that the diseases occurring in these locations are different entities and should be treated in different ways. Here, we discuss frequent mistakes that can be made during gastrointestinal stent placement, based on the literature and the authors’ clinical experience.
Figure 1 | Oesophageal stent obstruction. a | Stent obstruction caused by food stasis. b | Stent obstruction caused by distal migration of an oesophageal stent. Images courtesy of Amsterdam UMC, University of Amsterdam.
Figure 2 | Duodenal stent placement. a and b | Placement of a stent in the duodenum of a patient with gastric outlet obstruction caused by an irresectable pancreatic cancer. Images courtesy of Amsterdam UMC, University of Amsterdam. 
Figure 3 | Colonic stent placement. a and b | Placement of a stent in the colon of a patient with an obstructing colonic cancer. Images courtesy of Amsterdam UMC, University of Amsterdam. 

Mistakes in chronic diarrhoea and how to avoid them

Chronic diarrhoea is a common condition with a wide variety of possible causes

Chronic diarrhoea, lasting more than 3 or 4 weeks, is a common condition with a wide variety of different possible causes. Estimates suggest 5% of the population have experienced chronic diarrhoea and sought medical advice about it. All gastroenterologists see many patients whose principal complaint is frequent, loose stools, and will be aware of investigations that are needed to diagnose serious conditions such as inflammatory bowel disease (IBD) or colorectal cancer (CRC). Most people who present with chronic diarrhoea will not have these conditions and, if less common disorders are not considered, may be given a diagnosis of diarrhoea-predominant irritable bowel syndrome (IBS-D) or perhaps functional diarrhoea.1 Many different treatments are used for IBS-D and often benefit only a small proportion of patients, leaving many with unmet needs, seeking further investigation, advice and treatment.

Guidelines for the investigation of chronic diarrhoea in adults have recently been updated.2 These guidelines provide recommendations for investigating most patients who have chronic diarrhoea, and reflect the now greater availability of simple tests such as faecal calprotectin, coeliac serology, lower gastrointestinal endoscopy and tests for bile acid diarrhoea (BAD). The criteria for functional gastrointestinal disorders were revised in 2016 (Rome IV), with modifications made to the definitions of the various functional bowel disorders (FBD).1 The revised criteria recognise a continuum between functional diarrhoea and IBS-D, and the usefulness of the Bristol stool form scale (BSFS) types 6 and 7 for defining diarrhoea. Approaches to the clinical evaluation of patients are indicated in those articles,1–2 which provide much of the evidence discussed here, backed up by my clinical experience, highlighting certain mistakes that can be made in the management of chronic diarrhoea. 

Mistakes in pancreatic cystic neoplasms and how to avoid them

Surveillance and therapeutic approaches need to be tailored appropriately

Pancreatic cystic neoplasms (PCN) are a frequent and clinically challenging condition. PCN prevalence increases with age and reports estimate that they may be present in 2–45% of the general population1,2. In addition, the biological behaviour of the various types of PCN differs (ranging from benign to malignant [table 1]), requiring different surveillance and therapeutic approaches. Correct management of PCN is, therefore, critical for avoiding progression to cancer, but at the same time avoiding unneeded close and long-term follow-up, unnecessary invasive diagnostic procedures and overtreatment.


In this article, we discuss some frequent and relevant mistakes that can be made in the diagnosis, surveillance and management of PCN, and propose strategies to avoid them. These strategies are mainly based on the recently published European evidence-based guidelines on PCN.3

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Mistakes in mouse models of NASH and how to avoid them

Several animal models attempt to mirror each stage of human NAFLD

Nonalcoholic fatty liver disease (NAFLD) is a growing cause of chronic liver disease worldwide that can manifest as nonalcoholic fatty liver (NAFL) or nonalcoholic steatohepatitis (NASH). Compared with NAFL, NASH poses a substantially higher risk of progression to advanced liver disease, cirrhosis and hepatocellular carcinoma (HCC). Given the lack of directed pharmacological therapies and the complex, multifactorial disease aetiology and pathology, NAFLD is expected to become the leading cause of end-stage liver disease in the coming decades.
 

Preclinical research aimed at elucidating the molecular mechanisms driving disease and identifying reliable biomarkers and potential treatments is critical and has gained significant attention in recent years. Several animal models attempt to mirror the histopathology and pathophysiology of each stage of human NAFLD, including the development of NASH and fibrosis, up to HCC development. Most in vivo studies use mouse models owing to their relatively low cost, short lifespan and ease of genetic manipulation, which allow for a level of experimental control that is not possible with human studies. Independent of each model’s inherent advantages and disadvantages, making a mistake when choosing, performing, or even analyzing results for a particular animal NASH model may jeopardize our ability to obtain accurate results or draw firm conclusions. 
Here, we discuss some mistakes commonly made in NASH preclinical research. We also consider the challenges and opportunities when selecting animal models for the study of NAFLD.

Mistakes in small bowel bleeding and how to avoid them

Definitive management of small bowel bleeding can pose formidable challenges

Over the past 17 years, the disruptive impact of technologies including small bowel capsule endoscopy (SBCE), device-assisted enteroscopy (DAE) and dedicated cross-sectional imaging has transformed the investigation and management of small bowel pathology. Although a small bowel source only accounts for 5–10% of all cases of gastrointestinal bleeding,1–2 definitive management of small bowel bleeding even in the current era of advanced imaging, can still pose formidable challenges.  

In this brief article, we highlight frequent mistakes made in the investigation and management of small bowel bleeding and discuss strategies for their avoidance. 

Mistakes in acute jaundice and how to avoid them

Jaundice—one of the major signs in medicine—can result from numerous conditions

Jaundice or icterus (derived from the ancient Greek word ikteros that described the yellow-breasted oriole bird) is not a diagnosis in itself but constitutes one of the major signs in medicine. Jaundice refers to the yellowish discoloration of tissue that occurs as a consequence of the deposition of bilirubin. This discoloration is a physical manifestation of a marked increase in serum bilirubin levels. Normal serum bilirubin values are <17 μmol/L; for jaundice to be perceived visually serum bilirubin levels need to be elevated to >40 μmol/L (equivalent to 2.5 mg/dL).

Most serum bilirubin is formed from the breakdown of the haem contained in senescent red blood cells by the reticuloendothelial system. Thus, unconjugated bilirubin is released in the bloodstream, where it is bound by albumin. Through the blood circulation bilirubin is moved to liver hepatocytes, where it undergoes further processing. In brief, bilirubin becomes conjugated in the hepatocytes through glucuronidation, which allows it to be excreted from the body (unconjugated bilirubin is water insoluble and cannot pass into the urine). Conjugated bilirubin forms one of the main components of bile and most of it passes through the biliary tree to the intestine. Unconjugated and conjugated bilirubin are reported in laboratory measurements as indirect and direct bilirubin, according to their chemical properties (i.e. reaction with reagents).1 Jaundice can be caused by abnormalities in any of the steps comprising the formation, metabolism and excretion of bilirubin. In addition, these processes may be functioning properly, but jaundice can be seen because of an obstruction of the biliary tree at any point, from its intrahepatic origins to its end at the ampulla of Vater. For this reason, it is clear that numerous conditions can result in jaundice. When faced with a patient presenting with jaundice a reasonable and careful diagnostic approach is, therefore, warranted to elucidate the underlying cause of this sign. Conventional wisdom may be that “jaundice by itself never killed anyone,” but it is imperative to find the cause as soon as possible, as prompt intervention saves lives in many cases.  Here, we outline several of the mistakes made when approaching a patient presenting with acute jaundice based on our clinical experience and published data. 

Mistakes in capsule endoscopy and how to avoid them

Wireless technology means capsule endoscopy is well tolerated, but it is also a drawback

Capsule endoscopy is a noninvasive technique intended for studying the small bowel and/or colon. The capsule endoscope consists of a small, wireless, pill-sized camera that can be swallowed and allows direct visualization of the gastrointestinal mucosa. The design of the capsule differs depending on the part of the gastrointestinal tract to be studied. The small-bowel capsule has one optical dome and is generally used in patients who have suspected bleeding or to identify evidence of active Crohn’s disease. By contrast, the colon capsule has two optical domes, a higher frame rate and can be considered as an alternative to conventional colonoscopy, especially for cases when the examination was incomplete. There is also a new capsule with two optical domes that is designed for the panendoscopic study of both the small bowel and colon. 

The main characteristic of capsule endoscopy is the wireless technology, which enables it to be very well tolerated. However, this feature is also one of its drawbacks, as the capsule cannot be directly controlled by the physician. The capsule moves through the gut depending solely on intestinal motility, and the examiner is not able to drive it back and forth or to stop it to look more carefully at any finding. Moreover, the visualization relies heavily on the adequacy of intestinal cleansing as rinsing with water and aspiration are not possible. Capsule endoscopists should be aware of these shortcomings, as they directly affect the reading and diagnosis. Here we discuss frequent errors that are made when performing capsule endoscopy, based on the published literature and more than 15 years’ experience

Mistakes in clinical investigation of gastrointestinal motility & function

Symptoms related to abnormal motility and function are very common.

Symptoms related to abnormal gastrointestinal motility and function can occur from the moment food is swallowed to the time stool is passed into the toilet. A recent UEG survey indicated that dysphagia, heartburn, bloating, abdominal pain and changes to bowel habit are each reported by 5–15% of the general population.1 These symptoms are frequent reasons for seeking medical attention from general physicians and for referral to specialist gastroenterologists. Most patients with these symptoms do not have neoplasia, infection or inflammation on initial investigation, but rather so-called functional gastrointestinal symptoms.2,3

For patients with mild symptoms, negative tests provide reassurance and simple, symptomatic management might be all that is required (e.g. acid suppression, stool regulation). However, for those with severe symptoms that persist on therapy, ruling out life-threatening disease is not sufficient, and referral to the neurogastroenterology and motility (NGM) laboratory for physiological measurements is often indicated.

Clinical investigations aim to explain the cause of symptoms and establish a diagnosis that can guide rational treatment. Until recently, it could be argued that manometry, scintigraphy, breath tests and related tests rarely provided this information. As a result, only patients with suspected major motility disorders (e.g. achalasia, severe reflux disease or faecal incontinence) were routinely referred to the NGM laboratory for tests. Technological advances, such as high-resolution manometry (HRM), now provide objective measurements not only of motility, but also of function in terms of the movement (and digestion) of ingested material within the gastrointestinal tract. Furthermore, the ability to associate events (such as bolus retention, reflux or gas production) with symptoms provides an indication of visceral sensitivity and can identify what is causing patient complaints. Here, I discuss frequent mistakes in clinical investigation of gastrointestinal motility and function based on a series of consensus documents published by members of the International Working Group for Disorders of Gastrointestinal Motility and Function.

Mistakes in the endoscopic diagnosis and management of Barrett’s oesophagus and how to avoid them

Barrett’s oesophagus is the precursor to oesophageal adenocarcinoma, which carries a poor prognosis,1 and it is likely that all endoscopists and gastroenterologists will encounter Barrett’s oesophagus in their clinical practice.

Careful assessment and management of patients who have Barrett’s oesophagus with endoscopic surveillance and endoscopic endotherapy aim to reduce the risk of progression to invasive adenocarcinoma. Advances in endoscopic diagnosis and therapy should, therefore, help to reduce the risk of progression. As with all premalignant conditions and surveillance programmes,2 careful multidisciplinary management of the patient is important to reduce the risk of causing them to become unduly concerned. Here, we present some mistakes that in our experience are commonly made in the endoscopic diagnosis and management of Barrett’s oesophagus and give advice on how to avoid them. 

Mistakes in short bowel and how to avoid them

Short bowel manifests as high stomal output or diarrhoea, dehydration and malnutrition.

Short bowel is a condition that occurs after single or multiple intestinal resections. The incidence of short bowel in Europe is 2 per million of the population1–3 and it carries with it lifelong morbidity and mortality. The initial recognition and management of short bowel in the adult population tends to occur in the postoperative period and in the secondary care setting, where specialist input from clinicians experienced in short bowel is often lacking.

Normal small bowel length is 275–850 cm.4–7 It is accepted that when the length of small bowel is reduced to less than 200 cm it may be insufficient to enable adequate absorption of fluids and micronutrients. The symptoms of short bowel (often referred to in the literature as short bowel syndrome) are secondary to a reduction in intestinal surface area together with an increased motility of the remaining section of small bowel, with accompanying increased secretion into the lumen. These intestinal secretions vary in their electrolyte content and osmolality depending on the anatomical location, with the highest chloride and potassium loss from gastric secretions and high sodium loss from jejunal secretions.8 Clinically, short bowel manifests itself as a high stomal output or diarrhoea, dehydration and malnutrition. High stomal output or diarrhoea do not, however, necessarily equate immediately to short bowel; conversely, a small bowel longer than 200cm may be insufficient if it is diseased. Here, we discuss some of the pitfalls that are encountered in the recognition and management of short bowel and have suggested an algorithm for assessing and managing patients with a high stomal output. Although some of these pitfalls may appear obvious, they are addressed here because they are commonly encountered in clinical practice (summarised in table 1 at the end of the article).

Mistakes in paediatric IBD and how to avoid them

Better clinical outcomes are increasingly being sought in young people with IBD

Around 1 in 10 cases of inflammatory bowel disease (IBD) will present before adulthood, with the median age at presentation being 11–12 years.1 IBD in children and young people is associated with more extensive disease, increased disease activity and a higher rate of complications compared with adult-onset IBD.2 Worldwide, estimates of paediatric IBD prevalence rates are lacking, but data suggest its incidence is increasing.3


Risk factors for paediatric IBD include immigration to high prevalence regions, particularly to countries that have Westernised diets, increasing geographical latitude, and European ancestry (versus belonging to an indigenous population).4 The risk may also be higher in children of certain ethnicities (South Asian, Hispanic, and East Asian).5

While the pathophysiology and clinical presentation of paediatric IBD is well understood, the role of genetics and personalised treatment is currently the focus of a significant amount of international research. Better clinical outcomes—including optimal nutrition, improved growth, better quality of life and increased disease remission rates with decreased occurrence of complications—are increasingly being sought in children and young people with IBD.4

This article discusses mistakes commonly made when identifying, diagnosing and managing children whom are suspected or confirmed to have IBD. The mistakes and discussion are based on published evidence where possible, plus our clinical experience of looking after children with IBD.

Mistakes in tissue sampling during endoscopy and how to avoid them

Tissue acquisition is the most common manoeuvre performed during endoscopy.

Tissue sampling is the most common manoeuvre performed during endoscopic procedures and histological examination is part of almost every digestive disease investigation. The potential for mistakes is, therefore, widespread and knowledge of the adequacy of the indications and techniques used for tissue sampling during endoscopy, as well as the potential consequences, is indispensable for every gastroenterologist. As such, there are some questions that should always be posed before taking a biopsy sample or tissue acquisition during endoscopy: Why? What for? How? How many? (figure 1). This manuscript has been organized with these questions in mind. We’ve aggregated examples for the eight most frequent and most correctable mistakes made during tissue acquisition by endoscopy. In addition, most of the recommendations made in this article are supported by existing guidelines and evidence, with a few based solely on the authors’ experience. Figure 1 | Questions that should always be asked before a biopsy sample is taken or tissue acquired during endoscopy.

Mistakes in managing H. pylori infection and how to avoid them

Careful practice can overcome declining eradication rates for H. pylori treatment.

The sequelae of Helicobacter pylori infection, a known Group 1 carcinogen, can lead to significant morbidity and mortality worldwide. Billions of people are infected with H. pylori, but the incidence of H. pylori infection is declining in many parts of Europe, with a study from the Netherlands showing a decline in seroprevalence from 48% in subjects born between 1935 and 1946 to 16% in those born between 1977 and 1987.1

In recent years, however, eradication rates for H. pylori treatment have been falling, which has led to a large number of patients in the community having inadequately managed infections. Most of the problems that have led to the decline in the success of eradication treatment can be easily overcome through careful practice, supported by the robust framework provided by international guidelines. Careful practice includes the correct management of dyspepsia, the appropriate use of diagnostic tests for H. pylori, acceptable, efficacious treatments that enable good patient compliance and adequate follow up to insure eradication has been achieved in all cases. Here, we discuss the mistakes that are made when managing patients infected with H. pylori. Most of the discussion is evidence based, but where evidence is lacking the discussion is based on the authors’ clinical experience of more than 30 years in the field.
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