case study 7 gastroesophageal reflux disease

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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

StatPearls [Internet].

Gastroesophageal reflux disease.

Catiele Antunes ; Abdul Aleem ; Sean A. Curtis .

Affiliations

Last Update: July 3, 2023 .

• Continuing Education Activity

Gastroesophageal reflux disease (GERD) is a condition that develops when there is a retrograde flow of stomach contents back into the esophagus. It can present as non-erosive reflux disease or erosive esophagitis. This activity illustrates the evaluation and treatment of GERD and highlights the role of the interprofessional team in improving care for patients with this condition.

• Explain the pathophysiology of gastroesophageal reflux disease.
• Describe the signs and symptoms of a patient with gastroesophageal reflux disease.
• Describe the tests used to diagnose gastroesophageal reflux disease.
• Describe the importance of improving coordination among interprofessional team members to enhance the delivery of care for patients with gastroesophageal reflux disease.
• Introduction

Gastroesophageal reflux disease (GERD) is a chronic gastrointestinal disorder characterized by the regurgitation of gastric contents into the esophagus. It is one of the most commonly diagnosed digestive disorders in the US with a prevalence of 20%, resulting in a significant economic burden in direct and indirect costs and adversely affects the quality of life [1] [2] . GERD is caused by multiple different mechanisms that can be intrinsic, structural, or both, leading to the disruption of the esophagogastric junction barrier resulting in exposure of the esophagus to acidic gastric contents. Clinically, GERD typically manifests with symptoms of heartburn and regurgitation. It can also present in an atypical fashion with extra-esophageal symptoms such as chest pain, dental erosions, chronic cough, laryngitis, or asthma [3] [4] . Based on endoscopic and histopathologic appearance, GERD is classified into three different phenotypes: non-erosive reflux disease (NERD), erosive esophagitis (EE), and Barrett esophagus (BE) [5] . NERD is the most prevalent phenotype seen in 60-70% of patients followed by erosive esophagitis and BE seen in 30% and 6-12% of patients with GERD, respectively. [1] [5] [6] . Over the years, the mainstay in the management of GERD has been lifestyle modifications, and proton pump inhibitors (PPIs). However, medically refractory GERD is becoming increasingly common, requiring a tailored approach in the management of GERD.

Currently, there is no known cause to explain the development of GERD. Over the years, several risk factors have been identified and implicated in the pathogenesis of GERD. Motor abnormalities such as esophageal dysmotility causing impaired esophageal acid clearance, impairment in the tone of the lower esophageal sphincter (LES), transient LES relaxation, and delayed gastric emptying are included in the causation of GERD [7] . Anatomical factors like the presence of hiatal hernia or an increase in intra-abdominal pressure, as seen in obesity are associated with an increased risk of developing GERD [7] . A meta-analysis by Hampel H  et al.  concluded that obesity was associated with an increased risk of developing GERD symptoms, erosive esophagitis, and esophageal carcinoma [8] . The ProGERD study by Malfertheiner,  et al . evaluated the predictive factors for erosive reflux disease in more than 6000 patients with GERD and noted that the odds ratio for the erosive disease increased with the body mass index (BMI) [9] . Several other risk factors have been independently associated with the development of GERD symptoms that include age ≥50 years, low socioeconomic status, tobacco use, consumption of excess alcohol, connective tissue disorders, pregnancy, postprandial supination, and different classes of drugs which include anticholinergic drugs, benzodiazepines, NSAID or aspirin use, nitroglycerin, albuterol, calcium channel blockers, antidepressants, and glucagon [10] [11] [12] .

• Epidemiology

GERD is one of the most common gastrointestinal disorders, with a prevalence of approximately 20% of adults in western culture. A systematic review by El-Serag  et al.  estimated the prevalence of GERD in the US between 18.1% to 27.8%. However, the true prevalence of this disorder could be higher because more individuals have access to over-the-counter acid, reducing medications [2] [13] [2] . The prevalence of GERD is slightly higher in men compared to women [14] . A large meta-analysis study by Eusebi  et al.  estimated the pooled prevalence of GERD symptoms to be marginally higher in women compared with men (16.7% (95% CI 14.9% to 18.6%) vs. 15.4% (95% CI 13.5% to 17.4%) [12] . Women presenting with GERD symptoms are more likely to have NERD than men who are more likely to have erosive esophagitis [15] . However, men with longstanding symptoms of GERD have a higher incidence of Barrett's esophagus (23%) compared to women (14%) [16] .

• Pathophysiology

The pathophysiology of GERD is multifactorial and is best explained by various mechanisms involved, including the influence of the tone of the lower esophageal sphincter, the presence of a hiatal hernia, esophageal mucosal defense against the refluxate and esophageal motility.

Impaired Lower Esophageal Sphincter (LES) Function and Transient Lower Esophageal Sphincter Relaxations (TLESRs)

The LES is a 3-4 cm tonically contracted smooth muscle segment located at the esophagogastric junction (EGJ) and, along with the crural diaphragm forms the physiological EGJ barrier, which prevents the retrograde migration of acidic gastric contents into the esophagus [17] . In otherwise healthy individuals, LES maintains a high-pressure zone above intragastric pressures with transient relaxation of the LES that occurs physiologically in response to a meal facilitating the passage of food into the stomach. Patients with symptoms of GERD may have frequent transient LES relaxations (TLESRs) not triggered by swallowing, resulting in exceeding the intragastric pressure more than LES pressures permitting reflux of gastric contents into the esophagus [18] . The exact mechanism of increased transient relaxation is unknown, but TLESRs account for 48-73% of GERD symptoms [19] . The LES tone and TLESRs are influenced by factors such as alcohol use, smoking, caffeine, pregnancy, certain medications like nitrates, and calcium channel blockers [18] .

Hiatal hernia

Hiatal hernia is frequently associated with GERD and can exist independently without causing any symptoms. Nonetheless, the presence of hiatal hernia plays a vital role in the pathogenesis of GERD as it hinders the LES function [20] . Patti et al. reported that patients with proven GERD with or without a small hiatal hernia had similar LES function abnormalities and acid clearance. However, patients with large hiatal hernias were noted to have shorter and weaker LES resulting in increased reflux episodes. It was also pointed out that the degree of esophagitis was worse in patients with large hiatal hernias [21] . A study evaluating the relationship between hiatal hernia and reflux esophagitis by Ott  et al.  demonstrated the presence of hiatal hernia in 94% of patients with reflux esophagitis [22] . 

Impaired esophageal mucosal defense against the gastric refluxate

The esophageal mucosa comprises various structural and functional constituents that function as a protective defense barrier against the luminal substances encountered with GERD [18] . This defensive barrier can be breached by prolonged exposure to the refluxate, which consists of both acidic gastric contents (hydrochloric acid and pepsin) and alkaline duodenal contents (bile salts and pancreatic enzymes) leading to mucosal damage. The influence of gastroparesis on GERD is unknown. It is believed that delayed gastric emptying contributes to GERD symptoms due to gastric distention and increased exposure to the gastric refluxate [18] .

Defective esophageal peristalsis

Normally, the acidic gastric contents that reach the esophagus are cleared by frequent esophageal peristalsis and neutralized by salivary bicarbonate [23] [18] . In a prospective study by Diener  et al ., 21% of patients with GERD were noted to have impaired esophageal peristalsis leading to decreased clearance of gastric reflux resulting in severe reflux symptoms and mucosal damage [24] .

• Histopathology

The esophageal squamous epithelium serves to function as a protective defense barrier against the retrograde migration of refluxate. Disruption of this epithelial defense is a common phenomenon in GERD and NERD [25] . The histopathological features of GERD are not unique to this condition due to minimal biopsy criteria for diagnosis and varying sensitivity and specificity in the diagnosis [26] .In fact, the histopathologic diagnosis of GERD is made based on an array of microscopic findings that include features of inflammation, basal cell hyperplasia, papilla elongation, and dilatation of intercellular spaces [26] .

• History and Physical

The typical clinical presentation of GERD is heartburn and regurgitation. However, GERD can also present with various other symptoms that include dysphagia, odynophagia, belching, epigastric pain, and nausea [27] . Heartburn is defined as a retrosternal burning sensation or discomfort that may radiate into the neck and typically occurs after the ingestion of meals or when in a reclined position [28] . Regurgitation is a retrograde migration of acidic gastric contents into the mouth or hypopharynx [28] . GERD presentation is considered to be atypical when patients present with extraesophageal symptoms such as chest pain, chronic cough, asthma, laryngitis, dental erosions, dysphonia, and hoarseness, and globus sensation [3] [4] . 

The diagnosis of GERD is imprecise as there is no gold standard test available. The diagnosis of GERD is made solely based on presenting symptoms or in combination with other factors such as responsiveness to antisecretory therapy, esophagogastroduodenoscopy, and ambulatory reflux monitoring.

Proton pump inhibitor (PPI) trial

GERD can be presumptively diagnosed in most patients presenting with typical symptoms of heartburn and regurgitation [29] . Unless there are no associated alarm symptoms that include dysphagia, odynophagia, anemia, weight loss, and hematemesis, most patients can be initiated on empiric medical therapy with proton pump inhibitors(PPIs) without further investigations with a response to treatment confirming the diagnosis of GERD [29] . However, a meta-analysis published literature by Numans et al. refuted the accuracy of this empiric PPI trial diagnostic strategy [30] .

Esophagogastroduodenoscopy (EGD)

Patients presenting with typical GERD symptoms associated with any one of the alarm symptoms should be evaluated with an EGD to rule out complications of GERD. These include erosive esophagitis, Barrett's esophagus, esophageal stricture, and esophageal adenocarcinoma or rule out peptic ulcer disease. Distal esophageal biopsies are not routinely recommended to make a diagnosis of GERD as per the current American College of Gastroenterology (ACG) guidelines [29] . Patients with a high index of suspicion for coronary artery disease presenting with GERD symptoms should undergo evaluation for underlying cardiovascular disease. In contrast, patients presenting with noncardiac chest pain suspected due to GERD should have a diagnostic assessment with an EGD and pH monitoring before initiation of PPIs [31] . Current ACG guidelines recommend against screening for Helicobacter pylori infection in patients with GERD symptoms [29] .

Radiographic studies

Radiographic studies like barium radiographs can detect moderate to severe esophagitis, esophageal strictures, hiatal hernia, and tumors. However, their role in the evaluation of GERD is limited and should not be performed to diagnose GERD [29] .

Ambulatory esophageal reflux monitoring

Medically refractory GERD is increasingly common, and patients often have normal endoscopy evaluation as PPIs are incredibly effective in healing esophagitis caused by the refluxate. Ambulatory esophageal reflux monitoring can assess the correlation of symptoms with abnormal acid exposure. It is indicated in medically refractory GERD and in patients with extraesophageal symptoms suspicious for GERD. Ambulatory reflux (pH or in combination with impedance) monitoring employs the utility of a telemetry pH capsule or a transnasal catheter. It is the only available test that detects pathological acid exposure, frequency of reflux episodes, and correlation of symptoms with reflux episodes [29] . Current practice guidelines recommend mandatory preoperative ambulatory pH monitoring in patients without evidence of erosive esophagitis [29] .

• Treatment / Management

The goals of managing GERD are to address the resolution of symptoms and prevent complications such as esophagitis, BE, and esophageal adenocarcinoma. Treatment options include lifestyle modifications, medical management with antacids and antisecretory agents, surgical therapies, and endoluminal therapies.

Lifestyle Modifications

Lifestyle modifications are considered to be the cornerstone of any GERD therapy. Counseling should be provided about the importance of weight loss given that underlying obesity is a significant risk factor for the development of GERD, and studies have shown that weight gain in individuals with a normal BMI has been associated with the development of GERD symptoms [32] . Individuals should also be counseled about avoiding meals at least 3 hours before bedtime and maintaining good sleep hygiene as it has been shown that minimal disturbances in sleep are associated with suppression of TLESRs, resulting in decreased reflux episodes [27] [33] . Studies have also shown improvement in GERD symptoms and pH monitoring studies with the elevation of the head end of the bed. Diet modification with the elimination of chocolate, caffeine, and spicy foods, citrus, and carbonated beverages in GERD is controversial and is not routinely recommended as per current ACG guidelines [29] .

Medical Therapy

Medical therapy is indicated in patients who do not respond to lifestyle modifications. Medical therapy is comprised of antacids antisecretory agents like histamine (H2) receptor antagonists (H2RAs) or PPI therapy and prokinetic agents. Currently, there are two US Food and Drug Administration (FDA) approved H2RAs (famotidine and cimetidine) available in the US and are available over-the-counter. The other commonly used H2RA known as ranitidine has been recalled as a potential health hazard or safety risk due to an unexpected impurity in the active ingredient. The less commonly known prescription-only H2RA nizatidine has also been recalled as well due to similar concerns. In the US, there are six PPIs that are currently available, of which three (omeprazole, lansoprazole, and esomeprazole) are available over-the-counter, and the remaining three (pantoprazole, dexlansoprazole, and rabeprazole) are prescription-only medications. Of the available medical options, PPI therapy is considered to be the most effective for both erosive and non-erosive GERD based on multiple large-scale studies. These studies have also shown improved symptom control, healing of underlying esophagitis, and decreased relapse rates compared to H2RAs [34] [35] . ACG guidelines recommend PPI therapy be initiated at once a day dosing before the first meal of the day [29] . Patients with incomplete responses to once-daily dosing can be treated with twice-daily dosing or adjustment of dose timing, specifically in patients with nighttime symptoms [29] . As needed, bedtime administration of H2RAs is recommended for individuals with nighttime symptoms not optimized with maximal PPI therapy [29] . The role of prokinetic agents such as metoclopramide and domperidone in GERD is limited due to lack of data and also due to their profound adverse effects on the central nervous system and cardiovascular system.

Surgical therapy

Patients who present with either medically refractory GERD, noncompliance, or experience side effects with medical therapy, underlying large hiatal hernia, or individuals who desire to discontinue long-term medical treatment can be considered for surgical management [36] . The available surgical options for GERD are laparoscopic Nissen fundoplication, Laparoscopic anterior 180° fundoplication (180° LAF), or bariatric surgery in obese patients [29] . Laparoscopic Nissen fundoplication has been the gold standard surgical treatment in the management of GERD patients. However, given the rapid prevalence of obesity in the United States, gastric bypass surgery is becoming the most common surgical treatment for GERD [29] . It should be considered in obese patients with symptoms of GERD who prefer surgical therapy [27] [29] [36] [29] [27] . Current ACG guidelines recommend performing preoperative ambulatory pH monitoring in patients without erosive esophagitis and esophageal manometry to rule out achalasia or undiagnosed scleroderma-like esophagus prior to surgical therapy [29] . Two large meta-analyses comparing medical therapy with surgical therapy reported contrary conclusions with one reporting improvement of symptoms of GERD after surgery compared with medical therapy and the other reporting considerable uncertainty in the benefits of surgical therapy compared to medical therapy [37] [37] [37] . However, patients undergoing fundoplication are at risk for developing postoperative adverse events that include bloating, which is seen in 15 to 20% of patients, dysphagia, and belching. The most common bariatric surgeries performed are Roux-en-Y gastric bypass (RYGB), laparoscopic adjustable gastric banded plication (LAGP), and sleeve gastrectomy [36] . Studies have shown that the resulting weight loss from surgical management of obesity has had positive effects on GERD. Of all the bariatric surgeries available, RYGB has proven to be the most effective bariatric surgery for reducing GERD symptoms [36] . It is recommended as the bariatric procedure of choice in patients with severe GERD preoperatively [36] .

Endoluminal Therapy

In the era of minimally invasive surgery techniques, many different types of endoscopic therapies have been developed for GERD management. Most of them were discontinued after failing to demonstrate long-term efficacy. The current available endoluminal therapies include magnetic sphincter augmentation (MSA) and transoral incision-less fundoplication using the EsophyX  (EndoGastric Solutions, Redmond, WA, United States) [29] .   A recent meta-analysis by Gerson et al. that included data from 233 patients demonstrated that subjects who underwent TIF 2.0 procedure had improved esophageal pH, decreased need for PPIs, and significant improvement in the quality of life at three years after TIF 2.0 procedure [38] . Another prospective study by Testoni et al. demonstrated TIF with EsophyX as an effective long-term treatment option for patients with symptomatic GERD with associated hiatal hernia less than 2 cm. A meta-analysis comparing Nissen fundoplication and magnetic sphincter augmentation that included data from 688 patients with 415 who underwent MSA and the rest who were treated with Nissen fundoplication concluded that MSA was an effective therapeutic option for GERD as short-term outcomes with magnetic sphincter augmentation appeared to be comparable to Nissen fundoplication [39] .

• Differential Diagnosis
• Coronary artery disease
• Eosinophilic esophagitis (EoE)
• Non-ulcer dyspepsia
• Rumination syndrome
• Esophageal diverticula
• Gastroparesis
• Esophageal and gastric neoplasm
• Peptic ulcer disease (PUD)
• Complications

Erosive Esophagitis (EE)

EE is characterized by erosions or ulcers of the esophageal mucosa [28] . Patients may be asymptomatic or can present with worsening symptoms of GERD. The degree of esophagitis is endoscopically graded using the Los Angeles esophagitis classification system, which employs the A, B, C, D grading system based on variables that include length, location, and circumferential severity of mucosal breaks in the esophagus [40] .

Esophageal Strictures

Chronic acid irritation of the distal esophagus can result in scarring of distal the esophagus leading to the formation of a peptic stricture. Patients can present with symptoms of esophageal dysphagia or food impaction. ACG guidelines recommend esophageal dilation and continue PPI therapy to prevent the need for repeated dilations [29] .

Barrett Esophagus

This complication occurs as a result of chronic pathological acid exposure to the distal esophageal mucosa. It leads to a histopathological change of the distal esophageal mucosa, which is normally lined by stratified squamous epithelium to metaplastic columnar epithelium. Barrett's esophagus is more commonly seen in Caucasian males above 50 years, obesity, and history of smoking and predisposes to the development of esophageal adenocarcinoma [28] . Current guidelines recommend the performance of periodic surveillance endoscopy in patients with a diagnosis of Barrett's esophagus [41] .

• Enhancing Healthcare Team Outcomes

The majority of patients presenting with typical symptoms of GERD are usually recognized and managed by primary care providers. Patients with medically refractory GERD and alarm symptoms are generally referred to gastroenterologists.  The management of GERD requires an interprofessional approach involving primary care providers, gastroenterologists, otolaryngologists, pulmonologists, bariatric surgeons, and pharmacists.  Primary care physicians should obtain a good history to evaluate for any alarm symptoms or intrinsic cardiac causes and should promptly refer patients for further cardiac evaluation.  Considering lifestyle modifications are the cornerstone of GERD management, patients should be counseled about weight loss, tobacco and alcohol cessation, and avoidance of late meals.  Bariatric surgery should be discussed with morbidly obese patients presenting with GERD symptoms and should be promptly referred for bariatric surgery evaluation.  Otolaryngologists and pulmonologists should consider GERD in their differentials when evaluating patients presenting with atypical symptoms that include chronic cough, laryngitis, asthma, and hoarseness.  Cases of patients with medically refractory GERD should be discussed in a multidisciplinary approach with the surgeons, pharmacists, and endoscopy nurses. Complications of GERD should be promptly recognized, evaluated, and treated to prevent long-term morbidity. This interprofessional approach helps in the management of GERD, resulting in improved patients outcomes and increased quality of life.

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Disclosure: Catiele Antunes declares no relevant financial relationships with ineligible companies.

Disclosure: Abdul Aleem declares no relevant financial relationships with ineligible companies.

Disclosure: Sean Curtis declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Antunes C, Aleem A, Curtis SA. Gastroesophageal Reflux Disease. [Updated 2023 Jul 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Instructors can request access to the Casebook Instructor's Guide on AccessPharmacy. Email User Services ( [email protected] ) for more information.

After completing this case study, the reader should be able to:

Describe the clinical presentation of gastroesophageal reflux disease (GERD), including typical, atypical, and alarm symptoms.

Discuss appropriate diagnostic approaches for GERD, including when patients should be referred for further diagnostic evaluation.

Recommend appropriate nonpharmacologic and pharmacologic measures for treating GERD.

Develop a treatment plan for a patient with GERD, including both nonpharmacologic and pharmacologic measures and monitoring for efficacy and toxicity of selected drug regimens.

Outline a patient education plan for proper use of drug therapy for GERD.

Chief Complaint

“I’m having a lot of heartburn. These pills I have been using have helped a little but it’s still keeping me up at night.”

Janet Swigel is a 68-year-old woman who presents to the GI clinic with complaints of heartburn four to five times a week over the past 5 months. She also reports some regurgitation after meals that is often accompanied by an acidic taste in her mouth. She states that her symptoms are worse at night, particularly when she goes to bed. She finds that her heartburn worsens and she coughs a lot at night, which keeps her awake. She has had difficulty sleeping over this time period and feels fatigued during the day. She reports no difficulty swallowing food or liquids. She has tried OTC Prevacid 24HR once daily for the past 3 weeks. This has reduced the frequency of her symptoms to 3–4 days per week, but they are still bothering her.

Atrial fibrillation × 12 years

Asthma × 10 years

Type 2 DM × 5 years

HTN × 10 years

Patient is married with three children. She is a retired school bus driver. She drinks one to two glasses of wine 4–5 days per week. She does not use tobacco. She has commercial prescription drug insurance.

Father died of pneumonia at age 75; mother died at age 68 of gastric cancer

Diltiazem CD 120 mg PO once daily

Hydrochlorothiazide 25 mg PO once daily

Metformin 500 mg PO twice daily

Aspirin 81 mg PO daily

Fluticasone/salmeterol DPI 100 mcg/50 mcg one inhalation twice daily

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Case-based learning: gastro-oesophageal reflux disease in adults

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After reading this article, you should be able to:

• Recognise the signs, symptoms and mechanisms of gastro-oesophageal reflux disease (GORD);
• Offer medical management and lifestyle advice to patients with GORD;
• Understand when and where to refer patients.

Gastro-oesophageal reflux disease (GORD) is a chronic condition in which gastric contents — namely acid, bile and pepsin — reflux into the oesophagus, causing the patient to experience symptoms of heartburn and acid regurgitation ​[1,2]​ . GORD is usually diagnosed symptomatically, by the occurrence of heartburn on two or more days per week ​[3]​ . An initial trial of proton-pump inhibitor (PPI) therapy in adults presenting with typical GORD symptoms is a reasonable option ​[4,5]​ .

The prevalence of GORD worldwide is increasing and this has been linked to the obesity epidemic and an ageing population ​[6]​ . GORD has a significant economic burden globally — recent studies estimate the resource implications to be approximately £760m per year in the UK alone ​[7]​ .

If acid reflux continues for a prolonged period of time, it can lead to oesophagitis, benign oesophageal stricture and Barrett’s oesophagus ​[8]​ . Approximately 10–15% of patients who have GORD will go on to develop Barrett’s oesophagus and, of these, 1–10% will develop an oesophageal adenocarcinoma over the next 10–20 years ​[9]​ . 

Mechanisms of GORD include reduced tone of the lower oesophageal sphincter, hiatal hernia, increased hydrochloric acid production and high intragastric pressure (see Table 1) ​[10]​ .

The main symptoms of GORD are heartburn and acid reflux, but other symptoms include:

• Bloating and belching;
• Persistent cough or wheezing, which may be worse at night;
• Sore throat and hoarse voice;
• Bad breath;
• Tooth decay and gum disease.

Symptoms are often worse after eating large meals, when lying down and when bending over. Patients who have a diagnosis of asthma may see a deterioration in their condition as a result of stomach acid irritating the airways ​[11,12]​ .

More severe, or ‘red-flag’, symptoms can be remembered with the acronym ‘ALARMS’ ​[13]​ :

• A naemia; 
• L oss of weight;
• A norexia or vomiting;
• R efractory to antisecretory medicines;
• M alena (black, sticky stools); 
• S wallowing problems (dysphagia). 

These red flag symptoms are signs of differential diagnosis including, but not limited to,  upper gastrointestinal malignancy , peptic ulcer disease, coeliac disease,  pancreatitis ,  inflammatory bowel disease and coronary artery disease ​[1,5,10]​ .

An appropriate history of the symptoms should be taken from the patient, including frequency, severity, timing (day or night) and duration of symptoms, as well as any specific triggers (e.g. diet) ​[5]​ . It is also important to take a medication history to ensure the patient is not on any medicines that can cause or exacerbate GORD, such as non-steroidal anti-inflammatory drugs (NSAIDs), bisphosphonates, calcium channel blockers, corticosteroids, alpha blockers, anticholinergics and tricyclic antidepressants ​[2,14]​ . 

National guidelines recommend that patients presenting with classic symptoms of GORD — heartburn and regurgitation — who are not experiencing any red-flag symptoms should be started on a four-week trial of empiric PPI once daily as a way of confirming the diagnosis ​[15,16]​ . 

Endoscopy should be reserved for patients who do not respond to a trial of PPI therapy or for those whom oesophageal cancer is suspected ​[17,18]​ . Patients should be offered urgent direct access to endoscopy via the two-week wait pathway to assess for oesophageal cancer in those who present with dysphagia or who are aged over 55 years with weight loss and any of the following: 

• Upper abdominal pain;
• Reflux; 
• Dyspepsia. 

Non-urgent, direct access to an upper gastrointestinal endoscopy should be considered to investigate for oesophageal cancer in people aged 55 years or over with ​[18]​ :

• Treatment-resistant dyspepsia;  OR
• Upper abdominal pain with a low haemoglobin;  OR
• Weight loss;
• Upper abdominal pain;  OR
• Upper abdominal pain.

Treatment options

Medicines known to cause or exacerbate symptoms of GORD should be reviewed, reduced and ceased if appropriate ​[2]​ . This will require an appropriate consultation with the patient with shared decision making. 

Short-term, symptom-control management of GORD can be done with antacids and/or alginates; however, long-term, continuous use of these is not recommended ​[2]​ . It is also worth noting that antacids and alginates can affect the absorption of other medications and therefore antacids/alginates should not be taken within one to two hours of other medicines ​[19]​ .

Patients with proven or unproven GORD should be treated with a full-dose PPI for four to eight weeks, according to the National Institute for Health and Care Excellence (NICE) ​[16]​ .

If patients fail to respond, or have an inadequate response, to treatment with a PPI, an H2-receptor antagonist can be considered as an alternative therapy option ​[2,16]​ . 

Helicobacter pylori  testing is not recommended in patients with proven oesophagitis or symptoms suggestive of GORD; however, patients who have no red-flag symptoms, have failed to respond to lifestyle changes and antacids following a four-week trial of PPI therapy should be tested for  H. Pylori ​[2,20]​ .  H. Pylori  testing should not be performed within two weeks of treatment with a PPI, as this may lead to false-negative results ​[2]​ . 

Lifestyle advice 

Lifestyle changes can help with symptom control ​[2,8,21]​ . These include losing weight, stopping smoking, drinking less alcohol, reducing the amount of caffeine consumed, having small, regular meals, taking regular exercise and avoiding eating in the three to four hours before bed. Avoiding trigger foods (e.g. spicy foods, citrus fruits, tomatoes, onions, chocolate and fizzy drinks) can also be beneficial for some patients; however, triggers can be very individual and there is no single approach that will work for everyone ​[21]​ . Raising the head of the bed by around 15cm can also help manage GORD symptoms ​[17]​ . This can be done by placing blocks under the legs at the head of the bed, by using a wedge pillow or by placing a wedge underneath the mattress.

Case study 1 

Andrew, aged 36 years, presents at his community pharmacy to ask for treatment to help with heartburn.

Andrew says he has been experiencing pain and burning in his chest and throat for the past two weeks, which gets considerably worse after eating. He divulges that he has been stressed recently because of the breakdown of his relationship and has ‘not been taking care of himself’. He explains that he has put on around three stone and often eats unhealthy snacks and takeaways.

He smokes around ten cigarettes per day and has thought about quitting in the past, but has never seen this through. He does not drink alcohol on a regular basis but will have the odd pint at a family gathering. 

He has not tried anything to manage his symptoms yet but has seen adverts for indigestion products and wondered if that might help. 

The patient does not have any red-flag signs or symptoms, is not on any medicines and has no allergies. 

The pharmacist decides to offer Andrew a trial of a PPI, instead of an indigestion product, because his symptoms are suggestive of GORD. The patient is offered counselling points on the PPI and is also offered lifestyle advice to help reduce his symptoms.

Counselling points: 

• PPIs should be taken 30–60 minutes before food, usually in a morning if taken once a day;
• PPIs are generally well tolerated, but common side effects include constipation, diarrhoea, headache and nausea and vomiting;
• Andrew should trial the PPI for up to four weeks and if symptom control has not been achieved, further investigation is recommended ​[22]​ . If symptoms worsen or red-flag symptoms are experienced, Andrew should report to the appropriate place (e.g. the hospital if he shows signs of bleeding); 
• Andrew should try to eat smaller, healthier more frequent meals and try and eat his last meal of the day no later than three hours before he goes to bed. He could be signposted to the government ‘ Eatwell’ campaign that provides useful hints and tips on a health balanced diet ​[23]​ ;
• The pharmacist could reinforce the benefits of regular exercise and maintaining a healthy body weight;
• Smoking cessation advice and support could be offered with a discussion started about nicotine replacement therapy;
• Consider talking therapies for stress if the patient deems it appropriate. 

Case study 2 

Paula, aged 57 years, attends a pharmacist-led clinic for a medication review. She has well-controlled asthma that is managed with a steroid inhaler and, when required, a salbutamol inhaler (which she rarely uses). Recently she developed sciatica, for which she has been started on pain medicines including co-codamol, naproxen and amitriptyline. Her breathing has not been affected by naproxen, but she has been experiencing symptoms of heartburn, an acidic/sour taste in her mouth and nausea but no vomiting.

She has already tried milk of magnesia and indigestion tablets, which she obtained from her local supermarket, but they have had no effect. 

The pharmacist explains to Paula that her symptoms sound like gastro-oesophageal reflux disease, which could be linked to her naproxen and amitriptyline. Differential diagnosis include erosive oesophagitis, Barrett’s oesophagus, peptic ulcer disease, gastroparesis and oesophageal cancer. 

Management:

• Stop naproxen until investigations completed — if all tests/investigations are negative this could be restarted with a PPI if essential; 
• Consider an amitriptyline dose reduction or switch to an alternative agent for neuropathic pain, such as gabapentin; 
• Give laxative advice while Paula is taking co-codamol; 
• Ensure a blood test is completed to check for anaemia (a red-flag symptom);
• Consider non-urgent, direct-access upper gastrointestinal endoscopy to assess for oesophageal cancer, as Paula is >55 years, has nausea and reflux symptoms ​[18]​ . 

Case study 3 

Simon, aged 58 years, is admitted to hospital because of dysphagia, which has been getting progressively worse. He is no longer able to tolerate solid food and is only managing liquids. Simon has lost about half a stone in the last two months but is still significantly overweight (BMI 34kg/m 2 ). He has a long history of GORD and has been taking omeprazole 20mg once a day for about five years, although he admits that he often forgets to take it.

Simon is an ex-smoker and has been for about five years, since he suffered from a transient ischaemic attack. He is allergic to aspirin and is currently prescribed clopidogrel, atorvastatin, ramipril and omeprazole. 

Simon undergoes an oesophago-gastro-duodenoscopy and is found to have a 3cm segment of Barrett’s oesophagus. He also has a stricture that requires dilatation. Biopsies are taken during endoscopy to confirm the diagnosis. The endoscopist recommends double-dose PPI: omeprazole 40mg once a day. 

The pharmacist on the ward is reviewing new patients to the ward and finds that Simon has been prescribed omeprazole 40mg once a day for Barrett’s oesophagus. Simon is also on clopidogrel, so it is advised that the omeprazole is switched to lansoprazole owing to the known interaction between omeprazole and clopidogrel ​[2]​ . Also, lansoprazole oral bioavailability is around 80–90%, whereas omeprazole is around 40% ​[22,24]​ . The pharmacist recommends a dose of 30mg twice a day, which is off-licence for GORD, but as Simon had already been on a full-dose PPI prior to this admission it would be sensible to offer a higher dose in the acute phase (around four to eight weeks) and then reduce to full-dose lansoprazole 30mg once a day ​[16]​ . NICE guidelines indicate that Simon will need to remain on this long term because he has received dilatation ​[16]​ .

Barrett’s oesophagus is a pre-malignant condition; therefore, regular endoscopic surveillance is required to monitor for development of adenocarcinoma ​[17,25]​ . According to NICE guidelines, this should be done every two to three years (as the patient’s segment of Barrett’s is 3cm and therefore defined as a long segment) ​[26]​ .

• 1 Dyspepsia – unidentified cause. National Institute for Health and Care Excellence . 2024. https://cks.nice.org.uk/topics/dyspepsia-unidentified-cause (accessed March 2024)
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• 3 Pithawa A. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: pathophysiology, diagnosis, management. Medical Journal Armed Forces India. 2007;63:205. https://doi.org/10.1016/s0377-1237(07)80085-2
• 4 Chen JW, Vela MF, Peterson KA, et al. AGA Clinical Practice Update on the Diagnosis and Management of Extraesophageal Gastroesophageal Reflux Disease: Expert Review. Clinical Gastroenterology and Hepatology. 2023;21:1414-1421.e3. https://doi.org/10.1016/j.cgh.2023.01.040
• 5 Gastro-oesophageal reflux disease. BMJ Best Practice. 2022. https://bestpractice.bmj.com/topics/en-gb/82#:~:text=The%20classic%20symptoms%20are%20heartburn,%2C%20weight%20loss%2C%20anaemia). (accessed March 2024)
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• 7 Nirwan JS, Hasan SS, Babar Z-U-D, et al. Global Prevalence and Risk Factors of Gastro-oesophageal Reflux Disease (GORD): Systematic Review with Meta-analysis. Sci Rep. 2020;10. https://doi.org/10.1038/s41598-020-62795-1
• 8 Badiu C. Oxford Handbook of Clinical Medicine (10 Ed.). Acta Endo (Buc). 2019;15:144–144. https://doi.org/10.4183/aeb.2019.144
• 9 Dyspepsia – Proven GORD. National Institute for Health and Care Excellence . 2023. https://cks.nice.org.uk/topics/dyspepsia-proven-gord/ (accessed March 2024)
• 10 Antunes C, Aleem A, Curtis S. statpearls. Published Online First: 3 July 2023.
• 11 Heartburn and acid reflux. NHS. 2019. https://www.nhs.uk/conditions/heartburn-and-acid-reflux/ (accessed March 2024)
• 12 Gastro-esophageal Reflux Disease . NHS Inform. 2023. https://www.nhsinform.scot/illnesses-and-conditions/stomach-liver-and-gastrointestinal-tract/gastro-oesophageal-reflux-disease-gord/#symptoms-of-gord (accessed March 2024)
• 13 Collins P. Crash Course: Gastroenterology . 3rd ed. Elsevier 2008. https://shop.elsevier.com/books/crash-course-gastroenterology/collins/978-0-7234-3470-2 (accessed March 2024)
• 14 Summers A, Khan Z. Managing dyspepsia in primary care. Practitioner . 2009;253:23–7, 2–3.
• 15 Katz PO, Dunbar KB, Schnoll-Sussman FH, et al. ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol. 2021;117:27–56. https://doi.org/10.14309/ajg.0000000000001538
• 16 Gastro-Oesophageal Reflux Disease and Dyspepsia in Adults: Investigation and Management [CG184]. National Institute for Health and Care Excellence . 2014. https://www.nice.org.uk/Guidance/CG184 (accessed March 2024)
• 17 Lynch K. Gastroesophageal Reflux Disease . MSD Manual Professional Edition. 2024. https://www.msdmanuals.com/en-gb/professional/gastrointestinal-disorders/esophageal-and-swallowing-disorders/gastroesophageal-reflux-disease-gerd (accessed March 2024)
• 18 Suspected Cancer: Recognition and Referral [NG12]. National Institute for Health and Care Excellence . 2021. https://www.nice.org.uk/guidance/ng12 (accessed March 2024)
• 19 Peptac Peppermint Liquid. Summary of Product Characteristics (SmPC). Electronic Medicines Compendium. 2023. https://www.medicines.org.uk/emc/product/15318 (accessed March 2024)
• 20 Test and Treat for Helicobacter Pylori (HP) in Dyspepsia. Quick reference guide for primary care: for consultation and local adaptation. Public Health England. 2017. https://assets.publishing.service.gov.uk/media/5d6ceea740f0b607c946aa65/HP_Quick_Reference_Guide_v18.0_August_2019_change_highlighted.pdf (accessed March 2024)
• 21 All You Need to Know About Heartburn and Reflux. Guts UK. 2023. https://gutscharity.org.uk/advice-and-information/symptoms/heartburn-and-reflux/ (accessed March 2024)
• 22 Omeprazole 20 mg gastro-resistant tablets. Summary of Product Characteristics (SmPC). Electronic Medicines Compendium. 2024. https://www.medicines.org.uk/emc/product/663/smpc (accessed March 2024)
• 23 The Eatwell Guide. Public Health England. 2016. https://www.gov.uk/government/publications/the-eatwell-guide (accessed March 2024)
• 24 Lansoprazole 30 mg gastro-resistant capsules, hard. Summary of Product Characteristics (SmPC). Electronic Medicines Compendium. 2023. https://www.medicines.org.uk/emc/product/14551/smpc (accessed March 2024)
• 25 Barrett’s oesophagus and stage 1 oesophageal adenocarcinoma: monitoring and management [NG231]. National Institute for Health and Care Excellence . 2023. https://www.nice.org.uk/guidance/ng231/chapter/Recommendations#endoscopic-surveillance (accessed March 2024)
• 26 McDaniel M, Conran RM. Educational Case: Barrett Esophagus. Academic Pathology. 2019;6:2374289519848089. https://doi.org/10.1177/2374289519848089

Great article and a very useful case study.

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Gastroesophageal Reflux Disease (GERD) Diagnosis: A Primary Care Case Study

The following test-and-teach case is an educational program modeled on the interactive grand rounds approach. The questions are designed to test your current knowledge. After each question, you will be able to see whether you answered the question correctly. The author will then present referenced information to support the most appropriate answer choice. Please note that these questions are designed to challenge you, and you are not penalized for answering the questions incorrectly.

Patient History

A 34-year-old man visits a primary care clinic because his family says that his voice sounds hoarse and he finds that he needs to clear his throat often. During the initial visit, he tells you that he returned from military service 1 year ago and that his routine physical exam 6 months ago was normal. He is slightly overweight and currently smokes 1 pack of cigarettes a day and has done so since age 20. He denies experiencing any heartburn or regurgitation, although he has upper abdominal discomfort. He has no family history of esophageal cancer. His hoarseness has developed over the last 2 months.

Defining GERD

Medscape Family Medicine © 2008 

• Case Report
• Open access
• Published: 13 April 2016

A case of advanced systemic sclerosis with severe GERD successfully treated with acotiamide

• Ryo Kato 1 ,
• Kiyokazu Nakajima 1 , 2 ,
• Tsuyoshi Takahashi 1 ,
• Yasuhiro Miyazaki 1 ,
• Tomoki Makino 1 ,
• Yukinori Kurokawa 1 ,
• Makoto Yamasaki 1 ,
• Shuji Takiguchi 1 ,
• Masaki Mori 1 &
• Yuichiro Doki 1  

Surgical Case Reports volume  2 , Article number:  36 ( 2016 ) Cite this article

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The majority of systemic sclerosis (SSc) patients have gastrointestinal tract involvement, but therapies of prokinetic agents are usually unsatisfactory. Patients are often compromised by the use of steroid; therefore, a surgical indication including fundoplication has been controversial. There is no report that advanced SSc with severe gastroesophageal reflux disease (GERD) is successfully treated with acotiamide, which is the acetylcholinesterase (AChE) inhibitor designed for functional dyspepsia (FD). We report a 44-year-old woman of SSc with severe GERD successfully treated with acotiamide. She had received medical treatment in our hospital since 2003. She had been aware of the significant gastroesophageal reflux symptoms (e.g., heartburn, chest pain, and dysphagia) due to the development of esophageal hardening associated with SSc since 2014. As a result of upper gastrointestinal series, upper gastrointestinal endoscopy, and 24-h pH monitoring and frequency scale for the symptoms of the GERD (FSSG) scoring, she has been diagnosed with GERD associated with SSc. First of all, she started to take prokinetic agents Rikkunshito and mosapride and proton pump inhibitor; there was no change in reflux symptoms. So, we started to prescribe her the acotiamide.

After oral administration started, reflux symptoms have been improved. Five months after oral administration, FSSG score, a questionnaire for evaluation of the symptoms of GERD, was improved. Since its introduction of acotiamide, the patient has kept free from symptoms for 6 months.

Systemic sclerosis (SSc) is a multisystem and chronic disease characterized by abnormalities of small blood vessels and fibrosis of the skin and internal organs. SSc, when advanced, is often compromised with severe gastroesophageal reflux disease (GERD), which may be lethal in a worst-case scenario. A wide variety of medication has been used [ 1 – 5 ]; however, none of them are promising for patients with SSc. In addition, patients with SSc are often compromised by the use of steroid; therefore, a surgical indication including fundoplication has been controversial.

In this short communication, we describe our recent case of advanced SSc patients with severe GERD, who was successfully treated with a new drug originally designed for functional dyspepsia (FD).

Case presentation

A 44-year-old woman of SSc had received medical treatment in our hospital since 2003. She had been aware of the significant gastroesophageal reflux symptoms and esophagus stasis due to the development of esophageal hardening associated with SSc since 2014. On physical examination, cachexia, a “mouse face” appearance and ulceration in the distal phalanges were identified. The abnormal build-up of fibrous tissue in the skin can cause the skin to tighten so severely that her fingers curl and lose their mobility (Fig.  1 ). Because she had been aware of the worsening of gastroesophageal reflux symptoms, she received a medical examination from this department. Upper gastrointestinal series revealed no expansion and meandering esophagus, and reflux into the esophagus in the Trendelenburg position (Fig.  2 ). The upper gastrointestinal endoscopy showed reflux esophagitis of Los Angeles classification grade C and esophagus residue (Fig.  3 ).

The abnormal build-up of fibrous tissue in the skin can cause the skin to tighten so severely that fingers curl and lose their mobility in SSc

Upper gastrointestinal series revealed no expansion and meandering esophagus and reflux into the esophagus in the Trendelenburg position

The upper gastrointestinal endoscopy showed reflux esophagitis of Los Angeles classification grade C and esophagus residue

A 24-h esophageal pH monitoring revealed significant acid reflux: the number of refluxes was 81 times, pH was below 4.0 for 32.1 %, mean pH was 4.55, and DeMeester score (normal <14.75) was 117.5 (Fig.  4 ). Symptoms of gastroesophageal reflux disease (frequency scale for the symptoms of the GERD (FSSG)) score, a questionnaire evaluating the symptoms of GERD, was 34 points [ 6 ] (maximum 48 points). As a result of these tests, she has been diagnosed with GERD associated with SSc. Treatment with Rikkunshito and mosapride, which are prokinetic agents, and proton pump inhibitor was started. However, her symptoms were not improved. Therefore, we started the acotiamide on June 2015, which was a new drug originally designed for FD. Since then, her symptoms which were heartburn, burp, and nausea after a meal were improved. Five months after acotiamide was started, the FSSG score was reduced to 21 points (Fig.  5 ). However, the results of 24-h esophageal pH monitoring showed worsening acid reflux: the number of refluxes was 152 times, pH was below 4.0 for 60.5 %, mean pH was 3.73, and DeMeester score (normal <14.75) was 211.6 (Fig.  4 ). The upper gastrointestinal series and upper gastrointestinal endoscopy did not change.

A 24-h pH monitoring was performed before and after acotiamide oral administration. These four items showed worsening before and after the administration

After oral administration of acotiamide, FSSG score was improved from 34 points to 21 points

Since the introduction of acotiamide, the patient has been free from symptoms to date.

In 1994, Sjogren proposed a progression of SSc with gastrointestinal involvement, vascular damage, neurogenic impairment, and myogenic dysfunction with the replacement of normal smooth muscle by collagens fibrosis and atrophy [ 7 ]. It is distinguished in diffuse cutaneous SSc (dcSSc) or limited cutaneous SSc (lcSSc) whether skin hardening exceeds an elbow or a knee [ 8 ]. Next to the skin, the gastrointestinal tract is the second most common site of SSc organ damage that can affect patients with lcSSc and dcSSc [ 9 ]. It affects the gastrointestinal tract in more than 80 % of patients. Reflux esophagitis is found in 50–90 % of SSc patients [ 7 , 10 ].

The common characteristics of GERD seen in SSc patients are as follows. The upper GI series often shows peristaltic decrease and expansion of the lower esophagus. The upper gastrointestinal endoscopy shows linear redness and erosion of the lower esophagus caused by the reflux, which often merges with the Barett esophagus. In addition, the merger frequency of esophageal cancer is often in SSc. Esophageal dysmotility leads to impaired acid clearance, and 24-h monitoring shows prolongation of esophageal exposure time to gastric acid [ 11 ].

Its treatment, either medical or surgical, has been still challenging. The major medical treatment option includes use of histamine-2 receptor antagonist (H2RA) and/or proton pomp inhibitor (PPI) for the purpose of controlling stimulation and inflammation of the esophageal mucosa by the gastric acid reflux [ 12 – 14 ]. Surgery, e.g., Nissen fundoplication, can be considered for drug-resistant reflux disease [ 15 ]. These medical/surgical treatments have been shown not as promising as those for reflux patients without SSc [ 16 ].

The last option for SSc patients with severe GERD is a group of prokinetic drugs. A wide variety of prokinetic agents have been used, such as mosapride citrate, metoclopramide, domperidone, erythromycin, octreotide, and dinoprost [ 1 – 5 ]. However, therapies of traditional prokinetic agents are usually unsatisfactory for severe GERD patients.

Acotiamide is the novel prokinetic agent basically designed for FD; it is the acetylcholinesterase (AChE) inhibitor. FD is a chronic disorder of sensation and movement (peristalsis) in the upper gastrointestinal tract. The acetylcholine (Ach) is released from cholinergic nerve terminals and lets the gastrointestinal tract shrink by binding to the muscarinic receptor of the gastrointestinal smooth muscle. It is thought that the Ach is broken down immediately by AChE and enterokinesis is regulated by this reaction. Acotiamide inhibits AChE and regulates the resolution of Ach. As a result, it increases the quantity of ACh available in the synaptic cleft and therefore improves enterokinesis [ 17 ].

We have prescribed a variety of traditional prokinetic agents, without obtaining even temporary relief of her symptoms. Therefore, we prescribed acotiamide. We performed upper gastrointestinal series, gastrointestinal endoscopy, 24-h pH monitoring, and the quality of life (QOL) scores for the assessment of gastroesophageal reflux before and after oral administration of acotiamide on this patient. No changes were observed before and after treatment in the upper GI series and upper gastrointestinal endoscopy. Acotiamide does not show the emission promoting effect on the normal gastric emptying in rats. However, prior research reports that acotiamide does improve the gastric emptying during restraint stress. Acotiamide might have led to symptom improvement due to the suppressed response to stress by decreasing the expression of NmU, a stress-related gene in the hypothalamus, via the vagus nerve [ 18 ].We think this may be a partial reason why our patient showed improvement of her GI symptoms.

In the 24-h pH monitoring, DeMeester score even showed a worsening from 117 to 211. However, FSSG, which is one of the established QOL scoring system, showed improvement from total 34 to 21 points. FSSG is a questionnaire composed of 12 questions and classified into two groups, which are five items related to “dysmotility” symptoms and seven items to “acid reflux” symptoms. In our case, the score related to both symptoms were improved from 17 to 10 points and 17 points to 11 points, respectively. As we describe later, these improvements can be explained by the pharmacological effects of acotiamide on both the gastric and the esophageal functions.

In fact, this patient was clearly aware of the improvement of clinical symptoms, and QOL has been improved.

In our case, traditional prokinetic agents attempted prior to acotiamide were not effective. Only acotiamide showed substantial relief of the patient’s symptom. We speculated this might be because of these two factors: (1) pharmacologically, acotiamide may not only affect the gastric emptying but also improve fundic accommodation of adaptive relaxation, and (2) acotiamide may directly act on the esophageal body and improve esophageal peristalsis. The authors have reached the above speculation based on the results of FSSG score: improvements of early satiety and chest discomfort. The question score “Do you feel full while eating meals?” was improved from 4 points to 2 points and “Do some things get stuck when you swallow?” was improved from 3 points to 2 points, respectively.

We just experienced one case; therefore, further accumulation of similar cases is definitely required. In our case, no objective improvement was observed on classical 24-h pH monitoring. The authors believe this examination might not be appropriate as an evaluation tool of GERD in patients with severe esophageal motor dysfunction like advanced SSc patients. Novais et al. reported that the 24-h abnormal pH tracings were classified into three types: (i) 24-h abnormal pH, with a true GERD pattern, i.e., sharp sudden pH drops, reaching values below 3 and then returning to usual esophageal pH (pH 6–7) (Fig.  6 a); (ii) 24-h abnormal pH with a pattern suggesting esophageal fermentation due to retained food, i.e., steady drop of pH not reaching values below 3.0 (Fig.  6 b); and (iii) negative 24-h pH, i.e., presence of physiological reflux (reflux episodes occurring in less than 4.5 % of total examining time) or zero reflux (absence of any episode of pH lower than 4.0) [ 19 ]. In a 24-h pH monitoring after acotiamide was started, there were many frequent waveforms of (ii) than those of (i). The esophageal food fermentation may have affected the results of this case. The QOL score, including FSSG is likely to accurately reflect the symptoms of patients than 24-h pH monitoring. Future tasks are to perform a detailed study by using a new method of measuring such as high resolution manometry.

A 24-h pH tracing of this patient. True gastroesophageal reflux ( a ) and fermentation ( b )

Conclusions

We have experienced a case of advanced SSc with severe GERD successfully treated with acotiamide. Acotiamide might become a help of advanced SSc with severe GERD patient whose surgical indication has been controversial.

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Abbreviations

acetylcholine

acetylcholinesterase

functional dyspepsia

frequency scale for the symptoms of the GERD

gastroesophageal reflux disease

• systemic sclerosis

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Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2, E-2, Yamadaoka, Suita, Osaka, 565-0871, Japan

Ryo Kato, Kiyokazu Nakajima, Tsuyoshi Takahashi, Yasuhiro Miyazaki, Tomoki Makino, Yukinori Kurokawa, Makoto Yamasaki, Shuji Takiguchi, Masaki Mori & Yuichiro Doki

Division of Next Generation Endoscopic Intervention (Project ENGINE), Global Center for Medical Engineering and Informatics, Center of Medical Innovation and Translational Research, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan

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The authors declare that they have no competing interests.

Authors’ contributions

All authors participated in the management of the patient in this case report. KN is a chief surgeon of our hospital and supervised the case and also supervised the writing of the manuscript. YD is a chairperson of our department and supervised the entire process. All authors read and approved the final manuscript.

Ryo Kato is the first author.

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Kato, R., Nakajima, K., Takahashi, T. et al. A case of advanced systemic sclerosis with severe GERD successfully treated with acotiamide. surg case rep 2 , 36 (2016). https://doi.org/10.1186/s40792-016-0162-5

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DOI : https://doi.org/10.1186/s40792-016-0162-5

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Gastroesophageal reflux disease in an 8-year-old boy: a case study

Affiliation.

• 1 [email protected]
• PMID: 16584951
• DOI: 10.1016/j.jmpt.2006.01.004

Objective: To present the diagnosis and management of gastroesophageal reflux disease found in a pediatric patient, to discuss the importance of a detailed case history, and to bring forward some of the most important clues, both verbal and nonverbal, that can lead to the diagnosis.

Clinical features: An 8-year-old boy was brought to a chiropractic clinic by his mother complaining of headache and neck pain. Based on the history and physical examination, a diagnosis of cervicogenic headache was made.

Intervention and outcome: Treatment consisted of chiropractic manipulation of the upper cervical spine in combination with cranial treatment was applied in addition to dietary advice. The headache returned and the patient was then referred to a colleague for a second opinion. Based on a detailed history, gastroesophageal reflux disease was diagnosed and the patient was referred to a specialist for suitable treatment.

Conclusion: Because of the position as first-line health practitioners, it is inevitable that doctors of chiropractic will be faced with complaints of a nonbiomechanical nature. It is important to recognize conditions, such as gastroesophageal reflux, at an early stage and to refer appropriately.

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Resolution of gastroesophageal reflux disease following correction for upper cross syndrome—a case study and brief review.

1. Introduction

2. case report, 3. discussion, 4. conclusions, author contributions, institutional review board statement, informed consent statement, data availability statement, conflicts of interest.

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Chu, E.C.-P.; Butler, K.R. Resolution of Gastroesophageal Reflux Disease Following Correction for Upper Cross Syndrome—A Case Study and Brief Review. Clin. Pract. 2021 , 11 , 322-326. https://doi.org/10.3390/clinpract11020045

Chu EC-P, Butler KR. Resolution of Gastroesophageal Reflux Disease Following Correction for Upper Cross Syndrome—A Case Study and Brief Review. Clinics and Practice . 2021; 11(2):322-326. https://doi.org/10.3390/clinpract11020045

Chu, Eric Chun-Pu, and Kenneth R. Butler. 2021. "Resolution of Gastroesophageal Reflux Disease Following Correction for Upper Cross Syndrome—A Case Study and Brief Review" Clinics and Practice 11, no. 2: 322-326. https://doi.org/10.3390/clinpract11020045

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(Gastro-Esophageal Reflux Disease)

Mr. c is a 63-year-old man who owns a management consulting firm that focuses on improving the quality of business decisions by using enhanced data analysis..

He had been taking the “purple pill”,  a proton pump inhibitor (PPI), twice a day for five years for heartburn. His GERD symptoms were initially alleviated by the medication but had slowly become worse, despite continuing the drug.

Given his penchant for data analysis, we sent Mr. C medical studies that outlined other methods of addressing GERD. We also provided information on the side effects of long-term PPI use, including:

• A significant increase in bone fractures, kidney and liver disease,
• A 30% increase in all-cause mortality , mostly from heart disease, kidney failure, and gastric cancer, and 
• Difficulty in stopping the drug because the PPI itself causes a rebound hyperacidity which can increase the frequency and severity of GERD pain when stopped.

Although PPI’s became available in 1988, the most convincing data on the increased death rate with PPIs has only been available since 2019.

Mr. C appreciated the information but was disturbed that he had been taking PPIs for years without knowing the health risks . Mr. C had started a protocol to discontinue his PPI use over the next 6 to 12 months. Industry-sponsored “public service” websites minimize the risks while “spinning the truth.”

The Science – The Concerns with Proton Pump Inhibitors (PPI’s)

When PPIs were first released, the FDA stressed that treatment beyond four to eight weeks was not recommended because the long-term safety profile of the drug was unknown. Thirty years later, a 30% increase in mortality was found.

Reversing Needless Risk and Unnecessary Costs

Severe angina, knowledge can heal.

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