Bile Reflux
Duodenogastric Reflux
Gastroesophageal Reflux
Bile
Bile Acids and Salts
Postgastrectomy Syndromes
Barrett Esophagus
Esophagus
Vesico-Ureteral Reflux
Anastomosis, Roux-en-Y
Biliary Tract Diseases
Bile Ducts
Stomach
Gastric Juice
Esophagitis, Peptic
Gastric Mucosa
Pyloric Antrum
Metaplasia
Laryngopharyngeal Reflux
Helicobacter pylori
Helicobacter Infections
Enterogastric reflux mimicking gallbladder disease: detection, quantitation and potential significance. (1/64)
OBJECTIVE: Visualization of enterogastric reflux (EGR) may be present during hepatobiliary imaging. Reflux of bile may damage the gastric mucosa, altering its function, and cause such symptoms as epigastric pain, heartburn, nausea, intermittent vomiting and abdominal fullness. These symptoms also are associated with gallbladder disease. The aim of this study was to quantitate the EGR index (EGRI) and to determine if a difference exists in normal and abnormal responses using standard cholecystokinin (CCK)-augmented hepatobiliary imaging. METHODS: This study used 129 patients. LAO dynamic data on a 128 x 128 matrix at a rate of 1 frame/min were obtained. After the gallbladder ejection fraction (GBEF) was determined, the EGRI (%) was calculated by relating the counts in the gastric ROI to the counts in the hepatobiliary ROI at a specified time. The results were compared with the patient's final clinical diagnosis. RESULTS: Normal responders (GBEF > or = 35%) had a higher EGRI than abnormal responders with a P = 0.001 EGR observed in 75 patients (58.1%). Significant reflux (EGRI > or = 14.2% at 15 min) was observed in 29 additional patients (22.5%). Patients with EGRI > or = 24.5% showed a strong association with the pathophysiologic syndrome of gastritis, alkaline reflux, gastric ulcer and gastro esophageal reflux disease. There was no EGR observed in the remaining 25 patients (19.4%). CONCLUSION: This simple addition to the CCK-augmented hepatobiliary imaging may both detect and quantitate abnormal EGR as the cause of the patient's symptoms in the presence of a normal GBEF result, and/or those patients with risk factors for gastritis. (+info)Cell proliferation in type C gastritis affecting the intact stomach. (2/64)
AIMS: Type C gastritis caused by bile reflux has a characteristic appearance, similar to that seen in other forms of chemical gastritis, such as those associated with NSAIDs or alcohol. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging, particularly where there is chronic epithelial injury associated with bile reflux. It has been shown previously that type C gastritis is associated with increased cell proliferation in the postsurgical stomach. The aim of this study was to determine cell proliferation in type C gastritis caused by bile reflux affecting the intact stomach. METHODS: Specimens from 15 patients with a histological diagnosis of type C gastritis on antral biopsy were obtained from the pathology archives between 1994 and 1997. A control group of nine normal antral biopsies was also selected and all underwent MIB-1 immunostaining. The gastric glands were divided into three zones (zone 1, gastric pit; zone 2, isthmus; and zone 3, gland base) and the numbers of positively staining nuclei for 500 epithelial cell nuclei were counted in each zone to determine the percentage labelling index (LI%). RESULTS: Cell proliferation was significantly higher in all three zones of the gastric glands with type C gastritis compared with controls as follows: zone 1, median LI% in type C gastritis 64.7 (range, 7.8-99.2), controls 4.7 (range, 2.0-11.3); zone 2, median LI% in type C gastritis 94.7 (range, 28.8-98.7), controls 40.2 (range, 23.1-70.3); and zone 3, median LI% in type C gastritis 20.0 (range, 1.3-96.0), controls 2.6 (range, 0.9-8.7). CONCLUSIONS: Bile reflux is thought to act as a promoter of gastric carcinogenesis in the postsurgical stomach. The same may be true in the intact stomach. (+info)Bile reflux gastritis and Barrett's oesophagus: further evidence of a role for duodenogastro-oesophageal reflux? (3/64)
BACKGROUND: There is increasing evidence that reflux of bile plays a part in the pathogenesis of Barrett's oesophagus. Bile injury to the gastric mucosa results in a "chemical" gastritis in which oedema and intestinal metaplasia are prominent. AIM: To determine if patients with Barrett's oesophagus have more bile related changes in antral mucosa than patients with uncomplicated gastro-oesophageal reflux disease (GORD) or non-ulcer dyspepsia (NUD). PATIENTS AND METHODS: Patients were identified by a retrospective search of pathology records and those with a clinically confirmed diagnosis of either Barrett's oesophagus or reflux oesophagitis who had oesophageal and gastric biopsies taken at the same endoscopy and had no evidence of Helicobacter pylori infection entered the study. Control biopsies were taken from H pylori negative NUD patients. Antral biopsies were examined "blind" to clinical group and graded for a series of histological features from which the "reflux gastritis score" (RGS) and "bile reflux index" (BRI) could be calculated. The reproducibility of these histological scores was tested by a second pathologist. RESULTS: There were 100 patients with Barrett's, 61 with GORD, and 50 with NUD. The RGSs did not differ between groups. BRI values in the Barrett's group were significantly higher than those in GORD subjects (p=0.014) which in turn were higher than those in NUD patients (p=0.037). Similarly, the frequency of high BRI values (>14) was significantly greater in the Barrett's group (29/100; 29%) than in the GORD (9/61; 14.8%) or NUD (4/50; 8%) group. However, agreement on BRI values was "poor", indicating limited applicability of this approach. CONCLUSION: Patients with Barrett's oesophagus have more evidence of bile related gastritis than subjects with uncomplicated GORD or NUD. The presence of bile in the refluxate could be a factor in both the development of "specialised" intestinal metaplasia and malignancy in the oesophagus. (+info)Influence of pantoprazole on oesophageal motility, and bile and acid reflux in patients with oesophagitis. (4/64)
BACKGROUND: Reflux of duodeno-gastric juice into the oesophagus appears to be involved in the pathogenesis of both reflux oesophagitis and oesophageal adenocarcinoma. Although proton pump inhibitors have been shown to decrease acid reflux and heal oesophagitis, their effect on biliary reflux and motility is less clear. AIM: To investigate whether pantoprazole also reduces bile reflux and whether this is paralleled by a change in oesophageal motility. METHODS: Combined 24-h measurements of intraoesophageal bilirubin concentration, pH and pressure were performed in 18 symptomatic patients with endoscopically proven reflux oesophagitis before and on day 28 of treatment with pantoprazole, 40 mg/day, under standardized conditions. A reflux symptom score was determined initially and every 2 weeks thereafter. After 56 days on medication, a control endoscopy was performed. RESULTS: The symptom score and the acid and bile reflux improved significantly, whereas the motility parameters did not change during the study period. Helicobacter pylori-positive patients had a significantly higher bile reflux time (32.1 +/- 4.3%) than H. pylori-negative patients (16.3 +/- 3.1%) (P=0.009). The endoscopic healing rate was 89%. The cough symptoms disappeared in three of four patients. CONCLUSIONS: The proton pump inhibitor pantoprazole decreases both acid and bile reflux. The decrease of bile reflux cannot be explained by increased oesophageal clearance as oesophageal motility did not improve with therapy. Interestingly, H. pylori infection of the stomach was associated with higher levels of oesophageal bile reflux. (+info)Bile reflux gastritis and intestinal metaplasia at the cardia. (5/64)
BACKGROUND AND AIMS: Intestinal metaplasia (IM) at the cardia is likely to be a precursor of cardia cancer. Previous work has shown that it is associated with chronic inflammation attributable to either gastro-oesophageal reflux disease (GORD) or Helicobacter pylori infection. An alternative aetiological factor is bile reflux. Duodenogastric reflux brings about histological changes in the gastric mucosa that can be graded and used to calculate a bile reflux index (BRI). We used the BRI to assess whether reflux of bile plays a part in the development of cardia IM. METHODS: Histological changes in simultaneous gastric antrum and cardia biopsies from 267 dyspeptic patients were independently graded by two pathologists. The association between cardia IM and age, sex, clinical group, H pylori status, increased BRI (>14), and inflammation at the cardia were evaluated using logistic regression. RESULTS: A total of 226 patients had adequate cardia and antral biopsies; 149 had GORD and 77 had non-ulcer dyspepsia. Cardia IM was present in 66 (29%) patients, of whom 28 (42%) had complete IM. Increasing age, male sex, chronic inflammation, and a high BRI emerged as significant independent associations with cardia IM. Clinical group and H pylori status were not independent risk factors. CONCLUSIONS: Histological evidence of bile reflux into the stomach is associated with cardia IM. This could have an important bearing on carcinogenesis at this site. (+info)Efficacy and one year follow up of argon plasma coagulation therapy for ablation of Barrett's oesophagus: factors determining persistence and recurrence of Barrett's epithelium. (6/64)
INTRODUCTION: Barrett's epithelium (BE) has malignant potential. Neither acid suppression nor antireflux surgery produce consistent or complete regression of the metaplastic epithelium. Endoscopic thermoablation with argon plasma coagulation (APC) offers a different approach but factors influencing its outcome have not been systematically examined. AIM: To assess the efficacy of APC and factors influencing initial and one year outcome. METHODS: Fifty patients, mean age 61.4 years, mean BE length 5.9 cm (range 3-19), underwent APC therapy at four weekly intervals while receiving proton pump inhibitor (PPI) therapy. BE margins were marked by India ink tattooing and extent was documented by grid drawings, photography, and 2 cm interval quadrantic jumbo biopsies. Twenty four hour ambulatory oesophageal pH studies were done while on PPIs before and after APC therapy, and Bilitec bilirubin monitoring after APC completion. RESULTS: A total of 68% of patients achieved >90% BE ablation after a median of four APC sessions. Persistent BE (>10% original BE area) was associated with longer initial BE length despite more APC sessions. Persistent acid and bile reflux on PPIs, although commoner in this group, were not significantly different from those successfully ablated. Fifteen of 34 patients (44%) with successful macroscopic clearance had buried glands, present in 8.3% of a total of 338 biopsies. At the one year follow up, only 32% of those with initial successful ablation showed no recurrence. BE recurred or increased in most with mean segment length increases of 1.1 cm and 1.6 cm, respectively, in patients with previous full ablation and those with persistent BE. The presence of buried glands did not predict BE recurrence. Patients who reduced their PPI dose had significantly greater BE recurrence. CONCLUSIONS: APC is most effective for shorter segment BE ablation but "buried" glands do occur. Recurrence of BE is common at one year, especially in those with initial persistent and/or long segment BE and those who reduce their PPI dose. (+info)The effect of famotidine on gastroesophageal and duodeno-gastro-esophageal refluxes in critically ill patients. (7/64)
AIM: To investigate the effect of famotidine on gastroesophageal reflux (GER) and duodeno-gastro-esophageal reflux (DGER) and to explore it's possible mechanisms. To identify the relevant factors of the reflux. METHODS: Nineteen critically ill patients were consecutively enrolled in the study. Dynamic 24 hours monitoring of GER and DGER before and after administration of famotidine was performed. The parameters of gastric residual volume, multiple organ disorder syndrome (MODS) score, acute physiology and chronic health evaluation II (APACHE II) score and PEEP were recorded. Paired t test; Wilcoxon signed ranks test and Univariate analysis with Spearman's rank correlation were applied to analyse the data. RESULTS: Statistical significance of longest acid reflux, reflux time of pH<4 and fraction time of acid reflux was observed in ten critically ill patients before and after administration. P value is 0.037, 0.005, 0.005 respectively. Significance change of all bile reflux parameters was observed before and after administration. P value is 0.007,0.024, 0.005, 0.007, 0.005. GER has positive correlation with APACHE II score and gastric residual volume with correlation coefficient of 0.720, 0.932 respectively. CONCLUSION: GER and DGER are much improved after the administration of famotidine. GER is correlated with APACHE II score and gastric residual volume. (+info)Reflux and Barrett's oesophagitis after gastric surgery--long-term follow-up and implications for the roles of gastric acid and bile in oesophagitis. (8/64)
BACKGROUND: The role of gastric acid is difficult to separate from that of bile in oesophageal reflux, and the complications of this can take many years to develop. Gastric surgery patients provide a good model for both significant bile reflux and marked gastric acid inhibition. AIM: To study the oesophageal abnormalities in gastric surgery patients undergoing long-term follow-up, compared with patients with intact stomachs. METHODS: Two hundred and forty adult patients were endoscoped regardless of their age, sex or type of surgical procedure. Oesophageal damage was graded on a scale of 0-5, and biopsies were taken to exclude neoplasia, to diagnose Barrett's oesophagus and to identify Helicobacter pylori. RESULTS: Of the 240 patients studied, 140 had undergone gastric surgery 27 years (19-31 years) [median (interquartile range)] prior to endoscopy, and these patients had milder oesophageal scores and fewer cases of Barrett's oesophagitis. Of the 119 patients with post-surgical bile reflux gastritis, 31 (26%) had oesophagitis, two (1.7%) had Barrett's oesophagitis and oesophageal scores of 0 (0-1) were found. These results compared with corresponding values of 37 (37%; P = 0.11), 11 (11%; P = 0.007) and 0 (0-2) (P = 0.046), respectively, in 100 patients with intact stomachs. In addition, of the 83 patients with vagotomy, 19 had oesophagitis (23%; P = 0.05), none had Barrett's oesophagitis and lower oesophageal scores (P = 0.02) were found. CONCLUSIONS: The prevalence and severity of reflux and Barrett's oesophagitis are not increased in patients with a long history of gastric surgery, particularly after vagotomy, and despite being at risk of bile reflux. (+info)Learn More:
Bile Reflux | Symptoms, Causes, Treatments | American ...
https://www.gi.org/topics/bile-reflux/
GER can be caused by a variety of factors, including:
* Weakening of the lower esophageal sphincter (LES), which allows stomach acid to flow back up into the esophagus.
* Delayed gastric emptying, which can cause food and stomach acid to remain in the stomach for longer periods of time and increase the risk of reflux.
* Obesity, which can put pressure on the stomach and cause the LES to weaken.
Symptoms of GER can include:
* Heartburn: a burning sensation in the chest that can radiate to the throat and neck.
* Regurgitation: the sensation of food coming back up into the mouth.
* Difficulty swallowing.
* Chest pain or tightness.
* Hoarseness or laryngitis.
If left untreated, GER can lead to complications such as esophagitis (inflammation of the esophagus), strictures (narrowing of the esophagus), and barrett's esophagus (precancerous changes in the esophageal lining).
Treatment options for GER include:
* Lifestyle modifications, such as losing weight, avoiding trigger foods, and elevating the head of the bed.
* Medications, such as antacids, H2 blockers, and proton pump inhibitors, to reduce acid production and relax the LES.
* Surgical procedures, such as fundoplication (a procedure that strengthens the LES) and laparoscopic adjustable gastric banding (a procedure that reduces the size of the stomach).
It is important to seek medical attention if symptoms persist or worsen over time, as GER can have serious complications if left untreated.
1. Dumping syndrome: This occurs when food moves too quickly through the small intestine, causing symptoms such as nausea, vomiting, diarrhea, and dizziness.
2. Gastric band erosion: The gastric band can erode into the stomach wall, causing pain, inflammation, and infection.
3. Gastric dilatation-volvulus: This occurs when the stomach expands and twists, causing a blockage that can lead to vomiting, abdominal pain, and difficulty breathing.
4. Gastroesophageal reflux disease (GERD): This is a condition in which stomach acid flows back up into the esophagus, causing heartburn, chest pain, and difficulty swallowing.
5. Hiatal hernia: This occurs when the stomach bulges up through the diaphragm and into the chest cavity, causing symptoms such as heartburn, regurgitation, and difficulty swallowing.
6. Malabsorption: This occurs when the body is unable to properly absorb nutrients from food, leading to symptoms such as diarrhea, weight loss, and malnutrition.
7. Nutrient deficiencies: These can occur due to malabsorption or a limited ability to consume certain foods, leading to deficiencies in vitamins and minerals.
8. Obstruction: This occurs when there is a blockage in the digestive tract that can cause symptoms such as abdominal pain, vomiting, and constipation.
9. Ulcers: These are open sores that can occur in the stomach or small intestine, causing symptoms such as abdominal pain, nausea, and vomiting.
10. Vitamin deficiencies: These can occur due to malabsorption or a limited ability to consume certain foods, leading to deficiencies in vitamins such as vitamin B12 and iron.
It's important to note that some of these conditions can be caused by a variety of factors, including genetics, diet, allergies, and other medical conditions. If you suspect you have a gastrointestinal disorder, it's important to speak with a healthcare professional for proper diagnosis and treatment.
Symptoms of gastritis may include abdominal pain, nausea, vomiting, loss of appetite, and difficulty swallowing. In severe cases, bleeding may occur in the stomach and black tarry stools may be present.
Diagnosis of gastritis is typically made through endoscopy, during which a flexible tube with a camera and light on the end is inserted through the mouth to visualize the inside of the stomach. Biopsies may also be taken during this procedure to examine the stomach tissue under a microscope for signs of inflammation or infection.
Treatment of gastritis depends on the underlying cause, but may include antibiotics for bacterial infections, anti-inflammatory medications, and lifestyle modifications such as avoiding alcohol, losing weight, and eating smaller more frequent meals. In severe cases, surgery may be necessary to remove damaged tissue or repair any ulcers that have developed.
The condition is named after Dr. Norman Barrett, who first described it in 1956. It is a precancerous condition, meaning that if left untreated, it can progress to esophageal cancer over time. The exact cause of Barrett esophagus is not fully understood, but chronic acid reflux is thought to play a role in its development.
The symptoms of Barrett esophagus are similar to those of GERD and may include heartburn, difficulty swallowing, chest pain, and regurgitation of food. The condition can be diagnosed through an endoscopy, which involves inserting a flexible tube with a camera into the esophagus to visualize the cells lining the esophagus.
Treatment for Barrett esophagus typically involves controlling the underlying acid reflux through lifestyle changes and medications. In some cases, surgery may be necessary to repair any damage to the esophageal lining or to strengthen the lower esophageal sphincter (LES), which is the muscle that separates the esophagus from the stomach and prevents acid reflux.
It's important for individuals with chronic acid reflux to be screened regularly for Barrett esophagus, as early detection and treatment can help prevent the development of esophageal cancer.
VUR occurs when the muscles in the ureteral walls are weak or underdeveloped, allowing urine to flow back into the bladder instead of emptying properly into the ureters. It can also be caused by an abnormal connection between the bladder and the ureter, such as a birth defect or injury.
Symptoms of VUR may include recurring UTIs, fever, painful urination, and blood in the urine. To diagnose VUR, doctors may use imaging tests such as ultrasound or renal scan to visualize the flow of urine.
Treatment for VUR depends on the severity of the condition and may include antibiotics to treat UTIs, medication to relax the bladder muscle, and in some cases, surgery to repair any abnormal connections or narrowing of the ureters.
There are several types of biliary tract diseases, including:
1. Gallstones: Small, pebble-like deposits that form in the gallbladder and can cause pain and blockages.
2. Cholangitis: An infection of the bile ducts that can cause fever, chills, and abdominal pain.
3. Biliary cirrhosis: Scarring of the liver and bile ducts that can lead to liver failure.
4. Pancreatitis: Inflammation of the pancreas that can cause abdominal pain and digestive problems.
5. Cancer of the biliary tract: Cancer that affects the liver, gallbladder, or bile ducts.
Biliary tract diseases can be caused by a variety of factors, including genetics, obesity, alcohol consumption, and certain medications. Diagnosis is typically made through a combination of imaging tests, such as CT scans and endoscopic ultrasound, and laboratory tests, such as blood tests and liver function tests.
Treatment for biliary tract diseases depends on the underlying cause and severity of the condition. In some cases, treatment may involve medications to dissolve gallstones or treat infections. In more severe cases, surgery may be necessary to remove the gallbladder or repair damaged bile ducts.
Prevention is key in avoiding biliary tract diseases, and this includes maintaining a healthy diet and lifestyle, managing risk factors such as obesity and alcohol consumption, and getting regular medical check-ups. Early detection and treatment of biliary tract diseases can help to improve outcomes and reduce the risk of complications.
Esophagitis is a type of inflammation that affects the esophagus, which is the tube that carries food from the throat to the stomach. Peptic esophagitis is a specific type of esophagitis that is caused by reflux of stomach acid and digestive enzymes into the esophagus. This condition is also known as gastroesophageal reflux disease (GERD).
The symptoms of peptic esophagitis can vary from person to person, but common symptoms include:
* Heartburn: a burning sensation in the chest that can radiate up to the throat and neck
* Difficulty swallowing: food may feel like it's getting stuck in the throat or esophagus
* Chest pain: a sharp, stabbing pain in the chest that can be worse when lying down or eating
* Regurgitation: the sensation of food coming back up into the mouth
* Coughing or wheezing: acid reflux can irritate the lungs and cause these symptoms
* Hoarseness: stomach acid can irritate the vocal cords and cause hoarseness
Peptic esophagitis is usually diagnosed through a combination of endoscopy, which involves inserting a flexible tube with a camera into the esophagus to examine the lining, and pH testing, which measures the amount of acid in the esophagus. Treatment typically involves lifestyle changes, such as avoiding trigger foods, losing weight, and elevating the head of the bed, as well as medications to reduce acid production and protect the esophageal lining. In severe cases, surgery may be necessary to repair any damage to the esophagus.
Examples and Observations:
1. Gastric metaplasia: This is a condition where the stomach lining is replaced by cells that are similar to those found in the esophagus. This can occur as a result of chronic acid reflux, leading to an increased risk of developing esophageal cancer.
2. Bronchial metaplasia: This is a condition where the airways in the lungs are replaced by cells that are similar to those found in the trachea. This can occur as a result of chronic inflammation, leading to an increased risk of developing lung cancer.
3. Pancreatic metaplasia: This is a condition where the pancreas is replaced by cells that are similar to those found in the ducts of the pancreas. This can occur as a result of chronic inflammation, leading to an increased risk of developing pancreatic cancer.
4. Breast metaplasia: This is a condition where the breast tissue is replaced by cells that are similar to those found in the salivary glands. This can occur as a result of chronic inflammation, leading to an increased risk of developing salivary gland cancer.
Etiology and Pathophysiology:
Metaplasia is thought to be caused by chronic inflammation, which can lead to the replacement of one type of cell or tissue with another. This can occur as a result of a variety of factors, including infection, injury, or exposure to carcinogens. Once the metaplastic changes have occurred, there is an increased risk of developing cancer if the underlying cause is not addressed.
Clinical Presentation:
Patients with metaplasia may present with a variety of symptoms, depending on the location and extent of the condition. These can include pain, difficulty swallowing or breathing, coughing up blood, and weight loss. In some cases, patients may be asymptomatic and the condition may be detected incidentally during diagnostic testing for another condition.
Diagnosis:
The diagnosis of metaplasia is typically made based on a combination of clinical findings, radiologic imaging (such as CT scans or endoscopies), and histopathological examination of biopsy specimens. Imaging studies can help to identify the location and extent of the metaplastic changes, while histopathology can confirm the presence of the metaplastic cells and rule out other potential diagnoses.
Treatment:
Treatment for metaplasia depends on the underlying cause and the severity of the condition. In some cases, treatment may involve addressing the underlying cause, such as removing a tumor or treating an infection. In other cases, treatment may be directed at managing symptoms and preventing complications. This can include medications to reduce inflammation and pain, as well as surgery to remove affected tissue.
Prognosis:
The prognosis for metaplasia varies depending on the underlying cause and the severity of the condition. In general, the prognosis is good for patients with benign metaplastic changes, while those with malignant changes may have a poorer prognosis if the cancer is not treated promptly and effectively.
Complications:
Metaplasia can lead to a number of complications, including:
1. Cancer: Metaplastic changes can sometimes progress to cancer, which can be life-threatening.
2. Obstruction: The growth of metaplastic cells can block the normal functioning of the organ or gland, leading to obstruction and potentially life-threatening complications.
3. Inflammation: Metaplasia can lead to chronic inflammation, which can cause scarring and further damage to the affected tissue.
4. Bleeding: Metaplastic changes can increase the risk of bleeding, particularly if they occur in the digestive tract or other organs.
LPR can lead to a range of symptoms, including:
* Hoarseness or a raspy voice
* Chronic cough
* Trouble swallowing
* Throat clearing
* Regurgitation of food
* Difficulty breathing
The exact cause of LPR is not known, but it is thought to be related to a weakening of the lower esophageal sphincter (LES), which allows stomach acid and other digestive juices to flow back up into the throat. Factors that can contribute to the development of LPR include:
* Obesity
* Pregnancy
* Smoking
* Alcohol consumption
* Certain medications
* Eating close to bedtime
LPR is typically diagnosed through a combination of endoscopy, laryngoscopy, and pH testing. Treatment options for LPR include:
* Lifestyle changes (e.g., weight loss, avoiding trigger foods, elevating the head of the bed)
* Medications (e.g., antacids, histamine-2 receptor antagonists, proton pump inhibitors)
* Surgery (e.g., fundoplication)
It is important to note that LPR can have serious complications if left untreated, including chronic inflammation and scarring of the throat tissues, as well as an increased risk of developing asthma or other respiratory conditions.
Dyspepsia is not a specific disease but rather a symptom complex that can be caused by a variety of factors, such as:
1. Gastritis (inflammation of the stomach lining)
2. Peptic ulcer
3. Gastroesophageal reflux disease (GERD)
4. Functional dyspepsia
5. Inflammatory conditions such as Crohn's disease or ulcerative colitis
6. Food allergies or intolerances
7. Hormonal changes during pregnancy or menstruation
8. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics
The diagnosis of dyspepsia is based on a combination of medical history, physical examination, and diagnostic tests such as endoscopy, gastric emptying studies, and blood tests. Treatment depends on the underlying cause of dyspepsia and may include medications, lifestyle changes, and dietary modifications.
1. Gastritis: Inflammation of the stomach lining, which can be acute or chronic.
2. Peptic ulcer disease: Ulcers in the stomach or duodenum (the first part of the small intestine) that are caused by H. pylori infection.
3. Gastric adenocarcinoma: A type of stomach cancer that is associated with long-term H. pylori infection.
4. Mucosa-associated lymphoid tissue (MALT) lymphoma: A rare type of cancer that affects the immune cells in the stomach and small intestine.
5. Gastroesophageal reflux disease (GERD): A condition in which stomach acid flows back up into the esophagus, causing symptoms such as heartburn and regurgitation.
6. Helicobacter pylori-associated chronic atrophic gastritis: A type of chronic inflammation of the stomach lining that can lead to stomach ulcers and stomach cancer.
7. Post-infectious irritable bowel syndrome (PI-IBS): A condition that develops after a gastrointestinal infection, characterized by persistent symptoms such as abdominal pain, bloating, and changes in bowel habits.
Helicobacter infections are typically diagnosed through endoscopy, where a flexible tube with a camera and light on the end is inserted into the stomach and small intestine to visualize the mucosa and look for signs of inflammation or ulcers. Laboratory tests such as breath tests and stool tests may also be used to detect the presence of H. pylori bacteria in the body. Treatment typically involves a combination of antibiotics and acid-suppressing medications to eradicate the infection and reduce symptoms.
Preventing Helicobacter Infections:
While it is not possible to completely prevent Helicobacter infections, there are several measures that can be taken to reduce the risk of developing these conditions:
1. Practice good hygiene: Wash your hands regularly, especially before eating and after using the bathroom.
2. Avoid close contact with people who have Helicobacter infections.
3. Avoid sharing food, drinks, or utensils with people who have Helicobacter infections.
4. Avoid consuming undercooked meat, especially pork and lamb.
5. Avoid consuming raw shellfish, especially oysters.
6. Avoid consuming unpasteurized dairy products.
7. Avoid alcohol and caffeine, which can irritate the stomach lining and increase the risk of developing Helicobacter infections.
8. Maintain a healthy diet that is high in fiber and low in fat.
9. Manage stress, as stress can exacerbate symptoms of Helicobacter infections.
10. Practice good oral hygiene to prevent gum disease and other oral infections that can increase the risk of developing Helicobacter infections.
Conclusion:
Helicobacter infections are a common cause of stomach ulcers, gastritis, and other gastrointestinal disorders. These infections are caused by the bacteria Helicobacter pylori, which can be found in the stomach lining and small intestine. While these infections can be difficult to diagnose, a combination of endoscopy, blood tests, and stool tests can help confirm the presence of Helicobacter bacteria. Treatment typically involves a combination of antibiotics and acid-suppressing medications to eradicate the infection and reduce symptoms. Preventive measures include practicing good hygiene, avoiding close contact with people who have Helicobacter infections, and maintaining a healthy diet.
Hypopharyngeal cancer
Cholescintigraphy
Ursodeoxycholic acid
Reactive gastropathy
SADI-S surgery
Mucin 4
Gastric bypass surgery
Barrett's esophagus
Biliary reflux
Cholestatic pruritus
Hiatal hernia
Rapid urease test
Esophageal cancer
Pyloroplasty
Lipoprotein-X
Heidelberg test
Bile
Bilirubin glucuronide
List of MeSH codes (C06)
CDX2
Angle of His
Klatskin tumor
Bilious vomiting syndrome
Nissen fundoplication
Sphincter of Oddi
Gastroesophageal reflux disease
Medication
Human feces
Hemosuccus pancreaticus
Pyloric stenosis
Gastrointestinal disease
Sucralfate
Radiation therapy
Imperatorin
List of OMIM disorder codes
Omeprazole
Drug reaction with eosinophilia and systemic symptoms
Gastrectomy
Equine proximal enteritis
Self-expandable metallic stent
Major duodenal papilla
Delavirdine
Bariatric surgery
Laparoscopy
Intestinal bypass
Irritable bowel syndrome
Maternal physiological changes in pregnancy
Precancerous Condition Associated With Reflux Disease Triggered By Bile - Not Acid
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Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use - PubMed
Gastroesophageal Reflux18
- For many people with gastroesophageal reflux disease or GERD , acid reflux drugs are the answer to their woes, curbing the chronic heartburn and regurgitation of food or sour liquid characteristic of the disorder. (medicalnewstoday.com)
- Upper gastrointestinal contrast-enhanced studies are the initial radiologic procedure of choice in the workup gastroesophageal reflux disease. (medscape.com)
- Treatment of gastroesophageal reflux disease involves a stepwise approach. (medscape.com)
- Transthoracic and transabdominal fundoplications are performed for gastroesophageal reflux disease, including partial (anterior or posterior) and circumferential wraps. (medscape.com)
- Gastroesophageal reflux is a normal physiologic phenomenon experienced intermittently by most people, particularly after a meal. (medscape.com)
- Vomiting bile can be a sign of severe gastroesophageal reflux disease (GERD) . (verywellfamily.com)
- What Is Gastroesophageal Reflux (GER)? (kidshealth.org)
- Gastroesophageal reflux (GER), also called reflux , is when food and acid from the stomach go back up into the esophagus. (kidshealth.org)
- Reflux that happens a lot and causes problems like poor growth, vomiting, or damage to the esophagus is called GERD (gastroesophageal reflux disease) . (kidshealth.org)
- What Are the Signs & Symptoms of Gastroesophageal Reflux? (kidshealth.org)
- What Causes Gastroesophageal Reflux? (kidshealth.org)
- How Is Gastroesophageal Reflux Diagnosed? (kidshealth.org)
- How Is Gastroesophageal Reflux Treated? (kidshealth.org)
- Barrett's esophagus (BE) results from chronic, severe gastroesophageal reflux and predisposes to esophageal adenocarcinoma. (nih.gov)
- BACKGROUND: The main concerns following sleeve gastrectomy (SG) include the risk of gastroesophageal reflux disease (GERD) and its complications, such as Barrett's esophagus (BE). (bvsalud.org)
- Metoclopramide is an oral prokinetic and antiemetic agent used in the therapy of gastroesophageal reflux disease, gastroparesis and severe or chemotherapy induced nausea. (nih.gov)
- Prokinetic therapy for gastroesophageal reflux disease. (nih.gov)
- Effect of metoclopramide on normal and delayed gastric emptying in gastroesophageal reflux patients. (nih.gov)
Gastritis5
- Upper GI endoscopy evaluated reflux gastritis in the gastric remnant , and the presence of H. pylori infection and chronic, active inflammatory cellular infiltration in the biopsy specimens were examined microscopically with the updated Sydney system. (bvsalud.org)
- Chemical or reactive gastritis is caused by injury to the gastric mucosa resulting from reflux of bile and pancreatic secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic acid, chemotherapeutic agents, and alcohol. (medscape.com)
- Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. (nih.gov)
- So whether it is colitis, gastritis, bile reflux or even cirrhosis, acute liver failure, esophageal cancer and so on, our experts are enabled by our state of the art diagnostic and surgical technology to prescribe the most effective treatment protocols. (manipalhospitals.com)
- Endoscopy showed chronic gastritis with bile reflux. (biomedcentral.com)
Gastric7
- Inflammation of the gastric remnant after gastrectomy: mucosal erythema is associated with bile reflux and inflammatory cellular infiltration is associated with Helicobacter pylori infection. (bvsalud.org)
- Controversy exists concerning the role of bile reflux and Helicobacter pylori ( H. pylori) infection in the development of inflammation of the gastric remnant after gastrectomy . (bvsalud.org)
- This study was designed to investigate association of bile reflux and H. pylori infection or both with inflammatory changes in the gastric remnant . (bvsalud.org)
- Bile reflux into the gastric remnant was observed by Bilitec 2000. (bvsalud.org)
- Mucosal erythema and chronic, active inflammatory cell infiltration in the gastric remnant after gastrectomy may be caused by bile reflux or H. pylori infection , respectively. (bvsalud.org)
- Laparoscopic Roux-en-Y gastric bypass (LRYGB) is considered the gold standard in bariatric surgery, achieving durable long-term weight loss with improvement of obesity-related comorbidities. (biomedcentral.com)
- The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. (nih.gov)
Nonsteroidal anti-2
- The chronic gastritides are classified on the basis of their underlying cause (eg, H pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity or allergic response) and the histopathologic pattern, which may suggest the cause and the likely clinical course (eg, H pylori -associated multifocal atrophic gastritis). (medscape.com)
- Some types of pain relief medicines called nonsteroidal anti-inflammatory drugs (NSAIDs) , alcohol, and bile are among the most common irritating substances. (nih.gov)
Esophagus10
- But when it comes to Barrett's esophagus, a condition commonly found in people with GERD, acid control may be less important than beating back another bodily fluid - bile. (medicalnewstoday.com)
- A new study published in the Annals of Surgery shows that bile - a digestive fluid that leaks backwards from the stomach into the esophagus along with acid in patients with GERD - plays a critical and previously unrecognized role in the development of Barrett's esophagus. (medicalnewstoday.com)
- Peters' team found that bile that washes up from the stomach into the esophagus shuts off genes responsible for the normal, skin-like lining of the organ, and turns on genes that produce the intestine-like lining that is the hallmark of Barrett's. (medicalnewstoday.com)
- While previous research established that reflux components encouraged the development of intestinal tissue in the esophagus that alone was never enough to produce the changes that led to Barrett's. (medicalnewstoday.com)
- Bile is normally found in the intestinal environment, so when stem cells in the esophagus are exposed to bile that is what they change to. (medicalnewstoday.com)
- Currently, the only way to stop all reflux components, including bile, is to surgically reconstruct the faulty barrier between the esophagus and the stomach. (medicalnewstoday.com)
- In babies with GERD, breast milk or formula regularly refluxes into the esophagus, and sometimes out of the mouth. (kidshealth.org)
- The tip rests just above the esophageal sphincter for 24 hours to check acid levels in the esophagus and to detect any reflux. (kidshealth.org)
- Intestinalization of the esophagus, termed Barrett's esophagus (BE), is thought to develop in response to chronic acid and bile reflux and carries great clinical significance because it is the precursor to esophageal adenocarcinoma (EAC). (cancer.gov)
- Gastroenterology focuses on the entire digestive system which includes the esophagus, stomach, intestines, colon, pancreas, gall bladder, bile ducts as well as the liver and anus. (manipalhospitals.com)
Gastro-oesopha1
- Background Factors other than acid may play a role in gastro-oesophageal reflux disease (GERD) and its complications. (elsevierpure.com)
Pylori2
- Bile reflux did not correlate with the severity of chronic and active inflammatory cellular infiltration or H. pylori infection . (bvsalud.org)
- Smoking, bile reflux and H. pylori infection were influencing factors for VEGF expression in PLGC. (biomedres.info)
Stomach1
- The scans can show whether the stomach is slow to empty liquids and whether the refluxed liquid is being inhaled into the lungs. (kidshealth.org)
GERD5
- The finding that bile is important is key because current drug therapies for GERD focus largely on acid control. (medicalnewstoday.com)
- Aim To assessed the role of bile acids in the pathogenesis of GERD, Barrett's oesophagus and Barrett's-related neoplasia. (elsevierpure.com)
- In in vivo studies, bile acids concentrations were higher in the oesophageal aspirates of patients with GERD than controls, and bile acids infusions triggered GERD symptoms, especially in high concentrations or in combination with acid. (elsevierpure.com)
- Conclusions In aggregate, these studies suggest that bile acids may contribute to the pathogenesis of symptoms, oesophagitis and Barrett's metaplasia with related carcinogenesis in patients with GERD. (elsevierpure.com)
- But in people who have GERD, reflux happens more often and causes noticeable discomfort. (kidshealth.org)
Pancreatic1
- High-fat diets, chronic pantothenic acid deficiency, deficiency of gluconeogenic amino acids, platelet-activating factor, increased reflux of bile salts, and reduced exocrine pancreatic function are associated with ulceration but only with intact vagal innervations. (nih.gov)
Salts2
Barrett's5
- Though uncommon, Peters says it's one of the fastest-rising cancers in the world, likely due to the increase in obesity , which triggers reflux disease and Barrett's. (medicalnewstoday.com)
- In ex vivo/in vitro studies, bile acids stimulated squamous oesophageal cells and Barrett's epithelial cells to produce inflammatory mediators (e.g. (elsevierpure.com)
- 19. Curcumin abrogates bile-induced NF-κB activity and DNA damage in vitro and suppresses NF-κB activity whilst promoting apoptosis in vivo, suggesting chemopreventative potential in Barrett's oesophagus. (nih.gov)
- A novel mechanism of acid and bile acid-induced DNA damage involving Na+/H+ exchanger: implication for Barrett's oesophagus. (nih.gov)
- Abnormal gastro-oesophageal reflux and bile acids have been linked to the presence of Barrett's oesophageal premalignant lesion associated with an increase in mucin-producing goblet cells and MUC4 mucin gene overexpression. (nih.gov)
Endoscopy1
- Endoscopy showed positive correlation between mucosal erythema and bile reflux ( P (bvsalud.org)
Heartburn1
- Acid reflux disease can produce a variety of symptoms, such as: heartburn, regurgitation and dyspepsia (burping, nausea, bloating and discomfort). (naturalcompounder.com)
Biliary1
- 11. Biliary reflux as a causal factor in hypopharyngeal carcinoma: New clinical evidence and implications. (nih.gov)
Acids6
- Methods We conducted a systematic review of computerised bibliographic databases for original articles involving humans or human oesophageal tissue or cells that assessed exposure to or manipulation of bile acids. (elsevierpure.com)
- Transcriptional regulation of human mucin MUC4 by bile acids in oesophageal cancer cells is promoter-dependent and involves activation of the phosphatidylinositol 3-kinase signalling pathway. (nih.gov)
- However, the molecular mechanisms underlying the regulation of MUC4 by bile acids are unknown. (nih.gov)
- Since total bile is a complex mixture, we undertook to identify which bile acids are responsible for MUC4 up-regulation by using a wide panel of bile acids and their conjugates. (nih.gov)
- We show that among the bile acids tested, taurocholic, taurodeoxycholic, taurochenodeoxycholic and glycocholic acids and sodium glycocholate are strong activators of MUC4 expression and that this regulation occurs at the transcriptional level. (nih.gov)
- This new mechanism of regulation of MUC4 mucin gene points out an important role for bile acids as key molecules in targeting MUC4 overexpression in early stages of oesophageal carcinogenesis. (nih.gov)
Acid reflux4
- More than 60 million Americans experience acid reflux at least once a month. (naturalcompounder.com)
- If this sounds like you, then you probably haven't tried an old Amish remedy that we have at Johnson Compounding & Wellness, called Stops Acid Reflux in About One Minute . (naturalcompounder.com)
- This amazingly effective, fast-acting acid reflux remedy was discovered by the Amish while they were still in Europe and brought to this country sometime in the 1880's. (naturalcompounder.com)
- A carefully balanced mixture of certified organic unfiltered raw apple cider vinegar, juice from the ginger plant and just the right amount of all natural garlic juice in special combination so as to achieve almost instant relief from acid reflux. (naturalcompounder.com)
Duct1
- Metoclopramide has been linked to rare instances of clinically apparent liver injury that are typically cholestatic and can be associated with bile duct loss. (nih.gov)
Symptoms1
- In older kids, doctors usually diagnose reflux by doing an exam and hearing about the symptoms. (kidshealth.org)
Vivo2
- 2. In Vivo Short-Term Topical Application of BAY 11-7082 Prevents the Acidic Bile-Induced mRNA and miRNA Oncogenic Phenotypes in Exposed Murine Hypopharyngeal Mucosa. (nih.gov)
- 5. The in vivo preventive and therapeutic properties of curcumin in bile reflux-related oncogenesis of the hypopharynx. (nih.gov)
Clinical1
- The clinical outcome of HPI reflux and alcohol intake [2] . (who.int)
Vitro1
- 10. In vitro model for gastroduodenal reflux-induced nuclear factor-kappaB activation and its role in hypopharyngeal carcinogenesis. (nih.gov)
Cells6
- The team performed the first-ever analysis of all genes that are turned on and off in normal esophageal cells exposed chronically to bile or acid. (medicalnewstoday.com)
- 1. Curcumin prevents the bile reflux-induced NF-κB-related mRNA oncogenic phenotype, in human hypopharyngeal cells. (nih.gov)
- 7. NF-κB inhibition reverses acidic bile-induced miR-21, miR-155, miR-192, miR-34a, miR-375 and miR-451a deregulations in human hypopharyngeal cells. (nih.gov)
- 12. Temporal characteristics of NF-κB inhibition in blocking bile-induced oncogenic molecular events in hypopharyngeal cells. (nih.gov)
- 13. The Role of PARP-1 and NF-κB in Bile-Induced DNA Damage and Oncogenic Profile in Hypopharyngeal Cells. (nih.gov)
- The major goal of this study was to determine the mechanism responsible for bile acid-induced alteration in intracellular pH (pH(i)) and its effect on DNA damage in cells derived from normal oesophagus (HET1A) or Barrett's oesophagus (CP-A).Cells were exposed to bile acid cocktail (BA) and/or acid in the presence/absence of inhibitors of nitric oxide synthase (NOS) or sodium-hydrogen exchanger (NHE). (nih.gov)
Patients2
- Bile reflux was lower in patients who had undergone a gastrectomy with jejunal interposition, a pylorus -preserving gastrectomy , and a gastrectomy with Roux-Y anastomosis than those who had undergone a Billroth-II (B-II) anastomosis ( P (bvsalud.org)
- Currently, no role exists for computed tomography scanning, magnetic resonance imaging, or ultrasonography in the routine evaluation of patients with reflux disease. (medscape.com)
Molecular1
- 9. Targeting STAT3 prevents bile reflux-induced oncogenic molecular events linked to hypopharyngeal carcinogenesis. (nih.gov)
Role1
- 14. The role of bile reflux and its related NF-κB activated pathway in progression of hypopharyngeal squamous cell cancer. (nih.gov)
Flow3
- In this blog we're going to take more of a philosophical look at how circadian rhythms are important for gut health and why proper bile flow is crucial for it all to work. (hackyourgut.com)
- Retrograde bile flow. (nih.gov)
- Good bile flow is essential for the proper digestion and absorption of dietary fats and fat-soluble vitamins such as vitamins A, D, E and K. (naturalcompounder.com)
Babies1
- This is what bile looks like and this can be worrisome in babies," says pediatrician and lactation consultant Neela Sethi , MD, a MAM Baby ambassador. (verywellfamily.com)
Study1
- Examination of biopsies and cell lines revealed robust expression of NHE1 in Barrett's oesophagus but an absence of NHE1 in normal epithelium.The results of this study identify a new mechanism of bile acid-induced DNA damage. (nih.gov)
Review1
- 18. Bile reflux and hypopharyngeal cancer (Review). (nih.gov)