Prime Editing Unlocks a Universal Strategy for Restoring Lost Proteins
November 22, 2025
Background
GERD (Gastroesophageal reflux disease) is a chronic gastrointestinal condition defined by the reflux of stomach contents in the esophagus. It can develop itself as either erosive esophagitis or non-erosive reflux disease.
Heartburn and regurgitation complaints are the most common GERD indications. It may also exhibit unusual extra-esophageal symptoms such as chest pain, tooth erosions, a persistent cough, laryngitis, or asthma.
Epidemiology
It is the most widespread gastrointestinal condition, affecting 20% of adults in western countries. In the US, prevalence is estimated from 18.1-27.8%. Since more people have access to over-the-counter acid-neutralizing medications, the actual prevalence of this condition may be higher.
Men are more vulnerable than women to GERD. However, men have a greater incidence of Barrett’s esophagus than women with long-lasting GERD symptoms.
Anatomy
Pathophysiology
The pathophysiology is diverse and is implied by the multiple mechanisms which impact the lower esophageal sphincter’s tone, esophageal motility, and the esophageal mucosa’s protection against refluxate.
Defective esophageal peristalsis
Healthy esophageal peristalsis usually clears the acidic gastric contents that reach the esophagus and neutralizes them with salivary bicarbonate. The esophageal peristalsis is disrupted in GERD patients, which results in poor gastric reflux clearance, mucosal erosion, and severe reflux symptoms.
Impaired esophageal mucosal defense against the gastric refluxate
The esophageal mucosa comprises various structural and functional components that serve as a defense barrier against the luminal chemicals that individuals with GERD encounter.
Long-term exposure to the refluxate, which contains both acidic gastric contents like pepsin and hydrochloric acid and alkaline duodenal contents like pancreatic enzymes and bile salts, compromises this protective barrier and causes mucosal injury.
It is unknown whether gastroparesis affects GERD. GERD symptoms are thought to be triggered by delayed stomach emptying because it causes gastric distention and increases exposure to gastric refluxate.
Etiology
Numerous risk factors have been discovered and linked to the development of GERD over time. The cause of GERD includes motor aberrations like esophageal dysmotility, which impairs esophageal acid clearance, damage to lower esophageal sphincter tone, delayed stomach emptying, and transitory relaxation.
An increased chance of developing GERD is related to anatomical variables such as the development of a hiatal hernia or an increase in intra-abdominal pressure, as seen in obesity. Obesity is linked to an increased risk of erosive esophagitis, esophageal cancer, and GERD symptoms.
Age 50 years, tobacco use, low socioeconomic status, excessive alcohol consumption, pregnancy, postprandial supination, connective tissue disorders, and various drug classes, such as benzodiazepines, NSAID, anticholinergic drugs, nitroglycerin, aspirin, albuterol, antidepressants, and calcium channel blockers, glucagon, have also been independently linked to the development of GERD symptoms.
Genetics
Prognostic Factors
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
20
mg
every day
4
weeks
Indicated for Erosive Esophagitis Associated With GERD
40 mg orally daily 8-16 weeks; may be increased to 40 mg
30
mg
Orally 
every day
4
weeks
25mg orally four times a day. Take 1 hour before the meals or 2 hours later the meal
10-15 mg orally every 6 hours, 30 minutes before meals and bedtime
Do not exceed the dose more than 80 mg/day
10 mg taken orally four times daily, specifically 15 minutes prior to meals and before going to bed
If necessary, the dosage may be maximized up to 20 mg per dose
Children 1 to 10 yrs: based upon body weight, age, and the medical condition
Adults: Not indicated for use
Take 10 mg one time a day for the duration of four to eight weeks, which depends upon the condition and body response
The recommended maintenance dose is 5 to 10 mg one time a day
Take a capsule one time a day for four-to-eight-week duration before morning meal
Each tablet/capsule contains 40 mg of pantoprazole and 10 mg of domperidone: one tablet/capsule is administered once a day
Chewable tablet containing 150 mg alginic acid, 73.50 mg heavy magnesium carbonate and 625 mg calcium carbonate:
Chew 2 tablets usually one hour after meals and before bedtime
The suggested dose is 1 to 3 tablespoons by oral route
15mg to 40mg tablets orally once daily in 3–4 divided doses
(or)
15mg to 40mg granules orally once daily in 3–4 divided doses
(Or)
15-ml suspension orally once daily
Take one teaspoon after a meal daily
20 mg 2 times a day 6 weeks 
For Erosive diagnosed by endoscopy 20-40 mg orally 2 times a day 12 weeks 
Take a dose of 150 mg orally every 12 hours
weight (5-10 kg):
5
mg
orally
every day
weight (10-20 kg): 10 mg orally every day
weight (>20 kg): 20 mg orally every day
Age: > 12 years:
30
mg
Orally 
every day
4
weeks
0.3 to 0.6 mg/kg/day orally every 6 to 8 hours
Take 1 hour before the meals or 2 hours later the meal
Age>1 year: The oral dosage is 0.2 to 0.3 mg/kg/ dose, to be administered 3 to 4 times daily
The maximum dose per administration should not exceed 10 mg
For >12 years old:
Chewable tab containing 150 mg alginic acid, 73.50 mg heavy magnesium carbonate and 625 mg calcium carbonate:
Chew 2 tablets usually one hour after meals and before bedtime
Age 7 to 15 years:
The suggested dose is 1 to 3 teaspoons every eight times a day or every four times a day after a meal for 40 to 60 minutes or during sleep time
For 13 to 18 years old:
Take a dose of 40 mg orally daily for 8 to16 weeks
Take dose of 5 to 10 mg/kg orally divided every 12 hour and daily dose should not more than 300 mg
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK441938/
GERD (Gastroesophageal reflux disease) is a chronic gastrointestinal condition defined by the reflux of stomach contents in the esophagus. It can develop itself as either erosive esophagitis or non-erosive reflux disease.
Heartburn and regurgitation complaints are the most common GERD indications. It may also exhibit unusual extra-esophageal symptoms such as chest pain, tooth erosions, a persistent cough, laryngitis, or asthma.
It is the most widespread gastrointestinal condition, affecting 20% of adults in western countries. In the US, prevalence is estimated from 18.1-27.8%. Since more people have access to over-the-counter acid-neutralizing medications, the actual prevalence of this condition may be higher.
Men are more vulnerable than women to GERD. However, men have a greater incidence of Barrett’s esophagus than women with long-lasting GERD symptoms.
The pathophysiology is diverse and is implied by the multiple mechanisms which impact the lower esophageal sphincter’s tone, esophageal motility, and the esophageal mucosa’s protection against refluxate.
Defective esophageal peristalsis
Healthy esophageal peristalsis usually clears the acidic gastric contents that reach the esophagus and neutralizes them with salivary bicarbonate. The esophageal peristalsis is disrupted in GERD patients, which results in poor gastric reflux clearance, mucosal erosion, and severe reflux symptoms.
Impaired esophageal mucosal defense against the gastric refluxate
The esophageal mucosa comprises various structural and functional components that serve as a defense barrier against the luminal chemicals that individuals with GERD encounter.
Long-term exposure to the refluxate, which contains both acidic gastric contents like pepsin and hydrochloric acid and alkaline duodenal contents like pancreatic enzymes and bile salts, compromises this protective barrier and causes mucosal injury.
It is unknown whether gastroparesis affects GERD. GERD symptoms are thought to be triggered by delayed stomach emptying because it causes gastric distention and increases exposure to gastric refluxate.
Numerous risk factors have been discovered and linked to the development of GERD over time. The cause of GERD includes motor aberrations like esophageal dysmotility, which impairs esophageal acid clearance, damage to lower esophageal sphincter tone, delayed stomach emptying, and transitory relaxation.
An increased chance of developing GERD is related to anatomical variables such as the development of a hiatal hernia or an increase in intra-abdominal pressure, as seen in obesity. Obesity is linked to an increased risk of erosive esophagitis, esophageal cancer, and GERD symptoms.
Age 50 years, tobacco use, low socioeconomic status, excessive alcohol consumption, pregnancy, postprandial supination, connective tissue disorders, and various drug classes, such as benzodiazepines, NSAID, anticholinergic drugs, nitroglycerin, aspirin, albuterol, antidepressants, and calcium channel blockers, glucagon, have also been independently linked to the development of GERD symptoms.
https://www.ncbi.nlm.nih.gov/books/NBK441938/
GERD (Gastroesophageal reflux disease) is a chronic gastrointestinal condition defined by the reflux of stomach contents in the esophagus. It can develop itself as either erosive esophagitis or non-erosive reflux disease.
Heartburn and regurgitation complaints are the most common GERD indications. It may also exhibit unusual extra-esophageal symptoms such as chest pain, tooth erosions, a persistent cough, laryngitis, or asthma.
It is the most widespread gastrointestinal condition, affecting 20% of adults in western countries. In the US, prevalence is estimated from 18.1-27.8%. Since more people have access to over-the-counter acid-neutralizing medications, the actual prevalence of this condition may be higher.
Men are more vulnerable than women to GERD. However, men have a greater incidence of Barrett’s esophagus than women with long-lasting GERD symptoms.
The pathophysiology is diverse and is implied by the multiple mechanisms which impact the lower esophageal sphincter’s tone, esophageal motility, and the esophageal mucosa’s protection against refluxate.
Defective esophageal peristalsis
Healthy esophageal peristalsis usually clears the acidic gastric contents that reach the esophagus and neutralizes them with salivary bicarbonate. The esophageal peristalsis is disrupted in GERD patients, which results in poor gastric reflux clearance, mucosal erosion, and severe reflux symptoms.
Impaired esophageal mucosal defense against the gastric refluxate
The esophageal mucosa comprises various structural and functional components that serve as a defense barrier against the luminal chemicals that individuals with GERD encounter.
Long-term exposure to the refluxate, which contains both acidic gastric contents like pepsin and hydrochloric acid and alkaline duodenal contents like pancreatic enzymes and bile salts, compromises this protective barrier and causes mucosal injury.
It is unknown whether gastroparesis affects GERD. GERD symptoms are thought to be triggered by delayed stomach emptying because it causes gastric distention and increases exposure to gastric refluxate.
Numerous risk factors have been discovered and linked to the development of GERD over time. The cause of GERD includes motor aberrations like esophageal dysmotility, which impairs esophageal acid clearance, damage to lower esophageal sphincter tone, delayed stomach emptying, and transitory relaxation.
An increased chance of developing GERD is related to anatomical variables such as the development of a hiatal hernia or an increase in intra-abdominal pressure, as seen in obesity. Obesity is linked to an increased risk of erosive esophagitis, esophageal cancer, and GERD symptoms.
Age 50 years, tobacco use, low socioeconomic status, excessive alcohol consumption, pregnancy, postprandial supination, connective tissue disorders, and various drug classes, such as benzodiazepines, NSAID, anticholinergic drugs, nitroglycerin, aspirin, albuterol, antidepressants, and calcium channel blockers, glucagon, have also been independently linked to the development of GERD symptoms.
https://www.ncbi.nlm.nih.gov/books/NBK441938/

Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.

On course completion, you will receive a full-sized presentation quality digital certificate.
A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.

When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.
