Why can’t you take prilosec for more than 14 days?

Contents

FAQS About Prilosec OTC

What does “OTC” stand for?

“OTC” stands for “over-the-counter.” Prilosec OTC became available over the counter in 2003.

Is prescription Prilosec® the same as Prilosec OTC?

Prilosec and Prilosec OTC are different in indication and dose form. Prilosec OTC is indicated for the treatment of frequent heartburn (heartburn that occurs two or more days per week). Prilosec is a prescription medication indicated for the treatment of many other acid-related conditions. However, the omeprazole active ingredient in Prilosec became available over-the-counter in 2003 in the form of Prilosec OTC. Omeprazole magnesium, the active ingredient in Prilosec OTC, is equivalent to the active ingredient in Prilosec to treat frequent heartburn. Please follow the dosing instructions on the package or as directed by your physician.

How does Prilosec OTC work?

Prilosec OTC blocks frequent heartburn by shutting down many of the pumps in your stomach that produce excess acid.

Is Prilosec OTC strong enough to help me?

Prilosec OTC is in the strongest class of frequent heartburn medicines available over-the-counter. It blocks frequent heartburn before it begins with one pill a day for 14 days.*

Will Prilosec OTC allow me to eat my favorite foods?

Yes. Prilosec OTC blocks frequent heartburn before it begins so you can enjoy the foods you love.*

I heard medicines with the active ingredient ‘Ranitidine’ contain a probable carcinogen. Should I be worried about Prilosec OTC?

You can trust in Prilosec OTC as a FDA approved, safe and effective remedy to relieve frequent heartburn symptoms. Prilosec OTC (equivalent to Omeprazole 20 mg) has the longest history of safe & effective consumer use of any OTC PPI. Prilosec OTC is not in the same class of drugs referenced in the recent FDA study and does not contain the active pharmaceutical ingredient ‘Ranitidine’ mentioned in the study.

As with any OTC medication, it is important to read and follow all label directions to ensure proper dosing and to avoid drug interactions. Prilosec OTC is to be used once a day, every day for 14 days as a course of treatment. Do not take for more than 14 days or more often than every 4 months unless directed by a doctor.

Does Prilosec OTC interact negatively with other drugs?

It’s possible. Before taking Prilosec OTC, let your healthcare provider know if you are taking any of the following: warfarin, clopidogrel or cilostazol (blood-thinning medicines), prescription antifungal or anti-yeast medicines, diazepam (anxiety medicine), digoxin (heart medicine), or tacrolimus or mycophenolate mofetil (immune system medicines), prescription antiretrovirals (medicines for HIV infection) and methotrexate (arthritis medicine).

For more information on drug interaction with Prilosec OTC, visit this .

How often should I take Prilosec OTC?

Prilosec OTC is a 14-day regimen that is indicated for three courses per year, but not more often than every 4 months. If you need to use Prilosec OTC for more than the three indicated 14-day courses of treatment, you should first consult your doctor. Here’s why: By talking with your doctor first, you and your doctor will ensure you’re not missing a bigger health problem, such as GERD, and that Prilosec OTC continues to be right for you. Your doctor will confirm that Prilosec OTC should still be taken for your heartburn.

How long can I take Prilosec OTC?

Prilosec OTC is a 14-day regimen that is indicated for three courses per year. While Prilosec OTC is safe to treat frequent heartburn, it is also strong enough to mask more serious conditions. If you want to take more than the three indicated courses, first meet with your doctor, who will make sure that you don’t have a serious underlying condition, and that Prilosec OTC continues to be right for you.

What if I miss a day of heartburn treatment?

If you miss a day, just continue your treatment on the next day.

How do I open the package?

See how to open a Prilosec OTC package in .

What do I do after 14 days?

If your frequent heartburn continues or returns after 14 days of treatment, discuss with your doctor your options for ongoing treatment using Prilosec OTC. Your doctor will take steps to ensure Prilosec OTC is not masking any potentially serious underlying conditions behind your frequent heartburn, and that Prilosec OTC continues to be right for you.

Can I take Prilosec OTC if I’m pregnant?

If pregnant or breast-feeding, ask a healthcare professional before use.

If I am taking Prilosec OTC, can I eat the foods that used to give me frequent heartburn?

Yes. Prilosec OTC blocks heartburn before it begins so you can enjoy the foods you love.*

Does Prilosec OTC work right away?

Prilosec OTC starts to work on the very first day of treatment, but may take 1 to 4 days for full effect (although some people get complete relief within 24 hours). Even though you may feel heartburn relief in the first few days, make sure to take the entire 14 days of dosing to treat your frequent heartburn. Prilosec OTC is not meant for immediate relief. Taking Prilosec OTC every day for 14 days helps to ensure that acid production is consistently controlled.

What happens if I take Prilosec OTC after I started to feel heartburn coming on?

If you are a frequent heartburn sufferer, you don’t have to wait until you have heartburn symptoms to take Prilosec OTC. It begins working on the very first day of treatment, and with one pill each morning for 14 days you can get zero heartburn.*

If Prilosec OTC is available over-the-counter, why do I need to talk to my doctor?

As with any OTC drug, it is important to read and follow all label directions. If you have questions regarding the label or use of Prilosec OTC, talk with your doctor or pharmacist.

Can I take Prilosec OTC more than once a day?

No. As part of a course of therapy, take only one pill a day to treat frequent heartburn for 24 hours.* Take one pill a day with a glass of water before eating in the morning for 14 days. You may repeat this 14-day treatment every four months, or as directed by your doctor.

1P&G calculation based in part on Buying Households reported by the Nielsen Company through its Homescan Panel in the US market for Prilosec OTC for the period 8/31/03 through 6/28/14.

US Pharm. 2013;38(12):38-42.

ABSTRACT: Proton pump inhibitors (PPIs), available with or without a prescription, are commonly used for the treatment of acid-related disorders. Despite their ease of availability and common use, PPIs can have severe side effects. The long-term consequences of chronic PPI use include the potential increased risk of hypocalcemia, hypomagnesemia, Clostridium difficile infections, and pneumonia. Community pharmacists are poised to provide evidence-based recommendations and educate patients about the benefits and risks associated with chronic PPI use.

Proton pump inhibitor (PPIs) have been on the market since the late 1980s and have replaced the histamine2 receptor-antagonists (H2RAs) as the most potent class of drugs for the treatment of acid-related diseases.1 Anti-ulcer medications (therapeutic areas are based on proprietary IMS Health definitions) were the ninth largest class based on prescription volume in the United States in 2012 and the 11th in sales.2,3

Medications in the PPI class are widely available with or without a prescription. Currently, the U.S. market contains six PPIs, two of which are also available as OTC products (TABLE 1).4-9 In the early 2000s, the FDA announced the availability of omeprazole (Prilosec OTC) as the first OTC PPI.10 It was soon followed by the approval of OTC lansoprazole (Prevacid 24HR).11

PPIs are used for the treatment of many gastric conditions including peptic ulcer disease, eradication of Helicobacter pylori infections, treatment and prevention of nonsteroidal anti-inflammatory drug (NSAID) gastroduodenal ulcer, Zollinger-Ellison syndrome, and gastroesophageal reflux disease (GERD).1 Generally, these medications are prescribed because of the low incidence of side effects and superior efficacy compared to other drugs used to treat the same conditions.1

Long-term use of any medication raises safety concerns, especially if that product is available OTC. The American Gastroenterological Association (AGA) released guidelines on the management of GERD in 2008 that recommended against routine monitoring for PPIs due to insufficient evidence.12 However, since then studies have continued to show long-term consequences from chronic PPI use including malabsorption consequences and infections. Subsequently, in March 2013, the American College of Gastroenterology (ACG) released guidelines for the diagnosis and treatment of GERD.13 These guidelines do provide some insight into monitoring for long-term consequences of chronic PPI use. This article is a review of the recent literature and guideline recommendations regarding the possible long-term consequences of chronic PPI pharmacotherapy and opportunities to prevent these complications.

In animal studies, PPIs raised concerns about a potential for hypergastrinemia, but human studies failed to show an association.1 Therefore, long-term consequences of chronic PPI use can be grouped into two main categories, malabsorption and infections.1 Malabsorption secondary to PPI use affects calcium and magnesium, and the literature specifies two infections most often associated with PPI use, Clostridium difficile and pneumonia. Unfortunately, a definition in the literature for “long-term” is lacking; neither the AGA guidelines nor the ACG guidelines define what is considered long-term. For the rest of this article, the authors use long-term to designate therapy greater than 14 days, the maximum therapy for the OTC products.10,11

Malabsorption

The first potential long-term consequence of chronic PPI use is malabsorption of key minerals in the body, namely calcium and magnesium. The loss of these minerals could lead to bone fractures or cardiac abnormalities.

Decreased Calcium Absorption (Hypocalcemia): Long-term PPI use has been associated with an increased risk of osteoporosis and decreased bone mineral density (BMD), with a 35% increased risk of fractures.14 Calcium serves an important role in bone health and formation, as it is a key component of hydroxyapatite (the main structural element of bone). Bone material is a major reservoir for calcium and may contain greater than 99% of a body’s calcium.15 The hypothesis for the mechanism of PPI-induced bone fractures is that dietary calcium absorption is dependent upon an acidic environment in the gastrointestinal (GI) tract. Due to the decrease in acidity from the pharmacologic effect of PPIs, a potential loss of calcium absorption occurs. This reduction in calcium absorption leads to decreased osteoclastic activity and thus decreases in BMD, thereby increasing fracture risk.1

The 2013 ACG guidelines on GERD state that existing osteoporosis is not a contraindication to PPI therapy.13 Patients with osteoporosis may remain on PPI therapy unless another risk factor for hip fracture exists.13 Furthermore, in March 2011, the FDA modified its osteoporosis and fracture warning. It was concluded that OTC products do not warrant label changes to include warnings of fracture risk.16

However, several studies have demonstrated an association between long-term PPI use and risk of fractures, but they contain numerous confounders. Common risk factors for fractures such as a sedentary lifestyle and concomitant use of certain medications (e.g., thiazide diuretics, hormone replacement therapy, corticosteroids) are often observed in patients who routinely take PPIs.14 Additionally, patients who take high doses of PPIs are at higher fracture risk versus patients who take lower OTC doses.17 Finally, patients who take PPIs for extended periods of time (>1 year) are more likely to experience a fracture.18

An analysis of the data obtained from the Canadian Multicentre Osteoporosis Study revealed that the use of PPIs was associated with lower BMD, particularly at the hip and femoral neck, when compared to non-PPI use.19 However, long-term PPI use was not associated with an accelerated decline in BMD. Targownik et al reported that patients using PPIs did have lower BMD; however, these patients were significantly older (66.3 vs. 60.9 years; P <.001) and had a higher mean body mass index (BMI) (28.3 vs. 26.9; P <.001).19

Data remain relatively inconclusive and conflicting regarding the magnitude of the PPI and fracture association in the absence of additional risk factors. According to the 2013 ACG guidelines, there is insufficient evidence to warrant routine BMD tests, calcium supplementation, or other routine precautions because of PPI use.13 In contrast, Health Canada issued an alert in April 2013 stating that patients with existing risk factors for osteoporosis should be monitored closely and should also receive short-term PPI therapy at the lowest effective dose.20 This is parallel to current recommendations from the FDA despite the lack of recommendations from the ACG.16 If calcium supplementation is indicated, use of calcium citrate is the preferred calcium supplement in patients taking PPIs, as it can be absorbed in the absence of an acidic environment.1

Decreased Magnesium Absorption (Hypomagnesemia): In March 2011, the FDA released a warning regarding low serum magnesium levels associated with long-term use of PPIs.21 An analysis of reports from the FDA’s Adverse Event Reporting System (AERS) states that approximately 1% of patients who experienced an adverse effect while on a PPI experienced hypomagnesemia.21 The mechanism behind the changes in absorption is unknown. Symptoms of hypomagnesemia include seizures, arrhythmias, hypotension, and tetany. Hypomagnesemia is also potentially fatal.22 Hypomagnesemia related to chronic PPI use was not addressed in the 2013 ACG guidelines.13

All PPIs are associated with decreased magnesium absorption.21 Hypomagnesemia was more common in older patients taking a PPI (mean age 64.4 years).21 Mean time to onset of hypomagnesemia was 5.5 years after initiation of therapy.21 Similarly, a systematic review of case reports found that patients who presented with hypomagnesemia in association with PPI use also presented with other electrolyte disturbances, specifically hypokalemia and hypocalcemia.23 Hypomagnesemia generally resolved with the discontinuation of the PPI and recurred soon after the PPI was rechallenged.24

Concurrent use of medications that also decrease magnesium increases the risk of significant hypomagnesemia. Danziger et al reported that patients who take a PPI with a diuretic have nearly a 55% greater risk of hypomagnesemia than patients who take only a PPI.22

An FDA Drug Safety Communication warns of the risks of hypomagnesemia and recommends that providers monitor serum magnesium levels in patients taking PPIs.21 The FDA suggests that providers obtain serum magnesium levels prior to initiation of therapy and periodically thereafter for patients who will continue prolonged treatment and for patients who take medications that also cause hypo-magnesemia. Patients who present with clinically significant hypomagnesemia may require discontinuation of PPI therapy, magnesium replacement via oral or IV methods, and treatment with an alternative class of drugs for GI conditions such as an H2RA.1

Infections

In addition to decreased magnesium and calcium absorption, patients on long-term PPIs may be at an increased risk of infection. The hypothesis for the mechanism of action is that the gastric acid secretions act as a defense mechanism against enteric bacteria, and the increased gastric pH during PPI use allows for colonization of opportunistic microbes.1 The 2013 ACG guidelines warned about the risk of increased infections of C difficile and community-acquired pneumonia (CAP).13

Clostridium difficile: In a 2005 retrospective study, researchers found that patients who were taking PPIs had a hazard ratio (HR) of 2.9 (95% CI, 2.4-3.4); i.e., patients had a 2.9-fold increase in the risk of acquiring C difficile than patients who were not on a PPI.25 Seventy-five percent of the patients with reported cases were over the age of 65 years. Not only does long-term use of PPIs cause an increased incidence of C difficile, but patients who received a PPI during treatment of C difficile were also 42% (95% CI, 1.11-1.82) more likely to have a recurrent infection after finishing therapy.25

A 2010 study by Linsky et al looked at the association of PPI use and recurrent C difficile.26 The authors determined whether or not the patient had an infection with recurrent C difficile, 15 to 90 days after initial C difficile infection, if the patient received a PPI within 14 days of initial C difficle infection. The HR for patients exposed to PPIs during treatment was 1.42 (95% CI, 1.11-1.82). For patients over the age of 80 years, the HR increases from 1.42 to 1.86 (95% CI, 1.15-3.01).26

In 2012, the FDA issued a statement detailing the relationship between C difficile–associated diarrhea (CDAD) with the use of a PPI.27 The FDA safety alert warns patients and healthcare professionals to consider CDAD if a patient takes a PPI and experiences persistent diarrhea.27 The FDA also recommends that patients be on the lowest dose for the shortest period of time to treat their current condition.27 The 2013 ACG guidelines recommend use of PPIs with caution in patients with a risk of C difficile infections.13

Community-Acquired Pneumonia: Patients taking PPIs may potentially be at an increased risk for CAP. However, the degree of association is unclear due to conflicting data.28-30 The 2013 ACG guidelines state that short-term PPI use may increase the risk of CAP, but the risk does not seem to be elevated in long-term use.13

A 2012 cohort study by de Jagar et al showed that patients on PPIs were 2.23 times (95% CI, 1.28-3.75) more likely to develop a CAP infection compared to patients not on PPIs.31 Unfortunately, the duration of time that patients were prescribed was not included in the study design.31 In a meta-analysis completed in 2004, researchers discovered that patients who were on an acid-suppressing agent, either a PPI or an H2RA, were 4.5 (95% CI, 3.8-5.1) times more likely to develop pneumonia.30 Mean duration of use for H2RAs was 2.8 months; for PPIs the mean duration was 5 months.30

Conversely, a 2008 study conducted by Sarkar et al showed that current PPI use was not associated with an increased risk of CAP (odds ratio 1.02, 95% CI 0.97-1.08).29 However, the study did observe an increased risk of acquiring an infection in patients initiated on a PPI within the past 14 days (adjusted OR 3.21, 95% CI 2.46-4.18).29

The data support a short-term increase risk of pneumonia infections, but they are conflicting regarding long-term consequences. Despite the conflicting data, this risk is important to consider, especially because of the new Centers for Medicare & Medicaid (CMS) regulations on hospital readmissions.32 Laheij et al determined that the incidence rate of pneumonia was 2.5 per 100 patient-years for patients on PPIs.30 With 65.7 million prescriptions of omeprazole alone and an increased $15,682 cost to Medicare beneficiaries due to pneumonia hospitalizations, the risk of PPI use-associated infections warrants vigilance and evidence-based medicine on the part of the pharmacist.33,34

Conclusion

PPIs are an efficacious and safe drug class. They offer relief to patients in a patient-centered healthcare system. Unfortunately, these agents do potentially have some long-term consequences from continued use, including malabsorption issues and increased risk of infections. The pharmacist can be an advocate for the patient in the hospital system or in the community by understanding these risks and fostering patient-centered care by empowering a well-informed patient in healthcare decisions.

Omeprazole

Prescription omeprazole comes as a delayed-release (releases the medication in the intestine to prevent break-down of the medication by stomach acids) capsule, and packets of delayed-release (releases the medication in the intestine to prevent break-down of the medication by stomach acids) granules for suspension (to be mixed with liquid) to take by mouth or give through a feeding tube. Nonprescription (over-the-counter) omeprazole comes as a delayed-release tablet to take by mouth. Prescription omeprazole should be taken at least 1 hour before a meal. Prescription omeprazoleis usually taken once a day before a meal but may be taken twice a day when used with other medications to eliminate H. pylori, or up to three times a day, before meals when used to treat conditions in which the stomach produces too much acid. The nonprescription delayed-release tablets are usually taken once a day in the morning at least 1 hour before eating for 14 days in a row. If needed, additional 14-day treatments may be repeated, not more often than once every 4 months. To help you remember to take omeprazole, take it at around the same time(s) every day. Follow the directions on your prescription label or the package label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take omeprazole exactly as directed. Do not take more or less of it or take it more often or for a longer period of time than prescribed by your doctor or stated on the package.

If you are taking the delayed-release tablets, swallow them whole with a full glass of water. Do not split, chew, or crush them or crush and mix them into food.

Swallow the delayed-release capsules whole. If you have difficulty swallowing the delayed-release capsules, place one tablespoon of soft, cool applesauce in an empty bowl. Open the delayed-release capsule and carefully empty all the granules inside the capsule onto the applesauce. Mix the granules with the applesauce and swallow the mixture immediately with a glass of cool water. Do not chew or crush the granules. Do not store the applesauce/granule mixture for future use.

If you are taking the granules for oral suspension, you will need to mix it with water before use. If you are using the 2.5-mg packet, place 1 teaspoonful (5 mL) of water in a container. If you are using the 10-mg packet, place 1 tablespoonful (15 mL) of water in a container. Add the contents of the powder packet and stir. Wait 2 to 3 minutes to allow the mixture to thicken, and stir the mixture again. Drink the entire mixture within 30 minutes. If any of the mixture is stuck to the container, pour more water into the container, stir and drink all the mixture immediately.

The granules for oral suspension can be given through a feeding tube. If you have a feeding tube, ask your doctor how you should take the medication. Follow the directions carefully.

Do not take nonprescription omeprazole for immediate relief of heartburn symptoms. It may take 1 to 4 days for you to feel the full benefit of the medication. Call your doctor if your symptoms get worse or do not improve after 14 days or if your symptoms return sooner than 4 months after you finish your treatment. Do not take nonprescription omeprazole for longer than 14 days or treat yourself with omeprazole more often than once every 4 months without talking to your doctor.

Continue to take prescription omeprazole even if you feel well. Do not stop taking prescription omeprazole without talking to your doctor. If your condition does not improve or gets worse, call your doctor.

Ask your pharmacist or doctor for a copy of the manufacturer’s information for the patient.

Omeprazole (Prilosec) is a cheap, generic medication available both over the counter or with a prescription. It belongs to a class of medications known as proton-pump inhibitors (PPIs), and is one of the most popular medications in the U.S. It’s used to treat heartburn, reflux disease (GERD), and ulcers. Many people also use omeprazole to protect the stomach when taking NSAIDS (non-steroidal anti-inflammatory drugs).

Even if you’ve been taking omeprazole for a while, here are five things you may want to be aware of.

1) Disruption of gut bacteria

Studies have shown that people treated with omeprazole have different types of bacteria in their gut compared to untreated patients. Specifically, people taking omeprazole have higher counts of “bad” bacteria like Enterococcus, Streptococcus, Staphylococcus, and some strains of E. coli. Why this matters is not fully known. But, the bacteria in our guts play an important role in our defense against pathogens, so disrupting the gut flora may be a downside of omeprazole. It might be why people taking omeprazole have a higher risk of getting C. diff diarrhea.

2) Omeprazole vs. other GERD drugs

Is omeprazole the best medication for stomach issues? Well, studies show omeprazole works better than rabeprazole (Aciphex) for a variety of stomach issues, but it does not work as well as esomeprazole (Nexium) for GERD.

3) Omeprazole and heart attacks

A study published in August 2016 found that taking PPIs like omeprazole could be a risk factor for heart-related complications. How severely omeprazole impacts heart health has not been fully explored, but in this study, long-term use of PPIs was associated with a 70% increased risk of cardiovascular issues—and risk increased with longer use.

4) Omeprazole vs. acupuncture

In a study from 2016, acupuncture was found to work better than omeprazole for GERD. The researchers compared GERD symptoms in patients taking omeprazole versus those undergoing acupuncture treatments over 8 weeks. After the study, both groups’ symptoms improved, but acupuncture was significantly superior to omeprazole. Worth a try!

5) Omeprazole “as needed”

Unfortunately, omeprazole doesn’t work on an “as needed” basis. PPIs like omeprazole take five days to reach maximal effect. So, taking it on an “as needed” basis will not provide enough acid suppression and symptom relief. However, some histamine-2 antagonists, like cimetidine (Tagamet) and ranitidine (Zantac) are better for that.

Dr O.

  • 1. What is FDA announcing today?
    2. What is Prilosec OTC used to treat?
    3. How does Prilosec OTC work?
    4. Will Prilosec OTC work as well as the prescription strength Prilosec?
    5. How is Prilosec OTC taken?
    6. If Prilosec OTC takes a few days to take effect, can I take more each day to make it work faster?
    7. Who should take prescription strength Prilosec rather than Prilosec OTC?
    8. Who should NOT take Prilosec OTC?
    9. Does Prilosec OTC interact with food or other drugs?
    10. How is Prilosec OTC different from the other OTC treatments for heartburn?
    11. What are some possible side effects of Prilosec OTC?
    12. How can I report a side effect with Prilosec OTC to the FDA?
    13. When will Prilosec OTC be available?
    14. What if I have other questions about Prilosec OTC?

    1. What is FDA announcing today?

    The FDA is announcing the approval of Prilosec OTC (omeprazole) as an over-the-counter (OTC) drug product. Until today, Prilosec was available only with a doctor’s prescription. FDA originally approved prescription Prilosec in 1989.

    2. What is Prilosec OTC used to treat?

    Prilosec OTC is used to treat frequent heartburn. Heartburn occurs when the stomach contents back up and out of the stomach into the esophagus (the tube that connects the throat to the stomach). Frequent heartburn is when you have heartburn 2 or more days a week.

    Prilosec OTC is not the right medicine for you if you have occasional heartburn, one episode of heartburn a week or less, or if you want immediate relief of heartburn.

    It is very important that you carefully read and understand the Prilosec OTC label directions, warnings, and side effects. Most importantly, the label will tell you when you should seek medical attention instead of taking Prilosec OTC.

    3. How does Prilosec OTC work?

    Prilosec OTC stops the stomach from making acid. This causes less heartburn.

    4. Will Prilosec OTC work as well as the prescription strength Prilosec?

    Both prescription Prilosec and Prilosec OTC contain the same active ingredient, omeprazole, which effectively stops acid production. Prescription Prilosec treats diseases that require diagnosis and supervision by a doctor. Prilosec OTC treats only symptoms of frequent heartburn. Used as directed, Prilosec OTC will not treat the conditions that prescription Prilosec treats.

    5. How is Prilosec OTC taken?

    Prilosec OTC is a delayed-release 20mg tablet, taken once a day (every 24 hours) for 14 days before eating. You should not take it for more than 14 days or repeat a 14-day course more often than every 4 months unless directed by a doctor.

    Do not crush, break, or chew the tablet. This decreases how well Prilosec OTC works in the body.

    6. If Prilosec OTC takes a few days to take effect, can I take more each day to make it work faster?

    No. Prilosec OTC is not intended for immediate relief of occasional heartburn. Prilosec OTC may take 1 to 4 days for full effect, although some people get complete relief of symptoms within 24 hours.

    Although the two products contain omeprazole, prescription Prilosec is for treating conditions such as inflammation of the esophagus (esophagitis), ulcers, and other medical conditions for which a doctor’s supervision is needed.

    For this reason, stop taking Prilosec OTC and tell your doctor if you:

    • are not feeling better and your heartburn continues to worsen
    • need to take this product for more than 14 days
    • need to take more than 1 course of treatment every 4 months

    7. Who should take prescription strength Prilosec rather than Prilosec OTC?

    Prilosec OTC is not appropriate for adults who:

    • have only occasional heartburn
    • have one episode of heartburn a week or less
    • want immediate relief of heartburn

    8. Who should NOT take Prilosec OTC?

    Do not take Prilosec OTC if you have:

    • had an allergic reaction to Prilosec in the past
    • trouble or pain swallowing food
    • vomiting with blood
    • bloody or black stools

    9. Does Prilosec OTC interact with food or other drugs?

    When you are taking Prilosec OTC, it is especially important that your health care provider know if you are taking any of the following:

    • warfarin (blood-thinning medicine)
    • prescription antifungal or anti-yeast medicines
    • diazepam (anxiety medicine)
    • digoxin (heart medicine)

    10. How is Prilosec OTC different from the other OTC treatments for heartburn?

    There are other OTC drug products used to provide immediate relief for heartburn. These include antacids and acid reducer drug products such as Pepcid, Zantac, Tagamet, and Axid. Prilosec OTC should not be confused with these products because it works differently and is not intended for immediate relief.

    11. What are some possible side effects of Prilosec OTC?

    Although side effects from Prilosec OTC are not common, they can occur. Tell your doctor if any of these symptoms are severe or do not go away:

    • headache
    • diarrhea
    • constipation
    • upset stomach
    • vomiting
    • stomach pain
    • cough
    • cold symptoms
    • dizziness
    • rash

    12. How can I report a side effect with Prilosec OTC to the FDA?

    You can report a side effect the following ways:

    • Visit www.fda.gov/medwatch and click on “How to Report”
    • Call 1 – 800-FDA-1088
    • Fax 1 – 800-FDA-0178

    13. When will Prilosec OTC be available?

    The company marketing Prilosec OTC makes the decision on availability. For further information, please contact the manufacturer, Procter and Gamble, directly.

    14. What if I have other questions about Prilosec OTC?

    If you have further questions regarding Prilosec OTC or any medications, please contact the Center for Drug’s Division of Drug Information at: 888-INFOFDA (888-463-6332), or email us at: [email protected]

    Related Information

    • Prilosec OTC (omeprazole) Information

    Easy-to-read medicine information about omeprazole – what it is, how to take it safely and possible side effects.

    Type of medicine Also called
    • Medicine to reduce stomach acid
    • Belongs to a group of medicines known as proton pump inhibitors
    • Dr Reddy’s Omeprazole®
    • Losec®
    • Omezol Relief®
    • Omeprazole Actavis®

    What is omeprazole?

    Omeprazole reduces the amount of acid produced in your stomach. It belongs to a group of medicines known as proton pump inhibitors (PPIs). They are used to treat a number of conditions associated with high stomach acid affecting your stomach and gut, such as indigestion, reflux and ulcers. Omeprazole can prevent ulcers from forming or help the healing process where damage has already occurred.
    Omeprazole can also:

    • be given together with antibiotics to get rid of Helicobacter pylori, a bacteria found in your stomach that can cause ulcers.
    • be used to prevent ulcers caused by medicines such as non-steroidal anti-inflammatory drugs (NSAIDs). Examples of NSAIDs are diclofenac, ibuprofen, naproxen.

    In New Zealand omeprazole is available as capsules and can be given as an injection in the hospital.

    Dose

    • The usual dose of omeprazole is 20 mg a day.
    • For some people, 10 mg a day is enough; others may need a higher dose of 40 mg a day.
    • It is best to take the lowest effective dose, for the shortest possible time.
    • Your doctor will advise you how long to take omeprazole for (usually for 4 to 8 weeks). Some people may need to take it for longer.
    • The pharmacy label on your medicine will tell you how much omeprazole to take, how often to take it, and any special instructions.

    How to take omeprazole

    • Take omeprazole at the same time each day, usually in the morning.
    • Omeprazole is usually taken once a day, but some people may need to take it twice a day. Your doctor will tell you how often to take omeprazole.
    • Swallow the capsule whole with a glass of water. Do not crush or chew – the medicine doesn’t work properly if the capsule is crushed or chewed.
    • If you have difficulty swallowing the capsule, you can open it and sprinkle the pellets over some fruit juice or yoghurt and swallow the pellets without chewing.
    • Omeprazole can be taken before or after food, although taking it before food is best.
    • If you forget to take your dose, take it as soon as you remember. But, if it is nearly time for your next dose, just take the next dose at the right time. Do not take double the dose.

    Avoid long-term use – choose wisely

    If you don’t need them, PPIs like omeprazole should not be taken long term, because of the possible side effects. There may be a small increased risk of bone fractures, chest infections, kidney problems and nutrient deficiencies such as low magnesium and vitamin B12. If you’ve been taking a PPI for reflux for longer than 4 to 8 weeks, and your symptoms seem to be well managed, it’s a good idea to talk to your healthcare provider about reviewing your medicine. They may recommend stepping down your treatment. This could include:

    • reducing your daily dose of omeprazole
    • taking omeprazole only when you experience the symptoms of heartburn and reflux (also known as on-demand therapy)
    • stopping treatment completely, as your symptoms may not return. It may be best to reduce the dose over a few weeks before stopping.

    Read more about PPIs for heartburn and reflux Choose Wisely, NZ

    Precautions – before starting omeprazole

    • Are you pregnant, planning a pregnancy or breastfeeding?
    • Do you have problems with your liver?
    • Are taking any other medicines? This includes any medicines you are taking that you can buy without a prescription, as well as herbal and complementary medicines.

    If so, it’s important that you tell your doctor or pharmacist before you start omeprazole. Sometimes a medicine isn’t suitable for a person with certain conditions, or it can only be used with extra care.

    Possible side effects

    Like all medicines omeprazole can cause side effects, although not everyone gets them. Often side effects improve as your body adjusts to the new medicine.

    Rebound acid secretion

    When omeprazole is stopped, a common side effect is rebound acid secretion, where the acid secretion in your stomach increases significantly. This should return to normal within 2 weeks. Because the symptoms of rebound acid secretion are the same as for reflux (such as indigestion, discomfort and pain in your upper stomach and chest, feeling sick and an acid taste in your mouth), it can form an ongoing loop where stopping omeprazole treatment creates the need to start it again.

    Rather than restart omeprazole, your doctor may advise you to use medicines that contain both an antacid and an anti-foaming agent, such as Acidex oral liquid or Gaviscon Double Strength tablets. Alternatively, ranitidine tablets could be used. These can be effective for treating rebound acid secretion. You can use these medicines to relieve the symptoms when they occur.

    Talk to your doctor or pharmacist about how to manage rebound acid secretion.

    Other side effects

    Side effects What should I do?
    • Stomach upset, feeling sick
    • Feeling bloated, gas in your abdomen (tummy)
    • Loose stool (mild diarrhoea)
    • Constipation
    • These are quite common when you first start taking omeprazole.
    • Tell your doctor if troublesome.
    • Signs of low magnesium, such as muscle cramps, weakness, tiredness, feeling irritable and changes in heartbeat
    • Increase your intake of magnesium-rich foods such as wholegrain cereals, green leafy vegetables (spinach, parsley, cabbage), peas, lean meats, nuts, seeds and bananas.
    • Tell your doctor if troublesome – you may need a magnesium supplement.
    • Severe diarrhoea (loose, watery, frequent stools)
    • Omeprazole can increase the chance of getting severe diarrhoea (which may be caused by bacteria called clostridium difficle).
    • Stop omeprazole and tell your doctor immediately.
    • Signs of an allergic reaction such as rash, fever, painful joints
    • Tell your doctor immediately or ring HealthLine 0800 611 116.
    • Worsening stomach problems, such as really bad stomach pain, blood in your stool or black stools, vomiting blood or dark-coloured vomit
    • Tell your doctor immediately or ring HealthLine 0800 611 116.

    Interactions

    Omeprazole may interact with a few medications and herbal supplements, so check with your doctor or pharmacist before starting omeprazole or before starting any new medicines.

    Learn more

    The following links have more information on omeprazole:

    Omeprazole (Māori) New Zealand Formulary Patient Information
    Losec, Omezol Relief Medsafe Consumer Information Sheets

    1. Stopping proton pump inhibitors in older people BPAC, NZ 2019
    2. Proton pump inhibitors: When is enough, enough? BPAC, NZ, 2014
    3. Proton pump inhibitors and the risk of acute kidney injury. BPAC, NZ, 2016
    4. Omeprazole New Zealand Formulary

    Managing interactions with omeprazole

    A 30-year-old man comes into the pharmacy complaining of recurrent attacks of heartburn. He tells you that the symptoms are worse after large meals, and especially bad when he lies down. He has no history of other gastrointestinal conditions.

    He says he has seen an advertisement for Zanprol (omeprazole) and he asks you if he can buy a box.

    On further questioning he tells you he takes citalopram 20mg daily for depression.

    Is there an interaction with citalopram? Omeprazole is a moderate inhibitor of CYP2C19 and citalopram is a substrate of this isoenzyme. A crossover study in healthy subjects has shown that omeprazole approximately doubled the area under the concentration-time curve (AUC) of plasma S-citalopram (escitalopram), but did not affect the AUC of R-citalopram to a statistically significant extent. Any patient taking citalopram (or escitalopram) would, therefore, be expected to have a moderate increase in its exposure on concurrent use with omeprazole.

    However, because CYP2C19 is subject to genetic polymorphism (see PJ 2013;291:350–51), the extent to which citalopram is metabolised via this route could depend on the individual. Furthermore, determining the metaboliser status of an individual is currently a research tool rather than a clinical one.

    The clinical relevance of the interaction between omeprazole and citalopram is unclear. Until more is known, patients should be advised to be alert for an increase in citalopram adverse effects (such as dry mouth, increased sweating, or insomnia) when taking omeprazole. If patients experience an increase in citalopram adverse effects, they should be advised to stop taking it and to see their GP if the effects are severe, or switched to an alternative treatment for heartburn. For patients on longer-term treatment with omeprazole, consideration should be given to decreasing the dose of the SSRI if citalopram adverse effects become troublesome.

    Pantoprazole, another proton pump inhibitor available for OTC sale, does not inhibit CYP2C19 to a clinically relevant extent, and would be a more suitable alternative for this patient. Some H2 receptor antagonists, such as famotidine and ranitidine (but not cimetidine) also do not inhibit cytochrome P450 isoenzymes to a clinically relevant extent, and could also be sold to this patient for his heartburn.

    After you have explained the possible outcome of taking omeprazole with citalopram, and suggested alternatives, the patient decides he would still like to “give omeprazole a try”. After ensuring that he is aware of potential interaction effects and what to do if he experiences any, you sell it to him. You also explain that OTC omeprazole should only be used for up to two weeks and, if his symptoms persist, he should see his GP.

    A week later, the man returns to the pharmacy with a prescription for itraconazole capsules for a persistent ringworm infection. You ask him how his heartburn is. He tells you that it is still causing him problems, but the omeprazole is helping and he has been taking it on most days.

    On checking the prescription, you see there is an interaction between itraconazole and omeprazole.

    How significant is this interaction with itraconazole? Itraconazole is a poorly soluble base that must be converted by acid in the stomach into the soluble hydrochloride salt. Drugs that reduce acidity, such as proton pump inhibitors, H2 receptor antagonists, or antacids, therefore reduce the dissolution and absorption of itraconazole when given in capsule form.

    In a study in healthy subjects, the AUC and maximum plasma concentration of itraconazole given as a capsule were both reduced by about 65 per cent by omeprazole. In contrast, another study in healthy subjects found that omeprazole did not affect the pharmacokinetics of single doses of itraconazole given as an oral solution.

    The above studies indicate the possibility of an interaction between omeprazole and itraconazole capsules, but not between omeprazole and itraconazole solution. Therefore one option is to contact the man’s GP and suggest that he prescribes itraconazole solution to reduce the possibility of an interaction.

    It is interesting to note that studies have shown that giving itraconazole with acidic drinks can increase its dissolution and absorption. For example, a study in eight healthy subjects given itraconazole 100mg with either 325ml of water or Coca-Cola (pH 2.5) found that the maximum plasma concentration of itraconazole was more than doubled by Coca-Cola and the AUC of itraconazole was increased by 80 per cent, although two of the subjects did not show this effect.

    Although their effects on itraconazole absorption have not been studied, diet carbonated drinks are less acidic and are therefore expected to be less effective at reducing the stomach pH.9

    In theory, you could consider recommending that patients prescribed a combination of omeprazole with itraconazole take the latter with an acidic drink, such as non-diet cola, to increase gastric acidity and absorption of the antifungal, but this may not be such a good idea since acidic carbonated drinks might make heartburn worse.

    You decide to call the patient’s GP and explain that he is taking OTC omeprazole. You suggest that it would be a good idea to prescribe itraconazole liquid instead of the capsules. The GP agrees.

    Several months later the man returns with a prescription for fluoxetine 20mg daily, omeprazole 10mg daily, and a seven-day course of clarithromycin 250mg bd for an upper respiratory tract infection. He tells you that he did not respond particularly well to the citalopram, so his GP changed him to a different SSRI. Remembering your previous advice about potential drug interactions with omeprazole, the patient asks you if there will be any problems taking clarithromycin with his other prescribed medicines.

    What are the potential interactions with clarithromycin? CYP3A4 is one of the isoenzymes involved in the metabolism of omeprazole, and clarithromycin is a potent inhibitor of this isoenzyme. It would, therefore, be expected to increase the exposure of omeprazole, leading to an increase in omeprazole’s adverse effects.

    Studies have shown that clarithromycin moderately increases the AUC of omeprazole, but because omeprazole has a wide therapeutic range, the increase in exposure reported is unlikely to be clinically relevant.,6 In addition, omeprazole might slightly increase the AUC of clarithromycin and its active metabolite, but this is also not expected to be clinically relevant.6

    An isolated case report describes a man who developed apparent acute fluoxetine toxicity while taking clarithromycin, but the clinical significance of this case report is unknown. It has been suggested that clarithromycin (a potent inhibitor of CYP3A4), reduced the metabolism of fluoxetine, thereby increasing its serum concentration and precipitating the observed toxicity.7 However, fluoxetine does not appear to be primarily metabolised by CYP3A4.

    The Stockley’s team is not aware of an interaction between fluoxetine and omeprazole and the book contains no data for an interaction with this drug pair. The patient can be advised that no additional precautions or dose adjustments appear necessary on the concurrent use of omeprazole, clarithromycin, and fluoxetine.

    This case serves to illustrate some of the drug interactions that should be considered when omeprazole is sold over the counter and how they can be managed. It also highlights that not all potential drug interactions will be clinically relevant because of omeprazole’s wide therapeutic range. Panel 1 lists some more drug interactions that could occur with omeprazole.

    Other omeprazole interactions

    Cilostazol Omeprazole increases the exposure to cilostazol. Cilostazol dose reduction might be required.

    Clopidogrel Omeprazole might reduce the antiplatelet effects of clopidogrel. Consider giving an H2 receptor antagonist (not cimetidine) or pantoprazole instead.

    Clozapine Omeprazole possibly reduces clozapine concentrations. Monitor for reduced clozapine efficacy.

    Methotrexate Reduced methotrexate elimination has been reported in

    patients given proton pump inhibitors with high-dose methotrexate. Routine methotrexate monitoring should detect any toxicity; some advise against concurrent use and suggest that omeprazole should be stopped five days before starting methotrexate.

    Phenytoin Phenytoin exposure might be increased or not affected by omeprazole. Any interaction seems unlikely to be clinically significant, but be alert for signs of phenytoin toxicity.

    Tacrolimus Omeprazole might affect tacrolimus exposure; consider monitoring tacrolimus concentrations when either drug is started or stopped.

    Voriconazole Voriconazole increases the exposure to omeprazole. Omeprazole might increase the exposure to voriconazole and serious neurological adverse effects have been seen in some patients. Voriconazole dose reduction is recommended.

    Key points

    Omeprazole might increase exposure to citalopram but the clinical relevance is unclear. Patients should be alerted to the possibility of an increase in citalopram adverse effects.

    No additional precautions or dose adjustments appear to be necessary with the concurrent use of omeprazole and clarithromycin.

    Omeprazole reduces the exposure to itraconazole given as capsules, but not when given as itraconazole solution.

    Taking itraconazole capsules with an acidic drink, such as non-diet cola, can increase gastric acidity and therefore increase the absorption of the drug.

    About Stockley

    This article has been produced by Stephanie Jones, Sonia Khan and Claire L. Preston on behalf of the ‘Stockley’s drug interactions’ editorial team.

    The book is available in print through Pharmaceutical Press (www.pharmpress.com) or electronically with quarterly updates through MedicinesComplete (www.medicinescomplete.com).

    Drug interaction: Omeprazole and Phenprocoumon

    Oral anticoagulants like the coumarin derivatives are characterised by a particularly narrow therapeutic range. Concurrently taken drugs such as alcohol, barbiturates, and anti-inflammatory agents potentially interact with coumarin derivatives and can seriously affect anticoagulant activity. Any interfering comedication can pose a challenge to establishing a stable anticoagulant dosage regimen and thus present a serious risk for the patient . Here we describe two cases of possible drug interactions between phenprocoumon and the proton pump inhibitor omeprazole, requiring adjustment of the anticoagulant dose.

    Case 1

    A 68-year-old woman (height: 160 cm; body weight: 60 kg) with a history of recurring tachyarrhythmia, hypertension and severe hyperlipaemia was treated with phenprocoumon (Marcumar, Roche) since December 1998. After an initial phasing-in period of about 5 month, the required dosage for maintaining the patient’s International Normalised Ratio (INR) between 2.1 and 2.7 had stabilised at 5½ to 6½ tablets of phenprocoumon (3 mg/tablet) per week. At this stage, the INR was determined every 3 to 4 weeks to monitor anticoagulation therapy.

    On October 15th 1999, a gastroscopy was performed to investigate the patient’s persistent upper abdominal complaints. This revealed the presence of a large hiatus hernia as well as histological evidence of reflux esophagitis. After commencing (October 15th) treatment with omeprazole (Antra MUPS 1 × 20 mg/day), the patient’s INR increased from initially 2.15 (determined on October 6th) to 3.34 (November 3rd), although the phenprocoumon dosing regimen and all other medication had been continued without changes. For the following weeks, the phenprocoumon dose was therefore reduced to 5½ tablets per week, compared to 6 tablets per week just prior to omeprazole treatment. At the next check-up (November 17th), the INR had returned to 2.28, a value well within the targeted range.

    Case 2

    The second case concerns a 72-year-old diabetic woman with advanced arthropathy which had immobilised her for a considerable period of time. Her condition led to a bilateral pulmonary embolism which was scintigraphically confirmed on April 9th 1999. A thrombosis in her left leg was phlebographically confirmed six days later and on April 16th the patient was put on a loading schedule of phenprocoumon commencing with 4 tablets on day 1, 3 on day 2, 1 on day 3, and further as required. At the same time, the patient was given omeprazole (1 × 20 mg before bedtime) to treat a minimal antrum gastritis. Other co-medications were enalapril (Xanef: 1 × 1/day), glyburide (Euglucon: 1 × 1/day), and dipyrone (Novalgin: 3 × 20 drops/day).

    Before anticoagulation was initiated, the patient’s INR value was 1.02. On the third and fourth day of anticoagulation therapy it had increased to 2.02 and 3.28, respectively. Because the patient responded so strongly, she received no further phenprocoumon during the following days. However, surprisingly the INR value remained at the high level throughout the following 9 days. It was suspected that this unusually long persistence of anticoagulant activity was caused by interference of omeprazole with the metabolism (and thus elimination) of phenprocoumon. Consequently, omeprazole was discontinued on April 29th. Four days later the INR value had decreased to 1.5 and anticoagulation therapy with phenprocoumon was successfully resumed using initially 5½ tablets per week. By mid July, the required dose for maintaining the INR within the therapeutic range had stabilised at 3 to 3½ tablets/week.

    In December 1999, the patient had to undergo minor surgery and, thus, phenprocoumon was withheld for three weeks. Within 7 days the INR value had dropped to below 1.5, and no problems were encountered when anticoagulation therapy was resumed with a loading schedule similar to the one used in April. This observation lent further support to the notion that indeed omeprazole may have been responsible for the problems with the anticoagulation regimen encountered in April.

    Pharmacokinetic drug interaction profile of omeprazole with adverse consequences and clinical risk management

    Wei Li,1 Su Zeng,2 Lu-Shan Yu,2 Quan Zhou3
    1Division of Medical Affairs, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2Department of Pharmaceutical Analysis and Drug Metabolism, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, People’s Republic of China; 3Department of Pharmacy, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, People’s Republic of China
    Background: Omeprazole, a proton pump inhibitor (PPI), is widely used for the treatment of dyspepsia, peptic ulcer, gastroesophageal reflux disease, and functional dyspepsia. Polypharmacy is common in patients receiving omeprazole. Drug toxicity and treatment failure resulting from inappropriate combination therapy with omeprazole have been reported sporadically. Systematic review has not been available to address the pharmacokinetic drug-drug interaction (DDI) profile of omeprazole with adverse consequences, the factors determining the degree of DDI between omeprazole and comedication, and the corresponding clinical risk management.
    Methods: Literature was identified by performing a PubMed search covering the period from January 1988 to March 2013. The full text of each article was critically reviewed, and data interpretation was performed.
    Results: Omeprazole has actual adverse influences on the pharmacokinetics of medications such as diazepam, carbamazepine, clozapine, indinavir, nelfinavir, atazanavir, rilpivirine, methotrexate, tacrolimus, mycophenolate mofetil, clopidogrel, digoxin, itraconazole, posaconazole, and oral iron supplementation. Meanwhile, low efficacy of omeprazole treatment would be anticipated, as omeprazole elimination could be significantly induced by comedicated efavirenz and herb medicines such as St John’s wort, Ginkgo biloba, and yin zhi huang. The mechanism for DDI involves induction or inhibition of cytochrome P450, inhibition of P-glycoprotein or breast cancer resistance protein-mediated drug transport, and inhibition of oral absorption by gastric acid suppression. Sometimes, DDIs of omeprazole do not exhibit a PPI class effect. Other suitable PPIs or histamine 2 antagonists may be therapeutic alternatives that can be used to avoid adverse consequences. The degree of DDIs associated with omeprazole and clinical outcomes depend on factors such as genotype status of CYP2C19 and CYP1A2, ethnicity, dose and treatment course of precipitant omeprazole, pharmaceutical formulation of object drug (eg, mycophenolate mofetil versus enteric-coated mycophenolate sodium), other concomitant medication (eg, omeprazole-indinavir versus omeprazole–indinavir–ritonavir), and administration schedule (eg, intensified dosing of mycophenolate mofetil versus standard dosing).
    Conclusion: Despite the fact that omeprazole is one of the most widely prescribed drugs internationally, clinical professionals should enhance clinical risk management on adverse DDIs associated with omeprazole and ensure safe combination use of omeprazole by rationally prescribing alternatives, checking the appropriateness of physician orders before dispensing, and performing therapeutic drug monitoring.
    Keywords: administration schedule, drug interactions, drug toxicity, herb–drug interactions, omeprazole, pharmacokinetics, polypharmacy, prescription auditing, risk management, treatment failure

    Hi, My husband has been put on Prilosec daily indefinately. He was diagnosed with a hiatal hernia?

    Prilosec (omeprazole) is a medication used to treat several conditions related to the esophagus, stomach, and intestines. It is part of a class of drugs known as proton pump inhibitors (PPIs).

    Know

    A hiatal hernia occurs when part of your stomach pushes upward through your diaphragm. Your diaphragm normally has a small opening (hiatus) that allows your food tube (esophagus) to pass through on its way to connect to your stomach. The stomach can push up through this opening and cause a hiatal hernia.

    In most cases, a small hiatal hernia doesn’t cause problems, and you may never know you have a hiatal hernia unless your doctor discovers it when checking for another condition. But a large hiatal hernia can allow food and acid to back up into your esophagus, leading to heartburn and chest pain. Self-care measures or medications can usually relieve these symptoms, although a very large hiatal hernia sometimes requires surgery.

    If you feel uncortable with your original doctor get a second opinion… OK

    I AM NOT A DOCTOR… IF ANYTHING HAPPENS TO YOUR HUSBAND SEEK MEDICAL ASSISTANCE ASAP.

    All the best

    Hiatal Hernia: Management and Treatment

    How is a hiatal hernia treated?

    Most hiatal hernias do not cause problems and rarely need treatment. However, since some patients with a hiatal hernia have symptoms of GERD, treatment starts with methods used to manage GERD. These include making such lifestyle changes as:

    • Losing weight if you’re overweight.
    • Decreasing the portion sizes of meals.
    • Avoiding certain acidic foods—such as tomato sauce and citrus fruits or juices—that can irritate the esophageal lining.
    • Limiting fried and fatty foods, foods or drinks containing caffeine (including chocolate), peppermint, carbonated beverages, alcoholic beverages, ketchup and mustard, and vinegar.
    • Eating meals at least three to four hours before lying down, and avoiding bedtime snacks.
    • Keeping your head six inches higher than the rest of your body when lying on your back. Raising the level of your head helps gravity keep your stomach’s contents in the stomach. Raising the head of your bed by angling your mattress works best—piling your pillows doesn’t work as well because it makes you crunch your middle instead of simply angling your body upwards.
    • Quitting smoking.
    • Not wearing a tight belt or tight clothing that can increase the pressure on the abdomen — such as control top hosiery and body shapers.
    • Taking medications after eating to reduce acid in the stomach. These over-the-counter medications include antacids, Gaviscon®, or H-blockers (such as Pepcid AC® or Zantac®).

    Sometimes, a medication called a proton-pump inhibitor might be used to treat hiatal hernia. This medication is another way to decrease the amount of stomach acid you have, which can help prevent reflux. When you take this medication, your body doesn’t make as much stomach acid as normal. This is similar to H-blocker medications.

    Can over-the-counter medications help relieve my hiatal hernia symptoms?

    In many cases, over-the-counter medications can help you with some symptoms of hiatal hernia. Antacids are the most common medication you might use for relief. However, if you take over-the-counter medications for longer than two weeks without any improvement, see your healthcare provider. Prescription medications are typically the next step. These can include:

    • Pantoprazole (Protonix®).
    • Rabeprazole (Aciphex®).
    • Esomeprazole (Nexium®).
    • Omeprazole (Prilosec®).
    • Lansoprazole (Prevacid®).

    When is surgery for a hiatal hernia needed?

    If the portion of the stomach entering the esophagus is being squeezed so tightly that the blood supply is being cut off, you’ll need to have surgery. Surgery may also be needed in people with a hiatal hernia who have severe, long-lasting (chronic) esophageal reflux whose symptoms are not relieved by medical treatments. The goal of this surgery is to correct gastroesophageal reflux by creating an improved valve mechanism at the bottom of the esophagus. Think of this valve as a swinging door. It opens to let food pass down into the stomach and then closes to keep stomach contents from going back up the esophagus. When this valve doesn’t work correctly, your stomach contents can go the wrong way and damage your esophagus. If left untreated, chronic gastroesophageal reflux can cause complications such as esophagitis (inflammation), esophageal ulcers, bleeding or scarring of the esophagus.

    How is surgery for a hiatal hernia performed?

    Surgery for repairing a hiatal hernia involves:

    • Pulling the hiatal hernia back into the abdomen.
    • Improving the valve at the bottom of the esophagus.
    • Closing the hole in the diaphragm muscle.

    During surgery, your surgeon will wrap the upper part of the stomach (called the fundus) around the lower portion of the esophagus. This creates a permanently tight sphincter (the valve) so that stomach contents will not move back (reflux) into the esophagus.

    Called a fundoplication, there are two versions of this surgery. An open fundoplication surgery involves a larger incision. This type of procedure may need to be done in some very severe cases and it allows for greater visibility during surgery. However, open surgeries require a longer recovery time in the hospital. In many cases, the surgeon will decide to use a laparoscopic approach instead.

    A laparoscopic surgery is done through several small incisions instead of one big cut. This is considered a minimally invasive option. The specific laparoscopic procedure used to repair a hiatal hernia is called the Nissen fundoplication. This procedure creates a permanent solution to your hiatal hernia symptoms. During the procedure, your surgeon will make five or six tiny incisions in the abdomen. The laparoscope (a tool that allows the surgical team to see your internal organs on a screen in the operating room) and other surgical instruments are inserted through the small incisions. The fundus is wrapped around the esophagus and the sphincter is tightened during surgery. The advantages of laparoscopic surgery compared to an open surgery include:

    • Smaller incisions.
    • Less risk of infection.
    • Less pain and scarring.
    • A shorter recovery.

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    It is paradoxical that recently the number of operations for gastro-oesophageal reflux and hiatus hernia has increased dramatically even though extremely effective medication for these conditions is now available in many, if not all, Western countries.1a The traditional indications for antireflux surgery still exist but they have been impacted upon by cultural factors, cost, and associated serious disease; so why do more people require surgery?

    The most common indication for surgery used to be the failure of medical treatment in severely symptomatic disease; however, so effective are proton pump inhibitors (PPIs) at controlling the major symptom of reflux—namely, heartburn, that this is a less common reason for performing surgery today. Indeed, the failure of a patient to get some degree of symptomatic relief from an adequate dosage of PPIs should alert the surgeon to other problems—for example, bile reflux, irritable colon, functional dyspepsia, or gallstones. Yet, successful medical treatment is often indefinite in duration and many patients do not wish to be on medication for the rest of their lives; such patients are often considered for surgery. Lifelong medication is also costly, and surgery may be the cheaper option in the long term.1

    Stricture formation used to be another common indication for surgery, but PPI treatment has proved so successful that this is now rarely seen. Many patients are elderly and their predominant problem is dysphagia, which is usually effectively treated with PPIs and dilatation. A further indication for surgery—that is, regurgitation or high volume reflux, is now seen more often. It is possible that the successful treatment of heartburn through the use of PPIs has decreased awareness of reflux and the patient has thus allowed more fluid to regurgitate; as a consequence more patients are presenting with volume regurgitation as their main problem.

    Surgery as a result of patient and/or physician directed choice has also become more common since the introduction of laparoscopic surgery because patients no longer face long and painful incisions with prolonged hospital stays and time off work. There are reports of antireflux surgery performed as a day case procedure, with most patients out of hospital in two or three days and back at work within a few weeks of the operation.2 3

    A new, more controversial indication is the relation between reflux, columnar lined oesophagus, and adenocarcinoma. There is an argument that fundoplication should be considered at an earlier stage in the management of patients with reflux, so that the complications of Barrett’s oesophagus and its evolution into an adenocarcinoma of the distal oesophagus can be prevented. This hypothesis is based on evidence that the development of Barrett’s oesophagus is caused by the influence of duodeno-oesophageal reflux, which is not effectively controlled by antisecretory medication. Although earlier fundoplication has obvious appeal to surgeons, this hypothesis is, as yet, unsupported; in our opinion, the possible prevention of Barrett’s oesophagus and adenocarcinoma of the oesophagus is not yet an acceptable indication for surgery.  The reduction in morbidity resulting from laparoscopic antireflux surgery has been most noticeable in the treatment of giant hiatus hernias (intrathoracic stomach). These hernias can strangulate, cause anaemia or overt bleeding, and other symptoms such as chest pain or breathlessness after meals. Previously, surgery for giant hiatus hernias has been controversial because many patients with this condition are very old. However, because the majority of such hernias can be treated with a relatively straightforward laparoscopic procedure,4 5 a greater number of patients with this condition are now being referred for surgery before the hernia grows too large.

    Laparoscopy for antireflux surgery was first reported in 1991.6 The development phase allowed instrumentation and techniques to be refined, operating times to be shortened, and learning curve problems to be recognised and overcome; laparoscopic surgery for reflux has since become commonplace. In some centres, follow up extends for up to five years, and prospectively evaluated single centre experiences of more than 300 procedures have been reported.7 8 The published results of laparoscopic antireflux surgery, irrespective of the type of fundoplication, confirm the efficiency of the laparoscopic approach.3 7 8Furthermore, in comparison with an open approach, laparoscopy controls reflux symptoms well, and medium term outcomes have not been compromised.9 10 Moreover, the overall incidence of perioperative complications has been reduced, and the length of hospital stay shortened to two or three days. These outcomes have also been confirmed in randomised trials of open versus laparoscopic Nissen fundoplication.11 12

    Nevertheless, complications can occur following laparoscopic antireflux surgery. Mostly minor, such complications resolve rapidly and do not impact on the long term outcome of surgery. The risk of acute postoperative para-oesophageal hiatus herniation and acute dysphagia has been highlighted,13 14 but standardisation of surgical technique with routine hiatal repair, improved surgeon awareness of potential complications, and better appreciation of laparoscopic anatomy have all contributed to a significant reduction in postoperative problems.3

    The risk of postoperative dysphagia creates considerable anxiety for surgeons, gastroenterologists, and patients. It occurs almost universally in the early postoperative period, but only affects a minority of patients beyond the first year after operation, and in these patients dysphagia is usually mild.8 15 The long term incidence is about 5%, although this rate varies depending on whether the follow up data are collected by the operating surgeon or by an independent investigator. Additionally, the postoperative incidence of dysphagia should be compared with the incidence of dysphagia in patients with reflux who are awaiting surgery; the preoperative rate has been reported to be up to 40%.15-17

    The literature concentrates on adverse outcomes rather than good results after surgery, making it easy to overlook the fact that more than 90% of patients who have surgery for reflux are happy with the outcome. Much of the debate over technique is centred around comparisons between uncontrolled case series. However, evidence from prospective randomised trials has recently become available. Although trials which compare Nissen with partial fundoplication performed by either open18 or laparoscopic techniques19have shown no clear advantages for a posterior partial fundoplication, a recent trial has shown that the likelihood of adverse short term outcomes is reduced by performing an anterior partial fundoplication.16 Moreover, two further trials have not shown any advantages for division of the short gastric vessels during Nissen fundoplication.17 20 The overall outcome of these studies suggests that much of this debate is overstated, with the most important determinant of a good outcome likely to be the experience of the surgeon performing the operation.3

    Large hiatus hernias can cause chest pain because the stomach becomes trapped in the chest, and the more severe cases can be life threatening owing to compromise of the gastric blood supply. Even though patients presenting with this problem are, on average, 20 years older than patients presenting for reflux surgery and often have substantial co-morbidity, laparoscopic repair is usually feasible. Recent series of more than 50 patients undergoing laparoscopic repair for giant hiatus hernias have confirmed the safety and efficacy of this approach, and highlighted the need for early referral so that elective laparoscopic repair can be facilitated.4 5

    Most surgeons assess oesophageal motility before performing an antireflux procedure. This is useful because some conditions—for example, achalasia, can be misdiagnosed as reflux. However, patients with deficient oesophageal peristalsis are suitable candidates for surgery and some surgeons will select a partial fundoplication technique for patients with poor motility, although poor oesophageal motility is thought by some physicians to be a contraindication for fundoplication.21 The partial approach is not supported by evidence from controlled trials, and two recent studies have shown that an excellent outcome can be achieved with laparoscopic Nissen fundoplication in patients with poor oesophageal motility.22 23

    Most surgeons see medical and surgical treatment as having complementary roles, although some physicians see them as being in competition. Laparoscopic antireflux surgery should be considered in patients who need long term treatment, as surgery may be more cost effective than long term PPIs, particularly in younger patients. After surgery, symptom control is excellent, and side effects are usually infrequent. However, many patients taking PPIs develop recurrent symptoms24 and need an increasing dose to remain symptom-free. Nevertheless, surgery may be inappropriate for patients whose symptoms are easily controlled by changes in their lifestyle, or by intermittent courses of antisecretory medication. Therefore, it is likely that patients with mild to moderate reflux will be medically treated, and surgery will be considered for those with more severe disease, or for younger patients who would otherwise need lifelong medication. All patients in this latter category should have the opportunity to discuss surgical treatment with a clinician interested in the laparoscopic management of reflux disease.

    The treatment algorithms for reflux have now changed, with the development of reliable laparoscopic surgical techniques, as well as more potent medical treatments. Most patients with gastro-oesophageal reflux should now expect appropriate treatment to provide a good level of symptom control.

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