Nexium 20 mg side effects

Do PPIs have long-term side effects?

Published: January, 2009

Nexium and the other proton-pump inhibitors are great at reducing stomach acid, but that might have some unintended consequences.

 Madison Avenue has given stomach acid a bad name, but it’s really kind of a bum rap. Dip into any physiology textbook, and you’ll find that stomach acid serves several constructive purposes. Pepsin, an enzyme that is essential to the preliminary digestion of protein, needs an acidic environment in the stomach to be effective. The strongly acidic hydrochloric acid pumped out by cells in the lining of the stomach also plays a direct role in the early digestion of some foods. And stomach acidity is a built-in barrier to infection: many bacteria and other pathogenic fellow travelers don’t make it out of the stomach alive because of the low pH levels they encounter there.

Long-term use

Yet millions of us spend billions of dollars each year on products and medications designed to lessen or get rid of stomach acid. The old standbys, antacids like Maalox and Mylanta, have been supplanted in many cases by drugs that go to the source, acting on the cells that produce the hydrochloric acid, rather than just neutralizing the acid. Starting in the late 1970s, histamine2-receptor (H2) blockers like cimetidine (Tagamet), famotidine (Pepcid), and ranitidine (Zantac) came on the market. They were followed by the proton-pump inhibitors, or PPIs, which include esomeprazole (Nexium), lansoprazole (Prevacid), and omeprazole (Prilosec). The PPIs are increasingly the acid reducers of choice because they’re far more effective than the H2 blockers. They’re also quite a bit more expensive; for example, the over-the-counter version of Prilosec is about twice as expensive as the over-the-counter versions of Pepcid and Zantac.

People take acid-reducing medication for several reasons. PPIs are part of the “triple therapy” used to treat Helicobacter pylori, the bacteria that cause ulcers in the stomach and the upper part of the small intestine (the duodenum). Typically, though, that treatment lasts just one or two weeks. Long-term use of a nonsteroidal anti-inflammatory drug (NSAID) often comes with a long-term acid-reducing prescription. Randomized trials have shown that timely use of PPIs can protect people from getting the ulcers that can develop as a result of NSAID use. Whether PPIs ought to be routinely prescribed with the low doses of aspirin (aspirin is an NSAID) taken to prevent heart attack and strokes is unclear, although some findings suggest that it might be a good idea, and some doctors recommend it for people who are likely to have NSAID-related gut problems.

But the main use of acid reducers is to treat gastroesophageal reflux disease, or GERD, a condition characterized by stomach acid backing up into the esophagus from the stomach. We’ve all had occasional bouts of reflux and the heartburn pain that it causes. But GERD can be a serious, chronic problem that can lead to terribly painful inflammation of the esophagus (esophagitis), ulceration and bleeding of esophageal tissue, and, in rare instances, esophageal cancer. People with GERD might take an H2 blocker or PPI indefinitely: several studies have shown that in many cases it comes back unless people stay on maintenance therapy.

Like every medication, PPIs occasionally cause side effects, including nausea and headaches. Doctors are aware that PPIs can, in a roundabout way, promote an abundance of gastrin, an important stomach hormone. Too much gastrin could conceivably cause a number of problems, including a rebound effect of extra-heavy stomach acid secretion if people stop taking PPIs. PPIs may interfere with the metabolism of clopidogrel (Plavix). But by and large, PPIs have been viewed as safe medications with few drawbacks.

Yet some patients — and doctors and researchers — have wondered whether suppressing a natural process like stomach acid secretion for long periods might have unintended consequences. A number of studies suggest that there may, in fact, be a few things to worry about. But don’t jump the gun: this is an area of research that’s still taking shape, and we shouldn’t lose sight of the benefits of acid suppression for some people.

PPI-associated pneumonia

Obviously the respiratory and digestive tracts are quite separate, but they share a common beginning in the mouth and the back of the throat before forking into two separate “tubes” — the cartilage-encased trachea in the front of the neck and the slender, muscular esophagus that goes to the stomach (see illustration). Given the shared plumbing and cramped quarters, it’s amazing that things don’t go down the wrong way more often. The epiglottis, which covers the opening of the trachea when we swallow, is a big help in that regard. But, especially when we are lying flat while asleep, small amounts of stomach contents tend to travel up the esophagus and get into the trachea. Aspiration, as it is called, occurs even in people with perfectly healthy respiratory and digestive systems.

Bacteria are more likely to proliferate in the less acidic environment created by PPIs, so in people who take these medications, this little bit of aspiration may be more likely to carry bacteria into the lungs, where they can cause pneumonia. This is a recognized problem among hospitalized patients, whose defense mechanisms against respiratory illness are often impaired (a reduced cough reflex, for example). But several studies have suggested that relatively healthy people outside the hospital might also be at risk for PPI-associated pneumonia. In 2007, Danish researchers reported results showing that current PPI use was associated with a 50% increase of pneumonia. They found no such association for the less-potent H2 blockers. Studies have gone the other way: in 2008, University of Pennsylvania researchers did not find an association between pneumonia and long-term PPI use after crunching data culled from a large British database of patient records. Their analysis showed that newcomers to PPIs — people who had started taking the pills in the previous 30 days — did have more pneumonia than people not taking PPIs, but that’s probably for reasons unrelated to acid suppression and PPIs.

How reducing stomach acid can lead to infections

A connection to C. difficile

Clostridium difficile is a bacterium capable of causing life-threatening cases of diarrhea (10 bowel movements a day) and conditions like colitis, an inflammation of the lining of the colon. Growing numbers of people are coming down with C. difficile infections, and virulent “supergerm” strains have become a scary problem.

The conventional wisdom says the main risk factors for C. difficile infection are old age and use of antibiotics that disrupt the natural ecology of the gut. But in the past several years, a number of studies have identified a possible connection to PPIs — either by themselves or in combination with antibiotics. Using the same database as the University of Pennsylvania researchers, a group at McGill University in Montreal found an association between PPI use and C. difficile infection among people not in the hospital — the so-called community-acquired cases. And a well-designed case-control study of hospitalized patients published in the September 2008 American Journal of Gastroenterology found that people with diarrhea related to C. difficile were over three times more likely to be taking PPIs than people without a C. difficile infection.

People get infected with C. difficile by swallowing it. By making the stomach less acidic, PPIs may leave the door ajar to infections that wouldn’t have taken hold had the acid levels been normal — a pH of 4 or less. One wrinkle in the plot is that C. difficile is transmitted by way of acid-resistant spores, although researchers say the higher pH levels may still affect the life cycle of the spores in such a way as to encourage infection.

Bad for bone — and your B12 levels?

By lowering stomach acid levels, PPIs might affect the body’s absorption of calcium, which in turn could lead to osteoporosis and fractures. The University of Pennsylvania group that did not find a connection between PPIs and pneumonia did find a link between long-term use of PPIs and hip fractures. Their results also suggested that the risk increased the longer people were taking PPIs, which is the kind of dose-response relationship that researchers look for when deciding whether a correlation might indicate a causal relationship. In 2008, University of Manitoba researchers reported that continuous use of PPIs for five years resulted in excess risk of hip fractures. At seven years, there was an association with all kinds of osteoporosis-related fractures.

PPIs may also affect vitamin B12 levels because the body can’t absorb the vitamin without stomach acid to uncouple the vitamin from protein in food. Many doctors monitor the B12 levels of their patients taking PPIs. In its pill form, B12 doesn’t need stomach acid to be absorbed, so some people on long-term PPI therapy may take vitamin B12 pills — or a multivitamin that includes B12.

Time to take a step back

PPIs are a real advance, and millions of people have benefited from their ability to squelch the production of stomach acid that causes heartburn and contributes to NSAID-related ulcers and other serious conditions. But they’ve also been heavily marketed, especially Nexium as that appealing “little purple pill.”

Now that studies are beginning to show that PPIs could — the jury’s out still — cause some problems, it may be a good time to step back and ask whether we’ve been reaching for that PPI bottle too often and too soon. Occasional reflux can be treated effectively with the old-fashioned antacids. Some people find that only certain foods (chocolate, coffee, fatty food) trigger GERD-related heartburn, so they learn to avoid them. A chewing gum habit increases the production of saliva that can soothe an irritated esophagus and wash stomach acid back down into the stomach. And if the problem is nighttime heartburn, elevating the head of the bed can help.

People who need heavy-duty stomach acid suppression should still take a PPI but, working with your doctor, be sure that you’re one of them before getting into a long-term relationship with this medication.

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Nexium Study To Suppress Nausea During Chemotherapy (NEXIUM)

  1. Breast Cancer

    The American Cancer Society estimates that there will be approximately 215,990 new cases of breast cancer diagnosed in women during 2004 in the United States. Breast cancer is the most common malignancy in women in the United States and the second leading cause of cancer death in women.

    Treatment options for breast cancer have evolved from extensive surgical approaches to breast-conserving techniques and the use of adjuvant and neo-adjuvant chemotherapy, radiation, and endocrine therapy to reduce the risk of recurrence.

  2. Chemotherapy in Breast Cancer

    The use of adjuvant chemotherapy is a well established and routine part of care for breast cancer. Chemotherapy can reduce a woman’s risk of recurrence by 25-30%. The amount of risk reduction depends on the patient’s age, nodal status, and hormone receptor status.

    Anthracycline-based chemotherapy is standard in the treatment of breast cancer with doxorubicin being the most frequently used agent in this group. Currently the most commonly used chemotherapy regimens for breast cancer include: * doxorubicin/cyclophosphamide (AC) * fluorouracil/doxorubicin/cyclophosphamide (FAC) * cyclophosphamide/methotrexate/fluorouracil (CMF) * docetaxel/doxorubicin/cyclophosphamide (TAC) * fluorouracil/epirubicin/cyclophosphamide (FEC) * single agent taxanes (paclitaxel and docetaxel) Except for the taxanes, these agents are known to cause significant nausea and vomiting after administration.

    Cancer drugs differ both quantitatively and qualitatively in their emetogenic potential. Emetogenic potential can be influenced by chemotherapy-related characteristics and patient characteristics.

  3. Gastrointestinal Side Effects of Chemotherapy

Nausea and vomiting following administration of chemotherapy for cancer are among the most significant and feared side effects of patients undergoing treatment. Despite continued advances in pharmacology, the ability to prevent or control nausea, vomiting, or retching remains a problem for patients. Research has confirmed that chemotherapy related nausea and vomiting negatively affects quality of life. Among patients, the same level of nausea and vomiting varies in effect on quality of life. It is difficult to substantiate the degree of this effect, but it has been shown that even with serotonin antagonists, patients still rank nausea as their most bothersome chemotherapy side effect, while vomiting is ranked as third to fifth most bothersome.

The risk for chemotherapy induced nausea and vomiting is related to the anti-neoplastic agents administered and to patient related factors. Emetogenic potential is affected by the intrinsic emetogenicity of the chemotherapy drugs, the combination of agents, the doses administered and the rate of administration. Patient related factors include: 1. gender-increased risk in females 2. age-increased risk in younger, premenopausal patients 3. history of alcohol intake-low chronic intake decreases risk 4. history of motion sickness-increases risk 5. hyperemesis during pregnancy-increases risk.

Emesis is a complex phenomenon characterized by three components: nausea, vomiting, and retching. Nausea is a subjective phenomenon of an unpleasant sensation in the epigastrium and in the back of the throat that may or may not culminate in vomiting; it is also described as feeling “sick at the stomach.” Nausea exists only insofar as it is defined by the patient. Vomiting is the forceful expulsion of the contents of the stomach, duodenum and jejunum through the oral cavity as a result of changes in intrathoracic positive pressure. It is also described as “throwing up.” Retching, also called “dry heaves,” is the attempt to vomit without expelling any material.

Drugs used to improve the control of nausea and vomiting include serotonin antagonists, dopamine antagonist (metoclopramide, prochlorperazine), corticosteroids, benzodiazepines, and phenothiazines. The American Society of Clinical Oncology (ASCO) has developed clinical practice guidelines for the management of chemotherapy-induced nausea and vomiting based on the emetogenic potential of the agents being administered. For combinations with moderate emetogenic potential, acute emesis is managed with a corticosteroid and serotonin receptor antagonists. Serotonin receptor antagonists currently available include ondansetron, granisetron, and dolasetron. Studies indicate they are equally effective in the management of chemotherapy-related nausea/vomiting/retching. Delayed emesis (greater than 24 hours post-chemotherapy) can be controlled with a number of agents including steroids, serotonin receptor antagonists or metoclopramide. Recommended combinations include dexamethasone, 8 mg for 2-3 days, then 4 mg for 1-2 days and metoclopramide, 20-40 mg twice daily to four times daily for 3-4 days, or Zofran 8 mg twice daily for 3 days. With combination chemotherapy, patients should receive the antiemetic regimens appropriate for the chemotherapy agent with the highest emetic risk.

Drugs used to improve the control of nausea and vomiting include serotonin antagonists, dopamine antagonist (metoclopramide, prochlorperazine), corticosteroids, benzodiazepines, and phenothiazines. The American Society of Clinical Oncology (ASCO) has developed clinical practice guidelines for the management of chemotherapy-induced nausea and vomiting based on the emetogenic potential of the agents being administered. For combinations with moderate emetogenic potential, acute emesis is managed with a corticosteroid and serotonin receptor antagonists. Serotonin receptor antagonists currently available include ondansetron, granisetron, and dolasetron. Studies indicate they are equally effective in the management of chemotherapy-related nausea/vomiting/retching. Delayed emesis (greater than 24 hours post-chemotherapy) can be controlled with a number of agents including steroids, serotonin receptor antagonists or metoclopramide. Recommended combinations include dexamethasone, 8 mg for 2-3 days, then 4 mg for 1-2 days and metoclopramide, 20-40 mg twice daily to four times daily for 3-4 days, or Zofran 8 mg twice daily for 3 days. With combination chemotherapy, patients should receive the antiemetic regimens appropriate for the chemotherapy agent with the highest emetic risk.

Studies done with standard antiemetics in women undergoing treatment with anthracycline-based chemotherapy for breast cancer show a success rate for emetic control in the range of 60-65%. 4. Measurement of Nausea, Vomiting, and Retching

It remains difficult to compare clinical studies of nausea and vomiting because of the variety of measurement tools utilized and the variable time periods that were monitored following chemotherapy. The ideal tool would include assessment of: 1. duration and severity of nausea 2. frequency, duration, and severity of vomiting/retching 3. number of antiemetics utilized 4. impact of nausea and vomiting on quality of life 5. adverse effects experienced

5. Proton Pump Inhibitors

Despite utilization of the antiemetics recommended by ASCO, approximately one-third of patients undergoing anthracycline-based chemotherapy still develop nausea and vomiting. A current therapeutic challenge is to find and prove methods to control nausea and vomiting after chemotherapy.

Although the pathophysiology of nausea and vomiting is not well understood, we know that chemotherapy causes damage to the gastrointestinal (GI) mucosa. The pathobiology of the mucosal damage has been reviewed by Blijlevens and can be divided into four phases: the inflammatory phase, the epithelial phase, the ulcerative/bacteriological phase and the healing phase. This mucosal injury is usually self-limiting with a complete cycle of injury to healing lasting approximately 2-3 weeks. The mucosal damage can be increased in patients receiving chemotherapy and corticosteroids which breast cancer patients require as pre-medications. Since cytotoxic chemotherapy damages the mucosal lining, it leaves the GI mucosa exposed to the normal acid-producing gastric parietal cells. The resultant damage has been seen endoscopically in patients receiving chemotherapy with cytosine arabinoside. Hence, suppression of acid secretion from the gastric parietal cells should reduce mucosal injury and related symptoms.

Historical therapies for gastrointestinal distress have included anticholinergics, as well as H-2 receptor antagonists, to help reduce acid secretion. H-2 receptor blockers were effective by blocking the histamine driven acid secretion, but despite its targeted action, acid production continues through alternative pathways. Recently a group of new agents known as proton pump inhibitors have been developed which target the final common pathway of acid secretion. These agents are known to act directly on the H+/K+-ATPase in the gastric parietal cell. Since these agents act directly on the final stimulatory pathway, they provide rapid symptom resolution and reliable healing in gastroesophageal reflux disease and peptic ulcer disease.

To date, two large clinical trials have been performed to evaluate the effectiveness of proton pump inhibitors in preventing mucosal injury. The first trial selected 182 patients with breast cancer (77 pts) or colon cancer (105 pts) who were receiving cyclophosphamide, methotrexate and 5-FU (CMF), or 5-FU, respectively. These patients were randomized to receive either omeprazole (20 mg daily), misoprostol (a prostaglandin analogue) (400 mg twice daily), or placebo (once daily) for two full courses of chemotherapy (56 days). Endoscopic evaluation (EGD) was performed one week prior to initiation of chemotherapy and one week after the end of the second cycle of chemotherapy comparing the number of erosions/ulcers in the stomach and duodenum. The omeprazole group had a lower frequency and degree of erosions compared to placebo and misoprostol. Symptoms of epigastric pain and heartburn were also significantly less in the omeprazole patients. A second study performed by the same group evaluated patients with breast or colon cancer (n=228) receiving either CMF or 5-FU. These patients were randomized to receive omeprazole 20 mg daily, ranitidine 300 mg daily (a H2 blocker), or placebo once daily for 56 days. EGD was performed as above, before cycle 1 and after cycle 2 of chemotherapy. The omeprazole group experienced the lowest frequency of ulcers (n=2), followed by the ranitidine group (n=8), and the placebo group (n=18). Symptoms of epigastric pain or heartburn were also significantly less in the omeprazole arm (n=11) compared to the ranitidine (n=13) or placebo (n=24) arms. Chemotherapy was delayed in the placebo and ranitidine group, but not in the patients receiving omeprazole. These two trials demonstrate the ability of a proton pump inhibitor (omeprazole) to limit the mucosal injury induced by chemotherapy. Protecting the mucosa from damage also appeared to significantly decrease the frequency of upper GI symptoms. It should be noted that nausea or vomiting was not assessed in either trial since various antiemetics were given during chemotherapy.

Esomeprazole magnesium is the latest proton pump inhibitor that has been developed. It is unique in that it is the S- isomer of omeprazole, and as such, has better bioavailability and elevated levels compared to the racemic omeprazole. Since the proton pump is the last step in acid production, blockade of this pump causes reduction in gastric acidity. This effect is dose related up to a dose of 20-40mg daily. Esomeprazole is currently clinically indicated for the treatment of erosive esophagitis and symptomatic gastroesophageal reflux disease. In addition, it is approved to treat Helicobacter pylori in patients with duodenal ulcer disease in conjunction with either amoxicillin or clarithromycin and amoxicillin.

Nexium vs. Prilosec: Two GERD Treatments

Omeprazole (Prilosec) and esomeprazole (Nexium) are similar drugs. However, there are minor differences in their chemical makeup.

Prilosec contains two isomers of the drug omeprazole, while Nexium only contains one isomer.

Isomer is a term for a molecule that includes the same chemicals, but is arranged in a different way. So, you could say that omeprazole and esomeprazole are made of the same building blocks, but put together differently.

While the differences in isomers might seem minor, they can result in differences in how drugs work.

For example, the isomer that’s in Nexium is processed more slowly than Prilosec in your body. This means that levels of the drug are higher in your bloodstream, and that esomeprazole may decrease acid production for a longer period of time.

It may also work slightly faster to treat your symptoms compared to omeprazole. Esomeprazole is also broken down differently by your liver, so it may lead to fewer drug interactions than omeprazole.


Some studies indicate that the differences between omeprazole and esomeprazole may offer some advantages to people with certain conditions.

An older study from 2002 found that esomeprazole provided more effective control of GERD than omeprazole at the same doses.

According to a later study in 2009, esomeprazole offered faster relief than omeprazole in the first week of use. After one week, symptom relief was similar.

However, in a 2007 article in American Family Physician, doctors questioned these and other studies on PPIs. They cited concerns such as:

  • differences in the amount of active ingredients given in the studies
  • the size of the studies
  • the clinical methods used to measure effectiveness

The authors analyzed 41 studies on the effectiveness of PPIs. They concluded that there’s little difference in the effectiveness of PPIs.

So, while there’s some data to suggest that esomeprazole is more effective at relieving symptoms, most experts agree that the PPIs have similar effects overall.

The American College of Gastroenterology states that there are no major differences in how well different PPIs work for treating GERD.

The price of relief

The biggest difference between Prilosec and Nexium was price when reviewed.

Until March 2014, Nexium was available only by prescription and at a significantly higher price. Nexium now offers an over-the-counter (OTC) product that’s priced competitively with Prilosec OTC. However, generic omeprazole may be less expensive than Prilosec OTC.

Traditionally, insurance companies didn’t cover OTC products. However, the PPI market has led many to revise their coverage of Prilosec OTC and Nexium OTC. If your insurance still doesn’t cover OTC PPIs, a prescription for generic omeprazole or esomeprazole may be your best option.

“ME TOO” DRUG? Nexium is sometimes called a “me too” drug because it’s so similar to Prilosec, an existing drug. Some people think that “me too” drugs are just a way for drug companies to make money by copying drugs that are already available. But others have argued that “me too” drugs can actually decrease drugs costs, because they encourage competition between the drug companies.

Work with your doctor or pharmacist to decide which PPI is best for you. In addition to cost, consider things like:

  • side effects
  • other medical conditions
  • other medications you’re taking

Nexium Side Effects

Generic Name: esomeprazole

Medically reviewed by Last updated on Feb 12, 2019.

  • Overview
  • Side Effects
  • Dosage
  • Professional
  • Tips
  • Interactions
  • More

Note: This document contains side effect information about esomeprazole. Some of the dosage forms listed on this page may not apply to the brand name Nexium.

For the Consumer

Applies to esomeprazole: oral capsule delayed release, oral packet, oral tablet delayed release

Other dosage forms:

  • oral capsule delayed release
  • intravenous powder for solution

Along with its needed effects, esomeprazole (the active ingredient contained in Nexium) may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.

Check with your doctor immediately if any of the following side effects occur while taking esomeprazole:

Incidence not known

  • Blistering, peeling, or loosening of the skin
  • bloating
  • chills
  • constipation
  • cough
  • darkened urine
  • difficulty with swallowing
  • dizziness
  • drowsiness
  • fast heartbeat
  • fever
  • indigestion
  • joint or muscle pain
  • loss of appetite
  • mood or mental changes
  • muscle spasms (tetany) or twitching
  • nausea
  • pains in the stomach, side, or abdomen, possibly radiating to the back
  • puffiness or swelling of the eyelids or around the eyes, face, lips, or tongue
  • red skin lesions, often with a purple center
  • red, irritated eyes
  • seizures
  • skin rash, hives, itching
  • sore throat
  • sores, ulcers, or white spots in the mouth or on the lips
  • tightness in the chest
  • trembling
  • unusual tiredness or weakness
  • vomiting
  • yellow eyes or skin

Some side effects of esomeprazole may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them:

More common

  • Bad, unusual, or unpleasant (after) taste
  • change in taste

Less common

  • Sleepiness or unusual drowsiness


  • Acne
  • back pain

Incidence not known

  • Agitation
  • dry mouth
  • excess air or gas in the stomach or bowels
  • full feeling
  • hair loss or thinning of the hair
  • muscular weakness
  • passing gas
  • seeing, hearing, or feeling things that are not there
  • swelling of the breasts or breast soreness in both females and males
  • swelling or inflammation of the mouth
  • swollen joints

For Healthcare Professionals

Applies to esomeprazole: intravenous powder for injection, oral delayed release capsule, oral delayed release tablet, oral powder for reconstitution delayed release


The most frequently occurring adverse reactions were headache and diarrhea.

The most frequently reported adverse reactions for patients who received triple therapy for 10 days were diarrhea, taste perversion, and abdominal pain.

Nervous system

Very Common (10% or more): Headache (up to 10.9%)

Common (1% to 10%): Dizziness, somnolence, taste disturbance/perversion, vertigo

Uncommon (0.1% to 1%): Paresthesia

Very rare (less than 0.01%): Hepatic encephalopathy

Frequency not reported: Hypertonia, hypoesthesia, migraine/aggravated migraine, parosmia, taste loss, tremor


Very common (10% or more): Flatulence (up to 10.3%)

Common (1% to 10%): Abdominal pain, benign fundic gland polyps, constipation/constipation aggravated, diarrhea, dry mouth, duodenal ulcer hemorrhage, epigastric pain/aggravated epigastric pain, gastritis/aggravated gastritis, nausea/aggravated nausea, regurgitation, tooth disorder, vomiting/aggravated vomiting

Rare (0.01% to 0.1%): Gastrointestinal (GI) candidiasis, stomatitis

Very rare (less than 0.01%): Microscopic colitis

Frequency not reported: Barrett’s esophagus, benign polyps or nodules, bowel irregularity, duodenitis, dyspepsia, dysphagia, dysplasia GI, enlarged abdomen, eructation, esophagitis, esophageal disorder, esophageal stricture, esophageal ulceration, esophageal varices, frequent stools, gastric ulcer, gastroenteritis, GI hemorrhage, GI symptoms not otherwise specified, hernia, hiccup, melena, mouth disorder, mucosal discoloration, pharynx disorder, rectal disorder, tongue disorder, tongue edema, ulcerative stomatitis

Postmarketing reports: Clostridium difficile associated diarrhea, fundic gland polyps, hemorrhagic necrotic gastritis (in children), pancreatitis


Common (1% to 10%): Cough, respiratory infection, sinusitis, tachypnea (in pediatrics)

Uncommon (0.1% to 1%): Epistaxis

Rare (0.01% to 0.1%): Bronchospasm

Frequency not reported: Asthma aggravated, dyspnea, larynx edema, pharyngitis, rhinitis


Common (1% to 10%): Accident or injury, fever/pyrexia

Rare (0.01% to 0.1%): Malaise

Frequency not reported: Asthenia, earache, facial edema, fatigue, leg edema, otitis media, pain, rigors, tinnitus


Common (1% to 10%): Pruritus

Uncommon (0.1% to 1%): Dermatitis, rash, urticaria

Rare (0.01% to 0.1%): Alopecia, increased sweating/hyperhidrosis, photosensitivity

Very rare (less than 0.01): Erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis (TEN)/ fatal TEN

Frequency not reported: Acne, erythema, pruritus ani, rash erythematous, rash maculo-papular, skin inflammation, subacute cutaneous lupus erythematosus (SCLE)

Postmarketing reports: Cutaneous lupus erythematosus, systemic lupus erythematosus


Common (1% to 10%): Hypertension/aggravated hypertension

Uncommon (0.1% to 1%): Peripheral edema

Frequency not reported: Chest pain, flushing, generalized edema/swelling/inflammation, hot flush, hypertension, irregular heartbeat, phlebitis, substernal chest pain, superficial phlebitis, tachycardia, thrombophlebitis


Common (1% to 10%): Back pain

Uncommon (0.1% to 1%): Fracture of the hip, wrist or spine

Rare (0.01% to 0.1%): Arthralgia, myalgia

Very rare (less than 0.01%): Muscular weakness

Frequency not reported: Arthritis aggravated, arthropathy, cramps, fibromyalgia syndrome, hernia, hyperuricemia/increased uric acid, polymyalgia rheumatica

Postmarketing reports: Bone fracture

An increased risk of hip fracture has been reported in a cohort study. The risk was significantly increased among patients prescribed long-term high PPIs.


Common (1% to 10%): Increased serum gastrin

Very rare (less than 0.01%): Gynecomastia

Frequency not reported: Decreased/increased thyroxine, goiter, increased thyroid stimulating hormone


Common (1% to 10%): Administration/injection site reactions

Postmarketing reports: Tissue inflammatory reaction


Common (1% to 10%): Viral infection

Frequency not reported: Flu-like disorder, fungal infection


Common (1% to 10%): ALT increased

Uncommon (0.1% to 1%): Increased liver enzymes

Rare (0.01% to 0.1%): Hepatitis with/without jaundice

Very rare (less than 0.01%): Hepatic failure

Frequency not reported: Abnormal hepatic function, AST increased, bilirubinemia, increased alkaline phosphatase, increased total bilirubin


Uncommon (0.1% to 1%): Blurred vision

Rare (0.01% to 0.1%): Visual accommodation disorder/disturbances, visual field defect

Frequency not reported: Abnormal vision, conjunctivitis

Postmarketing reports: Irreversible visual impairment, loss of vision


Uncommon (0.1% to 1%): Insomnia, irritability

Rare (0.01% to 0.1%): Agitation, confusion, depression/aggravated depression

Very rare (less than 0.01%): Aggression, hallucinations

Frequency not reported: Apathy, nervousness, sleep disorder


Rare (0.01% to 0.1%): Leukopenia, thrombocytopenia

Very rare (less than 0.01%): Agranulocytosis, pancytopenia

Frequency not reported: Anemia, anemia hypochromic, cervical lymphadenopathy, decreased/increased hemoglobin, decreased/increased platelets, decreased/increased white blood cell count, leukocytosis


Rare (0.01% to 0.1%): Hyponatremia

Very rare (less than 0.01%): Hypomagnesemia with or without hypocalcemia and/or hypokalemia, severe hypomagnesemia

Frequency not reported: Anorexia, decreased/increased potassium, increased sodium, increased appetite, vitamin B12 (cyanocobalamin) deficiency, thirst, weight decrease/increase


Rare (0.01% to 0.1%): Anaphylactic reaction/shock, angioedema, hypersensitivity reactions

Frequency not reported: Allergic reaction


Very rare (less than 0.01%): Interstitial nephritis with/without renal failure

Frequency not reported: Glycosuria

Postmarketing reports: Acute interstitial nephritis, impaired renal function, increased creatinine, nephrosis


Frequency not reported: Abnormal urine, albuminuria, cystitis, dysmenorrhea, dysuria, genital moniliasis, hematuria, impotence, menstrual disorder, micturition frequency, moniliasis, polyuria, vaginitis

1. Cerner Multum, Inc. “UK Summary of Product Characteristics.” O 0

2. “Product Information. Nexium (esomeprazole)” Astra-Zeneca Pharmaceuticals, Wilmington, DE.

3. “Product Information. NexIUM I.V. (esomeprazole).” Astra-Zeneca Pharmaceuticals, Wilmington, DE.

4. “Product Information. Esomeprazole Strontium (esomeprazole).” Amneal Pharmaceuticals, Glasgow, KY.

5. Cerner Multum, Inc. “Australian Product Information.” O 0

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Popular Heartburn Pills Can Be Hard To Stop, And May Be Risky

Katherine Streeter for NPR Katherine Streeter for NPR

When Marcella Lafayette started having really bad heartburn, she went to her doctor to see if there was anything that might help.

“I was experiencing a lot of chest pain, back pain caused from heartburn,” says Lafayette, 62, of Portland, Ore.

Her doctor diagnosed her with gastroesophageal reflux disease, or GERD, and prescribed a drug called a proton pump inhibitor, or PPI. The drug worked, but Lafayette soon started having other problems, such as muscle weakness and severe leg cramping.

Lafayette discovered she was suffering from a magnesium deficiency, a side effect of the drug. She also learned that PPIs can cause not just deficiencies of nutrients but other side effects, such as an increased risk for infections.

So Lafayette decided to try to stop using her PPI. But whenever she did, her heartburn returned. And the symptoms were much worse.

“I can’t seem to get off the drug, because when I do, I experience severe stomach pain. I can’t eat anything without experiencing stomach pain,” Lafayette says. “It just feels like you’ve got a knife in your gut. It’s just really painful.”

Lafayette is not alone. Many people have trouble discontinuing PPIs because the amount of acid in their digestive system surges when they stop taking the drug.

Experiences like Lafayette’s, and rising evidence that the drugs may be associated with a variety of increased risks, are making doctors increasingly worried about their wide use.

“The teaching for many years was that these drugs were quite safe,” says John Clarke, a gastroenterologist at Johns Hopkins Hospital in Baltimore. “But there is data that’s emerging that suggests PPIs may not be as safe as we think they are.”

An estimated 15 million Americans use PPIs, which are sold by prescription and over the counter under a variety of brand names, including Nexium, Prilosec and Prevacid.

They work by blocking production of stomach acid. And that could be the root of the problem, according to Clarke. Stomach acid helps digest food and also has a “barrier function against different pathogens which are ingested,” he says.

So when there’s less stomach acid, it leaves people vulnerable to nutritional deficiencies and infections, including food poisoning like salmonella, a serious, sometimes life-threatening digestive system infection called Clostridium difficile, and perhaps pneumonia.

Stomach acid also helps digest food. So if you don’t have any of that acid, it can make it hard to get the vitamins, minerals and other nutrients you need from your food — including nutrients that keep bones strong and prevent fractures.

In addition, one recent study suggested people who take PPIs may be at greater risk of heart disease; another suggested the drugs could increase the risk for chronic kidney disease.

Updated Feb. 15, 11 a.m. ET: The latest concern is that PPIs might increase the risk for dementia. Britta Haenisch and colleagues at the German Center for Neurodegenerative Diseases in Bonn studied 73,679 people ages 75 and older. The researchers found regular PPI users had at least a 44 percent increased risk of dementia compared with those not using the drugs.

The researchers caution that the risk could only be considered an “association,” until more research could be conducted to produce more conclusive evidence. But the findings indicate “the avoidance of PPI medication may contribute to the prevention of dementia.”

How PPIs might increase the risk for dementia is unclear. But other researchers recently reported that, in the brains of mice, PPIs seem to increase levels of a damaging protein that accumulates in the brains of dementia patients, known as beta-amyloid.

In an editorial accompanying the study in the journal JAMA Neurology, Lewis Kuller of the University of Pittsburgh wrote that the findings “provided an important and interesting challenge to evaluate the possible association,” which is a “very important issue given” how commonly the drugs are used by the elderly, who are already at increased risk for dementia.

Our original post continues: As this evidence has emerged, Clarke says, “I think it’s imperative that people who take these drugs really make sure that they are looking at the risks versus benefit and people don’t use these drugs lightly.”

Many people take PPIs when they don’t really need them, Clarke says. They could get rid of their heartburn by making lifestyle changes, such as losing weight and cutting back on alcohol, caffeine and spicy and fatty foods. And many people stay on them a lot longer than they need them, he says. PPIs are usually supposed to be taken for two to eight weeks, although doctors may recommend more.

The companies that make PPIs say they’re safe for most people if they use them the way they’re supposed to. And doctors say many people really need to take a PPI for severe heartburn.

“Proton pump inhibitors do have some very positive benefits to patients,” says Kenneth DeVault, a gastroenterologist at the Mayo Clinic who is president of the American College of Gastroenterology. “They relieve symptoms better than any other medication that has ever been developed.”

The most important “positive effect of proton pump inhibitors is restoration of a quality of life,” DeVault says. “This is probably the big one.”

PPIs may also reduce the risk for esophageal cancer for some people, he says.

DeVault says if someone really needs a PPI, they should take one. But they should try everything else first, keep an eye out for any side effects, and talk to their doctor about how long they should stay on it.

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