https://www.sandiegohealthdirectory.com/kb en-us If the FDA decides that a drug's benefits outweigh its risks, the agency approves the drug for marketing. Approved drugs continue to be evaluated through post marketing surveillance--a system that monitors a drug's safety on an ongoing basis. Post marketing surveillance seeks to identify problems that weren't observed or recognized before approval and any problems that might arise because a product isn't being used as anticipated. https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=130 Fri, 21 Jul 2006 07:54:01 GMT https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=130
When it comes to any drug, "safe" means that the benefits of the drug outweigh the risks for the population the drug is intended to treat and for its intended use. "Safe does not mean harmless," Woodcock says. "Every drug comes with risks, and our tolerance for risk is higher for drugs that treat serious and life-threatening illnesses. There is no question that cancer drugs can be highly toxic. But they also save lives."

If the FDA decides that a drug's benefits outweigh its risks, the agency approves the drug for marketing. Approved drugs continue to be evaluated through post marketing surveillance--a system that monitors a drug's safety on an ongoing basis. Post marketing surveillance seeks to identify problems that weren't observed or recognized before approval and any problems that might arise because a product isn't being used as anticipated.

The goal is to catch any bad news right away so that the FDA and drug companies can act quickly and communicate new risk information to consumers and doctors. CDER evaluates required reports from drug companies, which must promptly pass on any report they receive of a serious adverse reaction that isn't already described in the drug's labeling. CDER also relies on MedWatch, the system through which consumers and health professionals voluntarily report adverse events associated with all products the FDA regulates.

When the FDA receives reports of significant new adverse events, the agency evaluates them for their seriousness and the likelihood that they were caused by the drug. To the extent possible, the agency also considers how the toxicity compares with other treatments for the same disease. Ultimately, of course, the critical question is: Do the benefits of this drug still outweigh its risks for the population described in the labeling? In many cases, that question cannot be answered immediately, and more reports must be considered. Sometimes, the impact of labeling revisions needs to be assessed.

Usually, when important new risks are uncovered, the risks are added to the drug's labeling and doctors are informed of the new information through letters and other education. It's only rarely that the approval decision on a drug needs to be reassessed and changed.

A conclusion that a drug should no longer be marketed is based on the nature and frequency of the adverse effect and how the drug compares with treatment alternatives.

When the FDA believes it is clear that a drug no longer has a place in treatment, it will ask the manufacturer to withdraw the drug voluntarily. Companies have agreed to withdraw the drug in all cases except one--the case of an ant diabetic drug called phenformin, which was taken off the market in 1976 as an imminent hazard, despite the company's objections. If a company does not agree, the FDA can bring formal procedures to require withdrawal.

At first glance, one might assume that every time a drug comes off the market, it means that somewhere along the way somebody made a horrible mistake--which the drug never should have been on the market in the first place. But FDA experts say that would not be correct. Most often, the withdrawal occurs because of adverse effects that were not seen prior to marketing. Sometimes, there was no clue at all. In other cases, one can see hints of the problem in retrospect, but not the serious events that eventually led to the withdrawal.

Many complex factors go into making judgments about benefits and risks, and into ultimately deciding whether a drug should be taken off the market. Here are some major issues, often overlapping, that weigh into the decision-making process.

Most drugs on the market are well tolerated and their adverse effects are known. Known side effects cause more injuries and deaths than unrecognized side effects. But some problems happen so infrequently that they can't be seen or predicted before a drug gets on the market. Serious drug-induced liver disease, for example, is the leading single reason drugs have been pulled from the market. But it is rare, occurring at a rate of 1 in 5,000 to 1 in 10,000 exposures or less. This will not show up in clinical trials, which will pick up relatively common problems.

"If we want reasonably rapid access to needed drugs, it's not practical to require that they be tested in 15,000 to 30,000 people, which is what you'd need to be reasonably sure you saw even one case that occurs at a rate of 1 in 5,000 to 10,000," according to Robert Temple, M.D., director of the FDA's office of medical policy. "And the case would need to be recognized as drug induced," he says. So drugs are typically tested in several thousand subjects, allowing detection of relatively common serious adverse events, such as those affecting 1 in 1,000 people. This practical size of clinical trials means we can't know everything about a drug when it gets on the market. Rare events will only surface when the drug is used in larger numbers of people. Temple says, "Sometimes less severe events that are seen in trials can be used to predict the occurrence of rare, more serious events, but that is not always the case, and such predictions have considerable uncertainty."

The number of subjects in clinical trials is increasing in some areas of drug development, says Peter Honig, M.D., director of the FDA's office of drug safety. "But the numbers will never be large enough to eliminate the need for post marketing surveillance." The FDA is working on ways to better predict rare events, especially those related to the liver and heart. But some uncertainties will always be there, including the possibility of rare characteristics that make some people particularly susceptible to an adverse reaction.

There are also times when a drug's toxicity is known, but the drug turns out to be more toxic than the clinical trials suggested, which again may only be seen when the drug is used in larger numbers or in different ways.

Initially approved in 1997, Baycol (cerivastatin) was a member of a class of cholesterol lowering drugs known as "statins." Baycol and the other five drugs in its class--Lipitor (atorvastatin), Lescol (fluvastatin), Mevacor (lovastatin), Pravachol (pravastatin), and Zocor (simvastatin)--have all been associated with rare reports of rhabdomyolysis, a condition that causes marked breakdown of muscle cells and can sometimes lead to fatal kidney failure and other problems.

Knowing this about the statin drugs, the FDA made sure to look for the problem when deciding to approve Baycol. But the agency didn't find unusual risk associated with the drug at that time. "In its first few years, Baycol had a small market share," says Sandra Kweder, M.D., acting director of the FDA's office of review management. "But when FDA approved a higher dose of the drug after initial marketing, use of the drug grew and we could see clearly that Baycol caused the problem more frequently than the other drugs in its class." Problems with Baycol were reported most frequently when it was used at higher doses, when used in elderly patients, and particularly, when used with another lipid-lowering drug called Lopid (gemfibrozil). Baycol was voluntarily withdrawn in the summer of 2001.

When the FDA approved Seldane (terfenadine) in 1985, the drug became the first prescription antihistamine to relieve allergies without causing drowsiness--a side effect that can cause accidents and injuries. A few years after approval, it was discovered that Seldane could cause fatal heart rhythm irregularities when it was used together with drugs that slowed its elimination from the body, or in patients with liver disease.

Major efforts to warn against use in such patients were partly successful, but fatal rhythm abnormalities continued to be reported. According to Temple, removal of the drug was considered, but that would have left only one non-sedating antihistamine, so Seldane remained available.

"But the equation shifted when Allegra came on the market in 1997," Temple says. "Allegra provided exactly the same benefits of terfenadine but without the risk of the potentially fatal heart condition." So the new availability of Allegra (fexofenadine) weighed heavily in the decision to withdraw Seldane.

Like Seldane, a heart drug called Posicor (mibefradil) posed problems mainly when used with other drugs. Although Posicor itself did not have unusual toxicity, it was taken off the market in 1998 because of its interactions with at least 25 drugs. It markedly increased the blood levels of those drugs, leading to potentially fatal side effects of the other medications.

When Posicor was first marketed in 1997, it’s labeling warned of possible interactions with three drugs. Two more drugs were later added, but reports of interactions and resulting adverse reactions with even more drugs kept coming. There was concern over whether it was realistic to expect physicians to be able to use Posicor safely, given the many drugs it interacted with. In the absence of any special benefit of Posicor compared to other members of its class, such as effectiveness in people who don't respond to other treatments, the FDA concluded that the drug should be removed from the market.
When taken at a higher than recommended dose and when taken with other drugs, Hismanal (astemizole), another non-sedating antihistamine approved in 1988, posed risks similar to Seldane. The drug was withdrawn in 1999, as safer alternatives became available.

Beginning about 1990, many potentially harmful interactions between drugs and even between drugs and foods such as grapefruit juice were noted with Seldane and other drugs. The discovery led to greater attention by the FDA and drug manufacturers to such interactions before drugs are marketed, Temple says. This represents a significant enhancement of safety assessment.

The term "safe" also depends on whether a drug is used according to the labeling. This is why the FDA makes sure labeling and advertising for prescription drugs are accurate and balanced--presenting both the benefits and the risks.

The major problem with Duract (bromfenac), a nonsteroidal anti-inflammatory drug, was that the directions were not followed. The pain drug was withdrawn in 1998 after liver failure occurred in patients who took the short-term treatment for pain for more than the 10 days recommended in the labeling. Clinical trials indicated that a higher incidence of elevated liver enzymes was associated with longer use. Duract's manufacturer, Wyeth-Ayerst Laboratories, Philadelphia, added a new warning to the labeling and sent letters out to doctors, but reports of long-term use of the drug continued.

The day you hear news about a drug coming off the market, it may appear to be a sudden, drastic step. But several other options to manage risks usually have been attempted before that point. The main risk management tools employed by the FDA are education through letters to health-care professionals (known within the FDA as "Dear Doctor" letters) and labeling changes, such as new warnings, sometimes boxed in black for emphasis. Also used are required Medication Guides, labeling specifically for patients that emphasizes significant risks and advises patients how to detect or avoid them. In some cases, a drug is labeled as "second line," meaning it is to be used only in patients for whom other treatments fail. In other cases, a drug that is known to be dangerous is still made available under certain circumstances through what's known as restricted distribution.

Sometimes these risk management techniques are effective, and other times they aren't. "We have our anecdotes, but there is little systematic study on the effect of drug labeling changes on physician behavior," says Temple.

Labeling changes were a partial success with the allergy drug Seldane. Studies showed use of Seldane with inappropriate drugs declined almost 90 percent, but that left considerable exposure to the dangerous combinations, some of which could be lethal.

The label of the heartburn treatment Propulsid (cisapride) was changed several times in 1998. The FDA cosponsored a study to evaluate the effect of various regulatory actions, and found that the percentage of patients inappropriately exposed to the drug was unchanged.

"We know that the farther out we are from the initial approval, the less likely we are to change behavior," Woodcock says. "Once a prescribing pattern has been established, it's hard to change it."

Clearly, the more special care that is required, the more physicians must remember, and the more we need other safeguards like spotting dangerous combination uses at the pharmacy level, the more of a challenge risk management becomes. "We do consider whether we are being unreasonable in our expectations, but sometimes that can't be known beforehand," Temple says.

Currently, the FDA is involved with several drug safety initiatives, including revamping the drug labeling for physicians to create a highlights section, a relatively short section that will describe the most critical information. Better education is a high priority. "We're looking into better ways to educate the public and doctors about changes in risk information, and to get information out faster," says Honig.

But FDA experts say the agency can't do it alone. The FDA judges drug risks for a population, doctors judge risks for individual patients, and patients judge the risks they'll take based on personal values. Ultimately, drug safety requires involvement of all parts of the health system.

During the 1980s and early 1990s, the FDA was criticized for taking too long to review and approve drugs. Then Congress, the FDA, and the pharmaceutical industry negotiated the Prescription Drug User Fee Act (PDUFA) of 1992. Under PDUFA, drug companies pay fees that allow the FDA to add more resources and speed up drug review time.

The FDA agreed to complete its review of marketing applications within specific times. For example, by 2002, the FDA's reviews of all marketing applications for new drugs were to be completed within 10 months. PDUFA allowed the agency to have a 60 percent increase in staff assigned to review new drug applications. The agency has essentially met all review-time goals. The faster review has led to more rapid approval, with median approval time cut in half--from about 30 months to 15 months. The FDA Modernization Act of 1997 extended PDUFA through 2002.

Myth #1: Drug withdrawals have become increasingly common because ever since user fees, the FDA has sped up drug approvals so much that mistakes are slipping through.

The reality is that it's a rare occasion when a drug is taken off the market. The FDA is the consumer watchdog for the more than 10,000 drugs on the market, and the drug withdrawal rate has been essentially constant over the last two decades. And when comparing the time before user fees and after, there has been no change in the rate of drug withdrawals, says Janet Woodcock, M.D., director of the FDA's Center for Drug Evaluation and Research. "There was a cluster of withdrawn drugs in 1997 and 1998, but if you look at the number withdrawn as a percent of those approved for each year, the rate was about 2.7 percent before user fees and is about 2.8 percent after user fees." Some of those drugs withdrawn in 1997 and 1998 had been on the market long before user fees took effect.

Faster reviews to get valuable and life-saving drugs on the market do not translate into safety shortcuts. It isn't that the same number of FDA reviewers is working faster. It also isn't the case that shorter FDA review times mean abbreviated clinical drug trials.

Myth #2: User fees make it difficult for the FDA to stay neutral.

FDA experts say PDUFA has clearly created a situation in which the FDA is responding faster to applications and is having more discussions with drug companies.

The FDA and drug companies share a common interest in getting drugs that are safe and effective to the market and in conducting well-designed trials that are persuasive. "We believe the many meetings and other forms of advice that we give help assure that," says Robert Temple, M.D., director of the FDA's office of medical policy. "Naturally, once they submit an application, the companies want our answer to their drug application to be 'Yes,' " he says, "but we are completely neutral, having no preferred answer except the right one." The FDA's mission is to protect the public health fairly and consistently. Decisions are scientifically based, not influenced by user fees.



]]> Currently, there are 26 antiretroviral drugs approved by the Food and Drug Administration to treat individuals infected with HIV. https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=107 Fri, 23 Jun 2006 03:23:42 GMT https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=107
The discovery and development of new therapeutic strategies against HIV is one of the highest priorities for the National Institute of Allergy and Infectious Diseases (NIAID). Research supported by NIAID has already greatly advanced our understanding of HIV and how it causes AIDS.

This knowledge provides the foundation for NIAID’s HIV/AIDS research effort and continues to support studies designed to further extend and improve the quality of life of those infected with HIV.

Currently, there are 26 antiretroviral drugs approved by the Food and Drug Administration to treat individuals infected with HIV. These drugs fall into three major classes.
1. Reverse transcriptase (RT) inhibitors interfere with the critical step during the HIV life cycle known as reverse transcription. During this step, reverse transcriptase, an HIV enzyme, converts HIV RNA to HIV DNA. There are two main types of RT inhibitors.
a. Nucleoside/nucleotide RT inhibitors are faulty DNA building blocks. When these faulty pieces are incorporated into the HIV DNA (during the process when the HIV RNA is converted to HIV DNA), the DNA chain cannot be completed, thereby blocking HIV from replicating in a cell.
b. Non-nucleoside RT inhibitors bind to reverse transcriptase, interfering with its ability to convert the HIV RNA into HIV DNA.
2. Protease inhibitors (PI) interfere with the protease enzyme that HIV uses to produce infectious viral particles.
3. Fusion inhibitors interfere with the virus’ ability to fuse with the cellular membrane, thereby blocking entry into the host cell.

Currently available drugs do not cure HIV infection or AIDS. They can suppress the virus, even to undetectable levels, but are unable to completely eliminate HIV from the body. Hence, infected patients still need to take antiretroviral drugs.

As HIV reproduces itself, different strains of the virus emerge, some that are resistant to antiretroviral drugs. Therefore, doctors recommend patients infected with HIV take a combination of antiretroviral drugs known as HAART. This strategy, which typically combines drugs from at least two different classes of antiretroviral drugs, has been shown to effectively suppress the virus when used properly. Developed by NIAID-supported researchers, HAART has revolutionalized how we treat people infected with HIV by successfully suppressing the virus and decreasing the rate of opportunistic infections.

Although the use of HAART has greatly reduced the number of deaths due to HIV/AIDS, this powerful combination of drugs cannot suppress the virus completely. Therefore, people infected with HIV who take antiretroviral drugs can still transmit HIV to others through unprotected sex and needle sharing.

People infected with HIV have impaired immune systems that can leave them susceptible to opportunistic infections (OIs) and AIDS-associated co-infections, caused by a wide range of microorganisms such as protozoa, viruses, fungi, and bacteria. One example is hepatitis C virus (HCV) infection that can lead to liver cancer.

Potent HIV therapies such as HAART, however, have produced dramatic responses in patients by suppressing HIV and slowing the progression of OIs and AIDS-associated co-infections. These therapies allow the immune system to recover, sustain, and protect the body from other infections. Hence, antiretroviral drugs provide a way for the immune system to remain intact and effective, thereby improve the quality and duration of life for people with HIV.

People taking antiretroviral drugs often have low adherence to complicated drug regimens. The current recommended regimen involve taking several antiretroviral drugs each day from at least two different classes, some of which may require fasting and cause unpleasant side effects such as nausea and vomiting. In addition, antiretroviral drugs may cause more serious medical problems, including metabolic changes such as abnormal fat distribution, abnormal lipid and glucose metabolism, and bone loss. Therefore, NIAID is investigating simpler, less toxic, and more effective drug regimens.

NIAID supports the development and testing of new therapeutic agents, classes, and combinations of antiretroviral drugs that will be able to continuously suppress the virus with few side effects. Through clinical trials involving volunteers, NIAID-supported studies will provide accurate and extensive information about the safety and efficacy of the new drug candidates and combinations, and will identify potential uncommon, but important, toxicities of newly approved agents. Studies are also underway to assess rare toxicities of older approved agents, especially as a result of long-term use.

Through the Multicenter AIDS Cohort Study and Women’s Interagency HIV Study, NIAID supports long-term studies of HIV disease and its treatment in both men and women. Since their inception, these cohort studies have enrolled and collected data from more than 10,000 people. In addition, NIAID supports treatment studies conducted through three HIV/AIDS clinical trials networks: Adult AIDS Clinical Trials Groups, Pediatric AIDS Clinical Trials Groups, and the Terry Beirn Community Programs for Clinical Research on AIDS.

To expand upon and better coordinate the global HIV/AIDS research activities, NIAID is restructuring all of its HIV clinical trials research networks to increase collaboration, efficiency, harmonization, and flexibility. This new structure is designed to encourage greater integration of vaccine, prevention, and treatment research; to improve upon research efforts; and to address high priority research questions, particularly in resource-limited settings where AIDS is most devastating.

NIAID supports studies aimed at understanding the side effects of antiretroviral drugs as well as strategies to reduce exposure to potentially toxic drug regimens, such as:
1. Structured treatment interruption (STI) protocols
2. Use of immune-based therapies with HAART
3. Studies to compare different dosing schedules
4. Studies to compare early versus delayed treatment

NIAID also supports projects evaluating regimens containing agents associated with toxicities. For example, NIAID-funded researchers are conducting studies to evaluate treatments for several drug-associated metabolic complications, including fat redistribution, lipid and glucose abnormalities, and bone loss. In addition, researchers are studying the long-term metabolic effects of various antiretroviral regimens in pregnant women and their infants and in HIV-infected children and adolescents.

The Pharmaceutical Research and Manufacturers Association of America maintains a database of new drugs in development to treat HIV infection. They include new protease inhibitors and more potent, less toxic RT inhibitors, as well as other drugs that interfere with entirely different steps in the virus’ lifecycle. These new categories of drugs include:
1. Entry inhibitors that interfere with HIV's ability to enter cells.
2. Integrase inhibitors that interfere with HIV's ability to insert its genes into a cell's normal DNA.
3. Assembly and budding inhibitors that interfere with the final stage of the HIV life cycle, when new virus particles are released into the bloodstream.
4. Cellular metabolism modulators that interfere with the cellular processes needed for HIV replication.
5. Gene therapy that uses modified genes inserted directly into cells to suppress HIV replication. These cells are designed to produce T cells that are genetically resistant to HIV infection.

In addition, scientists are learning how immune modulators help boost the immune response to the virus and may make the existing anti-HIV drugs more effective. Therapeutic vaccines also are being evaluated for this purpose and could help reduce the number of anti-HIV drugs needed or the duration of treatment. ]]> Whether depressed patients will respond to an antidepressant depends, in part, on which version of a gene they inherit, a study led by scientists at the National Institutes of Health (NIH) has discovered. Having two copies of one version of a gene that codes for a component of the brain's mood-regulating system increased the odds of a favorable response to an antidepressant by up to 18 percent, compared to having two copies of the other, more common version. https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=90 Tue, 20 Jun 2006 06:16:17 GMT https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=90
Since the less common version was over 6 times more prevalent in white than in black patients — and fewer blacks responded — the researchers suggest that the gene may help to explain racial differences in the outcome of antidepressant treatment. The findings also add to evidence that the component, a receptor for the chemical messenger serotonin, plays a pivotal role in the mechanism of antidepressant action. The study, authored by National Institute of Mental Health (NIMH) researchers Francis J. McMahon, M.D., Silvia Buervenich, Ph.D., and Husseini Manji, M.D., along with collaborators at the National Human Genome Research Institute (NHGRI), the National Institute on Alcohol Abuse and Alcoholism (NIAAA), and other institutions, was posted online March 8 and will appear in the May, 2006 American Journal of Human Genetics.

"This discovery brings us closer to the day when clinicians will be able to offer treatment options and medications that are tailored and personalized to be optimally effective for individual patients," said NIH Director Elias A. Zerhouni, M.D.

However, the findings cannot yet guide treatment decisions.

"To our knowledge, this is the first demonstration of significant, replicated association between genetic variation and outcome of antidepressant treatment," added Manji, director of the NIMH's Mood and Anxiety Disorders Program.

In the initial phase of the NIMH-funded STAR*D (Sequenced Treatment Alternatives for Depression) trial, about 47 percent of the 2,876 participants experienced some improvement with the serotonin selective reuptake inhibitor (SSRI) citalopram (Celexa). The NIH scientists set out to find genetic factors that might help to explain why some patients fared better than others.

They screened genetic material from 1,953 of the STAR*D patients, a sample with a higher percentage of responders (69 percent), in part because patients who were doing well tended to stay in contact longer and were more likely to allow a blood sample to be drawn. The researchers looked for associations between treatment response and 768 known sites of variability in 68 suspect genes - sites where letters in the genetic code vary across individuals.

They found the strongest connection in the gene that codes for the serotonin 2A receptor, one of several proteins to which serotonin binds when brain cells communicate.

Located on cells in the brain's thinking center (cortex), the serotonin 2A receptor regulates circuits implicated in depression. Antidepressants, including citalopram, reduce the number of serotonin 2A receptors in animal cortex over the course of a few weeks — the same time frame required for the drugs to work in humans — suggesting that the receptors are important in the drugs' mechanism of action.

Everyone inherits two copies of the serotonin 2A receptor gene, one from each parent. A tiny glitch in the gene's chemical sequence results in some people having an adenine (A) at the same point that other people have a guanine (G). So an individual can have gene types AA, AG or GG. Overall, the prevalence of the A version was 38 percent, compared to 62 percent for the G version in this sample. Fourteen percent had AA gene type, 43 percent AG and 43 percent GG. Since the site of variation is located in a stretch of genetic material with no known function, the researchers suspect that it may be just a marker for a still-undiscovered functional variation nearby in the gene.

Based on scores on a depression rating scale, close to 80 percent of patients who had AA responded to the antidepressant, compared to about 62 percent of those with GG. Thus, patients with the AA gene type were 16-18 percent more likely to benefit from the medication. Even patients with AG showed some increased benefit.

But this only applied to white patients, in whom the A version was more than six times more frequent than in black patients. There was no significant association between gene type and treatment outcome in black patients, who tended to fare less well in the trial overall.

"We now have to consider genetic factors as well as psychosocial issues in our attempts to explain why antidepressants do not help our black patients as much as they should," McMahon said. "The new findings help make a compelling case for a key role of the serotonin 2A receptor in the mechanism of antidepressant action."

Also participating in the study were: A. John Rush and Madhukar Trivedi, University of Texas Southwestern Medical Center; Gonzalo Laje, NIMH; Dennis Charney, Mount Sinai Hospital; Robert Lipsky, National Institute on Alcohol Abuse and Alcoholism (NIAAA); Alexander Wilson, Alexa Sorant, and George Papanicolaou, National Human Genome Research Institute (NHGRI); Maurizio Fava, Massachusetts General Hospital; and Stephen Wisniewski, University of Pittsburgh.]]> Over-the-counter (OTC) products are medicines you can buy without a doctor’s prescription. Many OTC products are advertised to relieve heartburn or acid reflux. These include antacids, bismuth subsalicylate, H2 blockers, proton pump inhibitors and combination medicines. https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=82 Mon, 19 Jun 2006 06:58:26 GMT https://www.sandiegohealthdirectory.com/kb/link.php?action=detail&id=82 Over-the-counter (OTC) products are medicines you can buy without a doctor’s prescription. Many OTC products are advertised to relieve heartburn or acid reflux. These include antacids, bismuth subsalicylate, H2 blockers, proton pump inhibitors and combination medicines. Combination medicines may include two or more of the following drugs.

How do antacids and acid reducers work?
Antacids neutralize the acid in your stomach. They can provide fast, short-term relief. Many OTC drugs combine different antacids.

H2 blockers reduce the amount of acid your stomach makes. While they don’t relieve symptoms right away, H2 blockers relieve symptoms for a longer period of time than antacids.

Some products combine antacids and an H2 blocker. One example combines famotidine, calcium carbonate and magnesium hydroxide (brand name: Pepcid Complete). These combination medicines can relieve symptoms right away and the relief can last for many hours.

Bismuth subsalicylate works by balancing the way fluid moves through your bowels. It also binds toxins (poisons) from bacteria so that they are not harmful and helps kill germs. It’s also used as an antiemetic (medicine to treat nausea and vomiting) and as an antidiarrheal (medicine to treat diarrhea).

Proton pump inhibitors stop your body’s production of acid. This type of drug requires 1 to 4 days to work. Only people who have heartburn often—at least 2 days a week—should use this drug.

To find out which product is right for you, talk to your doctor.

What problems can OTC antacids and acid reducers help?
These medicines can help relieve heartburn or dyspepsia (pain or an uncomfortable feeling in the upper middle part of your stomach). Heartburn is also called acid reflux disease or gastroesophageal reflux disease (GERD). OTC antacids and acid reducers may also be used as part of a plan to treat ulcers. For treating ulcers, these medicines may be used together and/or combined with antibiotics (drugs that kill bacteria) prescribed by your doctor.

If you aren’t getting enough calcium from your diet, your doctor might suggest that you take additional calcium to help treat or prevent osteoporosis. Antacids that contain calcium carbonate can be used with vitamin D to supplement the calcium in your diet.

What are some common side effects of heartburn medicines?
Antacids and acid reducers usually cause only minor side effects that go away on their own. These may include headaches, nausea, constipation or diarrhea. Bismuth subsalicylate can cause your tongue or stool to turn dark. This is a short-term side effect.

If side effects make it hard for you to take medicine for heartburn, talk to your family doctor. He or she may suggest a different drug or have ideas about how to make the side effects less of a problem.

Who shouldn’t take OTC antacids and acid reducers?
Don’t take these drugs if you have an allergy to any of the ingredients. Phenylalanine is an example of an ingredient in some antacids that can cause a problem for certain people.

If you have a condition called phenylketonuria, you shouldn’t take a medicine that contains phenylalanine.

Don’t take bismuth subsalicylate if you’ve ever had an allergy to aspirin or any other product that contains salicylates. Also don’t give bismuth subsalicylate to children who may have the flu or chickenpox because they will have a higher risk of Reye’s Syndrome.

Other ingredient-related warnings concern your diet while you’re taking an antacid or acid reducer. For example, unless your doctor tells you it’s OK; don’t use products that contain sodium bicarbonate or aluminum hydroxide and magnesium carbonate if you’re on a low-salt diet. Don’t take magnesium hydroxide if you’re following a magnesium-restricted diet.

If you have kidney disease, you shouldn’t use products containing calcium carbonate or aluminum hydroxide and magnesium carbonate without your doctor’s recommendation.

Can OTC antacids or acid reducers cause problems with any other medicines I take?
If certain drugs are taken at the same time, they can react with each other and change the way your body processes them. This is called a drug interaction. When this happens, the risk of side effects increases.

Don’t use more than one antacid or acid reducer at a time. Don’t mix acid reducers and antacids without first talking to your doctor.

If you take any prescription drugs and you’re thinking about taking an antacid, H2 blocker or proton pump inhibitor, talk to your doctor first. These drugs can cause problems with other medicines you take.

The following drugs may be of special concern for people who are taking H2 blockers or proton pump inhibitors:
1. Theophylline (oral asthma drug)
2. Warfarin (brand name: Coumadin) (blood-thinning drug)
3. Phenytoin (brand name: Dilantin) (seizure drug)
4. Prescription medicine for fungal or yeast problems
5. Diazepam (anxiety drug)
6. Digoxin (heart drug)

Bismuth subsalicylate may affect some drugs so that they don’t work as well. It also may cause side effects if combined with other drugs. If you take any of the following drugs, talk to your doctor before taking bismuth subsalicylate:
1. Blood-thinning drugs
2. Drugs to treat gout
3. Drugs to treat arthritis
4. Drugs for diabetes

Also, check with your doctor or pharmacist before taking bismuth subsalicylate if you take pain relievers, cold products or some prescription drugs. These medicines may contain aspirin, which is a salicylate, or they may contain some other type of salicylate. Because bismuth subsalicylate contains salicylate, you may take more salicylate than you intend if you take more than one of these products.

Should I call my doctor for any other reasons?
Before taking an antacid or acid reducer, talk to your doctor if you have any of the following symptoms:
1. Trouble or pain when you swallow
2. Bloody vomit
3. Bloody or black stools
4. Ongoing stomach pain
5. Lightheaded, dizzy or sweaty feeling
6. Chest pain, shoulder pain, or pain that spreads to your arms, neck or shoulders with shortness of breath
7. Weight loss for no reason
8. Nausea or vomiting
9. Wheezing (you’ll hear a squeaky or musical sound in your chest)
10. Heartburn that has lasted more than 3 months

You should stop using antacids or acid reducers and call your doctor if any of the following are true:
1. Your stomach pain doesn’t get better when you use the medicine, or it gets worse.
2. You need to take the medicine for more than 14 days.
3. You’re taking Omeprazole (brand name: Prilosec) and feel like you need to take more than 1 course in 4 months.
4. Don’t try to treat yourself if you have any of these symptoms. They may be signs that you have an ulcer or a more serious problem that needs to be checked by your doctor.

What should I look for on the drug label?
When choosing an OTC antacid or acid reducer, check the drug label for possible side effects or interactions with other drugs you’re taking. This information will appear in the “Warnings” section of the label.

Be sure to check that you’re not taking two medicines that contain the same ingredient.

Always read and follow the directions on the label. Be sure you understand what the label says before taking the medicine. If you have any questions, ask your family doctor or pharmacist.]]>