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The American Journal of GastroenteroloGy Volume 106 | march 2011 www.amjgastro.com

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The care of acid-related diseases such as gastroesophageal reflux disease (GERD) in the elderly patient presents challenges not found in younger populations. Concurrent comorbidities, medication interactions, and the physiology of aging all conspire to change the presentation and natural history of these diseases in older patients. Clinicians caring for geriatric patients must therefore be aware of these changes to provide optimal care for GERD and to use acid-suppressive therapies to their best advantage in the elderly population.

Below, we address several questions that commonly occur in caring for acid-related disease in the elderly population. Although the recommendations proposed below do not represent the only, or neces-sarily the “best,” way to care for all elderly patients, they are solutions supported by evidence found in elderly cohorts to produce satisfactory results. The United Nations’ definition of “elderly” is those aged 60 or older, but, given the average life expectancy in the United States, the discussion below is focused primarily on those 70 years and older.

Does the clinical presentation of GERD change as patients age?In the elderly population, as in the general population, more than 40% have occasional symptoms of GERD and 20% have weekly

symptomatic GERD. But as patients age, the severity of heartburn diminishes, while its complications become more frequent (1–3). In a study of 12,000 patients aged 18–75 with endoscopically documented erosive esophagitis, severe heartburn was seen in 30% of patients aged more than 70 years with erosive esophagitis (com-pared with 47% of patients aged 31–40), and severe esophagitis (defined as Los Angeles grade C or D) was seen in 35% of elderly patients vs. 25% of patients aged 31–40 among those with severe heartburn (Figures 1 and 2) (4). Thus, while elderly patients may have severe heartburn, severe esophagitis may be present without the hallmark accompanying symptoms. This is probably due to several factors, including decreased perception of mucosal damage. Elderly patients without the typical symp-tom of heartburn may instead complain of more atypical symptoms, including respi-ratory symptoms and vomiting (5). This has important implications for patient management. Aware clinicians should have a low threshold for investigation and/or empirical therapy in this patient popu-lation. Upper endoscopy in the elderly with GERD will demonstrate a higher yield of Los Angeles grade C or D erosive esophagitis, Barrett’s esophagitis, and ade-nocarcinoma and, in most subjects, can be done with a great degree of safety (6,7).

What are the most common side effects of proton pump inhibitors?Most mortality in GERD results from esophageal adenocarcinoma. All data suggesting that proton pump inhibitors (PPIs) retard the development of dysplasia

and/or cancer are retrospective and weak (8–10). Therefore, for most subjects suf-fering from GERD, the medication is used primarily to address symptoms. Although the decrement in quality of life associated with GERD is substantial (11,12), the low rate of morbidity and mortality means that medications used to address GERD must have excellent safety profiles to jus-tify their use. Diarrhea, abdominal pain, constipation, and headache are the most common side effects of PPIs but are limit-ing in relatively few patients and typically respond to dose reduction or discontinu-ation in those subjects. The risk of fundic gland polyps (lesions with negligible, if any, risk of dysplasia) may be increased (13). No data support the cessation of PPI use in subjects in whom they are other-wise indicated on account of the develop-ment of fundic gland polyps.

Serious complications of PPI use appear to be rare and may result from profound acid suppression and secondary hypergastrinemia, hypochlorhydria, and achlorhydria. The incidence of antibiotic-associated Clostridium difficile colitis is twice as high in PPI users. The putative mechanism of this increased risk is that hypochlorhydria prevents sterilization of the upper gastrointestinal (GI) tract, permitting colonization by pathogenic species (14). By the same mechanism, the risk of community-acquired pneumonia is increased approximately twofold (15). The same effect is seen, to a lesser degree, in users of H2-receptor antagonists, which supports the theory that reduc-tion of the gastric acid barrier may be to blame. However, studies investigating the

Treatment of GERD and Proton Pump Inhibitor Use in the Elderly: Practical Approaches and Frequently Asked QuestionsShannon Scholl, MD, MPH1, Evan S. Dellon, MD, MPH1 and Nicholas J. Shaheen, MD, MPH1

Am J Gastroenterol 2011;106:386–392; doi:10.1038/ajg.2010.409

1Center for Esophageal Diseases and Swallowing, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. Correspondence: Nicholas J. Shaheen, MD, MPH, Center for Esophageal Diseases and Swallowing, University of North Carolina School of Medicine, CB#7080, Chapel Hill, North Carolina 27599-7080, USA. E-mail: [email protected]

© 2011 by the american college of Gastroenterology The American Journal of GastroenteroloGy

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Is there a significant interaction between PPIs and clopidogrel?Concerns about PPI use in the setting of concurrent clopidogrel therapy were heightened in 2009, when a study by Ho et al. in JAMA showed a higher rate of acute coronary syndrome and/or mortal-ity in 8,205 veterans who used PPIs and clopidogrel (29.8%) vs. clopidogrel alone (20.8%) (23). This was a retrospective cohort study and had several limitations inherent to that design. However, there is a plausible biological mechanism sup-porting the interaction: ex vivo platelet aggregation studies showed an interaction between PPIs and clopidogrel due to inhi-bition of the CYP enzyme subclass that converts clopidogrel to its active metabo-lite (24). Subsequent platelet aggregation assays supported an interaction but did not evaluate the clinical results of such an interaction. Later in 2009, an analysis of 2,208 subjects enrolled in a French reg-istry following acute coronary syndrome failed to show a difference between clopi-dogrel users taking PPIs and those taking clopidogrel alone (25).

Two recent clinical studies and one in vitro aggregometry study evaluated the effect of pantoprazole, a weaker inhibi-tor of the CYP2C19 enzyme, on the effect of clopidogrel. All of them showed less interaction with pantoprazole than with omeprazole (26,27) or esomeprazole (27) or in comparison with all other PPIs (28),

reduced clearance (17,18) and increased bioavailability (17) of these PPIs in patients in the eighth and ninth decades of life as compared with younger patients, but, because of considerable overlap in the pharmacokinetic profiles of the groups, dose adjustment is not recommended. There is no difference in the metabolism of esomeprazole in elderly and middle-aged patients with GERD (19).

PPI metabolism occurs via the cyto-chrome P450 system in the liver (20). Clinically significant abnormalities of PPI metabolism are rare and do not increase in a healthy aged population. In elderly subjects with normal hepatic function, dose adjustment is not recommended.

Obesity is an independent risk factor for GERD and erosive esophagitis, so these patients frequently require PPI therapy. There are many reasons to suspect that an altered dose of PPI might be required for obese patientsthey may have more severe symptoms or a larger volume of distribution of drug, and they often have comorbid liver disease in the form of hepatic steatosis. However, to date, no study has shown an altered pharmacoki-netic profile in obese patients for either PPIs or H2-receptor antagonists. In fact, despite the increased severity of GERD with increasing body mass index (21,22), there is no difference in the response to comparable PPI doses in obese compared with lean patients.

effect of PPIs on community-acquired pneumonia have been confounded by the diagnosis of GERD, and it is unknown whether GERD itself or the PPI use is the predisposing factor. Concerns regard-ing hip fracture in the setting of PPI use are addressed below. Additionally, recent data suggest the potential for significant medication interactions, which have raised concerns about increased cardiac events in subjects on PPIs. These issues are also discussed below.

Given that both community-acquired pneumonia and C. difficile infection are more common and carry higher risks of morbidity and mortality as patients age (16), the associations described above deserve special attention in the elderly population. However, it should be noted that the majority of data supporting these more significant risks of PPI therapy are derived from retrospective studies of large databases, and such research is subject to multiple forms of bias. Despite the weak-ness of the data supporting these risks, to minimize side effects, PPIs should be applied only when clinically indicated, at the minimum effective dose.

Is it appropriate to change the PPI dose for elderly or obese patients?There are no data to support the use of reduced doses of PPIs on the basis of age alone. Pharmacokinetic studies of omeprazole and lansoprazole show

<21 21−30 31−40 41−50 51−60 61−70 >70

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Figure 2. Prevalence of severe heartburn by age-decade cohort. (Adapted from ref. 4.)

Figure 1. Prevalence of severe esophagitis by age-decade cohort.(Adapted from ref. 4.)


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larly metabolized drugs, such as warfarin, diazepam, and phenytoin, but these occur so rarely (less than one adverse event per million prescriptions) that they are not considered clinically significant (32–34). PPIs are metabolized via the CYP2C19 subclass, a minor pathway for metabolism of the weaker R-warfarin enantiomer of warfarin, raising the levels of this minor metabolite by up to 12% (35). Omeprazole may be the most active in this regard (36). Although not formally recommended, in subjects who have had marked lability of drug levels or in those with severe clini-cal syndromes, the clinician may wish to check for stability of the international normalized ratio or phenytoin level after a new PPI prescription is initiated.

Should PPIs be used to protect against GI complications of low-dose aspirin?Given the high prevalence of coronary artery disease in the elderly, the use of cardioprotective aspirin is frequent in this population (37). Since the risk of gastroduodenal ulceration also increases with age, prophylaxis against the GI complications of aspirin in the setting of cardioprotection is a commonly faced clinical issue in the elderly population. Aspirin exerts its gastropathic effects by direct epithelial damage and by inhibi-tion of mucosal prostaglandin produc-tion, which reduces mucosal defenses including mucus and bicarbonate secre-tion, reducing blood flow, and reducing epithelial-cell turnover and repair (38).

at risk for heart attacks or strokes who use clopidogrel to prevent blood clots will not get the full effect of this medicine if they are also taking omeprazole” (31). Given the divided nature of the data on this issue, the need for the warning is unclear. An alternative approach being used by some physicians—dosing one medication in the morning and the other at night—may be ineffective. The most recent package insert for clopidogrel reports an unreferenced study of 72 patients that showed that split dosing did not reduce the interaction. For now, physicians should warn patients of a potential interaction. When possible, avoidance of coadministration of omepra-zole and clopidogrel may be warranted until the potential interaction is better understood. In cases of patients who are considered to be at high risk for GI bleed-ing, the risk of reduced activity of clopi-dogrel must be weighed against the risk of GI bleeding, and decisions about treatment must be made on a case-by-case basis.

What other medication interactions do I need to consider when prescribing PPIs?Polypharmacy is common in elderly populations, and therefore medication interactions take on special importance in older patient populations. Fortunately, there have been very few significant med-ication interactions associated with PPI use. As noted above, metabolism by the CYP450 superfamily of enzymes may lead to rare inhibition or potentiation of simi-

raising hopes that pantoprazole could be safely used in these patients. How-ever, a more recent retrospective study of 1,033 patients readmitted to the hospital for acute myocardial infarction or stent placement showed similar rates of rehos-pitalization for users of pantoprazole vs. other PPIs (29).

Results of an industry-sponsored study evaluating the clinical significance of an interaction between PPIs and clopidogrel have recently been released in abstract form. The COGENT (Clopidogrel and the Optimization of Gastrointestinal Events) study randomized subjects in need of clopidogrel because of either recent acute coronary syndrome or stent placement into a clopidogrel and an omeprazole plus clopidogrel group. All patients were maintained on dual antiplatelet therapy with aspirin. Deaths from cardiovascular events were then assessed in both groups over a median of 4 months. The resulting survival curves for myocardial infarc-tion, revascularization, and composite cardiovascular events for the treatment and placebo groups are superimposable, providing striking evidence for a lack of interaction between omeprazole and clopidogrel. However, the survival curves for composite GI events do show a pro-tective effect of omeprazole (P = 0.007), suggesting that PPI use can ameliorate the GI effects of aspirin in this patient popula-tion. These results from a large, random-ized, well-controlled prospective trial provide evidence that omeprazole is safe when used with dual antiplatelet therapy and provides important protection from GI complications. However, the validity of the trial was challenged because of its premature terminationthe sponsor of the trial declared bankruptcy, and all trial proceedings immediately halted before completion of the study (30).

Because of the unclear nature of the data surrounding an interaction between PPIs and clopidogrel, on 17 November 2009, the US Food and Drug Administration (FDA) issued a warning regarding the concomi-tant use of clopidogrel and PPIs, stating, “New data show that when clopidogrel and omeprazole are taken together, the effec-tiveness of clopidogrel is reduced. Patients

Table 1. Risk categories for endoscopic procedures

High risk Low risk

Polypectomy Diagnostic: EGD ± biopsy

Biliary sphincterotomy Diagnostic: flexible sigmoidoscopy ± biopsy

Pneumatic or bougie dilation Diagnostic: colonoscopy ± biopsy

PEG placement ERCP without sphincterotomy

EUS with FNA Biliary/pancreatic stent without sphincterotomy

Laser ablation and coagulation EUS without FNA

Treatment of varices Enteroscopy

eGD, esophagogastroduodenoscopy; ercP, endoscopic retrograde cholangiopancreatography; euS, endo-scopic ultrasound; FNa, fine-needle aspiration; PeG, percutaneous endoscopic gastrostomy. adapted from ref. 43.


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other NSAIDs do not increase the risk of significant bleeding with polypectomy and sphincterotomy (43,53–55), aspirin should be discontinued for colonoscopy or endo-scopic retrograde cholangiopancreatog-raphy only if there is an additional strong clinical indication to do so. Cessation of clopidogrel alone beyond 30 days from bare-metal stent placement is common and does not confer increased risk of thrombo-sis over a short period of time. Similarly, short-term cessation of clopidogrel alone beyond 6 months from drug-eluting stent placement does not confer significant risk if aspirin is continued (46). But as a general principle, for elective procedures that would require interruption of anti-platelet therapy (such as routine screening colonoscopy with polypectomy), deferral until 12 months after percutaneous coro-nary intervention with drug-eluting stent placement is preferable.

There is no evidence that bridging with heparin reduces the risk of thrombotic events when antiplatelet therapy is dis-continued (56,57). Table 2 summarizes the recommendations for anticoagulation cessation.

When is it appropriate to do screening upper endoscopy on the elderly patient with chronic GERD?Weekly heartburn symptoms are present in 20% of elderly patients and, as noted above, often portend more severe endo-scopic disease than comparable symptoms in younger patients. Increasing age is a risk factor for Barrett’s esophagus and esopha-geal adenocarcinoma. But the presence of heartburn is not a reliable predictor for the presence of Barrett’s esophagus in this age group, because conversion to columnar epithelium may be associated with loss of symptomatic heartburn (58). Even when present, symptomatic heartburn is not a reliable risk factor for Barrett-related cancer because 40% of those with a new diagnosis of esophageal adenocarcinoma report an absence of prior weekly heart-burn. Clearly, any elderly patient with heartburn that is unresponsive to PPI and/or with dysphagia should be considered for endoscopy. But screening of patients with uncomplicated chronic heartburn of any

atography (without sphincterotomy), and colonoscopy (without polypectomy) do not require cessation of anticoagulants. Biopsy with forceps is considered a low-risk proce-dure. High-risk procedures (polypectomy, percutaneous endoscopic gastrostomy placement, fine-needle aspiration, sphinc-terotomy, and dilatation) do warrant cessa-tion of anticoagulation, which is typically discontinued 3–5 days (cilostazol) or 5–7 days (aspirin, clopidogrel) before the pro-cedure (Table 1) (43).

Clopidogrel–aspirin dual therapy is used to prevent stent thrombosis following percutaneous coronary intervention, as primary prevention of myocardial infarc-tion in patients with unstable angina or nonintervenable coronary artery disease, and as secondary prevention of myocar-dial infarction and cerebrovascular acci-dents and in those with a prior history of the same (44,45). If clopidogrel alone must be stopped within the first 30 days follow-ing bare-metal stent or drug-eluting stent placement, the risk of restenosis is low, estimated at 1–4%, the highest risk being in patients with longer stent lengths (suggest-ing more severe disease) and lower ejection fraction (46–51). Cessation of both aspirin and clopidogrel is associated with a higher risk of acute coronary syndrome and ST-elevation myocardial infarction and also confers a shorter time to stent thrombosis (7 days for those on no antiplatelet therapy vs. 122 days for patients still on aspirin) (52). As the current American Society for Gastrointestinal Endoscopy guidelines indicate that standard doses of aspirin and

The risk of GI bleeding in patients using low-dose aspirin is approximately twice the rate with placebo and carries a 5% case-fatality rate when severe enough to require admission (39). The risk of bleeding is increased in those who have a history of prior GI events, are older, or use anticoagulants, corticosteroids, or high-dose or multiple nonsteroidal anti-inflammatory drugs (NSAIDs). Cyclooxygenase-2-selective NSAIDs are less gastropathic, but use of low-dose aspirin largely obviates their gastropro-tective effects. PPIs have been found to be superior to full-dose ranitidine and placebo for the healing of NSAID-asso-ciated ulcers irrespective of Helicobacter pylori status, in a dose-dependent man-ner (40–42). The lowest effective dose of aspirin (and other NSAIDs) should be used, and risk factors for bleeding should be assessed, with application of PPIs in high-risk groups, as noted above.

How should we manage patients receiving antiplatelet therapy who need endoscopy?In considering an endoscopic procedure on an anticoagulated patient, the risk of ongo-ing or procedure-related bleeding must be weighed against the risk of thromboembo-lic events such as cerebrovascular accident or myocardial infarction following dis-continuation of anticoagulation. Low-risk procedures such as diagnostic esophago-gastroduodenoscopy, endoscopic ultra-sound (without fine-needle aspiration), endoscopic retrograde cholangiopancre-

Table 2. Summary of recommendations for anticoagulation cessation

Avoid cessation of antiplatelet therapies after PCI with stent placement when possible

Avoid cessation of clopidogrel (even when aspirin is continued) within the first 30 days after PCI and either DES or BMS when possible

Defer elective endoscopic procedures—possibly for up to 12 months, if clinically acceptable, from the time of PCI and DES placement

Perform high-risk endoscopic procedures 5–7 days after clopidogrel therapy and 3–5 days after cilostazol cessation. Aspirin should be continued when possible

Resume antiplatelet therapy after the procedure, once hemostasis has been achieved

Continue clopidogrel and aspirin in patients undergoing elective low-risk endoscopic procedures

BmS, bare-metal stent; DeS, drug-eluting stent; PcI, percutaneous coronary intervention. adapted from ref. 45.


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mineral density in a Manitoba registry of 21,933 patients (76). These investigators found no relationship between PPI use and osteoporosis or PPI use and loss of bone mineral density over 5 years. These data cast doubt on the hypothesis that PPIs pro-mote bone loss. Regardless of the divided nature of these data, on 25 May 2010, the FDA issued a warning regarding the pos-sible link between hip, wrist, and spine fractures and PPI use. The FDA mandated changes in the labels of all prescription and over-the-counter PPI preparations on the basis of these data and advised that “healthcare professionals and users of pro-ton pump inhibitors should be aware of the possible increased risk of fractures of the hip, wrist, and spine with the use of pro-ton pump inhibitors, and weigh the known benefits against the potential risks when deciding to use them” (77).

In summary, studies evaluating PPIs and fracture risk are methodologically limited, and divided in their conclu-sions. There is some suggestion of a small increase in fracture risk with an odds ratio less than 2. The mechanism of any increase in fracture risk is unclear but may not occur through reduction of bone den-sity. PPIs should be used only for appro-priate clinical indications at the lowest effective dose, and the possible increased risk of hip fracture should be disclosed to patients. In those who require high-dose, long-term PPIs, osteoporosis and fall risk should be assessed and modified as appropriate through the use of calcium supplements and/or bisphosphonates.

ConclusionIn summary, elderly patients represent a special population with respect to PPI therapy and acid-peptic disease. They have more severe esophagitis and are at the highest risk for complications of GERD, including Barrett’s esophagus and esopha-geal adenocarcinoma. They often have comorbidities that require NSAIDs or antiplatelet therapy, which put them at risk for GI bleeding and represent challenges for management during endoscopic inter-vention. And they are often on multiple medications, raising concern regarding medication interactions.

cer death may be averted and life extended in otherwise healthy subjects without life-limiting comorbidity even late in life with well-timed endoscopic intervention.

Does PPI use affect vitamin B12 absorption?Vitamin B12 is liberated from protein sources with the help of gastric acid. There has been concern that PPI use would inter-fere with this process, leading to B12 malab-sorption and deficiency. Studies comparing healthy controls with PPI users have had conflicting results (67–69). There may be a decline in B12 levels in long-term (>3-year) users of PPI, but this has not been shown to result in clinical disease (70). The elderly are at risk for development of pernicious anemia and should be screened for B12 deficiency if macroblastic anemia is detected. Otherwise, routine monitoring of vitamin B12 or other vitamins in chronic PPI users is not necessary.

Does PPI use increase the risk of hip fracture in the elderly?A 2006 article by Yang et al. (71) in JAMA gained media attention by suggesting that PPI use conferred an increased risk of hip fracture in patients 50 years of age or older. In this study, higher dose and duration of PPI use conferred an odds ratio (OR) of 1.59 (95% confidence interval 1.39–1.80) for use for more than 3 years. Two other studies found similar results, with the larg-est odds ratio being 1.92 (1.16–3.18) after 7 years of PPI use (72,73). All of the studies were retrospective case-control designs (a design that is subject to multiple forms of bias), and none of the studies controlled for vitamin D levels or fall risk. Importantly, a recent study was unable to show an asso-ciation of PPIs with increased fracture in those without risk factors (74).

Reduced calcium absorption in the hypochlorhydric stomach is a proposed mechanism of increased fracture risk. This concern originates from studies of human subjects whose plasma calcium and 24-hour urinary calcium levels were reduced following concomitant calcium carbonate and PPI administration (75). A recent case–control study evaluated the effect of PPIs on osteoporosis and bone

age is controversial, because of the lack of direct evidence demonstrating a mortality benefit. As a result, the value of endoscopic screening of subjects with chronic GERD symptoms of any age for Barrett’s esopha-gus is highly contested. Economic model-ing suggests that screening of white men aged more than 50 years with heartburn symptoms for at least 5 years is probably cost-effective (59). Moreover, regardless of age, any patient with alarm symptoms such as weight loss, anemia, dysphagia, or GI bleeding should undergo screening endoscopy.

When is it appropriate to stop performing surveillance endoscopy for elderly patients with Barrett’s esophagus?When Barrett’s esophagus is diagnosed, surveillance for dysplasia and adenocarci-noma is often performed. Approximately 5% of patients diagnosed with Barrett’s will develop adenocarcinoma, and the risk is greatest in patients aged 65–74 years (60–62). However, the risk of cancer in any given patient in a calendar year is small, estimated at 0.5% per year. For this reason, frequent surveillance of all patients with nondysplastic Barrett’s is not cost-effec-tive (59). Current guidelines recommend repeating endoscopy with four-quadrant biopsies within one year after the initial diagnosis of Barrett’s to detect any preva-lent dysplasia. Following that, decision-analysis studies suggest that endoscopic surveillance of persistent nondysplastic Barrett’s could be performed every 5 years (63). Surveillance should be ended when the life expectancy is less than 1 year or the patient could not be expected to tolerate endoscopic or surgical therapy in the event of a cancer diagnosis (64). Given the rise of endoscopic therapy for dysplastic Bar-rett’s esophagus (65,66), and the increasing life expectancy of the elderly in the United States, thinking about when to stop surveil-lance is evolving. Given that most patients who can tolerate surveillance endoscopy can also tolerate some form of endoscopic therapy, and that the onset of adenocarci-noma of the esophagus is late in life, cli-nicians should not use chronological age alone as a reason to stop surveillance. Can-


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22. Jacobson BC, Somers SC, Fuchs CS et al. Body-mass index and symptoms of gastroesophageal reflux in women. N Engl J Med 2006;354:2340–8.

23. Ho PM, Maddox TM, Wang L et al. Risk of adverse outcomes associated with concomitant use of clopidogrel and proton pump inhibitors following acute coronary syndrome. JAMA 2009;301:937–44.

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Potential competing interests: Dr Shaheen receives research funding from Takeda Pharmaceuticals, AstraZeneca, Procter & Gamble, BÂRRX Medical, CSA Medical, and Oncoscope Inc. He is a con-sultant for AstraZeneca, CSA Medical, and Oncoscope Inc.

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Fortunately, PPI use has a favorable side-effect profile and few significant drug inter-actions. Adverse effects of PPI therapy may include an increased risk of C. difficile coli-tis, community-acquired pneumonia, and hip fracture. The latter is an area of active research and current controversy. A com-mon-sense approach to pharmacotherapy should be applied: prescribe PPIs only to patients for whom therapy is indicated, and do so at the smallest effective dose.

The effect of PPIs on clopidogrel is an area of active research. A recent large pro-spective study showed no effect of PPIs on myocardial infarction, but the FDA has placed a warning on clopidogrel, citing this interaction. The package insert does not support split dosing as a means of avoiding the interaction. For now, physicians should dose PPIs judiciously in these patients and warn them of the potential interaction.

In the setting of recent coronary stent placement, prior stent thrombosis, or prior cerebrovascular accident, clopi-dogrel should be discontinued only if necessary, and preferably not within the first 30 days following stent placement, when the risk of in-stent stenosis is high-est. In all situations, aspirin should be continued as monotherapy if possible, even in high-risk procedures. A PPI is recommended as gastroprotection in elderly patients who require daily aspirin or other NSAID therapy.

Physicians should have a low threshold for prescribing PPIs for elderly patients who have symptomatic GERD and should be alert for atypical presentations. There is no evidence for adjusting the dose of PPI for elderly or obese patients. Chronologi-cal age should not be used as a sole crite-rion for discontinuing Barrett’s dysplasia surveillance; virtually any patient who can tolerate endoscopy can tolerate endoscopic ablative therapies.

COnFLICT OF InTERESTGuarantor of the article: Nicholas J. Shaheen, MD, MPH.Specific author contributions: Shannon Scholl and Evan S. Dellon authored the paper; Nicholas J. Shaheen edited the paper.Financial support: None.


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