# data[].attributes.body
🧪 Bismuth-Related Side Effects (if used in quadruple therapy)

Metallic taste

Black tongue or black stools (harmless but may alarm patients)

Nausea or constipation

Avoid in patients allergic to aspirin (contains salicylate component)

💊 Important Drug Interactions

Clarithromycin + Atorvastatin:

Clarithromycin inhibits CYP3A4 → increases atorvastatin levels

Risk of myopathy or rhabdomyolysis

Recommendation: Temporarily stop statin or switch to pravastatin/rosuvastatin

Pantoprazole + Atorvastatin:

PPI may reduce atorvastatin absorption

Monitor LDL cholesterol levels during/after PPI therapy

🔎 Long-Term Monitoring Considerations for PPI Use

Hypomagnesemia → Monitor for muscle cramps, arrhythmia if PPI is prolonged

Vitamin B12 deficiency → Monitor if used >1 year or in elderly

Osteoporosis/fractures → Consider bone health assessment in high-risk patients

Clostridium difficile infection → Watch for persistent diarrhea

Renal effects (CKD) → Monitor serum creatinine for long-term users

# data[].attributes.body
In normal human's stomach, there is a balance between aggravating factor and mucosal defensive factor. Hence, our stomach mucosal layer is well maintained.

In peptic ulcer disease, the aggravating factor is more than the mucosal defensive factor. This results the mucosal layer being destroyed and the damage is extended to the inner layer. On prolonged exposure of stomach lining to gastric acid, perforation and gastric bleeding occurs.

# data[].attributes.body
Naproxen = Non-selective NSAID
→ Inhibits both COX-1 and COX-2 enzymes
→ Especially blocks COX-1, which is important for stomach protection

COX-1 normally helps produce prostaglandins
→ Prostaglandins maintain mucus, bicarbonate, and blood flow in stomach lining
→ These protect the stomach from acid damage

Inhibition of COX-1
→ ↓ Mucus and bicarbonate secretion
→ ↓ Mucosal blood flow
→ ↑ Gastric acid damage
→ Gastric mucosa becomes vulnerable
→ Ulcer formation, bleeding, delayed healing

In RB’s case:
→ Long-term use of naproxen 500 mg BID
→ Developed severe epigastric pain and black tarry stools
→ Diagnosed with NSAID-induced PUD

# data[].attributes.headline
 H. pylori Eradication Therapy (Treatment Plan)

# data[].attributes.subject
 H. pylori Eradication Therapy (Treatment Plan)

# data[].attributes.body
Standard first-line triple therapy for 14 days:

1. Proton Pump Inhibitor (PPI) – e.g. Pantoprazole 40 mg BID

2. Clarithromycin – 500 mg BID

3. Amoxicillin – 1 g BID
🔁 OR Metronidazole – 500 mg BID (if penicillin allergy)

# data[].attributes.body
COX-1, or cyclooxygenase-1, is an enzyme that plays a crucial role in maintaining normal bodily functions, particularly in regulating blood flow, blood clotting, and protecting the stomach lining. It's involved in the production of prostaglandins, which are essential for these processes.

Blood clotting:

COX-1 in platelets helps produce thromboxane, which is involved in blood clotting.

Stomach lining protection:

COX-1 helps maintain the integrity of the stomach lining by producing prostaglandins that protect against ulcers and other damage.

Kidney function:

COX-1 contributes to renal blood flow regulation.

# data[].attributes.body
Antisecretory drugs used for peptic ulcer disease (PUD) include H2-receptor antagonists and proton pump inhibitors (PPIs). PPIs have largely replaced H2 receptor blockers due to their superior healing and efficacy. PPIs block acid production in the stomach, providing relief of symptoms and promoting healing. Treatment may be incorporated with calcium supplements as long-term use of the PPIs can increase the risk of bone fractures. NSAIDs induced PUD can be treated by stopping the use of NSAIDs or switching to a lower dose. Corticosteroids, bisphosphonates, and anticoagulants should also be discontinued if possible.

# data[].attributes.body
Stop Smoking
→ Improves healing and reduces future ulcers.

Limit Alcohol
→ Reduces stomach irritation and acid production.

Avoid Spicy, Acidic, Fatty Foods
→ Prevents further stomach irritation.

Eat Smaller, Frequent Meals
→ Reduces acid production and aids digestion.

Reduce Stress
→ Lowers acid production and improves well-being.

Avoid NSAIDs if Possible
→ Reduces risk of further irritation and ulcers.

Probiotics
→ Balances gut flora and aids ulcer healing.

# data[].attributes.headline
Helicobacter pylori (H. pylori) Infection

# data[].attributes.subject
Helicobacter pylori (H. pylori) Infection

# data[].attributes.body
H. pylori enters the stomach
→ Lives in the mucus layer of the stomach lining

Produces enzyme urease
→ Urease breaks down urea → ammonia
→ Ammonia neutralizes stomach acid around the bacteria
→ Allows H. pylori to survive harsh acidic environment

But ammonia and bacterial toxins
→ Damage the mucosal lining
→ Trigger chronic inflammation (gastritis)

Inflammation and mucosal damage
→ Weaken protective barrier of the stomach
→ Makes the stomach lining more vulnerable to acid attack
→ Leads to ulcer formation

# data[].attributes.body
Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum.

# data[].attributes.body
1. Based on Location:

Gastric ulcer –>occurs in the stomach.

Duodenal ulcer –> occurs in the first part of the small intestine (called the duodenum).

2. Based on Cause:

H. pylori-associated ulcer –>caused by infection with Helicobacter pylori bacteria.

NSAID-induced ulcer –> caused by frequent use of painkillers like ibuprofen or aspirin.

Stress ulcer –> due to severe physical stress, like after major surgery or serious illness.

Zollinger-Ellison syndrome –> caused by a rare tumor that increases acid production.

# data[].attributes.body
1. Patient Education & Risk Factor Management:

Teach patients about PUD and prevention of recurrence.

Advise cessation of smoking and limit/avoid alcohol.

Offer smoking cessation support (e.g., nicotine patches, counseling).

2. Safe NSAID Use:

Recommend safe alternatives to NSAIDs for pain relief.

Identify high-risk patients (e.g., elderly, history of ulcers) for NSAID complications.

Suggest COX-2 selective NSAIDs or adding a PPI for stomach protection if NSAID use is unavoidable.

3. Medication History Review:

Review patient’s medication records for:

Previous antibiotic use (potential to increase H. pylori resistance).

Harmful drug combinations.

4. OTC & Herbal Product Counseling:

Warn about OTC/herbal products containing hidden NSAIDs.

Encourage consultation with a healthcare provider before using new medications or supplements.

5. Promote Adherence & Proper Use:

Educate on correct timing and method for taking medications (e.g., full course of antibiotics, PPIs before meals).

Stress the importance of adherence to H. pylori eradication therapy to prevent resistance and treatment failure.

Herbal Product & Potential Effect/Risk:

Willow bark: Contains salicin (aspirin-like compound).

Turmeric (high doses): May irritate stomach lining or interact with medications.

Ginger (in large doses): Can thin blood or increase bleeding risk.

Ginseng: May increase risk of GI bleeding with NSAIDs.

# data[].attributes.headline
Rationale for PPI Use in H. pylori Eradication

# data[].attributes.subject
Rationale for PPI Use in H. pylori Eradication

# data[].attributes.body
Why PPIs are part of H. pylori triple therapy ?

1. Creates Favorable pH Environment

PPIs raise gastric pH → enhances stability and effectiveness of antibiotics (clarithromycin, amoxicillin)

2. Improves Antibiotic Penetration

Higher pH allows better penetration into gastric mucosa, where H. pylori resides

3. Supports Mucosal Healing

While antibiotics eliminate the bacteria, PPI promotes healing of the gastric lining

# data[].attributes.body
1. Corticosteroids (e.g., Prednisolone)

Mechanism:

Suppresses prostaglandin synthesis (via inhibition of phospholipase A2)

May delay epithelial cell turnover and healing

Potentiates NSAID-induced damage

RB's Case: On Prednisolone 5 mg OD—low dose, but when combined with NSAIDs, there's synergistic risk for mucosal injury and ulceration.

📌 Combination of NSAIDs + corticosteroids is strongly associated with increased risk of GI bleeding and PUD (Ref: NCBI, PMID: 28824092).

1. Smoking (12-pack-year history)

Delays ulcer healing

Reduces bicarbonate secretion

Increases gastric acid secretion

Enhances H. pylori virulence

RB's Case: Long-standing smoker. Smoking is a cofactor for duodenal ulcer formation and impairs mucosal defense.

3. Alcohol Use

Ethanol disrupts the mucosal barrier

Increases gastric acid secretion

Causes direct mucosal injury

RB's Case: Drinks alcohol with dinner regularly. Alcohol, especially spirits, is known to aggravate gastritis and promote ulcer symptoms like burning pain and dyspepsia.

4. Other Medications

Bisphosphonates (e.g., alendronate): Cause direct mucosal irritation

Potassium chloride: Causes esophageal and gastric ulcers

Fluorouracil: Chemotherapeutic that may cause mucosal damage

5. Hypersecretory States

Zollinger Ellison syndrome

Systemic mastocytosis

Cystic fibrosis

Hyperparathyroidism

Antral G cell hyperplasia

https://www.ncbi.nlm.nih.gov/books/NBK534792/

# data[].attributes.attachment_link.description
Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve the lower esophagus, distal duodenum, or jejunum. Epigastric pain usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer; on the other hand, the pain with a duodenal ulcer tends to occur 2-3 hours after a meal. Today, testing for Helicobacter pylori is recommended in all patients with peptic ulcer disease. Endoscopy may be required in some patients to confirm the diagnosis, especially in those patients with sinister symptoms. Today, most patients can be managed with a proton pump inhibitor (PPI) based triple-drug therapy.

# data[].attributes.body
Alternative regimens (if resistance is suspected or treatment fails):

Bismuth-based quadruple therapy:

PPI (Omprazole 20 mg OD) / H2RA+ Bismuth subsalicylate 120 mg QID + metronidazole 400mg TDS + tetracycline 500mg TDS

# data[].attributes.body
Epigastric abdominal pain

Bloating

Abdominal fullness

Nausea and vomiting

Weight loss/weight gain

Hematemesis

Melena

# data[].attributes.attachment_link.description
Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve the lower esophagus, distal duodenum, or jejunum. Epigastric pain usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer; on the other hand, the pain with a duodenal ulcer tends to occur 2-3 hours after a meal. Today, testing for Helicobacter pylori is recommended in all patients with peptic ulcer disease. Endoscopy may be required in some patients to confirm the diagnosis, especially in those patients with sinister symptoms. Today, most patients can be managed with a proton pump inhibitor (PPI) based triple-drug therapy.

# data[].attributes.body
Heartburn after eating is a common sensation caused by stomach acid backing up into the esophagus. This often happens due to a weakened lower esophageal sphincter (LES), the muscle that prevents acid from flowing back up. The LES is a ring of muscle at the bottom of the esophagus that normally stays closed to prevent stomach acid from flowing back up into the esophagus.

Frequent or persistent heartburn can be a sign of gastroesophageal reflux disease (GERD), a more serious condition.

# data[].attributes.headline
Warning symptoms or alarm symptoms that should prompt urgent referral include:

# data[].attributes.subject
Warning symptoms or alarm symptoms that should prompt urgent referral include:

# data[].attributes.body
Unintentional weight loss

Progressive dysphagia

Overt gastrointestinal bleeding

Iron deficiency anemia

Recurrent emesis

Family history of upper gastrointestinal malignancy

# data[].attributes.attachment_link.description
Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve the lower esophagus, distal duodenum, or jejunum. Epigastric pain usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer; on the other hand, the pain with a duodenal ulcer tends to occur 2-3 hours after a meal. Today, testing for Helicobacter pylori is recommended in all patients with peptic ulcer disease. Endoscopy may be required in some patients to confirm the diagnosis, especially in those patients with sinister symptoms. Today, most patients can be managed with a proton pump inhibitor (PPI) based triple-drug therapy.

# data[].attributes.body
Initially (Trigger 1):

RB was diagnosed with NSAID-induced peptic ulcer:

Long-term use of naproxen (500 mg BID)

Also on prednisolone (another ulcer risk factor)

Symptoms: epigastric pain, melena, rebound tenderness

Initiated on Pantoprazole for suspected NSAID-induced ulcer

After Test Results (Trigger 2):

Confirmed H. pylori-positive via:

Urea breath test

Rapid urease test (biopsy sample)

➡️ Final diagnosis: Mixed etiology peptic ulcer
✔ NSAID-induced
✔ H. pylori-associated

# data[].attributes.body
1. Gaviscon® is formulated for reflux, not peptic ulcers

Mechanism: Gaviscon works by forming a protective "raft" (via alginate) that floats on top of stomach contents to reduce reflux into the esophagus, and by neutralizing acid with antacids giving a quick, short-term relief from symptoms like heartburn and acid reflux

Limitation: It does not suppress acid production, heal ulcers, or reverse mucosal damage caused by NSAIDs or H. pylori

🔬 Source: NCBI – Gaviscon’s raft-forming mechanism is effective in GERD but not for ulcer healing (PMID: 27195314).

2. Gaviscon has no antibacterial activity against H. pylori

Helicobacter pylori is a spiral-shaped, gram-negative bacterium that colonizes the gastric mucosa, leading to:

Chronic inflammation

Mucosal injury

Ulcer formation

This infection requires antibiotic therapy + acid suppression to eradicate.

Gaviscon does not have antibacterial activity → it cannot eliminate H. pylori or halt its inflammatory effects.

📚 Source: NIH MedlinePlus – H. pylori Infection
📚 MOH Malaysia CPG 2020 – “Antacids do not eradicate H. pylori.”

3. NSAID-Induced Mucosal Injury – The Accelerating Factor

RB was taking naproxen (a non-selective NSAID), which:

Inhibits COX-1 → ↓ prostaglandins

Prostaglandins normally help maintain the gastric mucosal barrier by:

Increasing mucus and bicarbonate secretion

Promoting mucosal blood flow

Supporting cell repair

Without prostaglandins:

The mucosa becomes vulnerable to acid and pepsin, leading to erosions and ulcers

# data[].attributes.body
NSAIDs are second to Helicobacter pylori infection in causing peptic ulceration in the upper GI tract. They cause mucosal injury due to cyclooxygenase (COX)-1 inhibition by reduction of cytoprotective mucosal prostaglandins and reduction of the secretion of a protective bicarbonate mucus barrier in the stomach and small bowel.

# data[].attributes.attachment_link.readable_text
. Author manuscript; available in PMC: 2011 Aug 19.

Published in final edited form as: Ann Longterm Care. 2010;18(9):24-27.

Abstract

Older adults commonly take nonsteroidal anti-inflammatory drugs (NSAIDs) chronically. Studies of older adults show that chronic NSAID use increases the risk of peptic ulcer disease, acute renal failure, and stroke/myocardial infarction. Moreover, chronic NSAID use can exacerbate a number of chronic diseases including heart failure and hypertension, and can interact with a number of drugs (eg, warfarin, corticosteroids). Preferred analgesics in older adults that may have a lower risk of these adverse drug reactions include acetaminophen, a nonacetylated salicylate (eg, salsalate), a short half-life NSAID (eg, ibuprofen), or low-dose opioid/opioid-like agents in combination with acetaminophen (in appropriate patients).

Introduction

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a common class of analgesics used chronically for persistent pain due to osteoarthritis and other musculoskeletal disorders in older adults. Specifically, an estimated 40% of people age 65 years and older fill one or more prescriptions for a NSAID each year. Considering that NSAIDs are also currently available over the counter, it is clear to see that even larger numbers of older adults are exposed to NSAIDs in the United States.

While these agents can be effective in treating inflammation and pain, older adults are at increased risk for adverse drug reactions (ADRs) due to age-related loss of physiological organ reserve, increased comorbidities, polypharmacy, and changes in pharmacokinetics. As a result, NSAID use causes an estimated 41,000 hospitalizations and 3300 deaths each year among older adults. Some specific ADRs of concern with chronic use of NSAIDs include gastrointestinal (GI), renal, cardiovascular (CV), cerebrovascular, and central nervous system (CNS) adverse effects. This review will begin by describing key evidence for these organ-specific ADRs associated with the chronic use of NSAIDs in older adults and finish with general recommendations for healthcare providers to avoid/minimize these ADRs.

GI Risks Associated with Chronic NSAID Use

The spectrum of potential NSAID-related GI adverse effects is wide, ranging from dyspepsia to life-threatening gastric bleeding. A nested case control study from nearly two decades ago (before the introduction of cyclooxygenase-2 [COX-2] selective NSAIDs) showed that NSAIDs increase the risk of fatal peptic ulcers by nearly fivefold in older adults; other studies have shown that the risk of peptic ulcer complications is increased by three- to fivefold in older adults using NSAIDs. This risk is much more pronounced in those taking concomitant systemic corticosteroids and warfarin. In addition, the risk is increased as early as within the first month of treatment and is sustained over time. Often, these peptic ulcers are asymptomatic but can lead to significant morbidity and mortality. The evidence for which NSAIDs are less risky is limited. One retrospective cohort study found that celecoxib, as compared to nonselective NSAIDs (ibuprofen, diclofenac, naproxen) carried the least risk of hospitalization for GI bleeding among elderly persons. Of note, all NSAIDs (ie, nonselective and COX-2 selective) carry a boxed warning for adverse GI events. Overall, the rate of hospitalizations for peptic ulcer disease (PUD) increases with age, from 1 per 1000 per year in populations younger than age 50 years to 2-6 per 1000 per year in older adults (> 65 yr), with an estimated 15-35% of all peptic ulcer complications being due to NSAID use.

Renal Risks Associated with Chronic NSAID Use

Similar to NSAID-related GI adverse effects, NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure (ARF). While it is important to recognize that ARF can develop at any point during long-term NSAID therapy, the risk may be highest among those who have recently initiated therapy. Specifically, in a nested case control study of older adults, the risk of ARF was increased nearly twofold for all NSAIDs (nonselective and COX-2 selective NSAIDs) within 30 days of initial use/prescribing. This is consistent with previous studies reporting that NSAIDs increase the risk of ARF in the elderly. This risk is further increased in those older adults with preexisting chronic kidney disease (CKD) and in those who use long half-life NSAIDs. Thus, diligent monitoring of renal function (eg, blood urea nitrogen/serum creatinine to estimate creatinine clearance) is critical in older adults receiving NSAIDs, especially those who are at increased risk. Of note, salsalate may be preferred among the NSAIDs as it is rarely associated with nephrotoxicity. Overall, it is estimated that 2.5 million individuals in the United States experience adverse renal effects from NSAID use annually, with older adults being in the highest-risk group in the population.

CV/Cerebrovascular Risks Associated with Chronic NSAID Use

NSAIDs have been shown to worsen/increase the risk of various CV and cerebrovascular outcomes, with some studies suggesting a greater risk associated with COX-2 selective NSAIDs as compared to nonselective NSAIDs. One retrospective cohort study of older adults showed that naproxen carried the least risk of hospitalization for acute myocardial infarction (MI) among users of aspirin as compared to other nonselective NSAIDs (ibuprofen, diclofenac) and COX-2 selective NSAIDs (celecoxib, rofecoxib) used with aspirin. In contrast, a prospective, population-based cohort study found an increased risk of stroke with the use of nonselective NSAIDs (including naproxen), as well as with COX-2 selective NSAIDs (including celecoxib) in those not taking aspirin. On an individual NSAID analysis, naproxen users were found to have more than a twofold increased risk of stroke. Of note, all NSAIDs (ie, nonselective and COX-2 selective) carry a boxed warning for adverse CV events, including MI and stroke. Further research is needed to confirm individual NSAID adverse CV risk profiles.

One clinical trial of patients with hypertension (HTN) showed that piroxicam and ibuprofen blunted the effects of antihypertensive drugs (lisinopril/hydrochlorothiazide), significantly increasing systolic blood pressure (SBP) by 7.7-9.9%. An acetaminophen (APAP) period (in place of the NSAID) led to a significant decrease in blood pressure toward baseline, and a second exposure to the NSAIDs led to another significant increase in SBP of 7.0-7.7%, adding strong support to the evidence of causality. In addition, a cohort study of community-dwelling elderly individuals

The NSAID should be used at the lowest effective dose for the shortest period of time.

found that those who were taking antihypertensive therapy and NSAIDs had SBPs approximately 5 mmHg higher than those not taking NSAIDs, and were more likely to have SBP higher than 140 mmHg.

NSAIDs have also been shown to cause or exacerbate heart failure (HF) in older adults. Specifically, a cohort study of older adults found that rofecoxib and nonselective NSAIDS (naproxen, ibuprofen, and diclofenac), but not celecoxib, were significantly associated with an increased risk of admission for HF as compared to those not taking NSAIDs. In contrast, another cohort study found that among patients who had survived their first hospitalization because of HF, subsequent use of any NSAID (including celecoxib, as well as ibuprofen, diclofenac, naproxen, and other NSAIDs) led to a significantly increased risk of death.

Finally, an important point of clinical debate is the interaction between low-dose, cardioprotective aspirin and NSAIDs potentially interfering with the antiplatelet effect of aspirin. The American Geriatrics Society recommends avoiding the coadministration of aspirin and ibuprofen based on a 2006 Food and Drug Administration warning. However, it is important to recognize that evidence suggests that this warning should also apply to naproxen, but not celecoxib.

CNS Risks Associated with Chronic NSAID Use

NSAID use has been shown to be associated with a number of CNS effects including aseptic meningitis, psychosis, and cognitive dysfunction. This latter point may seem to be inaccurate, but the literature suggests otherwise. At the time of this writing, the studies to date have not consistently shown a benefit from chronic NSAID use in reducing the risk of dementia or cognitive impairment. Interestingly, though, several studies have shown that high-dose NSAIDs (ie, anti-inflammatory doses) may actually increase the risk of cognitive impairment. In particular, indomethacin appears to cause more CNS effects than other NSAIDs in the elderly.

What Should Clinicians Do to Avoid/Minimize ADRs Associated with Chronic NSAID Use in Older Adults?

One approach to reducing ADRs associated with NSAIDs is to avoid the use of specific agents and use preferred alternative analgesics ( Table). This is particularly important in those older adults with preexisting HTN, CKD, HF, and/or PUD, or those taking concomitant warfarin or corticosteroids. An alternative option would be to use APAP, which has been shown to be equally effective to NSAIDs in a number of studies of patients with mild-to-moderate osteoarthritis pain. Of note, patients who say that APAP does not work for them may not have used an optimal dose (3-4 g/day in divided doses for at least 2 wk), which would be required in order to show a lack of effectiveness. If APAP does not work and NSAID use is not contraindicated, a trial of analgesic dosing of a nonacetylated salicylate (eg, salsalate) or ibuprofen or celecoxib may be acceptable. For those with moderate-to-moderately severe osteoarthritis pain, a trial of a low-dose opioid or opioid-like agent (eg, codeine, tramadol) in combination with APAP is another option. The rationale for this approach is to combine two different mechanisms of analgesic action. In those elderly persons who require chronic NSAIDs, a proton pump inhibitor or misoprostol should be used to avoid the risk of PUD. In general, long half-life NSAIDs (eg, naproxen, oxaprozin, piroxicam) and specific other NSAIDs (eg, indomethacin, ketorolac) should be avoided because their risk outweighs their potential benefits.

Table.

Drug

Initial Dosing

Special Considerations in Older Adults

APAP

325-500 mg every 4 h or
500-1000 mg every 6 h; maximum
daily dose of 4000 mg

Does not interfere with platelet function; reduce maximum dose 50% to 75% in
patients with hepatic insufficiency or history of alcohol abuse

Celecoxib

100 mg daily

Higher doses associated with higher incidence of GI and CV side effects;
patients with indications for cardioprotection require aspirin

Ibuprofen

200 mg 3-4 times/day; maximum
daily dose of 3200 mg

Risk of GI bleeding increased in persons > 75 yr; misoprostol or PPI should be prescribed for long-term users

Salsalate

500-750 mg every 12 h; maximum
daily dose of 3000 mg

Does not interfere with platelet function; GI bleeding and nephrotoxicity are rare

Moderate-to-Moderately Severe Pain

APAP/Codeine

325/30 mg every 6 h; maximum
daily dose of 12 tablets

Monitor for constipation, confusion, and falls; same considerations for APAP as
listed above

APAP/Tramadol

325/37.5 mg every 6 h; maximum
daily dose of 8 tablets

Renally adjusted dose when estimated creatinine clearance < 30 mL/min:
maximum of 2 tablets every 12 h; treatment should not exceed 5 days; same
considerations for APAP as listed above

Conclusion

This review has summarized the potential risks associated with chronic NSAID use in older adults, including GI, renal, CV/cerebrovascular, and CNS adverse effects. Although only ADRs affecting these four organ systems were discussed in this review, it is important to recognize that NSAIDs can cause various other adverse effects (eg, hepatotoxicity, cutaneous toxicity). Moreover, it is important to note that nonpharmacological approaches (weight reduction, increasing physical activity) may also help patients who are experiencing musculoskeletal pain. For patients already taking NSAIDS chronically, healthcare providers should assess whether the patient could switch to APAP or salsalate. If the patient still requires a NSAID, GI prophylaxis should be considered in all older patients, especially those with other risk factors; importantly, the NSAID should be used at the lowest effective dose for the shortest period of time.

As the aging population rapidly grows over the next few decades, the risks associated with chronic NSAID use will remain an important public health issue. Hopefully, health-care providers armed with the above information who carefully and consistently monitor chronic NSAID use in their older patients will avoid these preventable complications.

Acknowledgments

The writing of this paper was supported by National Institute on Aging grants (R01AG027017, P30AG024827, T32 AG021885, K07AG033174, R01AG034056), a National Institute of Mental Health grant (R34 MH082682), a National Institute of Nursing Research grant (R01 NR010135), and an Agency for Healthcare Research and Quality grant (R01 HS017695).

Footnotes

The authors report no relevant financial relationships.

References

6. Hanlon JT, Guay DRP, Ives TJ. Oral analgesics: efficacy, mechanism of action, pharmacokinetics, adverse effects, and practical recommendations for use in older adults. In: Gibson SJ, Weiner DK, editors. Pain in Older Persons. IASP Press; Seattle, WA: 2005. pp. 205-222. [Google Scholar]

8. Shorr RI, Ray WA, Daugherty JR, Griffin MR. Concurrent use of nonsteroidal anti-inflammatory drugs and oral anticoagulants places elderly persons at high risk for hemorrhagic peptic ulcer disease. Arch Intern Med. 1993;153(14):1665-1670. [PubMed] [Google Scholar]

21. Pavlicević I, Kuzmanić M, Rumboldt M, Rumboldt Z. Interaction between antihypertensives and NSAIDs in primary care: A controlled trial. Can J Clin Pharmacol. 2008;15(3):e372-e382. Published Online: October 24, 2008. [PubMed] [Google Scholar]

26. Saag KG, Rubenstein LM, Chrischilles EA, Wallace RB. Nonsteroidal antiinflammatory drugs and cognitive decline in the elderly. J Rheumatol. 1995;22(11):2142-2147. [PubMed] [Google Scholar]

# data[].attributes.attachment_link.title
Recognizing the Risks of Chronic Nonsteroidal Anti-Inflammatory Drug Use in Older Adults

# data[].attributes.attachment_link.description
Older adults commonly take nonsteroidal anti-inflammatory drugs (NSAIDs) chronically. Studies of older adults show that chronic NSAID use increases the risk of peptic ulcer disease, acute renal failure, and stroke/myocardial infarction. Moreover, ...

# data[].attributes.body
Similar to NSAID-related GI adverse effects, NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure (ARF).

# data[].attributes.attachment_link.readable_text
. Author manuscript; available in PMC: 2011 Aug 19.

Published in final edited form as: Ann Longterm Care. 2010;18(9):24-27.

Abstract

Older adults commonly take nonsteroidal anti-inflammatory drugs (NSAIDs) chronically. Studies of older adults show that chronic NSAID use increases the risk of peptic ulcer disease, acute renal failure, and stroke/myocardial infarction. Moreover, chronic NSAID use can exacerbate a number of chronic diseases including heart failure and hypertension, and can interact with a number of drugs (eg, warfarin, corticosteroids). Preferred analgesics in older adults that may have a lower risk of these adverse drug reactions include acetaminophen, a nonacetylated salicylate (eg, salsalate), a short half-life NSAID (eg, ibuprofen), or low-dose opioid/opioid-like agents in combination with acetaminophen (in appropriate patients).

Introduction

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a common class of analgesics used chronically for persistent pain due to osteoarthritis and other musculoskeletal disorders in older adults. Specifically, an estimated 40% of people age 65 years and older fill one or more prescriptions for a NSAID each year. Considering that NSAIDs are also currently available over the counter, it is clear to see that even larger numbers of older adults are exposed to NSAIDs in the United States.

While these agents can be effective in treating inflammation and pain, older adults are at increased risk for adverse drug reactions (ADRs) due to age-related loss of physiological organ reserve, increased comorbidities, polypharmacy, and changes in pharmacokinetics. As a result, NSAID use causes an estimated 41,000 hospitalizations and 3300 deaths each year among older adults. Some specific ADRs of concern with chronic use of NSAIDs include gastrointestinal (GI), renal, cardiovascular (CV), cerebrovascular, and central nervous system (CNS) adverse effects. This review will begin by describing key evidence for these organ-specific ADRs associated with the chronic use of NSAIDs in older adults and finish with general recommendations for healthcare providers to avoid/minimize these ADRs.

GI Risks Associated with Chronic NSAID Use

The spectrum of potential NSAID-related GI adverse effects is wide, ranging from dyspepsia to life-threatening gastric bleeding. A nested case control study from nearly two decades ago (before the introduction of cyclooxygenase-2 [COX-2] selective NSAIDs) showed that NSAIDs increase the risk of fatal peptic ulcers by nearly fivefold in older adults; other studies have shown that the risk of peptic ulcer complications is increased by three- to fivefold in older adults using NSAIDs. This risk is much more pronounced in those taking concomitant systemic corticosteroids and warfarin. In addition, the risk is increased as early as within the first month of treatment and is sustained over time. Often, these peptic ulcers are asymptomatic but can lead to significant morbidity and mortality. The evidence for which NSAIDs are less risky is limited. One retrospective cohort study found that celecoxib, as compared to nonselective NSAIDs (ibuprofen, diclofenac, naproxen) carried the least risk of hospitalization for GI bleeding among elderly persons. Of note, all NSAIDs (ie, nonselective and COX-2 selective) carry a boxed warning for adverse GI events. Overall, the rate of hospitalizations for peptic ulcer disease (PUD) increases with age, from 1 per 1000 per year in populations younger than age 50 years to 2-6 per 1000 per year in older adults (> 65 yr), with an estimated 15-35% of all peptic ulcer complications being due to NSAID use.

Renal Risks Associated with Chronic NSAID Use

Similar to NSAID-related GI adverse effects, NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure (ARF). While it is important to recognize that ARF can develop at any point during long-term NSAID therapy, the risk may be highest among those who have recently initiated therapy. Specifically, in a nested case control study of older adults, the risk of ARF was increased nearly twofold for all NSAIDs (nonselective and COX-2 selective NSAIDs) within 30 days of initial use/prescribing. This is consistent with previous studies reporting that NSAIDs increase the risk of ARF in the elderly. This risk is further increased in those older adults with preexisting chronic kidney disease (CKD) and in those who use long half-life NSAIDs. Thus, diligent monitoring of renal function (eg, blood urea nitrogen/serum creatinine to estimate creatinine clearance) is critical in older adults receiving NSAIDs, especially those who are at increased risk. Of note, salsalate may be preferred among the NSAIDs as it is rarely associated with nephrotoxicity. Overall, it is estimated that 2.5 million individuals in the United States experience adverse renal effects from NSAID use annually, with older adults being in the highest-risk group in the population.

CV/Cerebrovascular Risks Associated with Chronic NSAID Use

NSAIDs have been shown to worsen/increase the risk of various CV and cerebrovascular outcomes, with some studies suggesting a greater risk associated with COX-2 selective NSAIDs as compared to nonselective NSAIDs. One retrospective cohort study of older adults showed that naproxen carried the least risk of hospitalization for acute myocardial infarction (MI) among users of aspirin as compared to other nonselective NSAIDs (ibuprofen, diclofenac) and COX-2 selective NSAIDs (celecoxib, rofecoxib) used with aspirin. In contrast, a prospective, population-based cohort study found an increased risk of stroke with the use of nonselective NSAIDs (including naproxen), as well as with COX-2 selective NSAIDs (including celecoxib) in those not taking aspirin. On an individual NSAID analysis, naproxen users were found to have more than a twofold increased risk of stroke. Of note, all NSAIDs (ie, nonselective and COX-2 selective) carry a boxed warning for adverse CV events, including MI and stroke. Further research is needed to confirm individual NSAID adverse CV risk profiles.

One clinical trial of patients with hypertension (HTN) showed that piroxicam and ibuprofen blunted the effects of antihypertensive drugs (lisinopril/hydrochlorothiazide), significantly increasing systolic blood pressure (SBP) by 7.7-9.9%. An acetaminophen (APAP) period (in place of the NSAID) led to a significant decrease in blood pressure toward baseline, and a second exposure to the NSAIDs led to another significant increase in SBP of 7.0-7.7%, adding strong support to the evidence of causality. In addition, a cohort study of community-dwelling elderly individuals

The NSAID should be used at the lowest effective dose for the shortest period of time.

found that those who were taking antihypertensive therapy and NSAIDs had SBPs approximately 5 mmHg higher than those not taking NSAIDs, and were more likely to have SBP higher than 140 mmHg.

NSAIDs have also been shown to cause or exacerbate heart failure (HF) in older adults. Specifically, a cohort study of older adults found that rofecoxib and nonselective NSAIDS (naproxen, ibuprofen, and diclofenac), but not celecoxib, were significantly associated with an increased risk of admission for HF as compared to those not taking NSAIDs. In contrast, another cohort study found that among patients who had survived their first hospitalization because of HF, subsequent use of any NSAID (including celecoxib, as well as ibuprofen, diclofenac, naproxen, and other NSAIDs) led to a significantly increased risk of death.

Finally, an important point of clinical debate is the interaction between low-dose, cardioprotective aspirin and NSAIDs potentially interfering with the antiplatelet effect of aspirin. The American Geriatrics Society recommends avoiding the coadministration of aspirin and ibuprofen based on a 2006 Food and Drug Administration warning. However, it is important to recognize that evidence suggests that this warning should also apply to naproxen, but not celecoxib.

CNS Risks Associated with Chronic NSAID Use

NSAID use has been shown to be associated with a number of CNS effects including aseptic meningitis, psychosis, and cognitive dysfunction. This latter point may seem to be inaccurate, but the literature suggests otherwise. At the time of this writing, the studies to date have not consistently shown a benefit from chronic NSAID use in reducing the risk of dementia or cognitive impairment. Interestingly, though, several studies have shown that high-dose NSAIDs (ie, anti-inflammatory doses) may actually increase the risk of cognitive impairment. In particular, indomethacin appears to cause more CNS effects than other NSAIDs in the elderly.

What Should Clinicians Do to Avoid/Minimize ADRs Associated with Chronic NSAID Use in Older Adults?

One approach to reducing ADRs associated with NSAIDs is to avoid the use of specific agents and use preferred alternative analgesics ( Table). This is particularly important in those older adults with preexisting HTN, CKD, HF, and/or PUD, or those taking concomitant warfarin or corticosteroids. An alternative option would be to use APAP, which has been shown to be equally effective to NSAIDs in a number of studies of patients with mild-to-moderate osteoarthritis pain. Of note, patients who say that APAP does not work for them may not have used an optimal dose (3-4 g/day in divided doses for at least 2 wk), which would be required in order to show a lack of effectiveness. If APAP does not work and NSAID use is not contraindicated, a trial of analgesic dosing of a nonacetylated salicylate (eg, salsalate) or ibuprofen or celecoxib may be acceptable. For those with moderate-to-moderately severe osteoarthritis pain, a trial of a low-dose opioid or opioid-like agent (eg, codeine, tramadol) in combination with APAP is another option. The rationale for this approach is to combine two different mechanisms of analgesic action. In those elderly persons who require chronic NSAIDs, a proton pump inhibitor or misoprostol should be used to avoid the risk of PUD. In general, long half-life NSAIDs (eg, naproxen, oxaprozin, piroxicam) and specific other NSAIDs (eg, indomethacin, ketorolac) should be avoided because their risk outweighs their potential benefits.

Table.

Drug

Initial Dosing

Special Considerations in Older Adults

APAP

325-500 mg every 4 h or
500-1000 mg every 6 h; maximum
daily dose of 4000 mg

Does not interfere with platelet function; reduce maximum dose 50% to 75% in
patients with hepatic insufficiency or history of alcohol abuse

Celecoxib

100 mg daily

Higher doses associated with higher incidence of GI and CV side effects;
patients with indications for cardioprotection require aspirin

Ibuprofen

200 mg 3-4 times/day; maximum
daily dose of 3200 mg

Risk of GI bleeding increased in persons > 75 yr; misoprostol or PPI should be prescribed for long-term users

Salsalate

500-750 mg every 12 h; maximum
daily dose of 3000 mg

Does not interfere with platelet function; GI bleeding and nephrotoxicity are rare

Moderate-to-Moderately Severe Pain

APAP/Codeine

325/30 mg every 6 h; maximum
daily dose of 12 tablets

Monitor for constipation, confusion, and falls; same considerations for APAP as
listed above

APAP/Tramadol

325/37.5 mg every 6 h; maximum
daily dose of 8 tablets

Renally adjusted dose when estimated creatinine clearance < 30 mL/min:
maximum of 2 tablets every 12 h; treatment should not exceed 5 days; same
considerations for APAP as listed above

Conclusion

This review has summarized the potential risks associated with chronic NSAID use in older adults, including GI, renal, CV/cerebrovascular, and CNS adverse effects. Although only ADRs affecting these four organ systems were discussed in this review, it is important to recognize that NSAIDs can cause various other adverse effects (eg, hepatotoxicity, cutaneous toxicity). Moreover, it is important to note that nonpharmacological approaches (weight reduction, increasing physical activity) may also help patients who are experiencing musculoskeletal pain. For patients already taking NSAIDS chronically, healthcare providers should assess whether the patient could switch to APAP or salsalate. If the patient still requires a NSAID, GI prophylaxis should be considered in all older patients, especially those with other risk factors; importantly, the NSAID should be used at the lowest effective dose for the shortest period of time.

As the aging population rapidly grows over the next few decades, the risks associated with chronic NSAID use will remain an important public health issue. Hopefully, health-care providers armed with the above information who carefully and consistently monitor chronic NSAID use in their older patients will avoid these preventable complications.

Acknowledgments

The writing of this paper was supported by National Institute on Aging grants (R01AG027017, P30AG024827, T32 AG021885, K07AG033174, R01AG034056), a National Institute of Mental Health grant (R34 MH082682), a National Institute of Nursing Research grant (R01 NR010135), and an Agency for Healthcare Research and Quality grant (R01 HS017695).

Footnotes

The authors report no relevant financial relationships.

References

6. Hanlon JT, Guay DRP, Ives TJ. Oral analgesics: efficacy, mechanism of action, pharmacokinetics, adverse effects, and practical recommendations for use in older adults. In: Gibson SJ, Weiner DK, editors. Pain in Older Persons. IASP Press; Seattle, WA: 2005. pp. 205-222. [Google Scholar]

8. Shorr RI, Ray WA, Daugherty JR, Griffin MR. Concurrent use of nonsteroidal anti-inflammatory drugs and oral anticoagulants places elderly persons at high risk for hemorrhagic peptic ulcer disease. Arch Intern Med. 1993;153(14):1665-1670. [PubMed] [Google Scholar]

21. Pavlicević I, Kuzmanić M, Rumboldt M, Rumboldt Z. Interaction between antihypertensives and NSAIDs in primary care: A controlled trial. Can J Clin Pharmacol. 2008;15(3):e372-e382. Published Online: October 24, 2008. [PubMed] [Google Scholar]

26. Saag KG, Rubenstein LM, Chrischilles EA, Wallace RB. Nonsteroidal antiinflammatory drugs and cognitive decline in the elderly. J Rheumatol. 1995;22(11):2142-2147. [PubMed] [Google Scholar]

# data[].attributes.attachment_link.title
Recognizing the Risks of Chronic Nonsteroidal Anti-Inflammatory Drug Use in Older Adults

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Older adults commonly take nonsteroidal anti-inflammatory drugs (NSAIDs) chronically. Studies of older adults show that chronic NSAID use increases the risk of peptic ulcer disease, acute renal failure, and stroke/myocardial infarction. Moreover, ...

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Peptic ulcer disease (PUD), if not diagnosed and treated promptly, can lead to serious complications. Following complications can occur in PUD:

Upper gastrointestinal bleeding

Gastric outlet obstruction

Perforation

Penetration

Gastric cancer

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Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve the lower esophagus, distal duodenum, or jejunum. Epigastric pain usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer; on the other hand, the pain with a duodenal ulcer tends to occur 2-3 hours after a meal. Today, testing for Helicobacter pylori is recommended in all patients with peptic ulcer disease. Endoscopy may be required in some patients to confirm the diagnosis, especially in those patients with sinister symptoms. Today, most patients can be managed with a proton pump inhibitor (PPI) based triple-drug therapy.

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1. Gastrointestinal (GI) Protection

Naproxen is a non-selective NSAID, which means it inhibits both COX-1 and COX-2 enzymes.

COX-1 protects the stomach lining, so blocking it can lead to stomach ulcers, bleeding, or gastritis.

Celecoxib is a COX-2 selective inhibitor, so it's gentler on the stomach and often preferred in patients with a history of GI issues.

2. Cardiovascular Risk

In some cases, celecoxib might be preferred if naproxen worsens blood pressure control or interacts with cardiovascular meds.

3. Chronic Pain Management

Celecoxib is often prescribed for chronic conditions like osteoarthritis or rheumatoid arthritis where long-term NSAID use is needed — again, due to its better GI tolerability.

It also has a longer half-life, so can be taken once daily in some cases.

Dose for celecoxib for osteoarthritis:

200 mg OD or 100 mg BD or PRN

References:

https://pmc.ncbi.nlm.nih.gov/articles/PMC11160842/#:~:text=Results:,inhibition%20(p%3C0.05).

https://www.mims.com/malaysia/drug/info/celebrex/dosage

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Degree of Cyclooxygenase-2 Inhibition Modulates Blood Pressure Response to Celecoxib and Naproxen

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Non-steroidal anti-inflammatory drugs (NSAIDs) increase the risk of adverse cardiovascular events via suppression of cyclooxygenase (COX)-2-derived prostacyclin (PGI2) formation in heart, vasculature, and kidney. The Prospective Randomized…

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Monitoring Therapy Effectiveness:

Symptom Relief: Monitor for relief of epigastric pain, heartburn, and nausea.

Melena: Check for dark stools and monitor hemoglobin levels if anemia is present.

H. pylori Eradication: Evaluate effectiveness 4 weeks after therapy.

Urea Breath Test (Gold Standard) and Stool Antigen Test (Alternative).

Avoid PPIs before testing to prevent false negatives.

Managing Side Effects of Therapy:

H. pylori Eradication Regimen (e.g., PPI + 2 antibiotics):

Diarrhea/Nausea: Common with antibiotics like clarithromycin and amoxicillin; consider probiotics for relief.

Metallic Taste: Associated with bismuth subsalicylate; typically temporary.

Drug Interactions:

Clarithromycin + Statins: Increases myopathy risk.

Long-Term PPI Use: Risk of hypomagnesemia, osteoporosis, and Clostridium difficile infection (C. diff).

PPI -> Reduce absorption of atorvastatin (monitor LDL), iron, B12, magnesium (long-term risk

Celecoxib (COX-2 inhibitor):

Lower ulcer risk compared to naproxen but increases cardiovascular risk; monitor blood pressure.

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Pharmacists play an integral role in the management of patients with PUD. They are in a unique position to provide patient education and management of risk factors associated with peptic ulcer development and recurrence. Patients should be encouraged to abstain from smoking and alcohol consumption, and smoking cessation therapy should be offered when appropriate. Pharmacists can work within the health care team to make recommendations for appropriate NSAID use and recognize patients at risk for ulcer complications. Further, through review of medication histories, pharmacists can identify previous antimicrobial exposure that could increase the likelihood of H pylori resistance. Patients must be made aware that a number of OTC medications and herbal products contain NSAIDs, and that they should consult their health care provider prior to taking these medications. Additional patient education emphasizing the importance of adherence and counseling on proper administration of drug therapy is an essential component for treatment success.

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First-line treatment for H. pylori-induced PUD is a triple regimen comprising two antibiotics and a proton pump inhibitor. Pantoprazole, clarithromycin, and metronidazole, or amoxicillin are used for 7 to 14 days. Antibiotics and PPIs work synergistically to eradicate H. pylori. The antibiotic selected should take into consideration the presence of antibiotic resistance in the environment. If first-line therapy fails, quadruple therapy with bismuth and different antibiotics is used.

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General Types of Peptic Ulcer Disease (PUD)

1. NSAID-Induced Ulcer

Caused by long-term use of NSAIDs (e.g. naproxen, ibuprofen)

Often asymptomatic until complications arise

Occurs in stomach or duodenum

More common in older adults or those on steroids

2. H. pylori-Associated Ulcer

Caused by Helicobacter pylori infection

Chronic inflammation weakens mucosal lining → ulceration

Typically affects duodenum > stomach

3. Stress-Related Ulcer

Seen in critically ill patients (e.g. ICU, severe trauma)

Due to hypoperfusion and acid hypersecretion

4. Zollinger-Ellison Syndrome

Rare — due to gastrin-secreting tumor → excessive acid

Leads to recurrent or multiple ulcers

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Why Gaviscon Did Not Provide Adequate Relief in RB’s Case:

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Why Gaviscon Did Not Provide Adequate Relief in RB’s Case:

# data[].attributes.body
1.Severity of Condition:

RB likely has severe peptic ulcer (evidenced by bleeding, melena, and positive FOBT).

Antacids like Gaviscon are typically effective for mild or occasional heartburn, not for active ulcers or severe gastric inflammation.

2. NSAID-Induced Mucosal Damage:

RB was taking Naproxen (an NSAID), which inhibits COX-1 enzyme.

This leads to reduced prostaglandin synthesis, which is essential for:

Mucosal protection (stimulating mucus and bicarbonate secretion).

Maintaining mucosal blood flow and healing.

Antacids do not repair mucosal injury or reverse prostaglandin inhibition caused by NSAIDs.

3. Rebound Acid Hypersecretion:

Frequent use of antacids may lead to rebound acid hypersecretion.

This occurs when the stomach increases acid production in response to temporary neutralization.

Can potentially worsen symptoms once the effect of the antacid wears off.

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Prevention of Recurrence of Peptic Ulcer & H. pylori Infection

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Prevention of Recurrence of Peptic Ulcer & H. pylori Infection

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1. Address the Underlying Cause

Discontinue NSAIDs (e.g., naproxen) – switched to celecoxib with lower GI risk

Complete H. pylori eradication therapy (e.g., PPI + amoxicillin + clarithromycin for 14 days)

Confirm eradication with urea breath test 4 weeks after treatment

2. Pharmacological Strategy

Avoid long-term PPI use once ulcer is healed and H. pylori is eradicated

If NSAID is still needed, consider PPI co-therapy as gastroprotection

3. Lifestyle Modifications

Stop smoking – RB has a 12-pack-year history; smoking delays ulcer healing

Limit alcohol intake – alcohol irritates gastric mucosa

Avoid trigger foods (e.g., spicy, acidic, fatty foods)

4. Patient Education

Stress the importance of adherence to full H. pylori treatment

Educate on symptoms of recurrence (e.g., melena, epigastric pain)

Advise to avoid self-medicating with NSAIDs

5. Regular Follow-Up

Monitor for symptom recurrence and check healing progress

Reassess ongoing need for celecoxib or any NSAIDs

Encourage reporting of any new GI symptoms promptly

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Aggravating factor and protective factor

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Aggravating factor and protective factor

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1. omeprazole ( 20 mg = 20 OE)

2. pantoprazole ( 20 mg = 4.5 OE)

3. lansoprazole (15 mg = 13.5 OE)

4. esomeprazole (20 mg = 32 mg)

5. rabeprazole (20 mg = 36 mg)

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1. Gastric acid suppression

2. For symptomatic relief

3. Minimize further damages of the stomach inner lining

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1. misoprostol

2. sucralfate

3. bismuth salts ( bismuth subsalicylate)

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Endoscopy with biopsy is more invasive but useful for diagnosing other GI issues and selecting effective antibiotics if first-line treatment fails.

Retesting may be needed if symptoms persist or based on initial findings.

Medication interference: Antibiotics, PPIs, bismuth, and possibly H2 blockers can affect test accuracy.

Stop antibiotics ≥4 weeks and PPIs/bismuth ≥2 weeks before testing if possible.

Post-treatment confirmation of eradication should be done ≥4 weeks after antibiotics using the same diagnostic tests (e.g., urea breath test, stool antigen test).

https://www.racgp.org.au/afp/2014/may/helicobacter-pylori-eradication

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To diagnose peptic ulcer disease (PUD), doctors take a detailed medical history, do a physical exam, and may use medical tests (invasive or non-invasive). Key symptoms include upper stomach pain, feeling full quickly, and fullness after eating.

Pain from gastric ulcers usually starts 15–30 minutes after eating and may lead to weight loss.

Pain from duodenal ulcers often gets better after eating and may lead to weight gain.

If a patient has anemia, black stools (melena), vomiting blood (hematemesis), or weight loss, doctors will check for serious problems like bleeding, a hole in the stomach or intestine (perforation), or cancer. On physical exam, there may be tenderness in the upper stomach and signs of anemia.

Investigations for Peptic Ulcer Disease (PUD)

1. Esophagogastroduodenoscopy (EGD)

Most accurate test (90% sensitivity/specificity)

Recommended for:
• Patients over 50 with new symptoms
• Anyone with alarm signs

2. Barium Swallow

Used if EGD isn’t possible

3. Blood Tests

Includes:
• Complete Blood Count (CBC)
• Liver Function Tests (LFTs)
• Amylase and Lipase

4. Serum Gastrin

Ordered if Zollinger-Ellison syndrome is suspected

5. H. pylori Testing

Urea Breath Test – accurate, used to confirm eradication

Rapid Urease Test – typically done during endoscopy

Stool Antigen Test

Serology, Urine, and Antibody Tests

6. Endoscopic Biopsy

Used when:
• Treatment fails
• Resistance is suspected

Taking samples from 4–6 sites improves accuracy

7. CT Scan (with Contrast)

Not used to directly diagnose ulcers

Helpful for detecting complications like:
• Perforation
• Obstruction

8. Fecal Occult Blood Test (FOBT)

Detects hidden (occult) blood in the stool

Used to screen for:
• Colorectal cancer
• Other sources of GI bleeding

Two main types:
• Guaiac-based FOBT (gFOBT)
• Fecal Immunochemical Test (FIT)

References:

https://www.ncbi.nlm.nih.gov/books/NBK534792/#:~:text=Evaluation,be%20evaluated%20by%20an%20EGD.

https://medlineplus.gov/lab-tests/fecal-occult-blood-test-fobt/#:~:text=What%20is%20a%20fecal%20occult,cancer%20before%20you%20have%20symptoms.

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Oral-Oral Transmission
→ H. pylori can be transmitted through saliva, especially when sharing utensils or cups.
→ Risk increases when personal hygiene is poor.

Fecal-Oral Route
→ H. pylori spreads through the fecal-oral route when hands are not washed after using the toilet.
→ Contaminated food, water, or hands can lead to infection.

Contaminated Food or Water
→ Consuming food or drinks from unhygienic sources increases infection risk, especially with unsafe water supplies or poorly prepared street food.

Poor Socioeconomic Conditions
→ Lack of access to clean water and sanitation increases infection rates, especially in childhood.

Family History of H. pylori
→ Having a family member with H. pylori infection increases the likelihood of transmission due to shared living and hygiene practices.

Low Immune Function
→ Individuals with weakened immune systems, such as the elderly, malnourished, or those on immunosuppressive therapy (e.g., prednisolone), are more vulnerable to chronic H. pylori infection.

https://pmc.ncbi.nlm.nih.gov/articles/PMC3561889/#:~:text=Seroepidemiological%20studies%20and%20endoscopic%20surveys,%25%20(1%E2%80%935).

# data[].attributes.attachment_link.title
Prevalence and Ethnic Distribution of Helicobacter Pylori Infection Among Endoscoped Patients in North Eastern Peninsular Malaysia

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The objective of this study was to determine the prevalence and ethnic distribution of Helicobacter pylori infection in an endoscoped population in North Eastern Peninsular Malaysia. Pathology records of 400 consecutive gastric biopsies received at…

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1. Relieve Symptoms of Ulcer and Dyspepsia

Alleviate epigastric pain, heartburn, nausea, and dysphagia

Improve quality of life and reduce discomfort

These symptoms directly affect quality of life and may worsen if untreated. Pain relief is often the first thing patients look for in PUD.

Outcome: Improved comfort, reduced episodes of pain, and better sleep quality, which all contribute to recovery.

MOH Malaysia Dyspepsia CPG (2020): Symptom relief is one of the primary endpoints in PUD therapy.

2. Eradicate Helicobacter pylori Infection

A important goal to cure H. pylori-induced ulcers and prevent recurrence and reducing the risk of gastric cancer.

H. pylori is responsible for most peptic ulcers, and if not eradicated, ulcers are likely to recur.

Outcome: Successful eradication of H. pylori within 14 days, leading to reduced ulcer recurrence and decreased gastric cancer risk.

NCBI – “H. pylori eradication promotes ulcer healing and prevents recurrence.” [PMID: 35405147]
NIH – “Without eradication, recurrence rates are as high as 70–90% within one year.”

3. Promote Healing of Gastric Mucosa

Facilitate the repair of the gastric or duodenal mucosa affected by the ulcer.

Reduce acid secretion using proton pump inhibitors (PPIs) to allow mucosa to regenerate.

Outcome: Complete healing of the ulcer over 4-8 weeks, depending on severity.

4. Prevent Recurrence and Complications

Minimize the risk of future ulcer formation in the patient.

Even after treatment, ulcers can recur if contributing factors (like NSAID use or ongoing H. pylori infection) are not addressed.

Prevent complications such as:

Upper GI bleeding

Gastric perforation

Gastric outlet obstruction

Outcome: Lower risk of future ulcers and improved long-term gastric health and minimise life-threatening complications, particularly bleeding or perforation.

5. Address Modifiable Risk Factors

Eliminate or reduce lifestyle factors that worsen ulcer healing and increase the risk of ulcer recurrence. Such as:

Stopping NSAIDs (or substitute with celecoxib + PPI)

Discontinue alcohol

Encourage smoking cessation

Manage stress, weight, and diet

Outcome: Improved healing rates, reduced risk of ulcer recurrence, and better overall gastric health.