NSAID Gastropathy: Difference between revisions

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<div class="noeditbox">Welcome to [[Pathophysiology of Complex Patient Problems|PT 635 Pathophysiology of Complex Patient Problems]] This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!</div><div class="editorbox">
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'''Original Editors '''- Amanda Huber &amp; Emily Sipe&nbsp;[[Pathophysiology of Complex Patient Problems|&nbsp;from Bellarmine University's&nbsp;Pathophysiology of Complex Patient Problems project.]]  
'''Original Editors '''- Amanda Huber &amp; Emily Sipe[[Pathophysiology of Complex Patient Problems|&nbsp;from Bellarmine University's&nbsp;Pathophysiology of Complex Patient Problems project.]]  


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== Definition/Description  ==
== Introduction ==
<nowiki/>[[File:Gastropathy.jpeg|right|frameless]]Nonsteroidal anti-inflammatory drugs ([[NSAIDs]]) are the most highly prescribed drugs in the world. Their analgesic, anti-inflammatory, and antipyretic actions may be beneficial; however, they are associated with severe side effects including gastrointestinal injury and peptic ulceration. Though several approaches for limiting these side effects have been adopted, like the use of COX-2 specific drugs, co-medication of acid suppressants like proton pump inhibitors and prostaglandin analogs, these alternatives have limitations in terms of efficacy and cardiovascular effects side effects.<ref name=":0">Sinha M, Gautam L, Shukla PK, Kaur P, Sharma S, Singh TP. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3610380/ Current perspectives in NSAID-induced gastropathy. Mediators of inflammation]. 2013 Oct;2013.Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3610380/<nowiki/>(accessed 1.11.2021)</ref>


<references />
== Current Therapies for Prevention of Gastric Damage ==
Several approaches have been adopted for addressing the prevention and cure of the possible side-effects produced by the NSAIDs in the gut.


'''What is an NSAID? Nonsteroidal Anti-inflammatory drug.'''
* Some of these strategies are routinely prescribed to the patients administering NSAIDs.
* Presently, the most common protective strategies adopted are: combination therapy of NSAIDs with gastroprotective agents and; use of selective COX-2 inhibitors.<ref name=":0" />


==== ====
== Gastrointestinal Effects ==
[[File:GI normal.jpeg|right|frameless]]
The use of NSAIDs is associated with gastrointestinal toxicity, affecting both upper gastrointestinal tract (peptic ulcer disease) and lower gastrointestinal tract (NSAID-induced enteropathy). NSAIDs use has been associated with an increased risk of clinical relapse in inflammatory bowel disease patients. <ref>Hijos-Mallada G, Sostres C, Gomollón F. [https://pubmed.ncbi.nlm.nih.gov/34157367/ NSAIDs, gastrointestinal toxicity and Inflammatory Bowel Disease]. Gastroenterologia y Hepatologia. 2021 Jun 19.Available: https://pubmed.ncbi.nlm.nih.gov/34157367/<nowiki/>(accessed 1.11.2021)</ref>
* Some 10%-50% of patients are unable to tolerate NSAID treatment because of side effects, including abdominal pain, diarrhea, and upset stomach.
* Approximately 15% of patients on long-term NSAID treatment develop a peptic ulcer (ulceration of the stomach or duodenum).
* Even though many of these patients with ulcers do not have symptoms and are unaware of their ulcers, they are at risk of developing serious ulcer complications such as bleeding or perforation of the stomach<ref name=":0" />.<br>


*“Despite well known complications, oral nonsteroidal anti-inflammatory drugs (NSAIDs) remain the most commonly prescribed medications in the US for musculoskeletal disorders such as osteoarthritis”&nbsp; <ref name="Roth">Roth S. Coming to terms with nonsteroidal anti-inflammatory drug gastropathy. Drugs(2012, May 7), 72(7): 873-879.</ref>  
== How do they effect the Gut ==
*NSAIDs are prescribed to decrease pain and inflammation.
NSAIDs work by stopping the production of prostaglandins (which promote [[Inflammation Acute and Chronic|inflammation]], pain, and fever), they do this do this by blocking cyclooxygenases (COX) enzymes. These [[enzymes]] produce prostaglandins, yet they also protect your stomach and intestinal lining. This is why NSAIDs can damage your gut. <ref name=":1">AMD [https://www.amymyersmd.com/article/nsaids-harm-gut/ 6 Reasons NSAIDs Are Harmful To Your Gut] Available: https://www.amymyersmd.com/article/nsaids-harm-gut/<nowiki/>(accessed 1.11.21)</ref>


<br>
Examples of NSAIDS Impact on Gut Health


'''What medications are NSAIDs?&nbsp;<ref name="Lanza">Lanza F. A guideline for the treatment and prevention of NSAID-induced ulcers. Members of the Ad Hoc Committee on Practice Parameters of the American College of Gastroenterology. The American Journal Of Gastroenterology. (1998, Nov), 93(11): 2037-2046.</ref>'''
1. Bacterial Imbalance: Recent research suggest that changes in the [[Gut Brain Axis (GBA)|gut microbiome]] balance are brought on by these medications. Studies show that the combination of medications you ingest are reflected in the types of bacteria that populate your gut. Scientists believe that each type of NSAID can affect different [[Bacterial Infections|bacteria]] in the gut, causing a different imbalance depending on which one you take. Because each person’s gut microbiome is unique, the effects may vary significantly from one person to another.


====  ====
2. Digestive Discomfort: The most commonly reported side effects of NSAID use are gastrointestinal symptoms, including gas, feeling bloated, stomach pain, constipation and diarrhea because they disrupt the enzymes that protect your gut lining. One study showed that diarrhea due to NSAID use could last for up to six days after their use.


*Ketorolac
3. Heartburn/[[Gastroesophageal Reflux Disease|GERD]]
*Piroxicam
*Naproxen
*Indomethacin
*Ketoprofen
*Diclofenac
*Ibuprofen
*Nabumetone
*Etodolac
*Oxaprozin
*Aspirin


<br>
4. [[Peptic Ulcers|Gastrointestinal Ulcers]] and Bleeding: approximately 15% of patients who take NSAIDs long-term develop a peptic ulcer. The risk of bleeding ulcers doubles if you take aspirin with other NSAIDs.


NSAID induced gastropathy can result from too high of dosage or too frequent intake of NSAID drugs as well as long-term use. These drugs are used to decrease pain and inflammation and are often taken by those diagnosed with osteoarthritis and rheumatoid arthritis or other musculoskeletal conditions. Doctors often prescribe this drug to these individuals as well as suggest over the counter (OTC) types of NSAIDs. Because of the easy accessibility of these drugs, the incidence rate of NSAID induced gastropathy is high, especially among individuals who are &gt;60 years. <ref name="Lanza" />
5. Leaky Gut: NSAIDS not only cause leaky gut, they can be one of the greatest barriers to recovering from it because they increase your intestinal permeability, which means they make leaky gut worse.


NSAID induced gastropathy can result in stomach or duodenal ulcers which may even lead to death. There are thousands of hospitalizations over each year just from symptoms resulting from NSAID use. Though these rates are high, most individuals do not know the risk of these medications and continue to take them. Also, this induced gastropathy goes on asymptomatically until it is too late and has caused further damage of the gastrointestinal tract. <ref name="Lanza" /><ref name="Roth" />
6. Acute Colitis and [[Autoimmune Disorders|Autoimmune Disease]]: NSAIDs may also set off a chain reaction that leads to conditions such as ulcerative colitis and Crohn’s disease. NSAIDs are associated with hospitalizations for severe colitis in patients with inflammatory bowel disease (IBD), and relapses of IBD. This is due to the inflammation that they cause, as well as the leaky gut, which can let through food particles that are so similar to your body’s own cells that your immune system attacks your body<ref name=":1" />.
== Characteristics/Clinical Presentation ==


“NSAIDs are COX-1 inhibitors which suppress the mucous barrier in the gastrointestinal system which can lead to break down of the GI tract as well as increase in the acidity of the gastric contents.” <ref name="Gigante">Gigante A, Tagarro I. Non-steroidal anti-inflammatory drugs and gastroprotection with proton pump inhibitors: a focus on ketoprofen/omeprazole. Clinical Drug Investigation. (2012, Apr 1),32(4): 221-233.</ref><br>
Up to 50% of NSAID induced gastropathy is asymptomatic.&nbsp;<ref name="Roth">Roth S. Coming to terms with nonsteroidal anti-inflammatory drug gastropathy. Drugs(2012, May 7), 72(7): 873-879.</ref>  
 
== Prevalence  ==
 
*“Patients with rheumatoid arthritis (RA) and osteoarthritis (OA) taking NSAIDs have an ulcer incidence of approximately 15-20%”&nbsp;<ref name="Lanza" />
*“Although a 15-25% incidence of gastric and/or duodenal ulcer has been demonstrated in all patients taking NSAIDs, the bleeding rate is estimated by most experts at only 2-4%”. <ref name="Lanza" />
*1 in 10 NSAID induced ulcer bleeds.&nbsp;<ref name="Lanza" />
*“In elderly patients taking NSAIDs, the relative risk of GI surgery is 10 times, and for GI cause of death, about 4.5 times greater than in control groups”&nbsp;<ref name="Lanza" />
*“Approximately 20 million patients in the US take NSAIDs on a regular basis; the risk for hospitalization for serious GI adverse effects is 1-2%, resulting in approximately 200,000 to 400,000 hospitalizations per year at an average cost of $4,000 per patient, or 0.8-1.6 billion dollars annually”&nbsp;<ref name="Lanza" />
*“An increased risk of GI bleeding has even been noted in patients taking low dose aspirin therapy for cardiovascular prophylaxis”&nbsp;<ref name="Lanza" />
*“Gastric and duodenal lesions were more common in patients who took NSAIDs for &lt;3 months, whereas patients with a longer duration of therapy tended to have more lesions in the small bowel and colon”&nbsp;<ref name="Lanza" />
*“Some recent studies have shown that the incidence of duodenal ulcer is increased in ''Helicobacter pylori''-positive patients taking NSAIDs…It has been recently reported that eradication of ''H.pylori ''before NSAID therapy strikingly reduces the incidence of ulcer disease in patients being treated with naproxen.”&nbsp;<ref name="Lanza" />
*“Among individuals with arthritis, almost 30% report daily use of OTC NSAIDs…Safety often is not considered or well understood among consumers of OTC NSAIDS until after the occurrence of adverse events such as gastropathy” <ref name="Roth" />
 
[[Image:Fig8deaths.jpg|border|center]]
 
== Characteristics/Clinical Presentation  ==
 
Up to 50% of NSAID induced gastropathy is asymptomatic.&nbsp;<ref name="Roth" />  


#Mild dyspepsia  
#Mild dyspepsia  
Line 72: Line 53:
#Exacerbation of existing colon disease
#Exacerbation of existing colon disease


<ref name="Gigante" /><ref name="Roth" /><ref name="Lanza" />
<ref name="Gigante">Gigante A, Tagarro I. Non-steroidal anti-inflammatory drugs and gastroprotection with proton pump inhibitors: a focus on ketoprofen/omeprazole. Clinical Drug Investigation. (2012, Apr 1),32(4): 221-233.</ref><ref name="Roth" /><ref name="Lanza">Lanza F. A guideline for the treatment and prevention of NSAID-induced ulcers. Members of the Ad Hoc Committee on Practice Parameters of the American College of Gastroenterology. The American Journal Of Gastroenterology. (1998, Nov), 93(11): 2037-2046.</ref>  


== Associated Co-morbidities  ==
== Associated Co-morbidities  ==


Osteoarthritis
* [[Osteoarthritis]]
 
* [[Rheumatoid Arthritis]]
Rheumatoid Arthritis
* [[Ankylosing Spondylitis]]
 
* Other musculoskeletal conditions
Ankylosing Spondylitis
* [[Cardiovascular Disease|Cardiovascular]] Complications
 
Other musculoskeletal conditions
 
Cardiovascular Complications
 
== Medications  ==
 
Prostaglandin E1 analog misoprostol can prevent gastric ulcer and duodenal ulcer&nbsp;<ref name="Lanza" />
 
Proton pump inhibitor (PPI) omeprazole reduces gastric ulcer and prevents duodenal ulcer <ref name="Lanza" />. Though PPIs can help with gastric irritation, it is also found that they can induce risk of osteoporosis which often cause hip fractures in elderly patients as well as increase cardiovascular risk due to low serum magnesium levels in the blood.&nbsp;<ref name="Roth" />
 
H2 receptor antagonists are effective in preventing duodenal ulcer but not gastric ulcer.&nbsp;<ref name="Lanza" />
 
“Studies have shown that antacids and buffered tablets do not protect against NSAID injury” <ref name="Lanza" /><br>
 
== Diagnostic Tests/Lab Tests/Lab Values  ==
 
An early finding of anemia may warrant more extensive diagnostic testing such as an endoscopy or radiography in determination of NSAID gastropathy. Hematocrit and hemoglobin levels may also provide information about the extent of bleeding from perforation or hemorrhage. As NSAID induced ulcers are often asymptomatic, patient history and diagnostic tests/lab values are important in diagnosis. Endoscopy has a success rate of 90% for diagnosis of a peptic ulcer, however, it is expensive and the rate of correct diagnosis of NSAID gastropathy is high among physicians. (See Tamblyn et al 1997 study.) Radiography with barium can also detect and diagnose peptic ulcers but is less common than endoscopy.<br>
 
 
&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;&nbsp;[[Image:Ulcers2.jpg|border|200x200px|NSAID induced stomach ulcer (same patient as image to left)]][[Image:Ulcers4.jpg|border|right|200x200px|NSAID gastropathy with upper GI hemorrhage]][[Image:Ulcers.jpg|border|left|200x200px|Stomach hematin-covered erosions typical of NSAID use]]
 
== Etiology/Causes == NSAIDs inhibit the enzyme cyclooxygenase which is a necessary enzyme for the synthesis of prostaglandins from arachidonic acid. While inhibition of COX allows NSAIDs to have their anti-inflammatory and analgesic properties by blocking proinflammatory prostaglandins, it also blocks prostaglandins that protect the gastrointestinal system. Prostaglandins in the gastric system help maintain gastric blood flow, increase bicarbonate production, and increase mucus that serves as a protective barrier against bacteria colonization and mechanical injury. Decreased blood flow and decreased mucosa decrease the healing ability and leave the stomach more exposed to injury from pepsin and gastric acid. Furthermore, these decreases lead to “increased back-diffusion of hydrogen ions into epithelial cells with resultant impaired mucosal resistance to injury”. <br> The function of cyclooxygenase in this process led to the establishment of two COX isoforms: COX-1 and COX-2. COX-1 is found throughout all tissues of the body whereas COX-2 is in the area of inflammation such as in an area of osteoarthritis contributing to the inflammation. Previous NSAIDs included both COX-1 and COX-2 inhibitors, however, in the 1990s COX-2 medications were developed to act on the areas of inflammation without causing the mucosal effects to the GI tract from inhibitng COX-1. COX-2 inhibitors are associated with fewer upper GI side effects, however, they are not as symptom free as hoped and still place people at risk of gastroduodenal mucosa injury. The opinion that only COX-1 affects GI issues is simplistic and not the full story. Medications that suppress acid have shown to be effective in combination with NSAIDs to a greater extent than COX-2 medications alone. These medications are discussed below in the medical management section.<br> [[Image:Fig2nsaid.jpg|thumb|left|NSAID Mechanism of Action]]  
<div><br></div>


== Systemic Involvement  ==
== Systemic Involvement  ==


The effects of NSAIDs can occur throughout the GI tract from the esophagus to the colon (384). A potential complication of ulcers left untreated is that the ulcer can perforate through the stomach mucosa and cause infection to spread or the ulcer can erode stomach arteries creating a life-threatening bleed (p.382). <br>In addition to effects on the GI system, NSAIDs also affect the renal and cardiovascular systems.  
The effects of NSAIDs can occur throughout the GI tract from the esophagus to the colon. A potential complication of ulcers left untreated is that the ulcer can perforate through the stomach mucosa and cause infection to spread or the ulcer can erode stomach arteries creating a life-threatening bleed. In addition to effects on the GI system, NSAIDs also affect the renal and cardiovascular systems<ref name="Goodman">Goodman, CC, Snyder, TEK. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis: Saunders Elsevier, 2007.</ref>.   
 
== Medical Management (current best evidence) ==


== Management ==
One of the difficulties of NSAID gastropathy is that its course is asymptomatic 50% of the time<ref name="Roth" />. &nbsp;Therefore, it is essential that health care professionals assess each patient's risk factors and recommend either discontinued use of an NSAID or inclusion an accompanying cytoprotectant agent in those patients considered high risk. &nbsp;A preventative approach of discontinued NSAID use is recommended over treating the gastropathy<ref name="Roth" />.  
One of the difficulties of NSAID gastropathy is that its course is asymptomatic 50% of the time<ref name="Roth" />. &nbsp;Therefore, it is essential that health care professionals assess each patient's risk factors and recommend either discontinued use of an NSAID or inclusion an accompanying cytoprotectant agent in those patients considered high risk. &nbsp;A preventative approach of discontinued NSAID use is recommended over treating the gastropathy<ref name="Roth" />.  


However, if it is not possible to discontinue use of the NSAID, PPIs or H2-receptor antagonists may be prescribed to reduce the gastric effects. &nbsp;The use of a PPI along with NSAIDs has shown decreased risk of NSAID-related ulcers and adverse drug events compared with H2-receptor antagonists. A COX-2 selective NSAID along with a PPI has shown the best results for reducing gastropathy risk in those who must continue to take NSAIDs<ref>Becker, JC, Domschke W, Pohle T.  Current Approaches to prevent NSAID-induced gastropathy—COX selectivity and beyond. Br J Clin Pharmacol.2004;58:6:587-600.</ref>. Other treatment options include misoprostol which is a synthetic prostaglandin designed to replace those loss by NSAIDs. However, misoprotol has a lot of side effects that have proved difficult such as abdominal pain, nausea, and diarrhea<ref name="Lanza 2">Lanza, F, Chan, FKL, Eamonn, MMQ, and the Practice Parameters Committee of the American College of Gastroenterology. Guidelines for Prevention of NSAID-related ulcer complications. Am J Gastroenterol.2009;104:728-738.</ref>.<br>
If long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) leads to reactive gastropathy, it may be  recommend that the client stops taking NSAIDs, take a lower dose, or take a different medicine for pain. It may also be recommend to take a PPI (protein pump inhibitors) along with NSAIDs to prevent or treat reactive gastropathy and its possible complications.  
== Physical Therapy Management ==


== Physical Therapy Management (current best evidence) ==
Many of the patients seen in physical therapy will be taking NSAIDs for their disorder. &nbsp;PTs must be aware of risk factors, clinical signs and systems (and be aware the patient may be asymptomatic but still have NSAID induced gastropathy), and they must take a detailed patient history including medication questions concerning multiple NSAIDs, prescription drugs combined with NSAIDs, and changes to medications. Any patient who presents with new onset of back or shoulder pain, who takes NSAIDs, and who presents with signs and symptoms of a peptic ulcer must be referred to the MD.<ref name="Goodman" />


add text here
Risk Factors for NSAID gastropathy&nbsp; (should serve as a red [[The Flag System|flag]]). &nbsp;The incidence of mortality and morbidity from NSAID use is high among the aging population and taking a detailed patient history is essential.


== Alternative/Holistic Management (current best evidence)  ==
*Age &gt; [[Older People - An Introduction|65 years]]
 
*History of peptic ulcer or GI disease
'''Up and coming nontoxic NSAIDs but little evidence&nbsp;<ref name="Lanza" />'''
*[[Smoking Cessation and Brief Intervention|Smoking]], [[Alcoholism|alcohol]] use
 
*Oral [[Corticosteroid Medication|corticosteroid]] use
'''COX-2 selective inhibitors'''
*Anticoagulation or use of other anticoagulants.
 
*[[Kidney|Renal]] complications in clients with [[hypertension]] or [[Heart Failure|congestive heart failure]] or who use [[diuretics]] or [[ACE Inhibitors: Congestive Heart Failure|ACE]] inhibitors
*COX-1 enzyme is blocked, inflammation is reduced, but protection of stomach lining is lost with normal NSAID
*Use of acid suppressants (H2-receptor antagonists, antacids); these agents can mask the warning symptoms of more serious GI complications, leaving the client unaware of ongoing damage'''<sub></sub>'''
*COX-2 inhibitors block COX-2 enzyme and does not play a role in the gastroprotection, therefore decrease the incidence of&nbsp;gastrointestinal adverse&nbsp;effects and still reduce inflammation and pain. But it may cause cardiovascular complications because it can cause thrombosis due to suppression of inflammatory mediators in atherogenesis. It can also cause renal toxicity and peripheral&nbsp;edema.&nbsp;<ref name="Roth" />
*NSAIDs combined with SSRIs&nbsp; &nbsp; &nbsp; &nbsp; &nbsp;  
*Two COX-2 inhibitors have been removed from the market recently (fecoxib in 2004 and valdecoxib in 2005)
 
'''Nitric oxide- releasing NSAIDs'''  
 
'''Topical NSAIDs&nbsp;'''&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;  
 
*Deliver the drug directly to the tissue but avoids absorption through the gastrointestinal tract. <ref name="Roth" /><br>


== Differential Diagnosis  ==
== Differential Diagnosis  ==


Peptic ulcers are typically caused by ''H. pylori'' infection or acid related consumption and are commonly in young males <ref name="Roth" />  
* Peptic ulcers are typically caused by ''H. pylori'' infection or acid related consumption and are commonly in young males <ref name="Roth" />
 
* [[Crohn's Disease]] is a type of inflammatory bowel disease which causes the gastrointestinal tract to be chronically inflamed.&nbsp; Common symptoms of this disease include abdominal pain, diarrhea, blood in the stool and vomiting and can even cause rectal or gastrointestinal bleeding, loss of appetite and liver inflammation. <ref name="Riley">IU health. Riley Hospital for Children: 2013. Available from: http://iuhealth.org/riley/gastroenterology/diseases-conditions/crohns-disease/</ref>
Crohn's Disease is a type of inflammatory bowel disease which causes the gastrointestinal tract to be chronically inflammed.&nbsp; Common symptoms of this disease include abdominal pain, diarrhea, blood in the stool and vomiting and can even cause rectal or gastrointestinal bleeding, loss of appetite and liver inflammation. <ref name="Riley">IU health. Riley Hospital for Children: 2013. Available from: http://iuhealth.org/riley/gastroenterology/diseases-conditions/crohns-disease/</ref><br>  
* Gastroesophageal Reflux Disease (GERD) is caused by stomach acid back flowing into the esophagus.&nbsp; The most common symptom is heartburn but those with GERD can also have a dry cough, asthma-like symptoms, and trouble swallowing. <ref name="GERD">Berry, J., PhD, APRN. IU Health. Health Encyclopedia. April 2012. Available from: http://iuhealth.staywellsolutionsonline.com/Library/Encyclopedia/85,P00381</ref>
 
Gastroesophageal Reflux Disease (GERD) is caused by stomach acid back flowing into the esophagus.&nbsp; The most common symptom is heartburn but those with GERD can also have a dry cough, asthma-like symptoms, and trouble swallowing. <ref name="GERD">Berry, J., PhD, APRN. IU Health. Health Encyclopedia. April 2012. Available from: http://iuhealth.staywellsolutionsonline.com/Library/Encyclopedia/85,P00381</ref><br>
 
== Case Reports/ Case Studies  ==
 
add links to case studies here (case studies should be added on new pages using the [[Template:Case Study|case study template]])<br>
 
== Resources <br>  ==
 
add appropriate resources here
 
== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed])  ==
 
see tutorial on [[Adding PubMed Feed|Adding PubMed Feed]]
<div class="researchbox">http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1NWuP8eFPUuwyj0pDSS3XOFYZlulP7caD8JmSAUkfjXCBqbYiw
<br>
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== References  ==
== References  ==
see [[Adding References|adding references tutorial]].


<references />&nbsp;<br>  
<references />&nbsp;<br>  


[[Category:Bellarmine_Student_Project]]
[[Category:Bellarmine_Student_Project]][[Category:Medical]][[Category:Pharmacology]]

Latest revision as of 06:44, 8 February 2023

Original Editors - Amanda Huber & Emily Sipe from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Top Contributors - Emily Sipe, Amanda Huber, Lucinda hampton, Admin, Kim Jackson, Elaine Lonnemann, 127.0.0.1, Wendy Walker and Aminat Abolade  

Introduction[edit | edit source]

Gastropathy.jpeg

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most highly prescribed drugs in the world. Their analgesic, anti-inflammatory, and antipyretic actions may be beneficial; however, they are associated with severe side effects including gastrointestinal injury and peptic ulceration. Though several approaches for limiting these side effects have been adopted, like the use of COX-2 specific drugs, co-medication of acid suppressants like proton pump inhibitors and prostaglandin analogs, these alternatives have limitations in terms of efficacy and cardiovascular effects side effects.[1]

Current Therapies for Prevention of Gastric Damage[edit | edit source]

Several approaches have been adopted for addressing the prevention and cure of the possible side-effects produced by the NSAIDs in the gut.

  • Some of these strategies are routinely prescribed to the patients administering NSAIDs.
  • Presently, the most common protective strategies adopted are: combination therapy of NSAIDs with gastroprotective agents and; use of selective COX-2 inhibitors.[1]

Gastrointestinal Effects[edit | edit source]

GI normal.jpeg

The use of NSAIDs is associated with gastrointestinal toxicity, affecting both upper gastrointestinal tract (peptic ulcer disease) and lower gastrointestinal tract (NSAID-induced enteropathy). NSAIDs use has been associated with an increased risk of clinical relapse in inflammatory bowel disease patients. [2]

  • Some 10%-50% of patients are unable to tolerate NSAID treatment because of side effects, including abdominal pain, diarrhea, and upset stomach.
  • Approximately 15% of patients on long-term NSAID treatment develop a peptic ulcer (ulceration of the stomach or duodenum).
  • Even though many of these patients with ulcers do not have symptoms and are unaware of their ulcers, they are at risk of developing serious ulcer complications such as bleeding or perforation of the stomach[1].

How do they effect the Gut[edit | edit source]

NSAIDs work by stopping the production of prostaglandins (which promote inflammation, pain, and fever), they do this do this by blocking cyclooxygenases (COX) enzymes. These enzymes produce prostaglandins, yet they also protect your stomach and intestinal lining. This is why NSAIDs can damage your gut. [3]

Examples of NSAIDS Impact on Gut Health

1. Bacterial Imbalance: Recent research suggest that changes in the gut microbiome balance are brought on by these medications. Studies show that the combination of medications you ingest are reflected in the types of bacteria that populate your gut. Scientists believe that each type of NSAID can affect different bacteria in the gut, causing a different imbalance depending on which one you take. Because each person’s gut microbiome is unique, the effects may vary significantly from one person to another.

2. Digestive Discomfort: The most commonly reported side effects of NSAID use are gastrointestinal symptoms, including gas, feeling bloated, stomach pain, constipation and diarrhea because they disrupt the enzymes that protect your gut lining. One study showed that diarrhea due to NSAID use could last for up to six days after their use.

3. Heartburn/GERD

4. Gastrointestinal Ulcers and Bleeding: approximately 15% of patients who take NSAIDs long-term develop a peptic ulcer. The risk of bleeding ulcers doubles if you take aspirin with other NSAIDs.

5. Leaky Gut: NSAIDS not only cause leaky gut, they can be one of the greatest barriers to recovering from it because they increase your intestinal permeability, which means they make leaky gut worse.

6. Acute Colitis and Autoimmune Disease: NSAIDs may also set off a chain reaction that leads to conditions such as ulcerative colitis and Crohn’s disease. NSAIDs are associated with hospitalizations for severe colitis in patients with inflammatory bowel disease (IBD), and relapses of IBD. This is due to the inflammation that they cause, as well as the leaky gut, which can let through food particles that are so similar to your body’s own cells that your immune system attacks your body[3].

Characteristics/Clinical Presentation[edit | edit source]

Up to 50% of NSAID induced gastropathy is asymptomatic. [4]

  1. Mild dyspepsia
  2. Heartburn
  3. Nausea
  4. Abdominal discomfort
  5. Erosion
  6. Ulcers
  7. Hemorrhage
  8. Perforation
  9. Obstruction
  10. Occult and frank bleeding
  11. Acute colitis
  12. Exacerbation of existing colon disease

[5][4][6]

Associated Co-morbidities[edit | edit source]

Systemic Involvement[edit | edit source]

The effects of NSAIDs can occur throughout the GI tract from the esophagus to the colon. A potential complication of ulcers left untreated is that the ulcer can perforate through the stomach mucosa and cause infection to spread or the ulcer can erode stomach arteries creating a life-threatening bleed. In addition to effects on the GI system, NSAIDs also affect the renal and cardiovascular systems[7].

Management[edit | edit source]

One of the difficulties of NSAID gastropathy is that its course is asymptomatic 50% of the time[4].  Therefore, it is essential that health care professionals assess each patient's risk factors and recommend either discontinued use of an NSAID or inclusion an accompanying cytoprotectant agent in those patients considered high risk.  A preventative approach of discontinued NSAID use is recommended over treating the gastropathy[4].

If long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) leads to reactive gastropathy, it may be recommend that the client stops taking NSAIDs, take a lower dose, or take a different medicine for pain. It may also be recommend to take a PPI (protein pump inhibitors) along with NSAIDs to prevent or treat reactive gastropathy and its possible complications.

Physical Therapy Management[edit | edit source]

Many of the patients seen in physical therapy will be taking NSAIDs for their disorder.  PTs must be aware of risk factors, clinical signs and systems (and be aware the patient may be asymptomatic but still have NSAID induced gastropathy), and they must take a detailed patient history including medication questions concerning multiple NSAIDs, prescription drugs combined with NSAIDs, and changes to medications. Any patient who presents with new onset of back or shoulder pain, who takes NSAIDs, and who presents with signs and symptoms of a peptic ulcer must be referred to the MD.[7]

Risk Factors for NSAID gastropathy  (should serve as a red flag).  The incidence of mortality and morbidity from NSAID use is high among the aging population and taking a detailed patient history is essential.

  • Age > 65 years
  • History of peptic ulcer or GI disease
  • Smoking, alcohol use
  • Oral corticosteroid use
  • Anticoagulation or use of other anticoagulants.
  • Renal complications in clients with hypertension or congestive heart failure or who use diuretics or ACE inhibitors
  • Use of acid suppressants (H2-receptor antagonists, antacids); these agents can mask the warning symptoms of more serious GI complications, leaving the client unaware of ongoing damage
  • NSAIDs combined with SSRIs         

Differential Diagnosis[edit | edit source]

  • Peptic ulcers are typically caused by H. pylori infection or acid related consumption and are commonly in young males [4]
  • Crohn's Disease is a type of inflammatory bowel disease which causes the gastrointestinal tract to be chronically inflamed.  Common symptoms of this disease include abdominal pain, diarrhea, blood in the stool and vomiting and can even cause rectal or gastrointestinal bleeding, loss of appetite and liver inflammation. [8]
  • Gastroesophageal Reflux Disease (GERD) is caused by stomach acid back flowing into the esophagus.  The most common symptom is heartburn but those with GERD can also have a dry cough, asthma-like symptoms, and trouble swallowing. [9]

References[edit | edit source]

  1. ↑ 1.0 1.1 1.2 Sinha M, Gautam L, Shukla PK, Kaur P, Sharma S, Singh TP. Current perspectives in NSAID-induced gastropathy. Mediators of inflammation. 2013 Oct;2013.Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3610380/(accessed 1.11.2021)
  2. ↑ Hijos-Mallada G, Sostres C, Gomollón F. NSAIDs, gastrointestinal toxicity and Inflammatory Bowel Disease. Gastroenterologia y Hepatologia. 2021 Jun 19.Available: https://pubmed.ncbi.nlm.nih.gov/34157367/(accessed 1.11.2021)
  3. ↑ 3.0 3.1 AMD 6 Reasons NSAIDs Are Harmful To Your Gut Available: https://www.amymyersmd.com/article/nsaids-harm-gut/(accessed 1.11.21)
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Roth S. Coming to terms with nonsteroidal anti-inflammatory drug gastropathy. Drugs(2012, May 7), 72(7): 873-879.
  5. ↑ Gigante A, Tagarro I. Non-steroidal anti-inflammatory drugs and gastroprotection with proton pump inhibitors: a focus on ketoprofen/omeprazole. Clinical Drug Investigation. (2012, Apr 1),32(4): 221-233.
  6. ↑ Lanza F. A guideline for the treatment and prevention of NSAID-induced ulcers. Members of the Ad Hoc Committee on Practice Parameters of the American College of Gastroenterology. The American Journal Of Gastroenterology. (1998, Nov), 93(11): 2037-2046.
  7. ↑ 7.0 7.1 Goodman, CC, Snyder, TEK. Differential Diagnosis for Physical Therapists: Screening for Referral. St. Louis: Saunders Elsevier, 2007.
  8. ↑ IU health. Riley Hospital for Children: 2013. Available from: http://iuhealth.org/riley/gastroenterology/diseases-conditions/crohns-disease/
  9. ↑ Berry, J., PhD, APRN. IU Health. Health Encyclopedia. April 2012. Available from: http://iuhealth.staywellsolutionsonline.com/Library/Encyclopedia/85,P00381

 

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