Review of NSAIDs Effects & Side Effects for Arthritis Pain

Updated 3/2017-- all links (except to my own posts) removed as many no longer active. 

Recently I gave in and went to see a rheumatologist after more than 3 months of intense morning stiffness and swelling of my hands (especially around the PIPs and MCPs) and wrists which improved during the day but never went away.  It had gotten to the point where I could no longer open small lid jars (decreased strength), do my push-ups or pull ups (pain and limited wrist motion), and OTC products (Tylenol, Advil, etc) weren’t working.  I can’t take Aleve due to the severe esophagitis it induces.  I didn’t want to write a prescription for my self-diagnosed (without) lab arthritis.

BTW, all the lab work came back negative with the exception of a slightly elevated sed rate and very weakly positive ANA.  The rheumatologist was impressed with the swelling, pain, and stiffness and was as surprised as I by the normal lab work.  He thinks (and I agree) that I am in the early presentation of rheumatoid arthritis.  He wrote a prescription for Celebrex and told me to continue with the Zantac I was already taking (thanks to the Aleve).  The Celebrex is helping.

So I was happy to see this article (full reference below) come across by twitter feed.  H/T to @marcuspainmd: Useful review of NSAIDs effects & side effects for arthritis pain http://cot.ag/oHxQDX

A major disadvantage of NSAID use is the gastrointestinal side effects. These range from abdominal pain, nausea, diarrhea, and dyspepsia to more serious events, such as gastric or duodenal ulcers, anemia, and bleeding, or perforated ulcer. These side effects are due to the simultaneous inhibition of COX-1 and COX-2.

As many as 25% of chronic NSAID users will develop ulcer disease
2%–4% will bleed or perforate, especially those who have been designated as being in a high-risk category
The overall risk for these complications in patients taking NSAIDs was approximately 2.4.

High-risk patients are those with a history of complicated peptic ulcer disease or multiple (at least two) risk factors; moderate-risk patents are those with one to two risk factors, ie, age 65 years, high-dose NSAID therapy, previous history of an uncomplicated ulcer, concurrent use of aspirin (including low-dose), corticosteroids, or anticoagulants; and low-risk patients are those with no risk factors.

The two methods employed to prevent the development of peptic ulceration and mucosal injury in patients taking NSAIDs:

(1) prophylaxis with a proton pump inhibitor or a prostaglandin analog (such as misoprostol) or high-dose histamine 2-receptor antagonist (H2RA)
(2) with substitution of a traditional NSAID by a COX-2 inhibitor
The article on ulcer formation in COX-2 (Celebrex) vs NSAIDS:

Goldstein et al14 determined gastroduodenal damage
from endoscopy after 4, 8, and 12 weeks of treatment with celecoxib 200 mg twice daily or naproxen 500 mg twice daily in 537 patients with osteoarthritis or rheumatoid arthritis.

The cumulative incidence of gastric and duodenal ulceration for celecoxib was 9% and for naproxen was 41%. In the group that received celecoxib, the occurrence of ulcers was significantly associated with a number of factors, including H. pylori positivity, concurrent aspirin usage, and a history of ulcers.

It’s a really nice review article and is open source.



REFERENCES
Combination therapy versus celecoxib, a single selective COX-2 agent, to reduce gastrointestinal toxicity in arthritic patients: patient and cost-effectiveness considerations;  Marina Scolnik, Gurkirpal Singh; Open Access Rheumatology: Research and Reviews 2011:3 53–62