coba cari di topik Acetaminophen/Paracetamol.

yup, aspirin termasuk NSAID. aspirin inhibitor non selektif terhadap COX. aspirin 166 x lebih kuat menghambat COX-1 daripada COX-2. beberapa jurnal menyebutkan aspirin juga menghambat COX-3 di otak.

Best Evidence Interview: CINODs -- The NSAID Holy Grail?

Nonsteroidal anti-inflammatory drugs (NSAIDs) are universally used in the treatment of conditions that cause chronic pain, such as osteoarthritis (OA). However, their use is limited by their safety profiles, particularly gastrointestinal side effects and adverse effects on the cardiovascular system. Traditional NSAIDs such as ibuprofen and naproxen, which act by blocking the COX-1 and -2 enzymes, and COX-2 selective inhibitors, such as celecoxib, are associated with the destabilization of blood pressure control. This effect is particularly marked in hypertensive patients treated with blockers of the renin-angiotensin system (RAS).

Naproxcinod, a nitric oxide (NO) derivative of naproxen, is an investigational drug and the first of a class of NSAIDs known as COX-inhibiting NO donors. It is being developed by NicOx S.A. (Sophia Antipolis, France). Naproxcinod has been studied in a clinical phase 3 program in patients with OA of the knee and hip, and, on the basis of the results of these studies, it is currently under regulatory review for approval for treatment of OA in the United States. As of the date of this interview, a regulatory submission is also planned in Europe for late 2009. In preclinical studies, naproxcinod had similar anti-inflammatory and analgesic activity to naproxen but caused less gastric injury. Phase 2 and 3 trials showed that naproxcinod is an effective analgesic agent with reduced gastrointestinal toxicity compared with naproxen, and in contrast to naproxen, it reduces systemic blood pressure by 2-3 mm Hg. On the basis of these findings, naproxcinod may represent an alternative to traditional NSAIDs or COX-2 inhibitors in patients who have or are at risk for cardiovascular disease.

In the best evidence study discussed in this interview, the effects of naproxcinod on blood pressure in patients with OA were compared with those of naproxen and placebo over 13 weeks in a phase 3, randomized clinical trial carried out at the University of Connecticut, Farmington, and Northwestern University, Chicago, Illinois. The results of the trial, which were first presented at US and European rheumatology and cardiology conferences,[1,2] were published recently in the American Journal of Cardiology.[3] The trial randomly assigned a total of 916 patients with OA, with or without a history of hypertension, to treatment twice daily with either naproxcinod 750 mg, naproxcinod 375 mg, naproxen 500 mg, or placebo. Reductions in systolic blood pressure (SBP) with naproxcinod 750 mg were larger and significantly different from those with naproxen 500 mg at 2, 6, and 13 weeks (P < .05). The difference in mean change from baseline between these 2 groups was -2.9 mm Hg (P = .015). The 2 doses of naproxcinod showed reductions from baseline in diastolic blood pressure relative to naproxen (P < .04) and similar changes compared with placebo. The proportion of patients in the overall population with SBP increases > 10 mm Hg was greater with naproxen 500 mg (22%) compared with naproxcinod 750 mg (14%; P = .04), naproxcinod 375 mg (14%; P = .055), and placebo (15.6%; P = .155).

Separate analysis of a subgroup of 207 patients with hypertension treated with RAS-blocking agents alone or with diuretics showed a difference in mean change from baseline in SBP between naproxen 500 mg and naproxcinod 750 mg of -6.5 mm Hg in favor of naproxcinod (P = .011). Analysis of 73 patients being treated with antihypertensive drugs that did not include a RAS blocker did not show any statistically significant differences from baseline in SBP within or between groups.

The study authors concluded that naproxcinod is likely to destabilize the control of SBP compared with naproxen in patients with OA and behaves in a similar fashion to placebo overall as well as in patients treated with antihypertensive therapies involving blockade of the RAS. They suggested that the hypertensive burden induced by traditional NSAIDs in patients with OA and hypertension could be reduced by an NO-donating agent such as naproxcinod.

References
   1. Schnitzer TJ, Kivitz A, Rankin B, et al. Comparison of naproxcinod to naproxen and placebo: results of a 13-week phase 3 pivotal trial in patients with osteoarthritis of the knee with particular focus on blood pressure effects. Ann Rheum Dis. 2008;67(suppl II):394. Abstract 0350.
   2. White WB, Schnitzer T. The cyclooxygenase inhibiting nitric oxide donator naproxcinod lacks the hypertensive effects seen with naproxen in patients with osteoarthritis. Program and abstracts of the American College of Cardiology 2009 Annual Meeting; March 29-30, 2009; Orlando, Florida. Abstract 0910-4.
   3. White WB, Schnitzer TJ, Fleming R, et al. Effects of the cyclooxygenase inhibiting nitric oxide donator naproxcinod versus naproxen on systemic blood pressure in patients with osteoarthritis. Am J Cardiol. 2009;104:840-845.

NSAIDs May Be More Effective Than Paracetamol for Menstrual Pain

January 20, 2010 — Nonsteroidal anti-inflammatory drugs (NSAIDs) may be more effective than paracetamol for menstrual pain, according to the results of a systematic review reported online January 20 in the Cochrane Database of Systematic Reviews.

"Dysmenorrhoea is a common gynaecological problem consisting of painful cramps accompanying menstruation, which in the absence of any underlying abnormality is known as primary dysmenorrhoea," write Dr. Jane Marjoribanks, Cochrane Menstrual Disorders and Subfertility Group in Auckland, New Zealand, and colleagues. "Research has shown that women with dysmenorrhoea have high levels of prostaglandins, hormones known to cause cramping abdominal pain. ...NSAIDs are drugs which act by blocking prostaglandin production."

The goal of this review was to compare the effectiveness and safety of NSAIDs used in the treatment of primary dysmenorrhea vs placebo, paracetamol, and each other. The reviewers searched the Cochrane Menstrual Disorders and Subfertility Group trials register, Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, and Web of Science to May 2009. They also searched the National Research Register, the Clinical Trials Register, abstracts of major scientific meetings, and bibliographies of identified articles.

Inclusion criteria were all randomized controlled comparisons of NSAIDs vs placebo, other NSAIDs, or paracetamol for treatment of primary dysmenorrhea. Two reviewers independently evaluated trials for methodologic quality, extracted data, and calculated odds ratios (ORs) for dichotomous outcomes and mean differences for continuous outcomes. The reviewers then combined the data using inverse variance methods.

Based on 73 randomized controlled trials meeting selection criteria, NSAIDs were significantly more effective for pain relief than placebo among women with primary dysmenorrhea (OR, 4.50; 95% confidence interval [CI], 3.85 - 5.27), but there was marked heterogeneity for this finding (I² statistic = 53%). Excluding 2 outlying studies with no or negligible placebo effect decreased heterogeneity (OR, 4.14; 95% CI, 3.52 - 4.86; I² = 40%). Compared with paracetamol, NSAIDs were also significantly more effective for pain relief (OR, 1.90; 95% CI, 1.05 - 3.44), but NSAIDs were associated with significantly more overall adverse effects than placebo (OR, 1.37; 95% CI, 1.12 - 1.66).

"Women using these drugs need to be aware of the side effects," Dr. Marjoribanks said in a news release. "It would be interesting to see whether these could be reduced, without loss of effectiveness, by combining lower doses with other drugs such as paracetamol, or with other therapies such as transcutaneous electrical nerve stimulation."

Comparison of various NSAIDs vs other NSAIDs showed limited evidence that any individual NSAID was superior for either pain relief or safety.

Limitations of this review include limited power to detect differences among NSAIDs because most individual comparisons were based on very few trials with small sample size.

"NSAIDs are an effective treatment for dysmenorrhoea, though women using them need to be aware of the significant risk of adverse effects," the review authors conclude. "There is insufficient evidence to determine which (if any) individual NSAID is the safest and most effective for the treatment of dysmenorrhoea."

Cochrane Database Syst Rev. Published online January 20, 2010.

yo... begitulah.

Yah..memang...sih semua digolongkn NSAID..Namun, denger denger.. walapun sama-sama menghambat COX-2, ada yang lebih sebagai anti nyeri..ada yang onset kerjanya sebentar..ada yang memang bisa sebagai anti inflamasi..tapi secara fungsi rendah..

@ pak ran: Walaupun mekanisme kerja NSAID sebagai inhibor COX, baik yang selektif (hanya menghambat COX2) maupun non selektif (menghambat COX2 dan COX1, contoh: celexocib), adalah sama, tetapi masing2 NSAID punya potensi yang berbeda. Perbedaan potensi ini dipengaruhi banyak faktor (salah satunya adalah faktor farmakokinetika)

@ pak astrawinata: oya? ada NSAID yang ngga menghambat COX 2? contoh obatnya apa pak?

aspirin dan ketorolac spesifik terhadap COX-1. sedangkan indomethacin dan piroxicam agak condong ke COX-1, MasRian