Now a day, the COX-II theory is established. What
about the selectivity of Rheumarene (Diclofenac
Sodium) for COX-II enzyme?
Diclofenac is (non selective) NSAIDs
otherwise it's most selective for COX-II than COX-I
among the classical (non selective) NSAIDs.
Therefore this is reflected on Rheumarene safety
profile, ensures minimal adverse effects with
patients and lowers discontinuation rate that helps
physicians to gain more successful cure rates.
We knew about the cardiac problems that may occur
with patients who are taking selective NSAIDs. Could
this serious adverse event happen with patients on
Rheumarene as non selective NSAIDs therapy?
The cardiovascular safety aroused from the
VIGOR trial & new research of the Journal of the
American Medical Association proofed that non
selective NSAIDs as Rheumarene is a cardio
protective according to the following information:
Selective COX-II inhibitor NSAIDs
Non selective NSAIDs
Myocardial Infarctions were more common :
►COX-2 enzyme is responsible for creating protective fatty acids in the
body. By blocking this enzyme with drugs, patients are left without
these protective fatty acids. And that, might increases their risk of
suffering fatal heart attacks and other cardiovascular events.
►COX-2 inhibitor has prothrombotic effects and do not block thromboxane
which enhances platelet aggregation while it inhibits prostacycline
which has anti-aggregatory and vasodilatory properties.
►High-dose of selective COX-II inhibitor
NSAIDs associated with an increased risk of coronary heart disease.
Pain killers that also inhibit COX-1are known to offer cardio
protection
►COX-2 enzyme is responsible for creating protective fatty acids in
the body is not inhibited.
►non-specific COX-II NSAIDs including Diclofenac could have been
providing cardiovascular benefits (anti-platelet effects) in a way
similar to low-dose aspirin.
Regarding osteoarthritis, acetaminophen is the 1st
line pharmacological therapy for relief of pain and
inflammatory symptoms. Is there any advantage with
Rheumarene over acetaminophen in such indication?
Rheumarene (Diclofenac sodium) more effective
than acetaminophen in osteoarthritis; according to
Journal of Family Practice, July, 2003 by R. Marc
Via:
►Most of the patients
(71%) were taking an NSAID alone or in combination
with acetaminophen before the study started. Because
acetaminophen has been advocated as first-line
therapy for osteoarthritis for almost 10 years,
these patients had very likely tried acetaminophen
without success long before the study was
started.Predictably, when those patients who had
previously taken an NSAID were analyzed, there was a
significant response in the diclofenac-treated group
but not in the acetaminophen or placebo groups.The
response from acetaminophen was similar to that seen
with placebo and was not significantly different
from baseline scores.
►Only patients treated
with diclofenac experienced a significant
improvement in the primary outcome-the WOMAC--at
week 2 (27%; P=.001) and week 12 (25.6%; P=.001)
compared with baseline. The individual components
(pain, stiffness, and function) of the WOMAC each
showed clinical and statistically significant
improvement compared with baseline scores at 2 and
12 weeks in the diclofenac-treated group only.
Therefore Rheumarene should be considered as a 1st
line in such indication.
Which is more effective, the gel form or the
emulgel?
The penetration power and absorption of the gel is
more better than the emulgel , so Rheumarene
gel(20g) is the ideal for rapid control of pain for
a longer duration than any other emulgel
preparation.
Why don't you mix a local anesthetic with diclofenac
in Rheumarene ampoule ?
There is no need to mix local anesthetic with
diclofenac in Rheumarene ampoule:
►The watery-base
preparation of Rheumarene ampoule form is rapidly
absorbed and has no painful irritation effect .
►The local anesthetic
might produce a vasoconstriction which will cause a
delay in absorption and subsequently the expected
rapid effect will be delayed.
