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Obat Pereda Sakit dan Penurun Panas

Dimulai oleh syx, Maret 24, 2009, 08:46:51 AM

« sebelumnya - berikutnya »

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Astrawinata G

ooh, saya kira Mbak LH menerjemahkannya sebagai COX-1 menghasilkan produk untuk fungsi tubuh dan cox-2 untuk peradangan :)
okeh Mas, tq tq....sekarang menunggu jawaban Mbak LH :)
Best Regards,


Astrawinata G

riandono


- COX 1 dan COX 2 diekspresikan berbeda, COX 1= constitutively; COX 2= inducible
- COX 1 dan COX 2 sama-sama mengkatalisis pembetukan PGH2

lidya handayani

#62
Well... yg bener mbak LH yaa.... bukan mas LH..  ;D
ini dah saya baca lg...
" There has been great interest in the COX-2 enzyme because it is induced by a variety of inflammatory stimuli and is absent in most tissue under normal "resting" conditions. COX-1, in contrast, is produced in response to inflammatory stimuli and is also constitutively expressed in most tissues. This difference has led to the notion that COX-1 is responsible for the production of prostaglandins that are involved in inflammation but also serve a homeostatic function (e.g. fluid and electrolyte balance in the kidneys, cytoprotection in the gastrointestinal tract). In contrast, COX-2 stimulates the production of the prostaglandins that are involved in inflammatory reaction "
yup... brarti saya yg kurang dlm ngertinya selama ini...maklum dah byk lupa..he2 ::) jd kalo selektif COX-1 msi mungkin juga.. selama ini saya pikir NSAID lama (ibuprofen, aspirin dll) menghambat COX-1 n COX-2... jd ga mgk inhibisi COX-1 saja.. karena untuk efek antiradang dia harus bekerja menghambat COX-2 (krn awalnya saya pikir COX-2 saja lah yg diekspresikan dlm sel radang). Sementara COX-2 selektif inhibitor pasti bisa... n jelas efeksamping gastritis nya sangat minimal... hmmmm.... thx for discussing.. :angel:

Astrawinata G

efek samping gastritis berkurang dengan cox-2 inhbtr, tapi efek samping stroke, trombosis, iskemi sangat meningkat :)

yang paling bagus efeknya itu diclofenak :) menurut penelitian
Best Regards,


Astrawinata G

riandono


@astra
kalo efek samping ke jantung, diklofenak dan ibuprofen hi dose sama jeleknya dengan coxib bang...
tuh diatas baru dipost ama Mr.Syx

Kutip dari: syx pada Juni 22, 2010, 07:05:56 AM
June 14, 2010 — The first study to examine the cardiovascular risk associated with nonsteroidal anti-inflammatory drugs (NSAIDs) in healthy individuals has found increased morbidity and mortality with diclofenac, rofecoxib (Vioxx, Merck), and high doses of ibuprofen [1]. Naproxen, in contrast, has a safer cardiovascular risk profile, say Dr Emil Loldrup Fosbøl and colleagues in their paper published online June 8, 2010 in Circulation: Cardiovascular Quality and Outcomes.

The increased cardiovascular morbidity and mortality seen with diclofenac, which is similar to that observed with rofecoxib--a drug that was withdrawn from the market in 2004 because of poor cardiovascular safety--is particularly concerning.

Astrawinata G

ya benar :) untuk menghasilkan resiko yang sama, butuh NSAID non-selektif dalam dosis besar :) tapi kalau dpakai dalam dosis yang rendah, resikonya juga turun. Pemakaian NSAID non-selektif dosis tinggi juga jarang diterapkan kok....
Best Regards,


Astrawinata G

riandono

koreksi pakde: yg hi dose cuma utk ibuprofen. utk diklofenak dlm dosis lazim.

Astrawinata G

oke oke :) suatu koreksi bagi saya....

memang NSAID ini banyak lika-likunya :)

btw, paracetamol juga ada yang menggolongkan sebagai cox-2 selektiv lho.....kalau mau boleh coba cari penelitiannya :)
Best Regards,


Astrawinata G

Idad

#68
Kutip dari: riandono pada Juni 28, 2010, 03:08:30 PM

- COX 1 dan COX 2 diekspresikan berbeda, COX 1= constitutively; COX 2= inducible
- COX 1 dan COX 2 sama-sama mengkatalisis pembetukan PGH2

Owh, iy2.., baru ngerti saya..,
berarti COX2 akan meningkat ekspresinya kalau ada stimuli inflamasi, dan COX1 inducible dan constitutive. Begitu ya?

Oia Om, mau tanya juga, mengenai ini
Bukankah COX1 dan COX2 itu enzim yang menkatalisa substrat yang sama untuk menghasilkan Prostaglandin yang sama. Tapi kok diatas dikatakan bahwa:
This difference has led to the notion that COX-1 is responsible for the production of prostaglandins that are involved in inflammation but also serve a homeostatic function (e.g. fluid and electrolyte balance in the kidneys, cytoprotection in the gastrointestinal tract). In contrast, COX-2 stimulates the production of the prostaglandins that are involved in inflammatory reaction

Soalnya waktu kemarin belajar COX, itu kok dari PGH2 klo g salah menghasilkan PGE2/PGEI2/PGD2/TXA2/PGF.
Apa mungkin maksudnya COX1 juga menghasilkan Prostaglandin lain yang berfungsi dalam homeostatis tubuh, atau mungkin PGE2/PGI2/PGD2/TXA2/PGF juga punya efek homeostatis?

riandono

itulah bang, knp juga tubuh kita iseng pake ekspresiin COX 2 kalo toh ntar cuma mengkatalisis produk PG yang sama dan dari substrat yang sama... ??

Aku jg bingung tuh hehehe..

Aku ga begitu tau perkembangan studinya, tp mungkin ini bisa menjelaskan dikit:
[pranala luar disembunyikan, sila masuk atau daftar.]

Idad

Hm.., ok, terimakasih atas jawabannya Om,
harus lebih banyak baca lagi..,

syx

Low-Dose Aspirin May Protect Against Colorectal Cancer

September 21, 2010 — Low-dose aspirin (75 mg/day) may protect against colorectal cancer, according to the results of a case-control study reported online September 15 in Gut.

"Previous studies have shown that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) lower colorectal cancer (CRC) risk," write Farhat V. N. Din, from the University of Edinburgh, Edinburgh, United Kingdom, and colleagues. "However, the lowest effective NSAID dose, treatment duration, and effects on survival are not defined. In a large population-based case-control study, we have explored the relationship between NSAID dose and duration, CRC risk and overall CRC-specific survival."

The study sample consisted of 2279 patients with colorectal cancer and 2907 control subjects who completed food frequency and lifestyle questionnaires. NSAID use was defined as taking more than 4 tablets per week for more than 1 month and was classified as low-dose aspirin (75 mg), nonaspirin NSAIDs, and any NSAID. Logistic regression models allowed calculation of odds ratios (ORs) with adjustment for potential confounding variables, and log-rank tests and Cox hazard models allowed estimation of the effect of NSAID use on all-cause and colorectal cancer-specific mortality.

Low-dose aspirin use was reported by 354 patients (15.5%) and 526 control subjects (18.1%). A reduced risk for colorectal cancer, seen in low-dose aspirin users (OR, 0.78; 95% confidence interval [CI], 0.65 - 0.92; P = .004), was apparent after 1 year and was greater with increased duration of use (P for trend = .004). Use of any NSAID or nonaspirin NSAIDs was also inversely associated with colorectal cancer risk. There was no apparent effect of NSAIDs on all-cause survival duration (hazard ratio, 1.11; P = .22; 95% CI, 0.94 - 1.33) or colorectal cancer-specific survival duration (hazard ratio, 1.01; P = .93; 95% CI, 0.83 - 1.23).

"This is the first study to demonstrate a protective effect against CRC associated with the lowest dose of aspirin (75 mg per day) after only 5 years use in the general population," the study authors write. "NSAID use prior to CRC diagnosis does not influence survival from the disease."

Limitations of this study include potential recall bias; inability to determine if patients continued to take NSAIDs after diagnosis; and lack of outcome measure, which reflects plasma levels of NSAIDs ingested.

"[H]igh aspirin doses are not required for protection against CRC and ... while protection increases with duration of use, there are effects apparent within 5 years," the study authors conclude. "This effect is apparent as early as 1 year but increases with time up to 10 years. Moreover, our results are applicable to the general population and not just high-risk groups."

syx

Does Acetaminophen in Comparison to Ibuprofen Effectively Reduce Fevers in Children Younger than 18 Years of Age?

Fever phobia is a term used to describe parents' unrealistic concerns about fever (Crocetti, Moghbeli, & Serwint, 2001). Schmitt (1980) found that 94% of caregivers thought fever could cause side effects, 63% of caregivers worry a great deal about serious harm resulting from fevers, and 18% of caregivers thought brain damage and other consequences can be caused by fevers of 38.9 C or less. Crocetti et al. (2001) completed a similar study and found that 91% of caregivers believed fever could cause harmful effects, with 21% of caregivers believing brain damage could result from fever.

Both acetaminophen and ibuprofen are effective antipyretic agents in children with history of febrile seizures (Carson, 2003; Goldman, Ko, Linett, & Scolnik, 2004; Hay et al., 2008; Van Esch et al., 1995). For treatment of fever, ibuprofen is more effective than acetaminophen in reducing fever (Goldman et al., 2004; Perrott, Piira, Goodenough, & Champion, 2004; Van Esch et al., 1995; Wahba, 2004; Wong et al., 2001), and ibuprofen provides longer duration of antipyretic effect than acetaminophen – four hours after treatment (Wahba, 2004). Alternating acetaminophen and ibuprofen in febrile children appears to be a common practice among pediatric health care providers (Mayoral, Marino, Rosenfield, & Greensher, 2000) and among parents advised to do so by their health care provider (Wright & Liebelt, 2007).

Studies examining an alternating regimen have not been consistent regarding the dosage of the medications or the schedule of administration. Kramer, Richards, Thompson, Harper, and Fairchok (2008) utilized two groups. Group A received acetaminophen (15 mg/kg/dose) followed by a placebo at hour 3 and a second acetaminophen dose at hour 4. Group B received acetaminophen, followed by ibuprofen (10 mg/kg/dose) at hour 3 and a placebo at hour 4. Nabulsi et al. (2006) also used two groups. Group A received a dose of ibuprofen (10 mg/kg/dose) followed by acetaminophen (15 mg/kg/dose) at hour 4. Group B received a similar dose of ibuprofen followed by a placebo four hours later and acetaminophen, whereas Sarrell, Wielunksy, and Cohen (2006) used six groups to assess medication administration at six and eight-hour dosing intervals for acetaminophen alone (12.5 mg/kg/dose q 6 hour or 25 mg/kg/dose q 8 hour) and ibuprofen alone (10 mg/kg/dose q 6 hour or 5 mg/kg/dose q 8 hour), versus an alternating regimen at four-hour intervals of acetaminophen and ibuprofen. However, these authors consistently found that an alternating regimen of acetaminophen and ibuprofen to reduce fever in children is more effective than either drug alone (Hay et al., 2008; Kramer et al., 2008; Mayoral et al., 2000; Nabulsi et al., 2006; Sarrell et al., 2006).

There is no consistent recommendation regarding the antipyretic schedule to use when alternating medications. The most commonly cited method is giving acetaminophen every four hours and ibuprofen every six hours. However, this timing is problematic in that it exceeds the recommended daily doses of each medication and does not specify which medication should be given at the 12th hour (Carson, 2003; Mayoral et al., 2000). Due to safety concerns, such as potential dosing errors (under dosing and overdosing) and toxicity, monotherapy of antipyretics is recommended (Carson, 2003; Goldman et al., 2004; Hay et al., 2008; Kramer et al., 2008; Mayoral et al., 2000; Sahib & El-Radhi, 2008).

In studies where adverse effects of acetaminophen and ibuprofen were studied, authors reported no significance between the two, and the risk of adverse effects are small (Goldman et al., 2004; Lesko & Mitchell, 1999; Perrott et al., 2004). However, it is recommended to use the lowest therapeutic dose that provides sufficient antipyresis to prevent adverse effects or toxicity related to the medication (American Academy of Pediatrics [AAP], 2001; Carson, 2003). The use of ibuprofen does not exacerbate asthma morbidity and provides a possible therapeutic effect compared with acetaminophen. Acetaminophen use in children may lead to an increased risk for wheezing (Kanabar, Dale, & Rawat, 2007).

Idad

Wa, artikel diatas kelihatannya penting juga,

tapi kenapa bisa begini ya? Kira2 mekanismenya apa y?
KutipFor treatment of fever, ibuprofen is more effective than acetaminophen in reducing fever (Goldman et al., 2004; Perrott, Piira, Goodenough, & Champion, 2004; Van Esch et al., 1995; Wahba, 2004; Wong et al., 2001), and ibuprofen provides longer duration of antipyretic effect than acetaminophen – four hours after treatment (Wahba, 2004).
KutipHowever, these authors consistently found that an alternating regimen of acetaminophen and ibuprofen to reduce fever in children is more effective than either drug alone (Hay et al., 2008; Kramer et al., 2008; Mayoral et al., 2000; Nabulsi et al., 2006; Sarrell et al., 2006).

Oia Om, mau tanya juga. Klo Ibuprofen itu memang aman y untuk anak2. Kan bukannya dia ada efek ke gaster mukosa Om?

syx

pasti praktisi yang menganjurkan penggunaan ibuprofen di antara NSAID lainnya sudah mempertimbangkan risk and benefit, termasuk efek sampingnya terhadap mukosa saluran cerna. kalo semua melihat ke risk aja ga ada obat demam yang aman untuk anak.