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   Neuro Gave me INDOMETHACIN any advice?
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   Author  Topic: Neuro Gave me INDOMETHACIN any advice?  (Read 477 times)
i_hate_the_pain
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Neuro Gave me INDOMETHACIN any advice?
« on: Jul 6th, 2004, 2:26pm »
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Well I just got back for the neuro I have been fighting with to get some pain relief.. Well he is finally saying with the amount of HA's I suffer with day and night he is now certain I suffer from Chronic paroxysmal hemicrania and gave me INDOMETHACIN 3 times a day. He wants me to take that along with the 25mg a day of TOPOMAX. After suffering since April 23rd this is what he has come up with..  
Now my question for those that have taken INDOMETHACIN did it help or not?
Also what is the difference between Chronic paroxysmal hemicrania treatment and regular cluster treatment? Also should I stop taken the Verap if I am going to start this new protocal of meds? Anythig you can share would be great.
 
Also he kept apologizing for the pain I am dealing with and saying he is sorry I am going through this.. I told him it is not his fault I have them but I do expect him to help me stop the pain.. So I have an appointment withhim in one month, but he said if I don't see a difference in the painw ithin 10 days call hima nd he will discuss other options.. Anyway thank you for any advice..
Pain free days to all..
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floridian
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Re: Neuro Gave me INDOMETHACIN any advice?
« Reply #1 on: Jul 6th, 2004, 2:40pm »
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CPH is usually very responsive to Indomethacin ...  90%+ of people with CPH get things under control with Indo.  If it brings glorious relief, then count yourself lucky and educate yourself about the side effects of Indomethacin as it will be a long term relationship (see below)  If it doesn't help, you might be in the minority of CPH people who don't respond, or you might have something else.    
 
Not sure about keeping you on topomax while starting indomethacin - usually indomethacin alone is enough, but doc may have a reason.  
 
Quote:
Almost all patients with chronic or episodic paroxysmal hemicrania have their headaches eliminated by indomethacin, which for CPH generally has to be taken for years. Sometimes large doses (200 mg per day) are needed to suppress the attacks. Indomethacin, like other non-steroidal anti-inflammatory drugs (NSAIDS) can produce intolerable dyspepsia, which may or may not be alleviated by antacids, such as cimetidine, and it can cause perforated or bleeding stomach or duodenal ulcers. When indomethacin is not tolerated (or effective) other drugs should be tried. One case report (Warner et al., 1994) stated that a patient with CPH unresponsive to indomethacin had her headaches suppressed by acetazolamide (Diamox) in a dosage of 250 mg three times daily. More recently, Mathew et al. (2000) reported a woman with CPH who had to discontinue indomethacin for intolerable gastric symptoms due to multiple ulcers. She was then treated with celecoxib (Celebrex), a drug in a new class of NSAIDs which decrease prostaglandin synthesis by inhibiting the enzyme cyclo-oxygenase-2 (COX-2) without affecting cyclo-oxygenase-1, as does indomethacin and the older NSAIDs such as aspirin, ibuprofen, etc. On a dose of 200 mg twice daily, her headache attacks remitted within 3 days and remained absent for the 3-month follow up--and without gastric symptoms.
http://www.upstate.edu/neurology/haas/hpclrx.htm
« Last Edit: Jul 6th, 2004, 2:45pm by floridian » IP Logged
floridian
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Re: Neuro Gave me INDOMETHACIN any advice?
« Reply #2 on: Jul 6th, 2004, 3:14pm »
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Here's more on treating CPH with cox-2 inhibitors, which was mentioned in the above abstract.  This is good news - cox2 inhibitors have fewer side effects than indomethacin for long term use.  There are also dietary sources of cox2 inhibitors (curcumin/turmeric, cherries, tomato and garlic (ie, spaghetti sauce).   Stick with the doctors plan to determine if you do indeed have CPH.  Assuming that you do, once things are under control you can discuss cox2 inhibitors and dietary changes w/ the doc.  
 
 
Quote:
Headache. 2002 Jun;42(6):530-1.
     
    Hemicrania continua responds to cyclooxygenase-2 inhibitors.
 
    Peres MF, Silberstein SD.
 
    Jefferson Headache Center, Department of Neurology, Thomas Jefferson University Hospital, Philadelphia, Pa., USA.
 
    BACKGROUND: Hemicrania continua is a primary headache disorder defined by its absolute responsiveness to indomethacin. We report the treatment response to two cyclooxygenase-2 inhibitors, celecoxib and rofecoxib, in a series of patients with hemicrania continua. METHODS: Fourteen patients were treated, 9 with rofecoxib and 5 with celecoxib. RESULTS: Three patients in each group had a complete response to treatment. CONCLUSION: The cyclooxygenase-2 inhibitors may represent an alternative to indomethacin in the treatment of hemicrania continua. Their mechanism of action for this potential indication is unknown.

 
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Cancer Lett. 2004 May 28;208(2):127-36.  
     
    Modulatory influence of garlic and tomato on cyclooxygenase-2 activity, cell proliferation and apoptosis during azoxymethane induced colon carcinogenesis in rat.
 
    Sengupta A, Ghosh S, Das S.
 
    Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700026, India. archanadi1@rediffmail.com
 
    Preventive intervention of colorectal cancer has become essential as a major portion of the population may develop the disease at some points during their lives. Diet and nutrition play an important role during this multistep colon carcinogenic process. Inhibitory activity of aqueous suspensions of garlic and tomato, individually and in combination, were tested on azoxymethane induced colon carcinogenesis in Sprague-Dawley rats. The effect was observed on aberrant crypt foci (ACF), the preneoplastic lesion. To investigate the mechanism of action of the agents used, cell proliferation and the level of apoptosis were determined and the expression of cyclooxygenase-2 (COX-2) protein was analyzed in the colon. Following treatment, significant inhibition of the level of cell proliferation (P<0.01 in garlic; P<0.001 in tomato and P<0.001 in combination treatment group with respect to the carcinogen control group), significant induction of apoptosis (P<0.01 in garlic treated; P<0.01 in tomato treated and P<0.001 in combination treatment group with respect to the carcinogen control group) and suppression of COX-2 expression among the treated groups resulted in significant reduction in the incidences of ACF (by 45.27% in garlic, 68.24% in tomato and 71.62% in combination treatment group). The preventive effect was better when the combination of garlic and tomato was administered in comparison to the individual treatment groups, suggesting the synergistic action of garlic and tomato.
« Last Edit: Jul 6th, 2004, 3:14pm by floridian » IP Logged
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Re: Neuro Gave me INDOMETHACIN any advice?
« Reply #3 on: Jul 6th, 2004, 3:42pm »
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More on cox2 inhibition by dietary flavonoids and vitamin E.  Onions & apples are two good sources of quercetin/quercetrin. Apigenin is found in parsley, artichoke, basil, celery and chamomile, while chrysin is present in some species of passionflower (both chamomile and passion flower can be relaxinng or sedating, passion flower more so than chamomile).  Genistein is found in soybeans, soy milk, tofu, etc.  Amentoflavone is present in St. Johns wort.  Resveratrol (from grape seeds or Polygonum cuspidatum root) also reduces cox-2.  Standardized Ginkgo extract contains 24% flavonoids, including quercetin and kaempferol (although it contains bilobalides, which not every one wants).    With all of these natural dietary cox2 inhibitors, it is amazing that the pharmacies can still sell Vioxx for $3 to $4 per pill.  
 
Quote:
Mutat Res. 2004 Jul 13;551(1-2):245-54.  
 
    Effect of flavonoids and Vitamin E on cyclooxygenase-2 (COX-2) transcription.
 
    O'Leary KA, Pascual-Tereasa Sd S, Needs PW, Bao YP, O'Brien NM, Williamson G.
 
    Institute of Food Research, Norwich Research Park, Colney, Norwich NR4 7UA, UK.
 
    Cyclooxygenase-2 (COX-2)-catalysed synthesis of prostaglandin E2 plays a key role in inflammation and its associated diseases, such as cancer and cardiovascular disease. There are numerous reports demonstrating that flavonoids inhibit COX-2 activity. However, transcriptional regulation of COX-2 can also be important. Nobiletin, amentoflavone, quercetin, quercetin penta-acetate, flavone, resveratrol, apigenin, chrysin, kaempferol, galangin, and genistein have been reported to modulate COX-2 transcription in a wide variety of systems. Here, we briefly review the literature on regulation of COX-2 transcription by flavonoids, and report some new preliminary data on Vitamin E and quercetin conjugates. Quercetin, quercetin 3-glucuronide, quercetin 3'-sulfate and 3'methylquercetin 3-glucuronide reduced COX-2 mRNA expression in both unstimulated and interleukin-1beta stimulated colon cancer (Caco2) cells. Quercetin and quercetin 3'-sulfate, unlike quercetin 3-glucuronide and 3'methylquercetin 3-glucuronide, also inhibited COX-2 activity. In contrast, tocopherols (alpha-tocopherol, alpha-tocopherol acetate, and gamma-tocopherol at 10microM) did not affect COX-2 mRNA expression in unstimulated Caco2 cells. However, the tocopherols inhibited COX-2 activity showing that the tocopherols act post-transcriptionally on activity, whereas quercetin and some quercetin conjugates affect both the transcription and activity of COX-2. Flavonoid modulation of COX-2 transcription may therefore be an important mechanism in anti-carcinogenesis.
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Re: Neuro Gave me INDOMETHACIN any advice?
« Reply #4 on: Jul 6th, 2004, 3:59pm »
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Just can't stop - too many natural cox2 inhibitors.  
 
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Carcinogenesis. 1999 Oct;20(10):1945-52.  
     
    Suppression of inducible cyclooxygenase and inducible nitric oxide synthase by apigenin and related flavonoids in mouse macrophages.
 
    Liang YC, Huang YT, Tsai SH, Lin-Shiau SY, Chen CF, Lin JK.
 
    Institute of Biochemistry, College of Medicine, National Taiwan University, No. 1, Section 1, Taipei, Taiwan.
 
    Prostaglandins biosynthesis and nitric oxide production have been implicated in the process of carcinogenesis and inflammation. In this study, we investigated the effect of various flavonoids and (-)-epigallocatechin-3-gallate on the activities of inducible cyclooxygenase (COX-2) and inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. Apigenin, genistein and kaempferol were markedly active inhibitors of transcriptional activation of COX-2, with IC(50) < 15 microM. In addition, apigenin and kaempferol were also markedly active inhibitors of transcriptional activation of iNOS, with IC(50) < 15 microM. Of those compounds tested, apigenin was the most potent inhibitor of transcriptional activation of both COX-2 and iNOS. Western and northern blot analyses demonstrated that apigenin significantly blocked protein and mRNA expression of COX-2 and iNOS in LPS-activated macrophages. Transient transfection experiments showed that LPS caused an approximately 4-fold increase in both COX-2 and iNOS promoter activities, these increments were suppressed by apigenin. Moreover, electrophoretic mobility shift assay (EMSA) experiments indicated that apigenin blocked the LPS-induced activation of nuclear factor-kB (NF-kB). The inhibition of NF-kB activation occurs through the prevention of inhibitor kB (IkB) degradation. Transient transfection experiments also showed that apigenin inhibited NF-kB-dependent transcriptional activity. Finally, we showed that apigenin could inhibit the IkB kinase activity induced by LPS or interferon-gamma. The results of further studies suggest that suppression of transcriptional activation of COX-2 and iNOS by apigenin might mainly be mediated through inhibition of IkB kinase activity. This study suggests that modulation of COX-2 and iNOS by apigenin and related flavonoids may be important in the prevention of carcinogenesis and inflammation.

 
Interesting article below:  'heating' foods from Chinese medicine boost Cox2 and prostaglandin synthesis, while cooling foods (including Chrysanthemum flower, which is rich in flavonoids and used as a summer tea) have the opposite effect.  
 
Quote:
J Biomed Sci. 2002 Nov-Dec;9(6 Pt 2):596-606.  
     
    Differential effects of foods traditionally regarded as 'heating' and 'cooling' on prostaglandin E(2) production by a macrophage cell line.
 
    Huang CJ, Wu MC.
 
    Department of Agricultural Chemistry, National Taiwan University, Taipei, Taiwan, ROC. cjjhuang@ccms.ntu.edu.tw
 
    Some components of natural foods may enhance or inhibit prostaglandin formation and potentially affect the inflammation condition. A macrophage cell line, RAW264.7, was employed to examine the effects of foods traditionally regarded as 'heating' or 'cooling' on the production of PGE(2), a well-known proinflammatory mediator. Foods traditionally regarded as 'heating' (litchi, longan, and dried longan) or 'cooling' (chrysanthemum flower, bitter gourd, and lotus seed plumule) were extracted sequentially with water and ethyl acetate. The water extracts (WE) and ethyl acetate extracts (EAE) were applied to RAW264.7 macrophages in the presence or absence of LPS (lipopolysaccharide). In the absence of LPS, the WEs from the 'heating foods', litchi, longan, or dried longan had a dose-dependent enhancing effect on PGE(2) production, with respective EC(50)s of 8.4, 16, and 11 mg/ml. This effect was accompanied by significant induction of COX-2 protein expression, as shown by Western blot analysis. In contrast, LPS-induced PGE(2) production was inhibited in a dose-dependent manner by the WEs of the 'cooling foods', chrysanthemum flower, bitter gourd, and lotus seed plumule, with respective IC(50)s of 0.6, 0.13, and 0.08 mg/ml. At the concentrations tested, none of the EAEs had any effect on basal PGE(2 )production, while LPS-induced PGE(2) production was inhibited or increased by the EAE from bitter gourd and longan, respectively. Water-soluble extracts of foods traditionally regarded as 'heating' enhanced basal PGE(2) production, while those from 'cooling' foods significantly inhibited LPS-induced PGE(2) production by the macrophage cell line. This subject merits further study to determine whether appropriate food selection may help patients suffering from chronic inflammatory conditions. Copyright 2002 National Science Council, ROC and S. Karger AG, Basel
« Last Edit: Jul 6th, 2004, 4:02pm by floridian » IP Logged
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