so i had my drs appt today and overall i am pleased to report that my pain has been managed quite well by the prednisone and my dr wants me to stay on it. bleck. it is the devil drug in my opinion but it did vastly improve the amount of pain i am in and i guess the side effects are a far cry from the agony i was experiencing before. he did tell add plaquenil to my meds lineup and feels good that we caught this thing so early. he wants to use the mildest agents possible to control pain and stave off permanent damage. so he started me on 400 mg of the plaquenil and continued the pred. however he did say i could try lowering the dosage of pred once the plaq started to work and see if that was enough to manage the pain. i was feeling quite awful this morning so i wasn't as articulate or questioning as i normally am. i have another appt set for 2 months and i have to get an eye exam in the next three.
so i have my (still numb and tingly) fingers crossed that the lowest dosages and mildest drugs will work for me for a long time before i have to switch to more potent and risky drugs.
i just took my first plaquenil so i will let you u all know how it works. anyone here have any experience with it? does it help more than hurt? my next net adventure will me plaquenil research.
on a paranoid sidenote...does it concern anyone that drugs originally designed for treatment of other things like malaria and cancer are used to treat AI disorders? i know science stumbles across dual usages all the time and experimentation with drugs leads to new medical discoveries, however i am somehow perturbed by the thought of blindly taking an antimalarial to fix my RA. maybe i am just cloudy brained today and nothing really makes sense.
Many drugs are discovered by accident... Viagra was originally supposed to be some sort of heart medication; Thorazine was supposed to be an antihistamine; thalidomide treats rare forms of leukemia, but it was originally used to treat morning sickness in pregnant women (with dire consequences!!!).
At least plaquenil and methotrexate have been on the market for many years, so their side effects are pretty well-known.
Hi Erica, I'm so gald you had a good report from your Dr. and that you are doing the right thing. Plaq takes a while to work, but I don't know how long. I grieved over taking 'small amt of drugs they give to people with cancer, but got over it', . I think if you need to see the Dr. sooner, or need questions asked to go for it. You never know what might come up and you don't want to 'be worrying', try to get a good relationship with the staff, as they are often able to get a message to your doctor, help you, help you get apptments, etc.
When you try to get off of the Prednisone you can take the 1mg amounts (people on here told me) so, if you want to decrease you can go from 7.5 to 6.5, etc. you need to ask for the 1mgs. though. You can cut the 5's in half, etc. So doing with less doesn't have to be going from 7.5 down to 5. These are powerful buggers, going up and down with them can be tricky.
I've finally gotten off, but I am very tired.
Lynda
Erica I have been on Plaquinile (sp?). It did not do much for me and this was before I got to the point I am now. It was an ok drug.
I hope it does work for you and then you can come off the pred. I am going on almost 3 years of being on pred. But without it right now I would be laying in bed unable to move and unable to tend to my son, and not to mention in GREAT HORRIFIC PAIN!
My new med I am on to take in combo with Remicade is Imuran. Imuran is used in combonation with other meds for kidney transplant patients to help them not to reject the new kidney.
Antimalarials were designed to kill a spirocette. Like syphillis.
Pip
That reminds me that I have always falsely tested positive for syphillis, everIt isn’t too unusual that your doctor is starting you out with the milder meds first. Plaquenil can take up to 6 months to work. Usually it does not. There are a few people here that have had great success with Plaq. I hope you do too. Many people new to RA and its medications are leery of the side of effects and long term effects of the stronger meds like mtx…imuran…Humira…etc. The only thing I can really say to you about that is the way I feel about it. I feel that I have to live in the here and now. That my family needs me to do whatever it is I can to be well. And if that means taking these stronger meds then so be it. I will worry about long term effects if and when that time ever comes. Because of the FDA and government regulations, these pharm companies are required to inform us in those stupid commercials about the long term effects and scare the crud out of everyone. Those long term effects that many people worry about very rarely happen. You are more likely to have long term effects from the RA if you do not opt to do the stronger meds. From what I understand about AP…it is the same theory as the traditional way to go with meds. If you do not do AP or the traditional meds…you are more likely to have long term effects from the RA rather than the meds.
As Jasmine said…many drugs that were intended to treat one disease are accidentally discovered to treat another one. In a way, I think that is kind of neat. I can’t figure out why tho lol. I am just happy that any treatment was discovered. Methotrexate is originally intended for breast cancer chemo treatment. It was found in women with BC that also had RA that their RA symptoms subsided with the mtx chemo treatments they were getting for their BC.
Most of us have a love/hate relationship with pred. I really hate being on the stuff but I know at this point in life, I really need it or I would not be able to get out of bed. You really will just *know* when you are ready to start weaning off of the prednisone. It is just a feeling that you get.
Hang in there!!
The biologically false-positive test for syphilis (BFP-STS) constituted the first assay for aPL .[10,13] False-positive syphilis tests are seen not only in APS, but also in other clinical situations, including recent infection, postvaccination, and SLE, as well as in otherwise-healthy young women.[15] Today, the Venereal Disease Research Laboratory (VDRL) test, which uses cardiolipin phospholipid as its major reagent, is used by most practitioners to screen for syphilis. A false-positive VDRL test is not considered to show a strong correlation with APS. It does not necessarily identify patients at increased risk for clotting, and it should not be used as the sole serologic criterion for diagnosing APS. However, a false-positive VDRL test should lead to further serologic evaluation, including both the LAC and aCL assays.[10,13]
As compared with BFP-STS, both the LAC and aCL tests have, to date, been the diagnostic tests of choice for APS. LAC antibodies are immunoglobulins that have been described as LACs since their discovery in the sera of lupus patients and their observed interference with in vitro phospholipid-dependent coagulation tests, frequently resulting in prolongation of the activated partial thromboplastin time (aPTT) and, less frequently, the prothrombin time (PT). This prolongation can be verified by additional laboratory mixing studies.[13] In addition to the PT and aPTT, tests for LAC antibody include the Kaolin clotting time (KCT) and the dilute Russell Viper Venom Time (dRVVT).[10,11,13,15] The term "lupus anticoagulant" is misleading, however, because patients positive for LAC antibody, or other aPL antibodies, are at risk for hypercoaguability, not for bleeding.
The aCL tests are the third category of assay used to detect aPL. The development of an assay for aCL by Hughes and associates has much facilitated the diagnosis of APS.[1] The test, now performed by enzyme-linked immunosorbent assay (ELISA), has been scrutinized by experts in the field, but continues to be the gold standard (along with LAC) for the serologic diagnosis of APS.[1] IgG, IgM, and IgA classes of aCL antibodies are expressed as G phospholipid units (GPL), M phospholipid units (MPL), and A phospholipid units (APL), based on previously established international standards.[13]
All 3 tests (BFP-STS, LAC, aCL) are assays for "antiphospholipid antibodies," a name that implies that the antibodies are directed against phospholipids. For many years the prevailing thought was that antibodies directed against vascular endothelial cell-membrane phospholipids caused the vascular thrombosis seen in APS. More recent data, however, suggest that these antibodies are directed against other plasma proteins (especially beta-2-GP1 or other protein-altered complexes), which bind to endothelial phospholipids and act as the true antigens, rather than cardiolipin or phospholipids themselves, which are poor antigens. It is likely that the antigen detected in the aCL assay is directed against this "cofactor protein," beta-2-GP1, bound to the phospholipid surface, possibly expressing a neoepitope, although other mechanisms may exist. With the advent of this concept, the term "antiphospholipid protein" or "antiphospholipid cofactor" syndrome (rather than APS) has evolved.[15-19] Hughes Syndrome, named after the premiere researcher in this field, may also come into use as a diagnosis.[1] Other proteins (or cofactors) that aPL antibodies (LAC, aCL) may recognize as antigens include prothrombin, protein C, and protein S, among others.[18,19]
Still debated is the question of whether aPL antibodies are causative or epiphenomenal.[15,16] For the practitioner, they remain the only reliable serologic test for the diagnosis of APS. At present only the aCL and LAC are commercially available, although anti-beta-2-GP1 assays may enter the market soon.
Interpretation of results from aCL and LAC antibody assays are disputed (Table II). Despite extensive attempts at international standardization of aCL test results, no consensus exists for a value beyond which the test is considered positive. Interestingly, a "dose-effect" relationship for aCL antibody titers has been noted: Higher titers of the antibody correlate with increased numbers of thrombotic events.[3] A lower limit of 20 phospholipid units has been suggested to make the diagnosis of APS.[13] What constitutes a positive test is further confounded by the fact that normal ranges vary from one commercial lab to another, and assay results do not demonstrate interlaboratory concordance.[20] As long as laboratories fail to adhere to internationally accepted standards for testing and reporting aCL levels,[21] clinicians should interpret results in the context of the patient's previous titers, if available, and of the clinical presentation. Significance of the titers (low-, mid-, and high-range) remains controversial.[10,11] Given the data on the variability of titers, it seems prudent for the clinician to believe aCL antibodies are significant when they are repeatedly positive, regardless of levels, especially when clinical criteria for the syndrome are present.
Some authorities consider only high- or mid-range titers important,[11] whereas others recognize that low-range titers are also important.[10] In fact, patients with documented APS may at times become seronegative, which makes the interpretation of titers even more difficult.[22] In addition, IgA aCL antibodies have been infrequently associated with APS.[13]
Patients with autoimmune diseases including SLE and rheumatoid arthritis, infections such as syphilis and HIV, or drug-induced states associated with certain psychotropic agents may test positive for aPL antibody but have no clinical manifestations of APS. An aPL antibody detected in patients with autoimmune disease is more likely to be associated with APS than in patients with either drug-induced or infection-related aPL. In the case of a positive test, the titer, type, or other characteristics of the aPL antibody, such as specificity for beta-2-GP1, may all affect the likelihood of expression of associated clinical disease.[11,13]
LAC testing is also problematic for the clinician. Not all hospitals and clinical laboratories use thromboplastin reagents that are sensitive to LAC for determination of aPPT. Furthermore, used alone, none of the LAC assays currently available is sufficiently sensitive. Therefore, batteries of tests, including the aPTT, KCT, dRVVT, and others, need to be done to increase the yield.[10] Test results may be unreliable in patients anticoagulated with warfarin, a therapy frequently employed in patients whose presentation is suspicious for APS.
Despite all of the problems associated with testing, the aCL and LAC assays are both of tremendous value to physicians managing patients with vascular events, fetal loss, or undiagnosed medical illnesses. We recommend that clinicians perform such screening assays on all patients in whom they suspect APS. If these tests are negative, follow-up serial testing may be warranted based on the clinician's index of suspicion. In addition, other aPL assays, including those for antiphosphatidyl serine, antiphosphatidyl choline, and antiphosphatidyl ethanolamine, may be requested. The standard laboratory work-up for unexplained clotting, including tests for antithrombin deficiency, protein C and protein S deficiencies, and others may be indicated.[13] Finally, if all locally available tests are negative, we strongly suggest that serum samples be sent to research centers where the anti-beta-2-GP1 assay is available. The assay for anti-beta-2-GP1 may become the most important test for aPL.
Thanks JasmineRain, I actually missed this post until someone just brought it to my attention. I'm not sure what it means but I'm going to print this out and show it to my GP tomorrow.