Fw: Subject Reference: Fw: Physicians' Protocol For Using Antibiotics in Rheumatic

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----- Original Message ----- From: ParfumGigi@...

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Subject: Physicians' Protocol for Using Antibiotics in Rheumatic Disease

Physicians' Protocol for Using Antibiotics in Rheumatic Disease The following is a modified version of Dr. Brown's protocol Introduction Rheumatoid arthritis affects about 1 percent of our population and at least two million Americans have definite or classical rheumatoid arthritis. It is a much more devastating illness than previously appreciated. Most patients with rheumatoid arthritis have a progressive disability. More than 50% of patients who were working at the start of their disease are disabled after five years of rheumatoid arthritis. The annual cost of this disease in the U.S. is estimated to be over $1 billion. There is also an increased mortality rate. The five-year survival rate of patients with more than thirty joints involved is approximately 50%. This is similar to severe coronary artery disease or stage IV Hodgkin's disease. Thirty years ago, one researcher concluded that there was an average loss of eighteen years of life in patients who developed rheumatoid arthritis before the age of 50. Most authorities believe that remissions rarely occur. Some experts feel that the term "remission-inducing" should not be used to describe ANY current rheumatoid arthritis treatment. A review of contemporary treatment methods shows that medical science has not been able to significantly improve the long-term outcome of this disease. My Experience with the Dr. Brown's Protocol I first became aware of Doctor Brown's protocol in 1989 when I saw him on 20/20 on ABC. This was shortly after the introduction of his first edition of The Road Back.The newest version is The New Arthritis Breakthrough that is written by Henry Scammel. Unfortunately, Dr. Brown died from prostate cancer shortly after the 20/20 program so I never had a chance to meet him. By the year 2000, I will have treated over 1,500 patients with rheumatic illnesses, including SLE, scleroderma, polymyositis and dermatomyositis. My application of Dr. Brown's protocol has changed significantly since I first started implementing it. Initially, I followed Dr. Brown's work rigidly with very little modification other than shifting the tetracycline choice to Minocin. I believe I was one of the first people who recommended the shift to Minocin, which seems to have been widely adopted at this time. In the early 90s, I started to integrate the nutritional model into the program and noticed a significant improvement in the treatment response. I cannot emphasize strongly enough the importance of this aspect of the program. It is absolutely an essential component of the revised Dr. Brown protocol. One may achieve remission without it, but the chances are much improved with its implementation. The additional benefit of the dietary changes is that they severely reduce the risk of the two to six month worsening of symptoms that Dr. Brown described in his book. In the late 80s, the common retort from other physicians was that there was "no scientific proof" that this treatment works. Well, that is certainly not true today. If one peeks ahead at the bibliography, one will find over 200 references in the peer-reviewed medical literature that supports the application of Minocin in the use of rheumatic illnesses. The definitive scientific support for minocycline in the treatment of rheumatoid arthritis came with the MIRA trial in the United States. This was a double blind randomized placebo controlled trial done at six university centers involving 200 patients for nearly one year. The dosage they used (100 mg twice daily) was much higher and likely less effective than what most clinicians currently use. They also did not employ any additional antibiotics or nutritional regimens, yet 55% of the patients improved. This study finally provided the "proof" that many traditional clinicians demanded before seriously considering this treatment as an alternative regimen for rheumatoid arthritis. Dr. Brown's effort to treat the chronic mycoplasma infections believed to cause rheumatoid arthritis is the basis for this therapy. Dr. Brown believed that most rheumatic illnesses respond to this treatment. He and others used this therapy for SLE, ankylosing spondylitis, scleroderma, dermatomyositis and polymyositis. Dr. Osler was also a preeminent figure of his time (1849- 1919). Many regard him as the consummate physician of modern times. An excerpt from a commentary on Dr. Osler provides a useful perspective on application of alternative medical paradigms: Osler would be receptive to the cautious exploration of nontraditional methods of treatment, particularly in situations in which our present science has little to offer. From his reading of medical history, he would know that many pharmacologic agents were originally derived from folk medicine. He would also remember that in the 19th century physicians no less intelligent than those in our own day initially ridiculed the unconventional practices of Semmelweis and Lister. Osler would caution us against the arrogance of believing that only our current medical practices can benefit the patient. He would realize that new scientific insights might emerge from as yet unproved beliefs. Although he would fight vigorously to protect the public against frauds and charlatans, he would encourage critical study of whatever therapeutic approaches were reliably reported to be beneficial to patients. Nutritional Considerations Limiting sugar is a critical element of the treatment program. Sugar has multiple significant negative influences on a person's biochemistry. Its major mode of action is through elevation of insulin levels. However, it has a similarly severe impairment of intestinal microflora. Patients who are unable to decrease their sugar intake are far less likely improve. One of the major benefits of implementing the dietary changes is that one does not seem to develop worsening of symptoms the first three to six months that is described in Dr. Brown's book. Most of my patients tend to not worsen once they start the antibiotics. I believe this is due to the beneficial effects that the diet has on the immune response. I ask all new patients to read my 6-page handout on the dietary changes. Rather than repeat it here, one could obtain the current version on my web site here. Antibiotic Therapy With Minocin There are three different tetracyclines available: simple tetracycline, doxycycline, or Minocin (minocycline). Minocin has a distinct and clear advantage over tetracycline and doxycycline in three important areas. 1. Extended spectrum of activity 2. Greater tissue penetrability 3. Higher and more sustained serum levels Bacterial cell membranes contain a lipid layer. One mechanism of building up a resistance to an antibiotic is to produce a thicker lipid layer. This layer makes it difficult for an antibiotic to penetrate. Minocin's chemical structure makes it the most lipid soluble of all the tetracyclines. This difference can clearly be demonstrated when one compares the drugs in the treatment of two common clinical conditions. Minocin gives consistently superior clinical results in the treatment of chronic prostatitis. In other studies, Minocin was used to improve between 75-85% of patients whose acne had become resistant to tetracycline. Strep is also believed to be a contributing cause to many patients with rheumatoid arthritis. Minocin has shown significant activity against treatment of this organism. There are several important factors to consider when using Minocin. Unlike the other tetracyclines, it tends not to cause yeast infections. Some infectious disease experts even believe that it even has a mild anti-yeast activity. Women can be on this medication for several years and not have any vaginal yeast infections. Nevertheless, it would be prudent to have patients on prophylactic oral Lactobacillus acidophilus and bifidus preparations. This will help to replace the normal intestinal flora that is killed with the Minocin. Another advantage of Minocin is that it tends not to sensitize patients to the sun. This minimizes the risk of sunburn and increased risk of skin cancer. However, one must incorporate several precautions with the use of Minocin. Like other tetracyclines, food impairs its absorption. However, the absorption is much less impaired than with other tetracyclines. This is fortunate because some patients cannot tolerate Minocin on an empty stomach. They must take it with a meal to avoid GI side effects. If they need to take it with a meal, they will still absorb 85% of the medication, whereas tetracycline is only 50% absorbed. In June of 1990, a pelletized version of Minocin became available. This improved absorption when taken with meals. This form is only available in the non-generic Lederle brand and is a more than reasonable justification to not substitute for the generic version. Clinical experience has shown that many patients will relapse when they switch from the brand name to the generic. Clinically it has been documented that it is important to take Lederle brand Minocin. Most all generic minocycline is clearly not as effective. A large percentage of patients will not respond at all or not do as well with generic non-Lederle minocycline. Traditionally it was recommended to only receive the brand name Lederle Minocin. However, there is one generic brand that is acceptable and that is the brand made by Lederle. The only difference between Lederle generic Minocin and brand name Minocin is the label and the price. The problem is finding the Lederle brand generic. Some of my patients have been able to find it at Wal Mart. Since Wal Mart is one of the largest drug chains in the US, this should make the treatment more widely available for a reduced charge. Many patients are on NSAID's which contribute to microulcerations of the stomach which cause chronic blood loss. It is certainly possible they can develop a peptic ulceration contributing to their blood loss. In either event, patients frequently receive iron supplements to correct their blood counts. IT IS IMPERATIVE THAT MINOCIN NOT BE GIVEN WITH IRON. Over 85% of the dose will bind to the iron and pass through the colon unabsorbed. If iron is taken, it should be at least one hour before the minocin or two hours after. One recent uncommon complication of Minocin is a cell-mediated hypersensitivity pneumonitis. Most patients can start on Minocin 100 mg. every Monday, Wednesday, and Friday evening. Doxycycline can be substituted for patients who cannot afford the more expensive Minocin. It is important to not give either medication daily, as this does not seem to provide as great a clinical benefit. Tetracycline type drugs can cause a permanent yellow- grayish brown discoloration of the teeth. This can occur in the last half of pregnancy and in children up to eight years old. One should not routinely use tetracycline in children. If patients have severe disease, one can consider increasing the dose to as high as 200 mg three times a week. Aside from the cost of this approach, several problems result may result from the higher doses. Minocin can cause quite severe nausea and vertigo. Taking the dose at night does tend to decrease this problem considerably. However, if one takes the dose at bedtime, one must tell the patient to swallow the medication with TWO glasses of water. This is to insure that the capsule doesn't get stuck in the throat. If that occurs, a severe chemical esophagitis can result which can send the patient to the emergency room. For those physicians who elect to use tetracycline or doxycycline for cost or sensitivity reasons, several methods may help lessen the inevitable secondary yeast overgrowth. Lactobacillus acidophilus will help maintain normal bowel flora and decrease the risk of fungal overgrowth. Aggressive avoidance of all sugars, especially those found in non-diet sodas will also decrease the substrate for the yeast's growth. Macrolide antibiotics like Biaxin or Zithromax may be used if tetracyclines are contraindicated. They would also be used in the three pills a week regimen. Clindamycin The other drug used to treat rheumatoid arthritis is clindamycin. Dr. Brown's book discusses the uses of intravenous clindamycin. It is important to use the IV form of treatment if the disease is severe. Nearly all scleroderma patients should take an aggressive stance and use IV treatment. Scleroderma is a particularly dangerous form of rheumatic illness that should receive aggressive intervention. A major problem with the IV form is the cost. The price ranges from $100 to $300 per dose if administered by a home health care agency. However, if purchased directly from Upjohn, significant savings will be appreciated. A case of two-dozen 900 mg prefilled IV bags can be purchased directly from Upjohn for about $200. For patients with milder illness, the oral form is preferable. If the patient has a mild rheumatic illness (the minority of cases), it is even possible to exclude this from their regimen. Initial starting doses for an adult would be a 1200 mg dose once a week. Patients do not seem to tolerate this medication as well as Minocin. The major complaint seems to be a bitter metallic type taste, which lasts about 24 hours after the dose. Taking the dose after dinner does seem to help modify this complaint somewhat. If this is a problem, one can lower the dose and gradually increase the dose over a few weeks. Concern about the development of C. difficile pseudomembranous enterocolitis as a result of the clindamycin is appropriate. This complication is quite rare at this dosage regimen, but it certainly can occur. It is important to warn all patients about the possibility of developing a severe uncontrollable diarrhea. Administration of the acidophilus seems to limit this complication by promoting the growth of the healthy gut flora. If one encounters a resistant form of rheumatic illness, intravenous administration should be considered. Generally, weekly doses of 900 mg are administered until clinical improvement is observed. This generally occurs within the first ten doses. At that time, the regimen can be decreased to every two weeks with the oral form substituted on the weeks where the IV is not taken. What To Do If Severe Patients Fail To Respond The most frequent reason for failure to respond to the protocol is lack of adherence to the dietary guidelines. Most patients will be eating too many grains and sugars, which disturb insulin physiology. It is important that patients adhere as strictly as possible to the guidelines. A small minority, generally under 15%, of patients will fail to respond to the protocol described above despite rigid adherence to the diet.These individuals should already be on the IV Clindamycin. It appears that the hyaluronic acid, which is a potentiating agent commonly used in the treatment of cancer may be quite useful. It seems that hyaluronic acid has very little to no direct toxicity but works in a highly synergistic fashion when administered directly in the IV bag with the Clindamycin. Hyaluronic acid is also used in orthopedic procedures. The dose is generally from 2 to 10 cc into the IV bag. Hyaluronic acid is not inexpensive as the cost may range up to $10 per cc.One does need to exert some caution with its use as it may precipitate a significant Herxheimer flare reaction. All negative emotions are disruptions in one’s bioenergy system. Energy psychology combines needless acupuncture and psychology for some of the most profoundly powerful tools in addressing stress. The most popular technique is called Emotional Freedom Technique (EFT). I believe this is one of the best tools to address pain in rheumatoid arthritis and I have been absolutely astounded at the rapid and profound benefits patients have received from this simple tool. Anti-Inflammatories The first non-aspirin NSAID, indomethacin was introduced in 1963. Now more than 30 are available. Relafen is one of the better alternatives as it seems to cause less of an intestinal dysbiosis. If cost is a concern, generic ibuprofen can be used. Unfortunately, recent studies suggest this drug is more damaging to the kidneys. One must be especially careful to monitor renal function studies periodically. It is important for the patient to understand and accept the risks associated with these more toxic drugs. Unfortunately, these drugs are not benign. Every year, they do enough damage to the GI tract to kill 2,000 to 4,000 patients with rheumatoid arthritis alone. That is ten patients EVERY DAY. At any given time patients receiving NSAID therapy have gastric ulcers in the range of 10-20%. Duodenal ulcers are lower at 2- 5%. Patients on NSAIDs are at approximately three times greater relative risk for developing serious gastrointestinal side effects than are non-users. Approximately 1.2% of patients taking NSAIDs are hospitalized for upper GI problems per year of exposure. One study of patients taking NSAIDs showed that a life-threatening complication was the first sign of ulcer in more than half of the subjects. Celebrex has received much recent press due to its decreased toxicity to the gut. That is certainly a step in the right direction. Celebrex inhibits a specific type of prostaglandin and is called a COX2 inhibitor. A similar new drug introduced in 1999 is Vioxx. There was a report in early 1999 in the Proceedings of the National Academy of Science, which showed that these drugs might increase the risk of heart attack, stroke and blood clotting disorders. Researchers found that the drugs suppress production of prostacyclin, which is needed to dilate blood vessels and inhibit clotting. Earlier studies had found that mice genetically engineered to be unable to use prostacyclin properly were prone to clotting disorders. Anyone who is at increased risk of cardiovascular disease should steer clear of these two new medications. Ulcer complications are certainly potentially life-threatening,but, heart attacks are a much more common and likely risk, especially in older individuals. Risk factor analysis helps to discriminate those that are at increased danger of developing these complications. Those associated with a higher frequency of adverse events are: 1. Old age 2. Peptic ulcer history 3. Alcohol dependency 4. Cigarette smoking 5. Concurrent prednisone or corticosteroid use 6. Disability 7. High dose of the NSAID 8. NSAID known to be more toxic Studies clearly show that the non-acetylated salicylates are the safest NSAIDs. Celebrex and Vioxx likely cause the least risk for peptic ulcer. But as mentioned, they pose an increased risk for heart disease. Factoring these newer medications out would leave the following less toxic NSAIDs: Relafen, Daypro, Voltaren, Motrin, and Naprosyn. Meclomen, Indocin, Orudis, and Tolectin are among the most toxic or likely to cause complications. They are much more dangerous than the antibiotics or non-acetylated salicylates. One should run an SMA at least once a year on patients who are on these medications. One must monitor the serum potassium levels if the patient is on an ACE inhibitor as these medications can cause hyperkalemia. One should also monitor their kidney function. The SMA will also show any liver impairment that the drugs might cause. These medications can also impair prostaglandin metabolism and cause papillary necrosis and chronic interstitial nephritis. The kidney needs vasodilatory prostaglandins (PGE2 and prostacycline) to counterbalance the effects of potent vasoconstrictor hormones such as angiotensin II and catecholamines. NSAIDs decrease prostaglandin synthesis by inhibiting cyclooxygenase, leading to unopposed constriction of the renal arterioles supplying the kidney. One might consider the use of non-acetylated salicylates such as salsalate, sodium salicylate and magnesium salicylate (i.e., Salflex, Disalcid, or Trilisate). They are the drugs of choice if there is renal insufficiency. They have minimal interference with anticyclooxygenase and other prostaglandins. Additionally, they will not impair platelet inhibition of those patients who are on every other day aspirin to decrease their risk for stroke or heart disease. Unlike aspirin, they do not increase the formation of products of lipoxygenase-mediated metabolism of arachidonic acid. For this reason, they may be less likely to precipitate hypersensitivity reactions. These drugs have been safely used in patients with reversible obstructive airway disease and a history of aspirin sensitivity. They also are much gentler on the stomach then the other NSAIDs and are the drug of choice if the patient has problems with peptic ulcer disease. Unfortunately, all these benefits are balanced by the fact they may not be as effective as the other agents and are less convenient to take. One needs to push them to 1.5-2 grams bid and tinnitus is a frequent complication. One should warn patients of this complication and explain that if tinnitus does develop they need to stop the drugs for a day and restart with a dose that is half a pill per day lower. They repeat this until they find a dose that relieves their pain and doesn't give them any ringing. Prednisone One can give patients with severe disease a prescription for prednisone 5 mg. They can take one of them a day if they develop a severe flare-up as a result of going on the antibiotics. They can use an additional tablet at night if they are in really severe flare. Explain to all patients that the prednisone is very dangerous and every dose they take decreases their bone density. However, it is a trade-off. Since they will only be on it for a matter of months, its use may be justifiable. This is the first medicine they should try to stop as soon as their symptoms permit. Blood levels of cortisol peak between 3 and 9am. It would, therefore, be safest to administer the prednisone in the morning. This will minimize the suppression on the hypothalamic-pituitary-adrenal axis. Patients often ask the dangers of these medications. The most significant one is osteoporosis. Other side effects that usually occur at higher doses include adrenal insufficiency, atherosclerosis acceleration, cataract formation, Cushing's syndrome, diabetes, ulcers, herpes simplex and tuberculosis reactivation, insomnia, hypertension, myopathy and renal stones. One also needs to be concerned about the increased risk of peptic ulcer disease when using this medicine with conventional non-steroidal anti-inflammatories. Persons receiving both of these medicines may have a 15 times greater risk of developing an ulcer. If a patient is already on prednisone, it is helpful to give them a prescription for 1 mg tablets so they can wean themselves off of the prednisone as soon as possible. Usually one lowers the dose by about 1 mg per week. If a relapse of the symptoms occurs, than further reduction of the prednisone is not indicated. Remission The following criteria can help establish remission: *A decrease in duration of morning stiffness to no more than 15 minutes No pain at rest Little or no pain or tenderness on motion Absence of joint swelling A normal energy level A decrease in the ESR to no more than 30 A normalization of the patient's CBC. Generally the HGB, HCT, & MCV will increase to normal and their "pseudo"-iron deficiency will disappear ANA, RF, & ASO titers returning to normal The natural course of rheumatoid arthritis is quite remarkable. Less than 1% of patients who are rheumatoid factor seropositive have a spontaneous remission. Some disability occurs in 50-70% of patients within five years after onset of the disease. Half of the patients will stop working within 10 years. This devastating natural prognosis is what makes the antibiotic therapy so exciting. Approximately one third of patients have been lost to follow-up for whatever reason and have not continued with treatment. The remaining patients seem to have a 60-90% likelihood of improvement on this treatment regimen. That is quite a stark contrast to the numbers quoted above. There are many variables associated with an increased chance of remission or improvement. The younger the patient is the better they seem to do. The more closely they follow the diet, the less likely they are to have a severe flare-up and the more likely they are to improve. Smoking seems to be negatively associated with improvement. The longer the patient has had the illness and the more severe the illness the more difficult it seems to treat. If patients discontinue their medications before all of the above criteria are met, there is a greater risk that the disease will recur. If the patient meets the above criteria, one can have them to try to stop their anti-inflammatory medication once they start to experience these improvements. If the improvements are stable for six months, then discontinue the clindamycin. If the improvements are maintained for the next six months, one can then discontinue their Minocin and monitor for recurrences. If symptoms should recur, it would be wise to restart the previous antibiotic regimen. Overall, nearly 80% of the patients do remarkably better with this program. Approximately 5% of the patients continued to worsen and required conventional agents, like methotrexate, to relieve their symptoms. Approximately 15% of the patients who started the treatment dropped out of the program and were lost to follow-up. The longer and more severe the illness, the longer it takes to cure. Smokers tend not to do as well with this program. Age and competency of the person's immune system are also likely important factors. Dr. Brown successfully treated over 10,000 patients with this protocol. He found that significant benefits from the treatment require on the average one to two years. I have treated nearly over 1,500 patients and find that the dietary modification I advocate accelerates the response rate to several months. The length of therapy can vary widely. In severe cases, it may take up to thirty months for the patients to gain sustained improvement. One requires patience because remissions may take up to 3 to 5 years. Dr. Brown's pioneering approach represents a safer less toxic alternative to many conventional regimens and results of the NIH trial have finally scientifically validated this treatment. Preliminary Laboratory Evaluation For Non-Rheumatologists It is important to evaluate patients to determine if indeed they have rheumatoid arthritis. Most patients will have received evaluations and treatment by one or more board certified rheumatologists. If this is the case, the diagnosis is rarely in question and one only needs to establish some baseline laboratory data. However, patients will frequently come in without having any appropriate workup done by a physician. Arthritic pain can be an early manifestation of 20-30 different clinical problems. These include not only rheumatic disease, but also metabolic, infectious and malignant disorders. These patients will require a more extensive laboratory analysis. Rheumatoid arthritis is a clinical diagnosis for which there is not a single test or group of laboratory tests which can be considered confirmatory. When a patient hasn't been properly diagnosed, then one needs to establish the diagnosis with the standard Rheumatism Association's criteria found in the table at the end of the article. One must also make certain that the first four symptoms listed in the table are present for six or more weeks. These criteria have a 91-94% sensitivity and 89% specificity for the diagnosis of rheumatoid arthritis. However, these criteria were designed for classification and not for diagnosis. One must make the diagnosis on clinical grounds. It is important to note that many patients with negative serologic tests can have a strong clinical picture for rheumatoid arthritis. The metacarpophalangeal joints, proximal interphalangeal and wrists joints are the first joints to become symptomatic. In a way, the hands are the calling card of rheumatoid arthritis. If the patient completely lacks hand and wrist involvement, even by history, the diagnosis of rheumatoid arthritis is doubtful. Rheumatoid arthritis rarely affects the hips and ankles early in its course. Fatigue may be present before the joint symptoms begin. Morning stiffness is a sensitive indicator of rheumatoid arthritis. An increase in fluid in and around the joint probably causes the stiffness. The joints are warm, but the skin is rarely red. When the joints develop effusions, the patients holds them flexed at 5 to 20 degrees as it is too painful to extend them fully. The general initial laboratory evaluation should include a baseline ESR, CBC, SMA, U/A, and an ASO titer. One can also draw RF and ANA titers to further objectively document improvement with the therapy. However, they seldom add much to the assessment. Follow-up visits can be every two months for patients who live within 50 miles, and every three to four months for those who live farther away. An ESR at every visit is an inexpensive and reliable objective parameter of the extent of the disease. However, one should run this test within several hours of the blood draw. Otherwise, one cannot obtain reliable and reproducible results. This is nearly impossible with most clinical labs that pick up your specimen at the office. Inexpensive disposable ESR kits are a practical alternative to the commercial or hospital labs. One can then run them in the office, usually within one hour of the blood draw. One must be careful to not run the test on the same countertop as your centrifuge. This may cause a falsely elevated ESR due to the agitation of the ESR measuring tube. Many patients with rheumatoid arthritis have a hypochromic, microcytic CBC. This is probably due to the inflammation in the rheumatoid arthritis impairing optimal bone marrow utilization of iron. This type of anemia does NOT respond to iron. Patients who take iron can actually worsen if they don't need it as the iron serves as a potent oxidant stress. Ferritin levels are generally the most reliable indicator of total iron body stores. Unfortunately it is also an acute phase reactant protein and will be elevated anytime the ESR is elevated. This makes ferritin an unreliable test in patients with rheumatoid arthritis. Fibromyalgia One needs to be very sensitive to this clinical problem when treating patients with rheumatoid arthritis. It is frequently a complicating condition. Many times, patients will confuse the pain from it with a flare-up of their arthritis. One needs to aggressively treat this problem. If this problem is ignored, the likelihood of successfully treating the arthritis is significantly diminished. Fibromyalgia is a very common problem. Some experts believe that 5% of people are affected with it. Over 12% of the patients at the Mayo Clinic's Department of Physical Medicine and Rehabilitation have this problem. It is the third most common diagnosis by rheumatologists in the outpatient setting. Fibromyalgia affects women five times as frequently as men. Signs And Symptoms of Fibromyalgia One of the main features of fibromyalgia is the morning stiffness, fatigue, and multiple areas of tenderness in typical locations. Most patients with fibromyalgia complain of pain over many areas of the body, with an average of six to nine locations. Although the pain is frequently described as being all over, it is most prominent in the neck, shoulders, elbows, hips, knees, and back. ============================================================

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----- Original Message ----- From: Martha Murdock & (gigi*) Lawrence

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Sent: Wednesday, February 13, 2002 10:14 PM

Subject: Subject Reference: Fw: Physicians' Protocol For Using Antibiotics in Rheumatic

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----- Original Message ----- From: ParfumGigi@...

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Sent: Wednesday, February 13, 2002 7:56 PM

Subject: Physicians' Protocol For Using Antibiotics in Rheumatic Disease (Continued)

Physicians' Protocol For Using Antibiotics in Rheumatic Disease (Continued) Bibliography Bibliography 1. Pincus T, Wolfe F: Treatment of Rheumatoid Arthritis: Challenges to Traditional Paradigms. AnnInternMed 115:825-6, Nov 15 1991. 2. Pincus T: Rheumatoid arthritis: disappointing long-term outcomes despite successful short-term clinical trials. J Clin Epidemiol 41:1037-41, 1988. 3. PM: Clinical management of rheumatoid arthritis. Lancet 341 :286-90, 1993. 4. Pincus T, Callahan LF: Remodeling the pyramid or remodeling the paradigms concerning rheumatoid arthritis - lessons learned from Hodgkin's Disease and coronary artery disease. JRheumatol 17:1582-5, 1990. 5. Reah TG: The prognosis of rheumatoid arthritis. Proc R Soc Med 56:813-17, 1963. 6. Wolfe F, Hawley DJ: Remission in rheumatoid arthritis. J Rheumatol 12:245-9, 1985. 7. Kushner I, Dawson NV: Changing perspectives in the treatment of rheumatoid arthritis. JRheumatol 19:1831-34, 1992. 8. Pinals RS: Drug therapy in rheumatoid arthritis a perspective. Br J Rheumatol 28:93-5, 1989. 9. Klippel JH: Winning the battle, losing the war? Another editorial about rheumatoid arthritis. JRheumatol 17:1118-22. 1990. 10. Healey LA, Wilske KR: Evaluating combination drug therapy in rheumatoid arthritis. J Rheumatol 18:641-2, 1991. 11. Wolfe F: 50 Years of antirheumatic therapy: the prognosis of rheumatoid arthritis. J Rheumatol 17:24-32, 1990. 12. SE, Luthra HS: Rheumatoid arthritis: Can the long term be altered? Mayo Clin Proc 63:58-68, 1988. 13. ED: Rheumatoid arthritis: Pathophysiology and implications for therapy. NEngl JMed 322:1277-1289, May 3, 1990. 14. Schwartz BD: Infectious agents, immunity and rheumatic diseases. Arthr Rheum 33 :457-465, April 1990. 15. Tan PLJ, Skinner MA: The microbial cause of rheumatoid arthritis: time to dump Koch's postulates. J Rheumatol 19:1170-71. 1992. 16. Ford DK: The microbiological causes of rheumatoid arthritis. 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Pincus T: Rheumatoid arthritis: disappointing long-term outcomes despite successful short-term clinical trials. J Clin Epidemiol 41:1037-41, 1988. 3. PM: Clinical management of rheumatoid arthritis. Lancet 341 :286-90, 1993. 4. Pincus T, Callahan LF: Remodeling the pyramid or remodeling the paradigms concerning rheumatoid arthritis - lessons learned from Hodgkin's Disease and coronary artery disease. JRheumatol 17:1582-5, 1990. 5. Reah TG: The prognosis of rheumatoid arthritis. Proc R Soc Med 56:813-17, 1963. 6. Wolfe F, Hawley DJ: Remission in rheumatoid arthritis. J Rheumatol 12:245-9, 1985. 7. Kushner I, Dawson NV: Changing perspectives in the treatment of rheumatoid arthritis. JRheumatol 19:1831-34, 1992. 8. Pinals RS: Drug therapy in rheumatoid arthritis a perspective. Br J Rheumatol 28:93-5, 1989. 9. Klippel JH: Winning the battle, losing the war? Another editorial about rheumatoid arthritis. JRheumatol 17:1118-22. 1990. 10. 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