Poor Results from Mainstream Scleroderma Therapies

• "We have seen too few (studies) that apply the basic standards used in modern scientific clinical research." (Journal of Rheumatology, 1992)1

• "There appear to be clear differences between the early stages and later stages of disease... The most basic question is whether a placebo effect is possible in diffuse scleroderma. . . Outcomes to consider include survival, quality of life, prevention of internal organ involvement, improvement in established internal organ involvement and control of more important symptoms." (Journal of Rheumatology, 1992)'

• "Scleroderma is difficult to treat. Although therapy with D-penicillamine has been suggested, it yields variable success and a high drop-out rate because of side effects. Intolerance Of D-penicillamine approaches 50% after 2 years. Because there is no truly effective therapy for scleroderma, alter native therapies need to be evaluated." (Seminars in Arthritis & Rheumatism, 1993)'

• "What distinguishes photopheresis from other proposed treatments (is) ... the extremely high cost of the therapy. A lot of money is involved... Data does not support the efficacy of photopheresis in scleroderma... Any therapeutic advantage is limited to minor skin softening, appears to disappear with time and the treatment does not affect the under-lying disease process as judged by skin biopsy. It is reasonable to consider whether a short term 15% improvement in skin thickening is worth $60,000 or more when compared to a therapy such as D-penicillamine $100/month) - ed. or antibiotics at $30 a month or less!" (Journal of Rheumatology, 1992)'

• "The mortality in SSc is increased compared to the general population, especially with diffuse disease... We found a 4.7-fold increase in the risk of death among patients with SSc compared to the Ontario population... The risk of death in the subset with diffuse scleroderma was 2-fold higher in men compared to women... the increase in death from pulmonary hypertension was greater with limited disease, while from renal failure and cardiac causes among those with diffuse disease." (Journal of Rheumatology, 1995)'

• "Scleroderma is associated with a 79% to 84% survival at 5 years and a 47% to 75% survival at 10 years. However, the presence of truncal sclerosis at disease onset reduces survival to 48% to 50% at 5 years and 22% to 26% at 10 years. In a study of 264 patients with SSc after 5 years of follow-up, at the end of the study, 50% were dead, 68% of deaths were definitely related to SSc." (Journal of the American Academy of Dermatology, 1993)1

• "It is estimated that there are 300,000 patients with SSc in the United States (as of 1993) with 5000 new cases per year." (Journal of the American Academy of Dermatology, 1993)1

What Medical Journals Say about Scleroderma and an Infectious Etiology

• In a discussion of scleroderma in her 1976 book, Cell Wall Deficient Forms, noted researcher Lida H. Mattman, Ph.D., an expert on altered bacterial forms (L-forms), comments, "The frequent isolation of wall deficient variants of pathogens from their respective diseases of known etiology and the further correlation of these forms with pathogenesis in animal virulence studies have launched many investigations seeking their possible role in diseases of unknown or variable etiology.... In spite of all modern therapeutic approaches, scleroderma remains a disease to respect." (Cell Wall Deficient Forms, CBC Press, 1976)1

• "This is a preliminary report on a probable bacterial cause of scleroderma and on its further treatment with an antibacterial agent... An acid-fast bacillus has been found in five cases of scleroderma examined bacteriologically." (Journal of Medical Society of New York, 1947)2

• "This report concerns the finding of acid-fast bacteria, closely allied to the mycobacteria, in the skin of three patients with scleroderma... It is pertinent to recall that it is difficult to demonstrate the causative organisms in certain stages of tuberculosis and leprosy, and that Koch's postulates have not been proven with M. leprae. Therefore no possible clue should be ignored in scleroderma." (Dermatologica, 1968)'

• "According to current medical thinking, scleroderma is a disease of unknown cause. However, the medical literature contains scientific studies showing that "acid-fast" bacteria are implicated as a cause of scleroderma."(The Physician's Page, Road Back Publication, 1996)1

What Medical Journals Say about Lupus and an Infectious Etiology

• "Some species of mycoplasma can cause an immune response with some features similar to the immunologic abnormalities seen in systemic lupus erythematosis (SLE)... 63% of the SLE patients were culture positive (for M. hominis) . Neither cortocosteroid treatment, SLE activity, nor age accounted for the difference." (Arthritis & Rheumatism, 1992)'

• "There are striking similarities between human parvovirus B 19 infection and systemic lupus erythematosus (SLE) both may present with malar rash, fever, arthropathy, myalgia, cytopenia, hypocomplementemia, anti-DNAm and antinuclear antibodies (ANA)... It is possible, therefore, that HPV B 19 infection may mimic SLE."(Seminars in Arthritis and Rheumatism),

• "The cutaneous lesions of seven consecutive patients with cutaneous lupus erythematosus (LE), two patient with systemic LE, and a patient with both dermatomyositis and cutaneous LE, were studied bacteriologically and microscopically for the presence of bacteria. . . Definite acid-fast coccoid forms were observed in vivo in two cases of cutaneous LE... In view of the continuing search for an antigen" or etiologic microbial agent in LE, it would seem worthwhile to consider the possibility that one or more types of CWD bacteria might be the offending agent. "(Journal of Dermatology)'

• "A 41-year-old woman with chronic systemic lupus erythematosis (SLE), died ...(necropsied material was reviewed ... Variably acid-fast coccoid forms, suggestive of CWDB, were observed in specially-stained sections of the heart, lungs, kidney, adrenal glands, brain, connective tissue and other organs. This finding may relate to the finding of acid-fast bacteria in scleroderma."(CUTIS, 1984) 4

What Journals Say about an Infectious Etiology for Reiter's Syndrome (Reactive Arthritis)

• The term (reactive arthritis or Reiter's syndrome) typically refers to arthritis seen in a sequela of either a sexually acquired urethritis caused by Chlamydia or Ureaplasma or an enteric infection caused by Salmonella, Shigella, Campylobacter, or Yersinia. " (Journal of Musculoskeletal Medicine, 1995)'

• Chlamydia and Ureaplasma which cause reactive arthritis, and Nisseria, which causes septic arthritis, are frequently found in the urogenital tract of affected individuals, isolation of these pathogens from synovial fluid or synovial tissue by traditional culture methods has been a low-yield Procedure However, accumulating evidence suggests that infectious agents in the joint may plan an important role in the pathogenesis of these diseases." PCR has proven a helpful too] in detection of these organisms. "In all cases, PCR positivity correlated well with the clinical diagnosis." (Arthritis & Rheumatism, 1996)2

• "Chlamydia trachomatis elementary bodies were found by direct immunoflourescence (DIF) in synovial-fluid cell deposits and synovial membrane biopsy samples from five of eight patients with sexually acquired reactive arthritis but in none of eight controls with other types of arthritis." (Lancet,1992)

• "The detection of bacterial DNA in the joint is a major reason to consider that 11 urealyticum may be an arthritis-triggering agent. DNA detection by PCR assay demonstrates the presence of bacterial components in the joint, but positive culture definitely proves the presence of viable organisms. There is increasing evidence to support the presence of bacteria in the joints of patients with so called reactive arthritis." (Arthritis & Rheumatism, 1997)'

• "A reactive arthritis is defined as a sterile inflammatory arthritis occurring in association with an infection at a distant site... Five unusual cases suggest that a reactive arthritis may have been precipitated by a streptococcal infection." (Annals of the Rheumatic Diseases, 1989)'

• "An important but as yet poorly understood aspect of chlamydia-related Reiter's syndrome (RS) Is the recurrence of active arthritis in the absence of any overt infection or reinfection with the organism... Chlamydia, Yersinia, Campylobacter, Shigella, and Mycoplasma have been strongly implicated as a triggering factor for the genesis of Reiter's syndrome (RS)." (Seminars in Arthritis and Rheumatism, 1992)6

• "Mycoplasma genitalium was sought in synovial fluid from 13 patients, of whom five had Reiter's syndrome, four had rheumatoid arthritis, and one each had systemic lupus erythematosus, psoriatic arthritis, rheumatic fever and undefined arthritis. The mycoplasma was detected by PCR assay . . The possibility exists that Mycoplasma genitalium might be responsible for in exacerbation of disease occurring in a low-grade seronegative arthritis of unknown etiology." (European Journal of Microbial Infectious Diseases, 1994)'

• "The colonization rate of Uu (Ureaplasma urealyticum) in patients with RS (74%) was significantly greater than in patients with other arthritides (14%)... Our findings suggest that Uu might bc a causative agentor a trigger in the development of sexually acquired RS." (Journal of Rheumatology, 1994)"

What Medical Journals Say about Reiter's Syndrome or Reactive Arthritis and Antibiotic Therapy

• "The inflammation seen is probably the result of a host immune response to the micro-organism. A substance which was both cytocidal for C trachomatis and capable of suppressing host immune responses would offer distinct therapeutic advantages. Minocycline may be such a substance." (Clinical Experimental Rheumatology, 1988)1

• "The basis for this study was a suspicion of bacterial persistence in reactive arthritis. The antibiotics used were doxycycline 100-200 mg. daily for patients with arthritis after chlamydia, yersinia, and campylobacter infections, and penicillin G 3 mega units daily for streptococcal infections. (Lancet, 1988)1

What Medical Journals Say about Ankylosing Spondylitis and polymyositis and an Infectious Cause

• "Bacterial infections have been known to be associated with HLA-1327, The role of bacteria is more evident in Reiter's syndrome, one of the diseases related to AS... Although Reiter's syndrome and ankylosing spondylitis are both associated with HLA-1327, they are clinically different conditions... About 27% of B27 positive individuals who have an attack of reactive arthritis will eventually develop some signs or symptoms of AS." (Spondylitis Plus, Spring 1996)'

• "Specific factors which initiate AS have yet to be established... Evidence supporting bowel pathology and AS comes from the reported association of the presence of Klebsiella pneumoniae in fecal cultures and activity of AS. Sequential studies on patients with AS have shown that a conversion from negative to positive fecal cultures for this organism precedes a relapse of Joint disease in some patients." ((Journal of Rheumatology, 1985)1 "Klebsiella pneumoniae has been shown to be persistently present in elevated numbers in the bowel flora of AS patients. The theory proposed molecular mimicry between the HLA-B27 molecule and one or more antigens made by enteric organisms... the difference between Reiter's and AS might be the difference in bacterial products reaching the joints in Reiter's but not in AS." (Bulletin on the Rheumatic Diseases, 1990)1

• "In a novel study on the causes of some forms of arthritis, researchers have now shown in animals that both a bacterial trigger and genetic susceptibility are necessary for the disease to occur. This discovery is the fruit of a research effort that began with a study to determine if a human gene called HLA-1327 was the major cause of a group of rheumatic disorders called spondlyarthropathies." (NIH Press Release, 1994)4

• "Coxsackie virus is a frequent agent in polymyositis." (Bulletin on the Rheumatic Diseases, 1990)1

• The Epstein-Barr virus normally resides in salivary duct epithelium and is suspected as a cause of Sjogren's syndrome. Not only does this virus replicate in normal salivary glands during initial infection and remain latent at this site afterwards, but it likewise infects normal B lymphocytes and remains as a latent infection in these cells in about one in a million." (Bulletin on the Rheumatic Diseases, 1990)'

The Cost Factor

• "Rheumatoid arthritis has been regarded as an easily treated disease, the management of which requires no sense of urgency. This traditional view ... remains accepted by most health professionals and reimbursement agencies. During the last decade, however, it has been recognized from long-term studies that most patients with RA experience a progressive disease. . . Long-term out comes of RA may even be as severe as those seen in cardiovascular or neoplastic disease." (Scandanian Journal of Rheumatology, 1994)1

• 1993 report from NIH notes more than 37 million Americans asafflicted with one or more rheumatic diseases, costing tens of billions of dollars annually. (NIH/NIAMS Research Highlights, 1993)1 The March 1997 issue of Self magazine notes the cost of chronic conditions (including arthritis) was $272 billion in 1987, and projects it could climb to $798 billion by the year 2030. (Self magazine, 1997)3

• There seems to be a trade-off between the cost of a treatment and the treatment's efficacy as well as the quality of life for the patient. The cost of monitoring for toxic side effects should be included in the overall cost of a drug therapy. (ed. The cost of monitoring for antibiotic therapy safety is virtually non-existent.) (Arthritis & Rheumatism, 1995)4

• "Rheumatologists are left facing a decision of whether to use a potential DMARD (minocycline) for RA that looks favorable in the literature but has not been approved for marketing as an RA drug by the Food and Drug Administration. This lack of approval may encumber reimbursement by third party payers." (Rheumatic Disease Clinics of North America, 1995)1

The Future

Baby Boomers will soon reach 65 years of age which will cause medical costs to escalate sharply. Arthritis and scleroderma are frequently diseases of middle age and the older patient, affecting women four times more than men. Women live longer than men, necessitating insurance payments for medical treatment for more years than for men.

Promising Research

RA and minocycline

Scleroderma and minocycline

• Study of 11 scleroderma patients treated with minocycline at Boston's Beth Israel Hospital by Chief of Rheumatology David E. Trentham, M.D. and Christine Le, M.D. of Melbourne, Australia. Study concluded February, 1997 (6 out of 11 patients with early, but severe diffuse scleroderma finished 1 year of minocycline. At the end of 1 year, 4 of the 6 had complete resolution of their skin disease and 3 of the 4 had normal patient and physician assessments. These results are significantly superior to those normally seen in drug studies for scleroderma patients. C Le, A Morales, DE Trentham, "Minocycline in Early Diffuse Scleroderma" , Lancet, 1998, 352:9142, pgs. 1755-1756. Larger, follow up studies underway.

References: Results from Mainstream Rheumatoid Arthritis Therapies

1. Kushner I and Dawson NV: Aggressive therapy does not substantially alter the long-term course of rheumatoid arthritis, Controversies in Clinical Rheumatology, Rhu Dis Cl of No Am, Vol. 19, No 1, Feb. 1993, pg. 163-172.

2. Scott DL, Symmons DPM, Coulton BL: Long-term outcome of treating rheumatoid arthritis, results after 20 years. Lancet , 1987; 1: 1108-1111.

3. Wolfe F, Hawley DJ, Cathey MA: Termination of slow acting antirheumatic therapy in rheumatoid arthritis: a 14 year prospective evaluation of 1017 consecutive starts, J. of Rhu , 1990; 17:8, pg. 994-1002.

4. Wolfe F: 50 years of antirheumatic therapy: the prognosis of rheumatoid arthritis. J of Rhu , 1990; (Supplement 22) Vol. 17, pg. 24-32.

5. Klippel JH: Winning the battle, losing the war? another editorial about rheumatoid arthritis, J. of Rhu , 1990; 17:9, pg. 1119-112 1.

6. Gabriel SE, Luhra HS: Rheumatoid arthritis: can the long-term outcome be altered? Mayo Clin Proc 1988; 63: pg. 58-68.

7. Short CL, Bauer W, Reynolds WE: Rheumatoid arthritis: a definition of the disease and a clinical description based on a numerological study of 293 patients and controls, Cambridge Massachusetts, Harvard University Press, 1957.

8. HR Barthel, GR Bun-nester, Specific drugs for a complex disease: can there be a magic bullet against rheumatoid arthritis?, Ann of Rheum Dis, 1995; 54i 948-950.

References - What Medical Journals Say about Rheumatoid Arthritis and Antibiotic Therapy

1. FC Breedveld, BAC Dijkmans, H Mattie, Minocycline Treatment for Rheumatoid Arthritis: An Open Dose Finding Study, J of Rhewn, 1990; 17:1, pg. 43-46.

2. M Kloppenburg, FC Breedveld, J Ph Terweil, C Malice, BAC Dijkmans. Minocycline in Active Rheumatoid Arthritis, Arth & Rheum, 1994, 37:5, pg. 629-636.

3. P Langevitz, I Bank, D Zemer, M Book, M Pras, Treatment of Resistant Rheumatoid Arthritis with Minocycline: An Open Study, J of Rheum, 1992, 19:10, pg. 1502-1504.

4. DE Trentham, RA Dynesius-Trentham, Antibiotic Therapy for Rheumatoid Arthritis: Scientific and Anecdotal Appraisals, Rheu Dis Clin of NAm, 1995; 21:3, pg. 817-834.

5. JR O'Dell, CE Haire, W Palmer, W Drymalski, S Wees, K Blakely, M Churchill, PJ Eckhoff, A Weaver, D Doud, N Erikson, F Dietz, R Olson, P Maloney, LW Klassen, GF Moore, Treatment of Early Rheumatoid Arthritis with Minocycline or Placebo: Results of a Randomized, Double-Blind, Placebo-Controlled Trial, Arthritis and Rheumatism, 1997; 40:5: pg. 942-848.

References - The Infectious; Theory of Rheumatoid Arthritis

1. J McCulloch, PM Lydyard, GAW Rook, Rheumatoid Arthritis: how well do the theories fit the evidence?, Clin Exp Immunol, 1993; 92: pg 1-6.

2. GAW Rook, PM Lydyard, X Stanford, A reappraisal of the evidence that rheumatoid arthritis and several other idiopathic diseases are slow bacterial infections, Ann of Rheum Dis, 1993; 52: S30-S38.

3. PLJ Tan, MA Skinner, The Microbial Cause of Rheumatoid Arthritis: Time to Dump Koch's Postulates, J of Rheum, 1992. 19:8, pg 1170-117 1.

4. JB Baseman, JG Tully, Mycoplasmas: Sophisticated, Reemerging and Burdened by Their Notoriety, CDC's Emerging Infectious Diseases, 1997; 3: 1.

5. SM Friedman, DN Posnett, JR Tumang, BC Cole, MK Crow, A potential role for microbial superantigens in the pathogenesis of systemic autoimmune disease, Arth & Rheum, 1991; 34:4, pg. 468479.

6. MH Williams, J Brostoff, IM Roitt Possible Role of Mycoplasma fermentans in pathogenesis of rheumatoid arthritis, Lancet, August 8, 1970, ii, 169-171.

7. D Taylor-Robinson, T Schaeverbeke, Mycoplasmas in rheumatoid arthritis and other human arthritides, J Clin Pathol (editorial), 1966; 49: 78 1 -82.

8. T Schaeverbeke, H Renaudin, M Clerc, L LcQuen, JP Vernhes, B DeBarbeyrac, B Bsnnwarth, Ch Bebear, J Dehais, Systemic detection of mycoplasmas by culture and polymerase chain reaction (PCR) procedures in 209 synovial fluid samples, Br J Rheum, 1997; 36: 310-314.

9. T Scheverbeke, CB Gilroy, C Bebear, J Denhais, D Taylor-Robinson, Mycoplasma fermentans in joints of patients with rheumatoid arthritis and other joint disorders, Lancet, 1996; 347: pg. 1418.

10. D Taylor-Robinson, Mycoplasmas in rheumatoid arthritis and other human arthritides, J Clin Pathol, 1996; 49:348: 516-517.

References - Poor Results from Mainstream Scleroderma Therapies

1. JR Seibold, DE Furst, PJ Clements, Why everything (or nothing) seems to work in the treatment of scleroderma, J of Rheum, 1992; 19:5, pg. 673-676.

2. JE Pope N Bellamy, Outcome Measurement in scleroderma clinical trials, Sem in Arth & Rhu, 1993; 23: 1, pg 22-33.

3. JF Fries, JR Seibold, TA Medsger, Jr., Photopheresis for scleroderma, no!, J of Rheum, 1992; 19:7. pg 1011- 10 13.4. M Abu-Shakra, P Lee, Mortality in systemic sclerosis: a comparison with the general population. J of Rheum, 1995; 22: 1, pg 2100-2102.

5. MI Peres, SR Kohn, Systemic sclerosis, Continuing Medical Education, J. of Am Acad of Derm, 1993; 28:4, pg. 525 -547.

References - What Medical Journals Say about Scleroderma and an Infectious Etiology

1. Lida H. Mailman, Ph.D., Cell Wall Deficient Forms, CBC Press, 1976, pg. 267-269.

2. V Wuertherle-Caspe, E Brodkin, C Mermod. Etiololgy of Scleroderma, a preliminary clinical report, J Med Soc MY, 1947, July; 44-7, pgs. 256-259.

3. AR Cantwell. E Craggs, JW` Wilson, F Swatek, Acid-Fast Bacteria as a Possible Cause of Scleroderma, Dermatologica, 1968; 136: pg. 141-150.

4. AR Cantwell, Jr., Acid-fast Bacteria in Scleroderma: Evidence for a known infectious agent as a cause of scleroderma, The Physician ~ Page, 1996, 1 :3, pg. 1-2.

References - What Medical Journals Say about Lupus and an Infectious Etiology

1. KS Ginsburg, RB Kundsin, CW Walter, PH Schur, Ureaplasma urealyticum and Mycoplasma hominis in women with systemic lupus erythematosus, Arth & Rheum, 1992; 35:4, pg. 429-433.

2. G Nesher, TG Osborn, TL Moore, Parvovirus infection mimicking systemic lupus erythematosus, Sem in Arth and Rheum, 12995; 24:5, pg. 297-303.

3. AR Cantewell, Jr., DW Kelso, JE Jones, Histologic observations of coccoid forms suggestive of cell wall deficient bacteria in cutaneous and systemic lupus erythematosus, International J of Derm, 1982; 21:9.

4. AR Cantwell, Jr., JK Cove, Variably acid-fast bacteria in a necropsied case of systemic lupus erythematosus with acute myocardial infarction, Cutis, a Yorke Medical Journal, June 1984.

References - What Journals Say about an Infectious Etiology for Reiter's Syndrome or Reactive Arthritis

1. DK Ford, Reactive arthritis: causes, recognition and management, J of Musculoskel Med, June 1995; pg. 30-37.

2. F Li, R Bulbul, HR Schumacher, Jr., T Kieber-Emmons, PE Callegari, JM Von Feldt, D Norden, B Freundlich, B Wang, V Imonitie, CP Chang, I Nachamkin, DB Weiner, WV Williams, Molecular detection of bacterial DNA in venerial-associated arthritis, Arth & Rheum, 1996; 39 * 6: pg. 950-958.

3. D Taylor-Robinson, CB Gilroy, BJ Thomas, ACS Keat, Detection of Chlamydia trachomatis DNA in joints of reactive arthritis patients by polymerase chain reaction, Lancet, 1992; 340: pg. 81-82.

4. T Scheverbeke, C Bebear, B Bannwarth, C Bebear, J Dehais, Reactive or septic arthritis? Comments on the article by I ~i et at, Arth & Rheum, 1997; 403: pg. 592- 593.

5. MU Arnold, A Tyndall, Poststreptococcal reactive arthritis, Ann of Rheum Dis, 1989; 48: pg. 686-688.

6. MU Rahman, HR Schumacher, AP Hudson, Recurrent arthritis in Reiter's Syndrome: a function of inapparent Chlamydian infection of the synovium? Sem in Arth & Rheum, 1992; 21:4: pg. 259-266.

7. D Taylor-Robinson, CB Gilroy, S Horowitz, J Horowitz, Mycoplasma genitalium in the joints of two patients with arthritis, Eur J Clin Microbiol Infect Dis, 1994; 13: pg. 1066-1068.

8. S Horowitz. I Horowitz, D Taylor-Robinson, S Sukenik, RN Apte, J Bar-David, B Thomas, C Gilroy, Ureaplasma urealyticum in Reiter's Syndrome, J Rheum, 1994; 21:5, pg 877-882.

References - What Medical Journals Say about Reiter's Syndrome or Reactive Arthritis and Antibiotic Therapy

1. A Lauhio, M Leirisalo-Repo, I Labdevirta, P Saikku, H Repo, Double-blind, placebo-controlled study of three-month treatment with lymecycline in reactive arthritis, with special reference to chlamydia arthritis, Arth & Rheum, 199 1; 34: 1, pg. 6-14.

2. GS Panayi, B Clark, Minocycline in the treatment of patients with Reiter's syndrome, Clin Exper Rheum, 1988;7: pg. 100- 10 1.

3. S Estreich. GE Forster, Long-term antibiotic treatment in reactive arthritis, Lancet, January 30, 1988; pg. 245-246.

References - What Medical Journals Say about Ankylosing Spondylitis and polymyositis and an Infectious Caus

1. J Taurog, Research '95: Spondyloarthropatht investigations, Spondylitis Plus, Spring 1996, pg. 3-4.

2. MD Smith, RA Gibson, PM Brooks, Abnormal bowel permeability in ankylosing spondylitis and rheumatoid arthritis, .1 Rheum, 1985; 12:2: pg. 299-305.

3. JH Vaughn, Infection and rheumatic diseases: a review, part 2 of 2, Bull on the Rheum Dis, 1990: 39:2, pg. I-T

4. E Ben-Ari, Normal intestinal bacteria play a role in some forms of arthritis, NIH Press Release, Nov. 30, 1994.

References - The Cost Factor

1. Rheumatoid Arthritis: A Medical Emergency?, T Puncus, Scand J Rheumatol, 1994; 23 (Suppl 100), 21-30,2. 1993 Research Highlights, Arthritis, Rheumatic Diseases, and Related Disorders, NIH/NIAMS, pg 1

2. Medical Flash!, Self, March 1997, pg. 67

4. The Total Costs of Drug Therapy for Rheumatoid Arthritis, Arthritis & Rheumatism, 1995, 38:3, pg 318-325.

5. DE Trentham, RA Dynesius-Trentham, Antibiotic Therapy for Rheumatoid Arthritis: Scientific and Anecdotal Appraisals, Rheu Dis Clin of N Am, 1995; 2 1 : 3, pg. 817-834.