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The Problem of Non-Responders
The lack of awareness of antibiotic therapy for the treatment of rheumatic disease has left many doctors unsure of how to prescribe, or even more important, how to adjust the prescription to promote a favorable patient response. Those patients who respond favorably with the first antibiotic chosen and first dosage prescribed are fortunate. The percent of responders is 70% or better among patients whose doctor is experienced at using antibiotic therapy. However, even at best there is sometimes a small percentage of patients who respond slowly or not at all. What is missing? Assuming the diagnosis is correct, here are several things to consider.
1. Of critical importance are: dosage, frequency of administration and route of administration (oral, IV or IM). These three must be tailored to the individual patient; one method does not work for all.
2. Changing the antibiotic to another tetracycline or a combination of antibiotics may be needed.
3. Is there another compromising factor preventing response? (allergy; food intolerance; streptococcus [ASO titre]; bad teeth; other microorganism; leaky gut syndrome, etc.) which should be treated at the same time?
4. Is a low immunoglobulin, hypo gammaglobulinaemia causing a poor immune response?
It is this last point that may be responsible for some patient non-response.
New patients should respond quickly; long-term patients will usually respond slowly. There will be ups and downs.
A number of journal articles have appeared in recent years examining the part immunoglobulins play in rheumatic disease and the part IV immunoglobulin therapy may play in making these patients more responsive to treatment.
Mycoplasma is considered to be a factor in rheumatic disease1. Arthritis patients deficient in antibody are uniquely susceptible to mycoplasma and urealyplasma infection2 which makes antibody critical to the patient's defense against mycoplasma. ADB Webster et a15 found that antibody alone inhibits the growth of mycoplasmas in vitro.
In a short report in the British Medical Journal, I 983, Dr. A K L So and colleagues found M salivariurn in the synovial fluid of a 39-year-old female with arthritis. She also tested positive for M. hominis and U. urealyticum. Oral and IV erythromycin was administered, but until immunoglobulins were administered and the antibiotic changed to oral minocycline, the patient did not achieve remission. (M. hominis has sometimes been shown to be erythromycin resistant. 4)
Nine out of ten patients with active, severe RA were treated with 6 months of IV Ig therapy by B Tumiati et a15. All patients had proved unresponsive to previous first and second line RA drugs, including MTX, GST and AUR. The IV Ig treatment resulted in an improvement in both the subjective and objective parameters of disease, and of the 7 on steroids, only one was unable to decrease or discontinue the drug with this treatment. No patients had adverse side effects (only mild nausea, dizziness, hypotension), and a significant decrease in CRP was observed.
All nine patients saw marked improvement in their RA with IV Ig treatment which exerted a very rapid and pronounced effect on the inflammatory signs and symptoms of the patients' RA. A return of symptoms occurred 12 weeks after discontinuing the IV Ig treatment. (Ed: It is possible that with the administration of a tetracycline with the IV 1g. the improvement would not only hold, but would continue until, in many cases, remission could be achieved.) IV Ig has been found effective in SLE, polymyositis, dermatomyositis, JRA, as well as RA and several other "autoimmune disorders.
It is now clear that patients with antibody deficiency are prone to arthritis and other infections with mycoplasmas and ureaplasmas, implying that humoral mechanisms have an important role in host defenses against these organisms. (So, et al.) (Mycoplasmas) are taken to the joints inside or attached to neutrophils, where they remain viable in the absence of anti body. (Webster, et al.)
References:
1. RW Wilder, Rheumatoid Arthritis: etiology. Printer on Rheumatic Diseases. lOt!, Ed., Arthritis Foundation, 1993.
2. EW Gelfand. Unique Susceptibility of Patients with Antibody Deficiency to slycoplasma Infection, C/in Infect Dis. 1993: 17 Isuppl I): S250-3.
3. AKL So. PM Furr. D Taylor-Robinson, AOB webster, Arthritis Caused by Mycoplasma Salivarium in Hypogammaglobulinaernia,BrMedJ. 5 March 1983; 286.762-3
4. 17K McMahon. 35 Dummer, Aw Pasculle. a Cassell. Extra-genital Myroplasma ho,ni,zis infections in adults. Amiof Med. 1990. vol 89. No.8, 275-281.
5. B Tumiati. PCasoli, M veneziani, G Rinaldi, High-Dose Immunoglobulin Therapy as an Immunomodulatory Treatment of Rheumatoid Arthritis. Art/i & R/teun,, 1992; 35:10, 1126-33.
6. ADD webster, PM Furr. NC Hughes-Jones, BD Gorick. 17 Taylor-Robinson, Critical Dependence on Antibody for Defense Against Nlycopiasmas, C/in Exp Intn,unol; 1988;71. 353-35,5.
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