TerryK
Frequent Contributor (5K+ posts)
Member # 8552
posted
This information is written specifically for long term antibiotic users who are treating for rheumatic conditions but I think many of the tips apply to any kind of treatment that is used to kill organisms.
Although many patients with various rheumatic diseases respond well to antibiotics, there are always some who do not respond at all and some who stop responding and plateau. Why does this happen and what, if anything, can you as a physician do to elicit the desired response?
There is no one thing that can be said to be responsible for a patient's lack of response, but there is a check list of possibilities. Determining what is interfering with your patient's positive response might take some trial and error and some medical detective work, but seeing a patient who is chronically ill and becoming disabled return to an active lifestyle should be gratifying to say the least.
1. Some generics don't work. This is probably the easiest thing to check. Ask your patient the color of their medication, and if on Minocin, if it is pellets. We know the brand name drugs work because they were tested in trials. Some of the generic versions do not work well at the same dose and frequency as the brand name drug. Some generics also cause side effects, usually GI disturbances, which go away when the patient is changed to brand name.
We asked patients who were on generics and who changed to brand name drugs to let us know if they saw a difference. Many responded that they saw immediate and dramatic improvements as well as diminished side effects.
2. Are there any other pre-existing conditions which are interfering with a positive response? For instance, candida, strep, allergies, chronic infections such as sinus, bladder or periodontal disease can be responsible for a marginal or negative response to treatment. When these conditions are treated concurrently, the response to antibiotics is often heightened.
3. Is the patient's immune system deficient or stressed? Many patients have been on strong immuno-suppressive drugs for years. Others are under heavy stress or are eating diets which are unhealthy. Physicians who strengthen their patient's immune systems find the response to antibiotic therapy is heightened. Recommending a healthier diet, vitamins or supplements can be helpful.
4. Is the patient on a drug (prescription or over-the-counter) which is contraindicated for use with tetracyclines? Not all patients consider over-the-counter medications to be on the same level as prescription drugs and when asked what medications they are using, neglect to mention over-the-counter or vitamin and supplemental products or antacids.
5. Hormone imbalances have been noted in high numbers of patients with chronic diseases. These levels are easy to test and if out of balance, getting them back into balance can be of considerable benefit to the patient. Take particular notice of thyroid, DHEA, testosterone, estrogen, progesterone and natural hydro-cortisone. Also be aware that many of these hormones work best together and that natural hormones work better than synthetics.
6. Does the patient have a strain of organism which is resistant to tetracycline antibiotics? Some mycoplasma strains have been found to be resistant to certain of the tetracycline antibiotics. Changing to a different antibiotic family might prove beneficial. Erythromycin, clindamycin, azithromax and Ceftin have been shown to provide a positive response as well as drugs in the tetracycline family.
7. Is the medication not being taken on an empty stomach or is it being taken with a substance which renders it ineffective? Tetracyclines bind to calcium and iron, and are affected by vitamin C. They are most effective when taken one hour before a meal or two to three hours after.
8. Does the patient have poor gut absorption? Among the many aspects of the immune response, poor gut motility, poor absorption, diminished gut flora, leaky gut and diminished function can all contribute to poor absorption of medications.
9. Is a high level of inflammation preventing the antibiotic from reaching the sites of activity? In patients with inflammatory disease, the effectiveness of the antibiotic can be diminished by the inflammatory barrier making it difficult for the drug to penetrate to the site of activity. Stress the need to reduce the inflammatory barrier so the drug can penetrate to the areas of activity. Many patients take NSAIDs or other anti-inflammatory measures only when they are in pain. Most of these products work best when taken regularly so a constant level is maintained. Patients do not always understand that and use the products more like pain medication than an anti-inflammatory.
10. Does the drug need to be rotated? Antibiotic therapy is a long-term therapy, months and years in most, - even for a lifetime in some. After 5-6 years, a patient can become tolerant of an antibiotic. Rotating to another antibiotic even within the same drug class can keep response optimal and avoid plateaus.
11. Is a higher loading dose needed to initiate a response? Some patients need an initial higher dose to "break things loose" so to speak. This higher dose can be a larger oral dose or an IV series. In some patients, it is a short term things loose" so to speak. This higher dose can be a larger oral dose or an IV series. In some patients, it is a short term elevation and the dose can be lowered and still maintain the desired improvement. In others, a lower dose is better, gradually increasing as the patient can tolerate it. This is particularly true with long-term patients, those with severe disease, and those who flare frequently or easily.
12. Are you expecting to see improvement too soon? This is a long-term therapy and response is usually slow and gradual - even subtle. Dr. James O'Dell, in his Minocycline-RA study, noted that the greatest patient response was seen beyond one year of antibiotics.
13. There does not seem to be improvement in labs. Does this mean the treatment is not working? Patient response and labs do not always parallel. Allow for a lag time between the patient's assessment and the lab results.
Patient response is very individualized. The dose and frequency which works for one patient doesn't work for the next patient.
As in other treatment regimens for rheumatic diseases, each patient is an individual with special responses to medication. Few physicians have all their RA patients on the same dose of the same drugs; the treatment is adjusted to accommodate individual needs and response. The same is true for antibiotic therapy. 100 mg. bid will work for some; but not for others.
14. Does the route of administration need to be changed? If there is no improvement in either patient & physician assessment or labs in 6 months, you might try a change in route of administration (adding IV or IM to oral) or an adjustment in dose or frequency. This can provide an added punch which will elicit improvement as IVs are needed to reach more deep seated disease in some patients. IVs can be particularly helpful in cases of mycoplasma infection as these organisms have been found to colonize the mucous membranes and these colonies are reached more effectively by the more potent IV antibiotics which do not pass through the digestive tract.
15. Are there multiple organisms involved which respond to different antibiotics? This can be the situation in some patients, and using more than one antibiotic can prevent an overgrowth of the untreated organism (e.g. mycoplasma and ureaplasma - mycoplasma and yeast or mycoplasma and strep).
Posts: 6286 | From Oregon | Registered: Jan 2006
| IP: Logged |
TerryK
Frequent Contributor (5K+ posts)
Member # 8552
posted
I was particularly interested in the inflammation issue since abx and antimicrobial alternatives seem to cause a great deal of inflammation for me as evidenced by the snap crackle pop of knees, neck, shoulder etc..
I've been taking digestive enzymes between meals AND rutin, bromelain and serraflazyme to help with inflammation and I think I've finally got it under control.
I didn't know that it needed to be controlled to get better tissue penetration of antimicrobials but that does make sense.
From what I've read from others here at LN, it seems that many of us get tissue inflammation once we start abx or other bug killing treatments. From what I've been told, the bugs die in the tissues and cause inflammation - it's basically the toxins that are the problem.
Terry
Posts: 6286 | From Oregon | Registered: Jan 2006
| IP: Logged |
CaliforniaLyme
Frequent Contributor (5K+ posts)
Member # 7136
posted
Hey, I remember this*)!)*! This is from Roadback.org*)*!)!!!!!!!!!!!!!! Good article!
-------------------- There is no wealth but life. -John Ruskin
All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer Posts: 5639 | From Aptos CA USA | Registered: Apr 2005
| IP: Logged |
map1131
Frequent Contributor (5K+ posts)
Member # 2022
posted
Thanks Terry, great info.
Pam
-------------------- "Never, never, never, never, never give up" Winston Churchill Posts: 6478 | From Louisville, Ky | Registered: Jan 2002
| IP: Logged |
merrygirl
Frequent Contributor (1K+ posts)
Member # 12041
posted
Interesting. I think that the inflammation info was interesting.
thanks Melissa
Posts: 3905 | From USA | Registered: May 2007
| IP: Logged |
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
Printer-friendly view of this topic