The following is a collection of questions about medications answered by SAA Medical Board Member Dr. Lianne Gensler. We’d like to thank Dr. Gensler for her time in assisting with this article.
Spondylitis Association of America (SAA): What are the primary categories of drugs prescribed for ankylosing spondylitis (AS) and related diseases?
Lianne S. Gensler (LG): There are three primary categories (and note the examples are not a comprehensive list):
SAA: After a diagnosis of AS is made, what thought process goes into prescribing a medication? What type of medication is prescribed first and why (e.g. allergies, disease severity)?
LG: There are a number of key factors that go into matching certain medications to a patient’s needs. These include:
First line drugs are NSAIDs unless there are contraindications. Contraindications might include kidney disease, peptic ulcer disease and sometimes inflammatory bowel disease (IBD) (Crohn’s or ulcerative colitis). If the most affected joints are the spine, hips and sacroiliac joints, and NSAIDs are not effective (after trying two different types), biologics (specifically TNF-α inhibitors) are the next step. All of these are equally effective for the joints, but certain types (monoclonal antibodies) are better for manifestations including IBD and uveitis.
SAA: Is there any reason to skip right to a TNF-α inhibitor?
LG: If there are contraindications to NSAIDs like those mentioned above, or if the patient has had an adequate trial of two different NSAIDs at a full strength dose, then it is reasonable to go straight to a TNF-α inhibitor.
SAA: What are the differences between the TNF-α inhibitors?
LG: The best way to describe the differences is with a table.
| Drug | Etanercept (Enbrel) | Infliximab (Remicade) | Adalimumab (Humira) | Golimumab (Simponi) |
|---|---|---|---|---|
| How the drug works to block TNF-α | Acts as a mop on soluble TNF-α | Acts on both soluble and cell bound TNF-α | Acts on both soluble and cell bound TNF-α | Acts on both soluble and cell bound TNF-α |
| Route of administration | Injection in the skin (SC) | Injection into the vein (IV) | Injection in the skin (SC) | Injection in the skin (SC) |
| Dose and frequency | 50mg weekly or 25mg 2× weekly | 3-10mg/kg every 6-8 weeks | 40mg every other week | 50mg every month |
| Disease specific comments | Works well in all arthritis forms | Works well in all arthritis forms and IBD | Works well in all arthritis forms and IBD | Works well in all arthritis forms (hasn’t been tested in IBD, but should work) |
SAA: What do you tell patients concerning side effects — specifically severe ones like the black box warning regarding risks of lymphoma with the biologic medications?
LG: The major risks are infection and cancer. The infection risk is because of the suppressed immune system as a result of the biologic. For the most part, they are common infections that anyone could get. It’s more likely in an immunosuppressed patient. Other infections we worry about that are less common include tuberculosis, certain fungi (coccidyomycoses [valley fever], histoplasmosis). The cancer risk has been better studied in Rheumatoid Arthritis than AS and the typical cancers are skin cancers and less commonly lymphoma (a type of blood cell cancer). The black box warning was a type of lymphoma described in children.
SAA: What do you tell a patient who doesn’t want to run the risk of the side effects of a TNF-α inhibitor (or for that matter, another medication) and has made a decision not to take them?
LG: They are the patient — they get to decide. As long as I can educate them about the choices, risks and benefits, they are ultimately responsible for choosing because it’s their body and they live with the results. It’s my role do the best job possible taking care of them independent of their treatment choices.
SAA: What is a DMARD in regards to spondylitis treatment (meaning, are there actually disease modifying anti-rheumatic drugs in the spondyloarthropathies) and in your experience, where do “DMARDs” (methotrexate / sulfasalazine) fit into treatment?
LG: If you are referring to the spine, the traditional DMARDs are likely not disease-modifying. They do play a role in those with smaller joint involvement like the knee, ankle, hands and feet. Even then, however, they may not be truly disease modifying, rather disease-controlling.
SAA: What about steroid use such as prednisone?
LG: The amount of steroids needed to have a response in the back is high and therefore the risk often far outweighs the benefit. In addition, if a patient has psoriasis (as many of these patients do), when the prednisone is tapered, the psoriasis gets worse.
SAA: What NSAIDs are most commonly used now?
LG: Each rheumatologist tends to have his/her own preference based on anecdotal experience. I don’t think it’s fair to state the most commonly prescribed as this varies from provider to provider.
SAA: When would you prescribe a narcotic/pain killer?
LG: If the patient has pain that is not managed by usual means (NSAIDs, biologics, etc), it is appropriate to prescribe these agents. They may be prescribed by the rheumatologist, primary care doctor, pain specialist or orthopedic surgeon.
SAA: During a flare, have you prescribed an additional medication to help with the inflammation/pain?
LG: Before prescribing additional medications for a patient in a flare, I like to first assess what may have caused the flare — i.e. a reduction in exercise, increased stress or travel, discontinuation of medications etc. I try to use non-pharmacologic measures like heat/ice, stretching and physical therapy. I will add or increase NSAIDs in a patient on a biologic agent. If the patient still is having significant symptoms, I may add pain medications as needed.
SAA: What differences are there between medications for the different forms of spondyloarthritis (e.g. ankylosing spondylitis vs. psoriatic arthritis or enteropathic arthritis)?
LG: Of the TNF-α inhibitors, all the monoclonal antibodies should work on the arthritis in addition to the uveitis and IBD. Etanercept is the only one that doesn’t have efficacy for treating manifestations outside of joints. However, etanercept still tends to reduce the number of uveitis flares that occur. Other drugs that work in Spondyloarthritis, especially the smaller joints, include sulfasalazine and methotrexate which are oral medicines.
SAA: Although there is no cure for ankylosing spondylitis and related diseases, are there any drugs that have been shown to slow or halt the progression of the diseases?
LG: It depends on which specific disease you are asking about and which manifestation of the disease. There is not good evidence that any drugs prevent bone formation (i.e., fusing of the spine). There is a possibility that NSAIDs may prevent fusion, but the evidence is not strong enough to make a formal statement. In psoriatic arthritis, TNF inhibitors have been shown to prevent radiographic damage.
SAA: What progress has been made in the last few years regarding treatments?
LG: TNF inhibitors have changed the face of this disease. Patients have gone from disability to fully functional. Other biologic agents are now being developed and studied. As we study the diseases and how patients respond (or don’t respond) to therapy, we learn more about the disease and figure out novel agents that might help to treat and hopefully cure the disease.
SAA: Given all the genetic discoveries as of late, what new medicinal treatments will we be seeing in the future?
LG: This is definitely a very exciting area that may allow us to target therapies to a patient’s particular genetic make-up. This would include the ability to predict response to different therapies in addition to potential complications based on a patient’s genes.
This article originally appeared in the Spring 2012 issue of Spondylitis Plus, the quarterly news magazine of Spondylitis Association of America. Members receive every copy of Spondylitis Plus in the mail for free. Get a Membership!
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