Posts Tagged ‘injection’

Given the fact that there are a slew of RA medications laying on the failure heap, I’m willing to move outside the box and so is my doctor. The latest drug to be tried will be secukinumab – brand name Cosentyx by Norvartis. This biologic is currently approved by the United States Food and Drug Administration (FDA) for the autoimmune diseases psoriasis, psoriatic arthritis (PSA), and ankylosing spondylitis (AS). Cosentyx is an interleukin 17 (IL-17) inhibitor. IL-17 is a cytokine produced by T cell lymphocytes and is connected with autoimmune inflammatory responses. I reported on clinical trials with secukinumab for RA back in 2012. In a recently reported clinical trial being conducted for RA, patients demonstrated improvement over a one year treatment period. Safety and side effect profiles match other biologics with increased risk of infections, allergic reactions, changes in liver and blood tests, and cases of inflammatory bowel disease.

My official diagnosis has been seropositive rheumatoid arthritis due to positive rheumatoid factor (RF) tests, classic RA symptoms like symmetrical bilateral presentation, and bone erosions. But I’ve also shown symptoms more associated with AS like tendon insertion tearing, large joint involvement, and uveitis but without a positive genetic marker for AS (HLA-B27). In addition, my grandmother dealt with psoriasis and her brother had a debilitating case of ankylosing spondylitis. My insurance approved this drug for my use and I will begin the weekly loading dose self-injections as soon as they are shipped. We’ll see how I respond to this newest option.


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Corticosteroids or glucocorticoids are powerful anti-inflammatory drugs commonly used to treat a variety of medical conditions. They are not to be confused with anabolic steroids that are notoriously abused by athletes.1 Anabolic steroids are associated with muscle mass gain and corticosteroids are connected with metabolism and immunity.

Most every RA patient has probably taken oral steroids in the form of pills or a dose pack that tapers down the dose over a period of time. Oral steroids are effective at providing quick reduction of RAsymptoms although long-term use is generally discouraged and even short-term use is being questioned.2 When taking an oral steroid, the drug goes throughout the entire body systemically. But there are other forms of steroids that are directly injected into a specific area of the body in an effort to treat RA related symptoms. Since being diagnosed with RA, I’ve had one steroid injection into my right knee, four into my left hip, one into my neck, and one into my right elbow.

Read the rest of the post at http://rheumatoidarthritis.net/living/steroid-injections-treating-ra-symptoms/

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I’m still in the midst of recovering from cervical fusion surgery on May 15 and am currently completing physical therapy. The process seems to be going well, pain and numbness is almost completely gone, and I’m slowly regaining muscle strength. After dealing with it for over 8 months, the neck and associated parts finally feels much better. But RA is never silent and has a way of rearing its ugly head just when you think things are calm. Sure, there is always the ongoing “background noise” of RA – fatigue, joint and muscle pain, finger swelling and pain, joint locking, and the persistent ankle pain after having three surgeries. But now the left hip is begging – no screaming – for attention.

Hip problems became apparent almost two years ago when I began getting steroid injections for trochanteric bursitis from my rheumatologist. Bursae are sac-like structures that are found in some joints and aid in providing friction reduction.[1] I had a bursa removed as part of an ankle surgery. The trochanteric bursa is on the outside of the hip and is commonly involved in RA.[2]

While my neck was healing, the left hip progressively grew worse. Sitting for any length of time was impossible, getting in and out of a chair and car was difficult, sleeping on the left side was not feasible, and the left side was favored while walking. At a recent rheumatology appointment, a fourth cortisone steroid injection was given into the trochanteric bursa. But the injection brought no relief. My rheumatologist referred me to an orthopedic specialist.

The orthopedic surgeon examined x-rays and noted that the space in the ball and socket joint, while somewhat reduced, looked fine. There was no bone erosion perceived. We spent some time discussing my earlier problems with the trochanteric bursa, the multiple steroid injections, and my current symptoms of groin and buttock pain. He then laid me down on my back and began to examine my hip movement through a series of tests. I couldn’t lift my leg off the table and extreme pain was felt when he manipulated it in various ways. After the physical exam his entire line of inquiry changed from the more external trochanteric bursa to focusing on tissues around the joint itself. He immediately began to suspect a labral tear. The labrum is cartilage that surrounds the hip joint.[3] But a physical exam and x-ray cannot directly pinpoint what’s really going on so an MRI is needed. A traditional MRI can’t always detect soft tissue in the complex hip joint so an arthrogram is added. Before the MRI, a radiologist injects a combination of fluid, steroid, and a contrast into the hip joint under the guidance of an x-ray. After the injection, you go directly to the MRI machine. The steroid can also provide a therapeutic purpose in reducing inflammation and pain. I am scheduled for an MR arthrogram tomorrow and hopefully it will help solve the mystery.

In addition to the more traditional bone erosion, I have a history of developing soft tissue damage to the musculoskeletal system from RA. This episode with the hip seems to be following that story.

[1] http://orthoinfo.aaos.org/topic.cfm?topic=a00409

[2] https://www.rheumatology.org/Practice/Clinical/Patients/Diseases_And_Conditions/Tendinitis_and_Bursitis/

[3] http://www.hss.edu/condition-list_labral-tears-hip.asp#.U_zH9WRDvA4

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When first diagnosed with RA over five years ago, I was prescribed oral methotrexate (MTX). After a month of taking the pills, I felt terrible and was basically non-functional. It felt like a truck ran over me as I had no energy, felt sick at my stomach non-stop, and had headaches. The RA symptoms were bad enough but this just added insult to injury. My rheumatologist finally told me that I clearly could not tolerate the drug and to stop taking it. The side effects subsided within a few weeks.

Several years later, and with a different rheumatologist, I asked about taking MTX injections because I was desperately trying to find a treatment combination that worked. It was recommended to add MTX with the biological medicines I was taking as the combination of the two typically produces better results. I started take methotrexate via weekly self-injection and found that the nausea side effects were much less than with oral pills. I seemed to tolerate the MTX much better when injecting it and adding both folic acid and leucovorin. I rarely felt nausea and did not loose any hair.

But an increase in migraine headaches over the past year coincided with the time I started taking MTX. While not one of the more commonly reported side effects like nausea or hair loss, headaches can come from taking MTX.[i] [ii] As my neurologist stated, the causes of the migraines are likely based on multiple factors including genetics, my fight with RA, and the medicines I take. During the past few months when the headaches increased in number, I completely stopped taking methotrexate in an effort to eliminate any possible triggers. We’ve been able to reduce the number of migraines through the use of gabapentin, a drug used for neuropathic pain, and botox injections (no, I don’t look any younger!). My rheumatologist suggested that I start retaking methotrexate by beginning with low doses initially and then increase back up to the dose I was taking before. I waited until I had been headache free for two weeks and then injected MTX. Within 48 hours I began to get migraines and fought off four bad headaches over the next five days. While it’s hard to determine direct cause and effect, this was enough for me to wonder if MTX was indeed a migraine trigger. I did not inject MTX the next week and did not have any bad migraines. I contacted my rheumy and she suggested I just stop MTX altogether. The good news is that during this time, Rituxan infusions that I started last September were starting to work at controlling my RA and this was during the time I had stopped taking MTX.

So for the time being, I’ll just stick with Rituxan as my main RA treatment. And I’ll be sitting in the infusion center this Wednesday starting my second series of doses.

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My rheumatologist reiterated with me yesterday that I have a tough to treat case of RA – called refractory RA. She displayed disappointment that all of the treatment plans we’ve tried over the years have not had the intended impact. We’ve cycled through four TNF inhibitors (Enbrel, Cimzia, Humira, and Remicade), Orencia, and Actemra. And that’s in addition to various DMARDs including sulphasalzine, azathioprine, and leflunomide (Arava). The reasons for stopping the use of these drugs runs the gamut of lack of efficacy to intolerable side effects. My doctor was apologetic, felt bad I wasn’t helped by all of the treatment plans, and genuinely expressed concern for the impact RA has had on my life recently. But I reassured her that I trusted her medical judgement and that the impact comes over time allowing time to adjust. I appreciated her empathy and deep desire to help.

We discussed the few remaining options which includes Xeljanz, Kineret, and Rituxan. Xeljanz (tofacitinib) was approved in the United States but not approved in Europe. We both felt that more data was needed on this “oral biologic” before giving it a try. Kineret, or anakinra is a biological response modifier that targets interleukin 1. My rheumy said that is not used that much anymore because of more effective options. A recently published report indicates that a Swedish company just purchased the rights for Kineret from biological pharmaceutical giant Amgen. Such a move seems like Amgen is dumping the drug likely because it is not profitable and is moving onto other new drugs. After much discussion, we both agreed to try Rituxan and I will continue to inject 20mg of methotrexate weekly. 

As I was describing my new treatment regimen to friends and family, I found myself trying to explain the drugs, how they are administered, how they act to treat RA, and the possible side effects. As I read more about these drugs, it struck me as interesting that both medicines were originally developed to treat certain forms of cancer. Methotrexate is a chemotherapy drug developed in the 1950s and is still used to treat forms of leukemia, breast cancer, lung cancer, non-Hodgkin lymphoma, and head and neck cancers (see American Cancer Society). It stops the growth of cancer cells by affecting their metabolism. Given the immunosuppressing nature of methotrexate, it is now commonly used in lower doses to treat various autoimmune diseases including rheumatoid arthritis. It’s also used to treat tubal ectopic pregnancies by inducing abortion. In spite of the low doses used in treating RA, some of the chemotherapy side effects remain including hair loss and nausea. This paints a picture of a rather toxic medicine! But I’ve been injecting 20mg weekly for some time now and seem to tolerate it rather well.

Rituxan is also known by the names MabThera and Rituxamab. This monoclonal antibody is a biological medicine that was originally developed in the late 1990s to target the protein CD20 present in certain phases of B lymphocytes. It was originally approved for the treatment of B cell related lymphomas and leukemias (see the Rituxan website). In the early 2000s, it was shown in clinical trials to be effective in treating rheumatoid arthritis and gained FDA approval for use in refractory RA cases in 2006. The involvement of B cells in autoimmune diseases likely led to the investigation of Rituxan as a treatment for RA. The side effect profile appears similar to other biologicals but with some additional infusion side effects requiring some pre-medications along with a few more rare serious infections.

The use of cancer drugs to treat RA points to the connection of both diseases to the immune system. It also demonstrates the serious nature of RA. Given the fact that both methotrexate and Rituxan were originally designed to treat certain cancers, and that they are now secondarily being used to treat RA, may point to the fact that a much larger proportion of research funding goes to cancer (see this earlier post). While I don’t mind receiving the “leftovers” or being an “afterthought” if the medicines effectively treat RA, the ideal would be for the development of new treatments or even cures specifically designed for the processes involved in autoimmune diseases. In the meantime, I’ll go to the infusion clinic and begin Rituxan infusions along with cancer patients and see if it can take care of this refractory case of RA!

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When dealing with a chronic illness, it can sometimes feel like being a patient is a full time job. Last week drove home this feeling. It began Wednesday with a visit to a new internist (general practitioner-GP). I decided to switch GPs for several reasons primarily to get all of my doctors under one clinic roof who all share the same electronic system and who can easily connect with one another if needed. Being that this was a first visit, additional medical history paperwork was required. The evening before, I typed up a brief history, printed it out, and brought it along. My daughter joked that it looked like I was writing a school report! I’ve learned that this is a great way to lay everything out in black and white so the doctor can get the whole picture quickly. This visit ended with the scheduling of a follow-up in two weeks along with lab tests for fasting glucose and lipid panels (related to metabolic syndrome – see earlier posts).

On Friday, most of the day was spent on medical tasks. It began with a weekly methotrexate injection right after breakfast. I learned that the syringes sent by the mail order pharmacy had huge needles which were not fun pushing into my stomach. I made a note to pick up smaller insulin needles later in the day.

I then headed out the door for a visit to my rheumatologist. I was so happy when the nurse and not the medical assistant came to bring me to the examination room. This was because I needed her to help process a co-pay assistance for the last two Actemra infusions I had in March and April. The almost $900 of co-pays were sitting on my bill from the clinic and I wanted to get those cleared. The nurse needed to make copies of the bill and my co-pay debit card in order for money to be loaded on the card so I can pay the bill. Once the funds are loaded, I will need to go to the business office of the clinic to pay the bill.

My rheumy came in and we had a long discussion about how things were going. She decided to up the dose of Remicade to 600mg per infusion and give infusions every four weeks instead of every six weeks. We’re just not seeing the impact expected by these RA treatments. After being on so many treatments, it’s easy to get cynical and I work hard at trying to avoid falling into a negative mindset. We also discussed recurring headaches and she added leucovorin once a week to be taken after the methotrexate injection. Leucovorin in a form of folic acid and is used to combat side effects of methotrexate. She also decided to give a cortisone shot in my right knee which has been getting worse over the past few months. It was a pretty painless procedure and after several days I can notice much less pain and popping. I just wish every other joint could feel that way!

After the rheumy appointment ended, I went straight to the infusion clinic to see how soon I could get in for an infusion at the new dose and treatment schedule. They said they could get me in that afternoon. I scheduled it and then as I walked away, I realized that insurance approval would likely be required first. I went back to the rheumy’s office and talked to the nurse. She confirmed that approval would be required and that she would call me when it came. Back up to the infusion clinic to cancel the appointment! But I wasn’t done with the rheumy yet. She ordered five lab tests – routine liver, kidney, and inflammation tests – so I headed to the lab for a blood draw. The c-reactive protein test came back high once again confirming that systemic inflammation is actively at work and the RA is not under control (but then again, I already knew that based on the way I feel).

After this appointment ended, I had an appointment with my neurologist. Nasty headaches had been raising their ugly head again and he wanted to figure out what was going on. The good thing is that the addition of an injection of solu-medrol cortisone prior to Remicade infusions helped control headaches associated with the infusion. He believes that my body is reacting to all the medicines and he added a preventative medicine in addition to the Imitrix abortive medicine I already use. He said that he would want to get an MRI if I wasn’t better in a couple of weeks.

It was noon by the time I left the clinic and then I went to the pharmacy to pick up some scripts – and the smaller syringes! That took about an hour as there were questions on the script along with new health insurance to process (thanks to changes in U.S. healthcare laws).

Almost the entire day was spent navigating medical systems and providers. I know the clinic like the back of my hand…best place to park, location of restrooms, coffee shop on 1st floor, lab on 2nd floor, rheumatology office 4th floor, infusion clinic 5th floor, neurology 8th floor, internal medicine 9th floor. Whew! I was tired and ready for something non-medical related at the end of this crazy day. Add to such a day the time spent in the infusion clinic, time processing insurance and payment paperwork, communicating with doctors via phone and email, and down time just trying to rest, being an RA patient feels like a job.

The good news is that during one of the of doctor visits, I picked up the July issue of the city magazine because the cover story was about “Top Doctors” in the city. I glanced through the different sections and was so pleased to find my rheumatologist and neurologist both listed as one of the top six in the city in their respective specialties. This helped confirm that I choose the right doctors and was under quality care.

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It seems that with the FDA approval of Xeljanz this week, most of the attention for new treatments for RA is focused on orally administered protein kinase inhibitors.[i] This attention is not unwarranted in that Xeljanz is the first oral treatment for RA approved in over 10 years. The kinase inhibitor drugs are complex molecules that impact some part of the biological pathways involved in cancer and immune diseases.[ii] With all the hoopla around Xeljanz, I wondered what was going on in the world of new biological treatments for RA.


Most biological treatments for autoimmune diseases are focused on signaling pathways involved with immune cells. These signals are typically carried by proteins including cytokines. In autoimmune diseases, it is thought that the pathways and associated cytokines are out of whack resulting in an overactive immune response in which a person’s own tissue comes under attack. Tumor necrosis factor (TNF) is a cytokine that has been the target of many recent biological treatments for RA. The most popular biological treatments for RA are Enbrel, Humira, and Remicade which all attempt to block TNF with antibody proteins. The large size of these sensitive proteins means that they must be injected or infused into the body rather than be ingested orally. Other biological treatments approved for RA include Orencia targeting the protein called B7 which reduces T cell stimulation, Rituxan which targets the protein CD-20 in B cell pathways, and the newest one Actemera which targets interleukin 6 (IL-6).

There are literally thousands of clinical trials related to RA occurring around the world[iii] and finding specific information related to new possible biological treatments is difficult for someone outside the research community. It seems that pharmaceutical companies are somewhat elusive with drug development. They want to maintain some level of trade secrecy, publish results in the peer-reviewed research world, and give out just enough information for investors to get excited. With a little snooping that would not have been possible 15 years ago in the early stages of the internet, I found that there are some important clinical trials going on for new biological treatments. In some cases, I had to create a login to access certain journals or use my university library access to find information.

B cell lymphocytes and their signaling proteins appear to be one of the main targets of recent biological drug development.[iv][v]. It seems that IL-6 and CD-20 are the most researched parts of the RA biochemical pathway. I found 17 biologicals that show promise and are in various stages of testing. Below is a list of some of the biologicals I found. Most of their scientific names end in “MAB” because they are monoclonal antibodies meaning that they are cloned proteins coming from one type of immune cell. Genetically engineered mice are used in the complex production process.

We see the usual set of major pharmaceutical players, who already have the lion’s share of the RA drug market, doing most of the testing of these new drugs demonstrating that there is big money to be had in this area. Sometimes smaller companies develop the drug and the rights are purchased by a large company who then funds the extensive clinical trails. Not all of these experimental drugs will obtain approval and make it to market.

It is a good thing for patients that the search for new biological and chemical treatments for RA continues. The wide variety of biologicals targeting different biochemical pathways may ultimately result in more patients responding to treatment. With over 1.5 million RA patients and as one of the leading causes of disability in the United States, treatments are needed that improve the quality of life and reduce disability. In spite of the proliferation of treatments, I still hold out hope for a real cure to this insidious disease.

IL-6 Inhibitors

Sarilumab is being developed by Sanofi in Europe. It shows promise in clinical trials in treating RA with infections the most common side effect.[vi]

BMS-945429 is an experimental drug from Bristol Meyers Squibb that also targets IL-6.[vii] It is made in yeast cells instead of the standard medium for making other biologicals-hamster ovaries. It shows promise in treating RA.[viii]

Sirukumab, being tested by GlaxoSmithKline, is an IL-6 inhibitor to which RA patients show a good response.[ix] Side effects include infections, gastrointestinal problems, and blood problems.[x]

Olokizumab is being developed in Europe by UCB which also developed the TNF blocker Cimzia. [xi] It shows promise in early trials with side effects including headache and blood problems.[xii]

GSK315234, also from GlaxoSmithKline, targets interleukin 6 (IL-6) and is in early clinical trials. [xiii] [xiv]

CD-20 Inhibitors

Like Rituxin, the antibody Ofatumumab (trade name Azerra also known as HuMax-CD20) targets the B cell protein CD-20. It is already approved for leukemia but is being tested in clinical trials for rheumatoid arthritis.[xv] It is produced by GlaxoSmithKline.

Pfizer, in partnership with Emergent, announced the development of a biological which also targets CD-20. It is currently called SBI-087 (PF-05230895).[xvi] It is in clinical trial for the treatment of RA.[xvii]

While not a completely new biological, Pfizer is testing an antibody called PF-05280586 that is similar to Rituxin. These are called “biosimilars” and other companies around the world are trying to get in on the action by developing their own Rituxin look-alikes.[xviii]

IL-20 Inhibitors

The monoclonal antibody NNC 0109-0012 targets interleukin 20 (IL-20). Clinical trials occurred in Europe and are funded by the company Novo Nordisk. Early results show that this biological positively impacted RA symptoms while showing the typical safety profile of other biologicals including increased infections and injection reactions.[xix]

IL-17 Inhibitors

Secukinumab, developed by Novartis, targets the cytokine interleukin 17 (IL-17).[xx] It is in clinical trial for several autoimmune diseases including RA in which some improvement was seen with typical side effect profiles for other biologicals.[xxi] [xxii]

Ixekizumab, from Eli Lily and Co., also targets IL-17 and is being tested for RA and plaque psoriasis.[xxiii] Early results demonstrate impact on RA symptoms along with typical side effects including infections.[xxiv]

B Cell Activating Factor (BAFF) Inhibitors

Tabalumab, from Eli Lily and Co., is being developed as a treatment for autoimmune diseases and some cancers. It shows some efficacy at reducing RA symptoms yet includes infections as a side effect.[xxv]


Pateclizumab, by Genentech and Roche, targets a set of cytokines called lymphotoxin (LT)-alpha Inhibitors. It shows promise in treating RA. It is also being tested by co-administering it along with a TNF blocker like Enbrel. Side effects include headache and gastrointestinal issues but no serious infections.[xxvi]

Denosumab is an antibody from Amgen that targets the production of RANKL, a protein that signals bone erosion. It is currently approved under the trade name Prolia for the treatment of osteoporosis and is currently under clinical trial for the treatment of RA.[xxvii] But problems with the drug have held up the use of Denosumab for osteoporosis let alone other diseases.[xxviii]

Ozoralizumab, developed by Ablynx in Europe, is a new TNF blocker that shows promise in treating RA and may compete with Humira and Enbrel if approved.[xxix][xxx]

Stelara (Ustekinumab), developed by Janssen, is already approved for the treatment of psoriasis. It targets interleukins 12 and 23 (IL-12, IL-23). It is in clinical trial for RA.[xxxi]

Fezakinumab, being developed by Pfizer, targets interleukin 22 and is in clinical trial for RA.[xxxii]

Creative Commons Photo Credit: http://commons.wikimedia.org/wiki/File:Chimeric_and_humanized_antibodies.svg

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