Sometimes, You Have to Ask

I saw my rheumatologist for a three month follow-up recently. Incidentally, the day before my 40th birthday. Do I know how to get a party started or what?! While I was sitting in the waiting room, two well-dressed ladies came in and asked the receptionist if it would be possible to see my doctor. They were clearly drug representatives packing freebies. I had already been waiting forty-five minutes at this point, as had the gentleman a few seats away from me. I couldn’t help but think–I hope you are seeing the doctor after me!

Within five minutes, they were called to come back. I said to the gentleman near me, “I wish we were called that quickly.” He agreed and we began to talk. It was nice to swap personal health facts and experiences with someone else that has dealt with wacky pain and inflammation. It was nice because he “get’s it” and because we both had compassion for what the other has endured. He wasn’t much older than me, drives a truck for Walmart, had a knee require surgery, soon after bodily joint pain and stiffness entered the scene and now for the past few years he has been on methotrexate and a biologic that he self injects, and has had a second knee surgery. The drugs are not getting the job done and he lives in pain.

I told him my body really let go after my fourth c-section, but because I was nursing, I researched alternative approaches. Shared with him the importance of looking at what you eat. He was surprised to hear that eliminating certain foods or chemicals can help take a load off your system. He had never heard that sugar was inflammatory. (Not only that–it’s like crack, people! Try to give it up for a month and tell me how you do. 🙂 ) I told him that I have done two different approaches with antibiotics. The first I said was nine months long, tough at the outset, progress was very gradual but awesome, and following it, I was drug-free and functioned quite well for a year and a half. Praise God. Now I have begun a second protocol and have been at it for a year, things are much better now than a year ago. He had never heard of the approach. I told him to check out the Road Back website. He was very interested and hopefully encouraged by the fact that I had experienced positive results. He was there to see my doctor after me. When I saw my doctor, I let him know his next patient might have questions. 🙂

Here are my current lab results from 10/2013 if you are interested:

Image

Not bad, eh? Except for that MCV number. My doctor said that meant enlarged red blood cells. “Which could mean what?” I asked. He said, “Could be thyroid, but we’ve checked that and you’re fine, alcohol is not a problem for you, labs show liver and kidney look good, could be your B12 or folate levels…let’s get that checked today and I will have the nurse call you with the results.”

Here’s a tip for anyone coming up on a birthday. Don’t consult with Dr. Google regarding anything about your health until waaaayyyy after your birthday! Note to self. I couldn’t help myself and looked for information about enlarged red blood cells. I’m not going to even write about some of the things I read about. I remember seeing the MCV number high a long time ago on my lab results in addition to MCH, but I recall my doctor not seeming concerned. I dug through my copies of blood work going back three years. The number has been up there for the past three years for both MCV and MCH. Interesting to me that it has my doctors attention now.

Lab results from three years ago (10/2010):

lab results 10/2013

In looking at my lab results from my primary care doctor, I discovered that my B12 and folate levels looked good two years ago when they were checked and I have supplemented with a multi-vitamin daily since then and have maintained a healthy, whole-foods diet. I’m guessing my levels will still be fine.

My doctor originally told me that he would keep me on minocycline for up to a year. I’ve passed the one year anniversary and was pleased that he didn’t mention taking me off and told me to schedule a follow-up three months from now. I am going to continue the minocycline indefinitely for now, as well as the sulfasalazine. I realized I wouldn’t see my doctor until the new year (hopefully won’t have to before!) and wished him a Happy Thanksgiving, Merry Christmas and Happy New Year before going next door for more blood work.

Just for kicks, I did an online search today for information about long-term antibiotic therapy and this came up on page one of my search hits from Doctor Oz:

http://www.doctoroz.com/blog/jacob-teitelbaum-md/antibiotics-helpful-rheumatoid-arthritis

Go Doctor Oz and thank you for spreading the word!

And this:

http://recoveringarthritics.blogspot.com/2009/11/three-recovering-arthritics.html

She might as well be me talking!

I also searched the list of abstracts presented recently at the American College of Rheumatology Annual Meeting in San Diego in hopes that this treatment is being investigated further. Unfortunately, not really. To me, it’s heart breaking. I found numerous studies involving biologic drugs, however. I found the following chart in one of the abstracts. The chart displays the average copay for drugs used for RA under Medicare–which is $250-$650 for a biologic. Plain crazy. I scrolled down and found minocycline–$7. So, what are the chances of pharmaceutical companies funding research studying long-term antibiotic protocols and their role in certain autoimmune diseases? I’m thinking next to none because they stand nothing to gain! Sad.

Table.   Coverage for Rheumatoid Arthritis Drugs in U.S. Medicare Part D Plans.

Drug

 

Plans covering drug

(%)

 

Plans covering drug without prior authorization

(%)

 

Plans Charging Percent

Co-insurance

(%)

 

Mean

Co-insurance

(%)

 

Average Copay

Mean (SD)

($)

 

Biologic
Abatacept

54

 

4

 

100

 

30.1

 

601 (22)

 

Adalimumab

100

 

7

 

100

 

30.0

 

583 (12)

 

Anakinra

40

 

4

 

100

 

29.9

 

517 (19)

 

Certolizumab

59

 

1

 

100

 

29.6

 

650 (16)

 

Etanercept

100

 

7

 

100

 

30.0

 

547 (11)

 

Golimumab

42

 

1

 

100

 

29.6

 

580 (17)

 

Infliximab

100

 

7

 

100

 

30.0

 

255 (5)

 

Rituximab

100

 

8

 

87

 

29.5

 

611 (25)

 

Tocilizumab

40

 

1

 

99

 

29.7

 

335 (14)

 

.
At least 1 biologic DMARD

100

 

9

 

87

 

30.3

 

275*

 

.
Non-biologic
Azathioprine

100

 

34

 

10

 

18.1

 

7 (1)

 

Cuprimine

60

 

60

 

59

 

30.6

 

83 (6)

 

Cyclophosphamide

94

 

2

 

20

 

27.4

 

32 (3)

 

Cyclosporine

100

 

12

 

22

 

25.1

 

34 (2)

 

Hydroxychloroquine

100

 

100

 

10

 

18.1

 

5 (1)

 

Leflunomide

100

 

100

 

13

 

19.3

 

11 (1)

 

Methotrexate

100

 

85

 

13

 

19.8

 

5 (1)

 

Minocycline

100

 

94

 

10

 

18.1

 

7 (1)

 

Sulfasalazine

100

 

100

 

10

 

18.1

 

5 (1)

 

.
At least 1 non-biologic DMARD

100

 

100

 

11

 

18.2

 

4*

 

.*mean copay of least expensive drug covered

Here are studies discussing the use of minocycline for rheumatoid arthritis from pub med:

http://www.ncbi.nlm.nih.gov/pubmed/14528503

http://www.ncbi.nlm.nih.gov/pubmed/10047718

The following is taken from:

British Journal of Pharmacology © 2013 The British Pharmacological Society.

Minocycline is a second-generation, semi-synthetic tetracycline that has been in therapeutic use for over 30 years because of its antibiotic properties against both gram-positive and gram-negative bacteria. It is mainly used in the treatment of acne vulgaris and some sexually transmitted diseases. Recently, it has been reported that tetracyclines can exert a variety of biological actions that are independent of their anti-microbial activity, including anti-inflammatory and anti-apoptotic activities, and inhibition of proteolysis, angiogenesis and tumour metastasis. These findings specifically concern to minocycline as it has recently been found to have multiple non-antibiotic biological effects that are beneficial in experimental models of various diseases with an inflammatory basis, including dermatitis, periodontitis, atherosclerosis and autoimmune disorders such as rheumatoid arthritis and inflammatory bowel disease. Of note, minocycline has also emerged as the most effective tetracycline derivative at providing neuroprotection. This effect has been confirmed in experimental models of ischaemia, traumatic brain injury and neuropathic pain, and of several neurodegenerative conditions including Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, Alzheimer’s disease, multiple sclerosis and spinal cord injury. Moreover, other pre-clinical studies have shown its ability to inhibit malignant cell growth and activation and replication of human immunodeficiency virus, and to prevent bone resorption. Considering the above-mentioned findings, this review will cover the most important topics in the pharmacology of minocycline to date, supporting its evaluation as a new therapeutic approach for many of the diseases described herein.”

Found this on minocycline and ovarian cancer:

http://www.ncbi.nlm.nih.gov/pubmed/23593315

Unfortunately, there is a great deal of information out there that our doctors are not telling us about. I’ve never had a medical doctor talk to me about what I eat and it’s role in disease. I’ve never had a medical doctor talk to me about the importance of managing stress and it’s impact on my body. And antibiotics as a treatment option are not being offered as readily as biologics, if even at all. Take the patient I spoke with in the waiting room for example. We have the same rheumatologist and he has never heard of antibiotics as a possibility. And he has been dealing with wonky joint pain and inflammation for a few years now. Antibiotics have certainly not been the end all be all for me. And they come with their own scary list of side effects. But my journey with them has changed my life for the better and it’s important to me to share that in the hopes it could help someone else.

The Latest From the Professionals

I wanted to let you know that my dermatologist called me personally and told me that my biopsy came back as highly probable for psoriasis. I’ll be honest, I would have prefered–it is or it isn’t psoriasis. Highly probable? Good enough, I suppose. Doc sounded pretty excited on the phone. “This is great! You actually have a diagnosis now that is pretty certain!” Yay for me. I’m sorry if I don’t sound as thrilled. I felt really phony in my response to her and said, “Yeah!” And that’s all I said. What was I supposed to say? “I know this is great! And now you can tell all your doctor friends that I am no longer a strange mysterious rash case with swollen joints.”

Discovering that what has been going on with me has a different name recently was quite a moment for me. I was anxious to share with family and my blogging friends (who are undoubtedly the most amazing group of people on the planet!). But I really didn’t like my dermatologist sounding so excited about the fact that something about me finally came back highly probable just because everything else I have presented her with has completely stumped her, her colleagues and the labs.

I also saw my rheumatologist for a follow up last month. It was an uneventful visit for the most part. Which in essence is a good thing. “How does my latest blood work look, Dr. H?” I asked. Anxious to know whether the antibiotics had affected my liver. To which he replied, “It still looks great.” “How do you feel?” he asked. “Similar to the last visit. Improvements have remained steady and feet are still very painful,” I replied. This means three more months on azithromycin and rifampin to go before I decide on the next step. (I already know what I’d like to try next and doc is on board. Love him!) Since I have seen some progress on AP and my liver is handling it ok thus far, it’s full steam ahead with the antibiotics.

Have you guys seen the recent press release from the American College of Rheumatology? Pretty exciting to a gal who is on AP for psoriatic arthritis. Here it is:

Press Release

THE BODY AGAINST ITSELF: BACTERIA INSIDE ONE’S OWN BODY LINKED TO RHEUMATOID ARTHRITIS AND OTHER AUTOIMMUNE DISEASES

ATLANTA – Researchers are using 21st-century technologies to investigate the century-old hypothesis that certain autoimmune diseases, including rheumatoid arthritis, are caused by bacteria living in the human body and will present their initial data this week at the American College of Rheumatology Annual Scientific Meeting in Atlanta.

Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.

Researchers have long associated periodontal disease, or gum inflammation, and bacteria in the gastrointestinal tract with RA, although no specific bacteria have ever been identified by researchers as the bacteria to target as possible therapy. Nevertheless, studies have suggested that bacteria or bacterial products contribute to RA and other autoimmune diseases.

Led by co-principle investigators Steven Abramson, MD, and Dan Littman, MD, PhD, researchers from New York University’s Langone Medical Center, aimed to determine whether bacteria in the human mouth and intestines can trigger RA. They used DNA amplification technology to identify what type of bacteria exist in the mouths and intestines of study participants, which included eight people with newly developed RA, three people with psoriatic arthritis, and nine people without these diseases – who were considered healthy.

Previous studies have relied on traditional bacteria cultures, which are only able to identify 20 percent of bacterial species in the human body because of the inability to find the right nutrients to grow the culture, which highlights the uniqueness of this study. “By sending our samples for a deep DNA sequencing, we’re able to identify 100 percent of the bacteria that are present,” says Jose U. Scher, MD, director of New York University’s new Microbiome Center for Rheumatology and Autoimmunity and one of the lead investigators in the study. “So we’re taking a huge step forward by not missing 80 percent of the bacteria. Taking that step will allow us to identify bacteria that are related to rheumatoid arthritis.”

Although it’s too early for this to be applied in the diagnosis of rheumatic diseases in a clinical health care setting, the research is already yielding results that distinguish people with RA from those without. Through this study, researchers were able to identify an over-abundance of the prevotellaceae family of bacteria in the intestinal fecal samples of participants who were newly diagnosed with RA—and had not been treated with drugs for the disease—when compared to those participants in the study who were identified as healthy.

Additionally, researchers found that mouth samples of participants with RA exhibited an overabundance of the porphyromonas genus compared to healthy controls. To examine bacteria in the mouth, researchers studied the gums of participants with RA or psoriatic arthritis, and healthy individuals. When examining the gums of these participants, researchers noted that 78 percent of the examined sites bled during examination in participants with RA, which was a significantly higher percentage than those with psoriatic arthritis (38 percent) and those participants identified as healthy (12 percent). Overall, 66 percent of participants with RA had moderate gum disease – compared to 25 percent of the participants with psoriatic arthritis and 12 percent of the participants in the healthy group.

Additional studies by the group have demonstrated that specific microbes induce the differentiation of Th17 cells in the intestine. There is already strong genetic and therapy-based evidence that pro-inflammatory Th17 cells and anti-inflammatory regulatory T cells (Treg) have critical roles in autoimmune diseases, including RA, psoriatic arthritis, and Crohn’s disease.

“The basic premise is that there are different oral and gut bacteria that activate Th17 cells to promote inflammation,” Dr. Scher explains. “Our hypotheses are that characterization of Th17-inducing microbes in the human intestine will provide insight into disease pathogenesis, and that directed manipulation of the gut microbiota will result in the alteration of arthritis biomarkers, including Th17/Treg balance.”

The next step for the team is a study in which 90 participants with RA will be subdivided into three arms. The first two arms will be given antibiotics for a two-month period, and the third arm will be given placebo. The researchers believe that by modifying the microbial flora with antibiotics, they can identify molecular mechanisms by which RA-associated bacteria affect Th17 and Treg homeostasis and thereby develop new strategies to diminish or even prevent the inflammatory process that leads to chronic destructive arthritis.

The American College of Rheumatology is an international professional medical society that represents more than 8,000 rheumatologists and rheumatology health professionals around the world. Its mission is to advance rheumatology. The ACR/ARHP Annual Scientific Meeting is the premier meeting in rheumatology. For more information about the meeting, visit www.rheumatology.org/education. Follow the meeting on twitter by using the official hashtag: #ACR2010.

Editor’s Notes: Jose U. Scher, MD will present this research during the ACR Annual Scientific Meeting at the Georgia World Congress Center at 3:30 PM on Tuesday, November 9 in the Room A 411. Dr. Scher will be available for media questions and briefing at 8:30 AM on Monday, November 8 in the on-site press conference room, B 212.