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:
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.