Rheumatoid and Osteo Arthritis: Where to Begin in THIS case?
September 11, 2018 | 8 Comments | SAFM Team
(This is a sample entry from our Q&A Treasure chest, a database with hundreds of entries to support students with their patient and client work. Unlimited access is included as part of our Core 101 Semester program.)
This is a patient who is 67, Dx rheumatoid arthritis and osteoarthritis. Renal reconstruction surgery at age 30 and has frequent bladder and yeast infections. Also stomach bloating and high BP.
She wants to lose weight and has lost 10 lb since going gluten free and is now 150 lb @ 5’4″.
Her daily Medications are Amlodipine, Benicar, Crestor, Zetia, Methotrexate 2.5mg-5 tabs weekly, Veramyst nasal spray, and Allegra.
Her supplements are cranberry capsules, Fish oil 1200mg, Vit C 1000mg, and Raw probiotics vaginal care (38 strains, 80 Billion CFU).
We’ve just gotten started. She was also taking folic acid 1mg (I recommended a switch to methylfolate) and aspirin 81mg (which I suggested may be aggravating intestinal permeability given the AI activation). Her PCP recently added Vitamin D3 5000 based on moderate lab values, but I am concerned about her serum calcium of 10.8 mg/dl. She states this value has been high “for a long time” but has never been flagged as notable or investigated. All other basic labwork seems optimal – or at least WNL.
My challenge is that she is not open to any functional testing (e.g. stool test) at all. She is open to follow-on bloodwork, but not until after her return from an upcoming six-week trip abroad. I know we have much to investigate and explore over time. My question is this: where would you begin?
A fascinating case! If you haven’t yet already, I highly recommend you read some of the other posts on various autoimmune diseases and common contributors and etiological factors on our site, especially this one. Searching by “autoimmune” in the Q&A Treasure Chest will bring up many more. But the details of this case are also a perfect example of why we need to approach every patient with Beginner’s Mind and look for the unique factors and contributors.
My input is to put some focus (50/50) both on Rapid Relief and on Root Cause investigation and resolution. You don’t mention whether there is ongoing pain in spite of the methotrexate (MTX). However, it’s key in my view to aim to reduce joint inflammation in pursuit of minimizing any ongoing damage in addition to symptoms of pain, discomfort, and/or stiffness. Then I have some interesting thoughts for you with regard to root cause interconnectedness.
In terms of Rapid Relief:
- I would check the quality of her fish oil supplement and add to it the anti-inflammatory GLA (an essential omega-6 fatty acid) such as 500mg evening primrose oil bid, taking both together in split doses with meals (to maximize absorption). GLA can be helpful in arthritis via a few pathways; it’s also helpful in countering IL-6 which is implicated as a major inflammatory mediator in rheumatoid arthritis (part of what the MTX is countering), and it has also been shown to reduce platelet aggregation.
- Given the likelihood of its contribution to enhance intestinal permeability (and reduction of immune function in the gut to the damage to the gut lining), I would stop the daily aspirin use for now unless there are immediate signs of cardiovascular disease (and check with the patient re:any plans for a long plane flight).
- I would add a ubiquinol (reduced CoQ10) supplement, 100mg bid, to counter the depleting effects of the statin drug.
- Given the existing autoimmune diagnosis, I appreciate your focus on excessive intestinal permeability. We also know that food sensitivities associated with leaky gut are often at play in osteoarthritis. I would recommend a focused elimination diet – including both gluten and dairy foods from the diet in general for that reason and, in the case of RA, I would add nightshade vegetables to that list. While a full elimination diet might be most helpful for this woman, I am sensitive to the travel ahead and what might be feasible vs. theoretically optimal for her to achieve.
- Lastly, I would add Undenatured Type 2 Collagen. The link is to an excellent research review. The mechanism is not agreed conclusively, but it appears UC-II works primarily by promoting oral tolerance to collagen that can stop the cycle of ongoing inflammation to endemic tissue, arresting the process. It appears at least 40mg/day is required; I usually recommend 60mg in divided doses on an empty stomach (key!). This is available in many products, some combined with anti-inflammatory agents, especially bromelain and boswellia e.g. Life Extension ArthroMax Advanced, Real Advantage Semperflex, Metagenics OsteoVantiv (but the magnesium oxide may not be well tolerated in this latter option).
In terms of Root Cause (but there are some urgent factors in here too):
- I too am concerned about the high serum calcium level. For now, until you can get additional labwork, I would stop the Vitamin D3 supplement and add in a Vitamin K2 and Magnesium glycinate supplement instead. High Vitamin D is just going to encourage more calcium absorption which, for the moment, is not helpful and potentially dangerous. This will help to channel available calcium into bone tissue and prevent calcification of soft tissue (which she is likely already vulnerable to from both a cardiovascular as well as renal perspective given her meds and history). The parathyroid gland is largely responsible to keep optimal levels of calcium in the blood. At your first opportunity, I would recheck Vitamin D, serum calcium, and parathyroid hormone (PTH) all at once. Sustained high serum Calcium in an adult may be indicative of a parathyroid gland tumor; I have actually seen this a few times in my own practice. This is an online resource I have found to be particularly helpful and clinically sound on the topic of parathyroid issues.
- When you can seek bloodwork, I would also order a full thyroid panel. There is a strong association (just one example) between hypothyroidism and the development of hyperparathyroidism. We also know that elevated LDL cholesterol (evidence her hypercholesterolemia meds) and gastrointestinal dysmotility (e.g. constipation, IBS-like symptoms) are common symptoms of a hypothyroid state. Thyroid hormone is also key for bile synthesis (see below).
- Unfortunately sustained, elevated levels of serum calcium may also have been a key driver of her arthritis by promoting build-up of calcification in the joints. Arthritis-like complaints are an acknowledged symptom of hyperparathyroidism. Is it also possible that elevated serum calcium contributed to her kidney dysfunction years ago? Or impaired filtration downstream from damaged kidneys is promoting higher calcium in the years since (and now)? Either or both are possibilities worth exploring. Powerful examples of interconnectedness.
- We know that LPS-mediated inflammation from the gut (due to enhanced intestinal permeability) can be a common driver for rheumatoid arthritis. The appropriate food eliminations (e.g. gluten and its cross-reactives) and healing the gut lining are key. But…
- I would also investigate the likelihood of impaired bile flow AND synthesis (check alkaline phosphatase and biliruin and liver enzymes in the next CMP you order; also ask to make sure she still has her gallbladder – a common item overlooked on intake form submissions!). This woman may need help with clearing out bile ducts and gallbladder (e.g. d-limonene, artichoke) and/or improving liver synthesis (evidence all of the medications and the statins impairing liver function). Those with RA are significantly more likely (50%!) to have gallstones or have had their gallbladder removed.
This woman is taking medication to both suppress synthesis of cholesterol (statin) and block reabsorption of cholesterol (zetia) from the gut. It’s very logical that this may be impairing bile function overtly and present a fascinating example of interconnectedness where medication to try to prevent disease in one system (cardiovascular) may actually be promoting it in another (gut, joint, kidneys).
As a final comment, this woman may or may not have a pathogenic microbial issue at play in her gut or as an etiology of the RA. Part of the “catch 22” of using an agent like MTX for relief is that it suppresses immune function and can be actively exacerbating a triggering infection while simultaneously providing triage. Supporting this type of patient to be able to remove the MTX (by addressing rapid relief via other agents and at least significantly beginning the journey to address root causes) will likely be key to her having sustainable relief from this dis-ease process.