Elevated rheumatoid factor -- and anti-CCP antibodies present. Lyme or rheumatoid arthritis.

A 54-year-old male presented to me within the last few weeks, having self-diagnosed himself with Lyme disease.  He asked for a Lyme test because of some unexplained tendinitis and a few unexplained aches and pains, which he appeared not be terribly concerned about.  His past history was remarkable for a skin disorder diagnosed as intractable eczema, although treated with UV therapy, typical of psoriasis. He states there had been no allergy workup, that he knew about. He went to his family doctor and asked for a Lyme test. He told his GP that previously, doxycycline made his eczema flare, so amoxicillin was prescribed. When he was getting worse, now with significant joint pain, after 1-2 weeks, he sought my attention. 

This amiable gentleman has a very positive demeanor and a healthy dose of denial – maybe a little to “healthy.”  

His IgE level of over 4000 was “off the chart.”  I have another patient with primary hyper-IgE syndrome which is an immune deficiency in and of itself. In this case, the elevation is due to severe allergies (demonstrated with food, RAST testing). This was not his chief complaint, but I have to see where all symptoms and problems lead and connect the dots. Oddly, his repeat Lyme test was negative, but his Babesia test was positive. (He has a history of night sweat dating back years which he had discounted).  To add another layer of confusion, his rheumatoid and anti-CCP antibody tiers were sky high.

There was no history of significant joint swelling or joint deformities. His joint pain was asymmetrical and involved primarily large, rather than small joints. 

I will segue from here to a discussion of elevated rheumatoid factor level.  A lot of patients see a rheumatologist long before seeing me, in this case his only doctors were his GP and his dermatologist. I was the first to order the tests. 

RA or rheumatoid arthritis, is an autoimmune disorder, primarily involving joints, but which may involve other organ systems at times (extra-articular manifestations). It is also traditionally classified as a collagen vascular disorder. 

Typically, the disease affects young women, not middle age men. Typically, involvement begins with small joints, hands and fingers (middle knuckles), is symmetric and is associated with swelling, frequently progressing to deformity. 

There are atypical cases. A middle age man presenting with a unilateral (single) knee swelling and pain, may indeed have rheumatoid arthritis: this would be a rarity. 

Rheumatoid arthritis has no connection to Lyme disease or any other tickborne disease. Or does it?  This patient has severe allergic disease and may also have a form of autoimmune disease. Is there any connection?  I don’t think there is. 

A positive rheumatoid factor is frequently elevated in my Lyme patients and usually resolves with treatment.

I have tended to be dismissive of an elevated RA when the anti-CCP antibody is negative – the confirmatory test.

All permutations are possible.  It is possible to have RA with both tests negative (RA factor and CCP antibodies) or with one negative and one positive. Similarly, it is possible to NOT have RA with both tests positive. An absolute diagnosis cannot be made simply based on finding one or both of these antibodies. This concept applies to ANA and others markers of rheumatologic disease.  Both rheumatoid arthritis and Lyme are diagnosed clinically, not reliably by a blood test.  I have heard it said that there is no real rheumatoid arthritis and no real lupus, it is all really Lyme. This is incorrect. These diseases existed long before Lyme came onto the scene. 

Lyme does not cause RA, at least not directly. I have several patients with classic RA triggered by Lyme disease. These patients were genetically predisposed to the illness. If not Lyme, something else may have triggered the disease at some point, including emotional stress. 

In the most common scenario, Lyme triggers false positive tests for rheumatoid arthritis, usually rheumatoid factor, but occasionally anti-CCP antibodies; and, these antibodies disappear when Lyme is successfully treated. The term false positive may be confusing. These antibodies are in fact present (real) but they are NOT elevated because of RA but because of Lyme inflammation of joints. Successful treatment of Lyme refers to a therapy with antimicrobial agents which eliminates all joint pain and swelling.  Getting there may be difficult. Over time, with treatment, RA factor and CCP antibodies slowly come down and then disappear. 

Plaquenil has may have some mild “anti-Lyme” properties.  Some patients benefit from its anti-inflammatory, immune modulating effects. (Also used in RA and lupus). 

The theory that Lyme persists in intracellular structures and that alkalization of the intracellular milieu (with Plaquenil) facilitates the antibacterial properties of drugs like Biaxin is NOT correct. 

We know Lyme persistence has to do with pleomorphism (round bodied forms) and biofilm formations. We also know that Lyme bacteria are predominantly extracellular and rarely intracellular. Known facts contradict the theory. 

The skin disease is this patient is allergic and/or mast cell mediated, not autoimmune and unrelated to Lyme disease. 

It is important not to confuse different, abnormal (pathological) immune responses: mast cell disease, allergic disease, autoimmune disease, Herxheimer reactions (excessive immune responsiveness) and immunodeficiency. These are all very different entities.

PS:  High IgE not caused by Babesia, only caused by parasitic worms.  (worms, wheezes and whacky diseases).