UCL researchers have shown that damage to the lining of the gut plays an important role in RA dev.

@Cymeryska You are not alone, I would strongly suggest you get confirmation that you have true RA, and not reactive RA, which has the same symptoms but triggered by external factors such as bacteria or certain drugs. It is cheap for the NHS to check this out and can save a lifetime of pain and cost, but the NHS is not fully bought into prevention yet, preferring things getting obviously bad and expensive to treat before doing anything, as many here will attest. (I don’t know if it’s still the case, but getting treatment for sight loss was not possible until you went blind in one eye)!

A differential diagnosis eliminates objectively other possible causes, before giving you cytotoxic drugs and lifelong immune suppression.

I include here both a summary of how a differential diagnosis is done, and UCL’s research link (it’s very readable). There are 2 people on this site this year who have “miraculously recovered” after being on RA meds with a “confirmed” RA based on only blood tests, which what happens most of the time. RA consultants seldom consult with their gastroenterologist colleagues who see this a lot more frequently.

RA Differential Diagnosis

When a patient presents with classic symptoms of rheumatoid arthritis (RA), such as bilateral joint pain in the elbows and hands, and tests positive for anti-cyclic citrullinated peptide antibodies (ACCPA) and rheumatoid factor (RF), the following would be among the possible differential diagnoses to consider:

  1. Rheumatoid arthritis: This is the most likely diagnosis given the symptoms and positive ACCPA and RF. Additional tests may be done to evaluate the severity and progression of the disease, such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) to assess inflammation levels, and imaging studies like X-rays, ultrasounds, or magnetic resonance imaging (MRI) to examine joint damage.
  2. Systemic lupus erythematosus (SLE): SLE shares some clinical features with RA, including joint pain and positive RF. However, it typically presents with a broader range of symptoms, such as skin rash, photosensitivity, kidney involvement, and specific antibodies like anti-double-stranded DNA (anti-dsDNA) and anti-Smith (anti-Sm). Further tests, such as an ANA (antinuclear antibody) test, complement levels, and specific antibody tests, can help differentiate between RA and SLE.
  3. Psoriatic arthritis: Psoriatic arthritis is a form of inflammatory arthritis associated with psoriasis. It can also present with symmetric joint involvement and positive RF. A thorough examination for skin and nail changes indicative of psoriasis is crucial. X-rays and MRI scans can reveal characteristic findings like enthesitis (inflammation where tendons and ligaments attach to bone) and joint erosions.
  4. *Reactive arthritis*: Reactive arthritis typically occurs following an infection, often involving the gastrointestinal or genitourinary tract. It can cause joint pain, swelling, and inflammation, but it is usually asymmetrical. In addition to a detailed medical history, tests for specific infections, such as Chlamydia trachomatis or gastrointestinal pathogens, may be conducted to support the diagnosis.
  5. Osteoarthritis: Although osteoarthritis is primarily a degenerative joint disease, it can sometimes cause bilateral joint pain. However, it typically lacks the systemic features seen in RA. Imaging studies, such as X-rays or MRI, may reveal joint space narrowing, osteophyte formation, and other signs of osteoarthritis.

It is important to note that the presence of positive ACCPA and RF is highly suggestive of rheumatoid arthritis, but these tests alone are not sufficient to establish a definitive diagnosis. A comprehensive evaluation by a rheumatologist, considering the patient's symptoms, physical examination findings, and additional diagnostic tests, is necessary to confirm the diagnosis and differentiate it from other possible conditions.

Item 4 is the only one that can be cured, fast & cheap under NHS, but everyone assumes it’s very rare, it’s not, it’s just easier to go with an easier diagnosis & symptom suppression rather than look for the curable cause. The same used to happen with peptic ulcers before 1981, where docs finally had to let go of their long held dogma and accept that the excruciating condition was not due to “executive stress” and lifestyle, but a bacterial infection. There’s no harm in getting it checked, but plenty of benefit if you are one of the “lucky” few.

Second the UCL research summary

Despite understanding of some of the genetic and environmental factors that might be involved in the development of arthritis, scientists still do not completely understand what initiates disease and how it accelerates. Recent research in this area is exploring how the bacteria in the gut might be involved in the development of arthritis, with researchers suggesting that growth of ‘bad’ bacteria in the gut might play a part in initiating the disease.

Co-lead author, Professor Claudia Mauri (UCL Division of Infection & Immunity), said: “We wanted to know what was happening in the gut and whether changes to the intestinal lining – which usually acts as a barrier to protect the body from bacteria – are a feature of the disease and contribute to its development.”

I’ll put the UCL research link in follow up below. (But you can also search for it with the Prof’s name).