Of all forms of arthritis, we know more about gout than perhaps any other. Gout has been documented since biblical times and has a history of being the “disease of kings.” Today, about 6 in 1,000 men and about 1 in 1,000 women in this country are afflicted with this disorder. Gout in women is uncommon before menopause, which is thought to be because oestrogen has a preventive effect.
Uric acid builds up and forms crystals when serum levels cross a particular threshold, which is what causes gout. While the majority of people with elevated uric acid levels do not develop gout, the hazard for this ailment increases considerably as these levels rise.
Patients with elevated uric acid levels either make too much uric acid (over-producers) or don’t eliminate enough uric acid in their urine (under-excretors). About 90% of those with gout fall into the latter category. Those considered over-producers tend to be younger and also have an increased risk for forming kidney stones.
Certain medications, such as diuretics (medications causing fluid excretion), cyclosporine, and tuberculosis drugs can elevate the uric acid level, as can alcohol and certain foods. Red meat could have a similar, albeit less noticeable, effect to organ meats in elevating uric acid levels (liver, kidneys, etc.). Gout risk is also higher for people with kidney disease, adult-onset diabetes, psoriasis, & organ transplants.
In those who are predisposed to gout, uric acid crystals result in severe joint inflammation, which leads to acute "attacks" marked by pain, warmth, swelling, and frequently redness over an affected joint. A fever may come on in some patients when in an acute flare. Traditionally, the flare may start at night and cause the patient to become aware. Many people claim that the injured joint is so painful that the bed sheets' pressure is bothersome.
The most commonly affected joint in gout is at the base of the big toe. At some point during the course of their illness, 90% of all individuals with gout will experience a flare in this joint at least once. Next in frequency is the mid-section of the foot near the instep, followed by the ankle, the knee, and finally the elbow, wrist, and finger joints.
Another characteristic of gout is the propensity for certain people to develop tophi, or soft tissue nodules. These nodules typically develop over bony areas like the elbows & knuckles of the hands, although they have also been seen to develop around the ear. People that develop tophi frequently have longer-lasting illnesses. We classify these people as having “chronic tophaceous gout.”
After the first flare of gout, as many as 1/2 of all patients will never have another episode. Otherwise, the natural history of untreated gout is to experience acute recurrent flares that become progressively more prolonged but less intense. The end result, after an average of 10 years, is chronic tophaceous disease, characterized by chronic and persistent joint swelling with nodules. Many of these individuals resemble patients with rheumatoid arthritis (RA; see Rheumatoid Arthritis section).
In IBD patients, the spine has arthritis a little more frequently than other joints. The sacroiliac joint experiences inflammation the most frequently, just as in people with ReA. X-rays of this joint may show involvement even when the patient is asymptomatic, however lower back pain is frequently observed. Bowel & lower back symptoms do not appear to be closely correlated with one another or to mirror one another, and sacroiliac inflammation may start either prior to or following the IBD diagnosis.
In contrast to spinal arthritis, inflammation in other joints may correlate more closely with disease activity in the bowel. The hands' knuckles and fingers, knees, ankles, elbows, and shoulders are the joints most frequently affected. Individuals with IBD experience upper limb involvement more frequently than those with ReA, and these patients generally have an increased number of inflamed joints. While joint injury is possible, the inflammation usually does not result in bone or joint deterioration. Because patients with IBD are at risk for joint infections as well as loss of blood supply to the bones (a complication known as avascular necrosis), an acutely swollen or painful joint should be investigated accordingly to rule out these problems.
Iritis, erythema nodosum (red nodules over the shins), pyoderma gangrenosum (painful skin ulcerations), aphthous ulcers (sores in the mouth), iritis, and liver-related issues are some of the other IBD side effects that can affect other sections of the body. While all of these features have been well described in IBD patients, they all occur in less than 20% of these individuals and are less frequently seen than the arthritis described above
Both ReA and IBD arthritis are best diagnosed by carefully examining the joints for swelling, tenderness, limited motion, and other signs of inflammation. Arthritis fitting the patterns described above in a patient with a known recent infection or either known or suspected IBD should raise the suspicion for these disorders. The diagnosis is further supported in patients with aberrant skin findings, oral ulcers, eye infections, vaginal involvement, or other traits typical of either ReA or IBD. Additional proof for these types of arthritis can be provided by X-rays of the affected joints, especially the pelvis if sacroiliac illness is suspected. While x-rays are often normal initially and may remain normal throughout the course of the disease (particularly in IBD patients), joint films may demonstrate erosions or joint damage suggesting the need for more aggressive treatment or provide evidence for another explanation for the patient’s joint symptoms.
Laboratory testing is of less value in the diagnosis of both ReA and IBD arthritis. While these disorders are frequently accompanied by increases in inflammatory markers, these results are not particular and can be observed in a variety of inflammatory conditions. It is possible to measure the HLA-B27 gene, however neither condition needs to be diagnosed in order for this result to be obtained. Although the presence of this gene may aid in confirming the diagnosis, a large proportion of people with ReA and IBD arthritis do not have this finding, as well as a negative test does not necessarily rule out these types of arthritis. Patients with ulcerative colitis and Crohn's disease may show anti-Saccharomyces cerevisiae antibodies and anti-neutrophil cytoplasmic antibodies (ANCA), respectively, although once more, these tests are commonly negative and may not need to be conducted in every case.
The tests needed to identify IBD are outside the purview of this article, but in general, either an endoscopy—a technique in which a lighted flexible tube is placed into the rectum to examine into the colon—or barium studies performed in the x-ray department—are used to make the diagnosis. The treatment and treatment of the bowel components of the disease are typically handled more intensively by other professionals, such as gastroenterologists or surgeons.
The intensity of the joint involvement and potential for damage determines how ReA and IBD arthritis should be treated, as it does with many other types of arthritis. Although many of the medicines used to treat bowel disease in patients with IBD also treat joint disease, we will concentrate on the therapy of IBD arthritis in this article.
Non-steroidal anti-inflammatory drugs (NSAIDs) In moderate cases of ReA or IBD arthritis, non-steroidal anti-inflammatory medications (NSAIDs) may be sufficient to alleviate joint discomfort. Ibuprofen, naproxen, & indomethacin are a few examples of medications in this group; the latter is a medication that many doctors like for spondyloarthropathies. One issue with these medications for IBD is that they run the risk of escalating gut inflammation in in addition to putting patients at risk for ulcers or stomach lining damage. However, this concern has not yet been explored in well-designed research. Newer NSAIDs that are "COX-2 selective" significantly reduce the risk of stomach injury and may also produce less worsening of intestinal inflammation. Prednisone and other corticosteroids work well to treat IBD flare-ups, however they work less well to treat related arthritis or ReA. However, the acute symptoms that come along with flare-ups of arthritis or tendinitis may be effectively managed by injecting steroids directly directly inflamed joints or soft tissues.
Sulfasalazine (SSZ) In patients with inflammatory bowel disease and those with ReA who do not react to NSAIDs, sulfasalazine (SSZ), a well-established therapy for inflammatory bowel disease, is frequently beneficial in reducing joint inflammation. Although SSZ is slow-acting and takes two to three months to start working, it frequently offers more persistent symptom relief than NSAIDs alone. While taking SSZ, it's important to watch out for less common side effects like a decline in white blood cells and raised liver enzymes as well as the most frequent ones, such as nausea, stomach pain, and allergic responses.
Antibiotics Patients with ReA who receive antibiotics may see a reduction in the intensity or length of their arthritis, although this is more likely to happen if the antibiotics are directed at a particular infection. Both ciprofloxacin and tetracycline-based antibiotics, such as doxycycline, have been demonstrated to be effective when administered over the course of three months to ReA brought on by genital infections & infectious diarrhoea, respectively. Despite the studies' slightly conflicting findings, it makes sense to administer the proper antibiotic therapy to a trigger infection that has been identified.
Immune suppressing drugs such as methotrexate (MTX), and azathioprine (AZA) may be useful in certain patients. Few well-designed studies have looked specifically at their impact on various types of arthritis, but because they are often used to treat IBD, many have noticed that these patients' joint symptoms also go better. These medications can sometimes be more effective at treating inflammatory arthritis in joints beyond the spine than they are at treating ReA. It is prudent to screen for HIV exposure before putting a patient having ReA on one of these drugs because these patients are more likely to experience negative effects. View the Medications section or even the Rheumatoid Arthritis section for further information on the adverse effects of these medications.
Tumor necrosis factor (TNF) antagonists have represented a major advance in the treatment of spondyloarthropathies and IBD. TNF, a protein implicated in inflammation in different regions of the body and widely used in RA, is blocked by these medications. They appear to be helpful in treating ReA and IBD arthritis, even though more studies have focused on AS and PsA patients.
Etanercept (marketed under the name Enbrel), infliximab (marketed under the name Remicade), & adalimumab are the medications in this class that are presently in use (trade name Humira). Remicade is given intravenously every eight weeks, while Enbrel and Humira are given via weekly or every two-week injections, respectively. While each medication appears to help individuals with spondyloarthropathy in overall, only Remicade appears to help those with IBD's bowel condition.
Due to the immune system suppression caused by TNF antagonists, infections must be closely monitored while using these treatments, and susceptibility to tuberculosis should be evaluated by doing a skin test before beginning treatment. Additional possible side effects include injection site responses, infusion site reactions, impairment of cardiac function in people with heart failure, including worsening of illness in patients with multiple sclerosis.
TNF antagonists are not appropriate for many patients with ReA or IBD arthritis due to the aforementioned dangers and the high expense of these drugs, but for those with advanced or resistant illness, they represent a significant advancement in treatment. Together, the doctor and patient can select which combination of the aforementioned therapies is most suitable for each person with ReA or IBD-associated arthritis.
