What is the difference between jra and ra

In addition to classifying of patients into various distinct phenotypic groups, the classification criteria also help to predict long-term outcome, on the basis of the phenotype at onset. However, a recent study by Guillaume et al. In this study, gender and age at onset were not identified as predictive of a poor articular outcome. A population-based outcome study of JCA from Sweden reported that at onset of the disease, gender is the greatest predictor of disability and that at follow-up, continued disease activity, followed by the presence of IgM-RF, are the greatest predictors of disability [ 7 ].

Interestingly, those whose monoarticular or pauciarticular disease extended later to polyarticular disease were as frequently classified into Steinbrocker functional classes II to IV as those who had polyarthritis at onset. In one study, patients with intermittent or persistent systemic JRA had poorer functional outcomes than those with a monocyclic course [ 8 ]. Another group reported that a polyarticular pattern and hip involvement at 6 months predicted a poor outcome in patients with systemic-onset JRA [ 9 ].

Disease activity strongly influences functional capacity in RA, even in long-standing disease. After 12 years of follow-up in another study, disease activity was the main determinant of the functional status as measured by the Health Assessment Questionnaire score [ 12 ].

Several studies have reported increased mortality rates in RA patients, with infections, pulmonary and renal disease and gastrointestinal bleeding being the major causes of death [ 13 ]. Patients with extra-articular RA had higher mortality rates than not only an age-matched general population, but also than the non-extra-articular RA group in another study [ 14 ].

The prevalence of definite RA among adults in the USA has been estimated to be approximately 10 per , with an overall prevalence of 7 per for men and 16 per for women [ 15 ]. The prevalence of JRA, however, is considerably lower, estimated to be between 57 to per , children under the age of The incidence of JRA is estimated to be approximately 10 per , per year in children under 16 years of age.

Thus JRA is a much less frequent autoimmune disease than its adult counterpart. Like RA, both pauciarticular and polyarticular JRA are characterized by a female-to-male ratio greater than 1. Systemic JRA, on the other hand, has no such female predilection.

Patients with RA frequently have a positive family history of RA. In fact, several extended families with RA have been reported and there are many affected sibling pairs with RA. The availability of such affected sibling pairs has been conducive to the performance of at least three genome-wide scans of linkage in RA [ 19 — 21 ].

Although there are studies that report an increased prevalence of inflammatory arthritis among relatives of patients with JRA [ 22 , 23 ], a family history of inflammatory arthritis is less common in children, and extended multiplex pedigrees are extremely rare in JRA. Relatives of patients with RA have an increased prevalence of other autoimmune disorders besides inflammatory arthritis [ 25 , 26 ]. Thomas et al. Similarly, Lin et al. Case reports describe JRA patients with other autoimmune disorders such as type 1 diabetes mellitus, vitiligo, thyroiditis and autoimmune oophoritis.

In an epidemiological study, we have shown that the relatives of patients with JRA have an increased prevalence of autoimmunity [ 27 ]. Information was collected from interviews of patients with JRA, 23 families of affected sibling pairs and 45 healthy controls. Information was available on more than relatives. Overall, the relatives of JRA patients had a significantly increased prevalence of autoimmunity. The most frequent autoimmune disorder seen was Hashimoto's thyroiditis.

The prevalences of RA among relatives of patients with simplex JRA and controls were not significantly different. Relatives of JRA-affected sibling pairs also had a higher prevalence of autoimmunity than controls.

While there were no differences in the overall prevalences of autoimmunity among relatives of simplex and multiplex JRA families, the prevalence of inflammatory arthritis JRA, ankylosing spondylitis and RA combined was increased among the relatives of JRA-affected sibling pairs. The most extensively studied susceptibility locus for autoimmune disorders is the major histocompatibility complex MHC located on chromosome 6p.

This region is densely packed with more than genes [ 28 ] and several of these are essential to the immune system, including the human leukocyte antigen HLA genes. HLA associations are distinct for RA and JRA, demonstrating that the immunogenetic factors involved in susceptibility to these two diseases are indeed different. However, the various HLA alleles that are associated with susceptibility to RA have a common determinant in the third hypervariable region of the DRB1 chain, encompassing the amino acid positions [ 30 ].

This common region, designated the shared epitope, is thought to play a crucial role in the interaction of the T cells with the peptide HLA complex. Those RF-positive RA patients with severe disease, with erosions and extra-articular features, are more likely to carry two DRB1 susceptibility loci alleles than are patients with milder forms of the disease [ 31 ].

Recently de Vries et al. They confirmed the association of susceptibility to RA with alleles encoding the susceptibility sequences of the shared epitope. Interestingly the protective alleles also shared a third motif in the hypervariable region. Independent homozygosity effects were observed both for susceptibility and for protective alleles.

Interestingly, this gene might be protective in patients with EOPA. Confirming the associations that have been reported, linkage between pauciarticular JRA and the HLA region has been shown both by using transmission disequilibrium testing in simplex families [ 40 ] and by allele sharing among affected sibling pairs [ 41 ].

Similarly, linkage between polyarticular JRA and the HLA region has also been shown by allele sharing among affected sibling pairs [ 41 ]. One of the unique features of JRA is that there appears to be a window of susceptibility, during which children with predisposing HLA alleles or combination of alleles are maximally susceptible to the development of JRA, suggesting gene—gene and gene—environment interactions [ 42 ].

Gender strongly influenced the age at which many of the alleles have their effect. These results demonstrate the complex interactions between different HLA susceptibility alleles that influence the age of onset of JRA.

This gene has been implicated in susceptibility to RA [ 43 ]. Sanjeevi et al. Polymorphisms of the genes related to the cytokine network have also been implicated in the pathogenesis of both JRA and RA and these findings have been supported by association studies.

The results of genome-wide scans from RA patients and families, in addition to confirming the linkage between RA and the HLA region, suggest the hypothesis that RA susceptibility loci overlap with loci implicated in other autoimmune disorders. Cornelis et al. Linkage was significant only for HLA and nominal for 19 markers in 14 other regions.

Four of these regions overlapped loci implicated in IDDM. In a further study of a second set of families, linkage to one region 3q13 was extended significantly. In another genome-wide scan for allele sharing in RA-affected sibling pairs collected in the USA, significant sharing was observed both within and outside the HLA region [ 20 ].

Not surprisingly, several of the regions positive for linkage were found to overlap with chromosomal locations implicated in other autoimmune disorders, including systemic lupus erythematosus, psoriasis and inflammatory bowel disease.

Myerscough et al. Another genome-wide scan performed on affected sibling pairs with RA from the UK confirmed the significant linkage to the MHC region [ 21 ].

In addition, 11 non-HLA regions had suggestive or nominal linkage. Six of these regions had been previously identified in the other genome-wide scans [ 19 , 20 ].

Genome-wide scans are under way in JRA and have not yet been reported. In general, the arthritis of RA is a symmetric polyarthritis. The metacarpophalangeal and proximal interphalangeal joints are typically involved in RA.

Ulnar drift of the metacarpophalangeal joint with volar subluxation is characteristic of longstanding RA, which is accompanied by a radial deviation of the wrist [ 48 ].

In JRA, any joint can be affected, but large joints are most frequently involved. Access your health information from any device with MyHealth. You can message your clinic, view lab results, schedule an appointment, and pay your bill.

The disease can be classified into three categories based on the number of and which joints are involved, the symptoms present and their duration, and the presence of specific antibodies produced by the immune system. These three variables often help physicians determine the progression of JRA and include the following:. See a Stanford specialist to learn about your treatment options. Visit our clinic to make an appointment. Share on Facebook. Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare.

We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience. View the changes to our visitor policy » View information for Guest Services ». New to MyHealth? Feeling very tired or rundown fatigue. Blurry vision or dry, gritty eyes. Appetite loss. High fever. Certain symptoms are specific to the type of arthritis a child has.

There are six types of JIA: Oligoarthritis: Affects four or fewer joints, typically the large ones knees, ankles, elbows. Most common subtype of JIA.

Polyarthritis: Affects five or more joints, often on both sides of the body both knees, both wrists, etc. May affect large and small joints. Systemic: Affects the entire body joints, skin and internal organs.

Skin symptoms may occur before or after joint symptoms appear. May affect one or more joints, often the wrists, knees, ankles, fingers or toes. Enthesitis-related: Also known as spondyloarthritis. Affects where the muscles, ligaments or tendons attach to the bone entheses. More common in boys; typically appears in children between the ages of eight and If JIA inflammation goes unchecked, it can damage the lining that covers the ends of bones in a joint cartilage , and the bones themselves.

Here are some other ways JIA can affect the body: Eyes. Dryness, pain, redness, sensitivity to light and trouble seeing properly caused by uveitis chronic eye inflammation. More common with oligoarthritis. Chronic inflammation and use of corticosteroids may cause growth delay in some children with JIA. Bones may get thinner and break more easily osteoporosis. Difficulty chewing, brushing or flossing. More than half of children with JIA have jaw involvement. Inflammation of the cervical spine can cause neck pain or stiffness.

Swollen neck glands could also signal an infection for kids with SJIA or who take immunosuppressing drugs. Foot pain and difficulty walking. More common in polyarthritis and enthesitis-related arthritis. Symptoms can range from a faint salmon colored rash SJIA to a red, scaly rash psoriatic arthritis. Inflammation and scarring that can lead to shortness of breath and lung disease. May occur in SJIA. Inflammation may cause damage to the heart muscle. Digestive Tract.

Abdominal pain and diarrhea. More common in children with spine arthritis or ankylosing spondylitis. Reproductive organs. Late onset of puberty. Certain drugs such as cyclophosphamide may lead to fertility problems later.

Weight loss or gain. Due to changes in appetite, jaw involvement or difficulty exercising. Being overweight puts extra stress on the joints. Controlling inflammation and managing disease can prevent damage and complications from these health effects.

According to American College of Rheumatology ACR a child must have inflammation in one or more joints lasting at least six weeks, be under 16 years old and have all other conditions ruled out before being diagnosed with JIA.

Some rheumatologists only treat children. Others only treat adults. Some of them treat both. A medical history, physical examination and blood tests helps to make the correct diagnosis. Medical history. This helps rule out other causes like trauma or infection. The doctor will also ask about the family's medical history. Physical examination. The doctor will look for joint tenderness, swelling, warmth and painful or limited movement and test range of motion.

Eyes and skin may also be checked. Laborator tests. The doctor may order blood tests that look for certain proteins and chemicals found in some people with arthritis.

Rheumatoid factor RF test: May show up in children with polyarthritis. A positive rheumatoid factor may signal more serious disease. Complete blood count CBC : Raised levels of white blood cells and decreased levels of red blood cells is linked to certain types of arthritis.

The doctor may order imaging tests, such as X-rays, ultrasound and MRI or CT scans, to look for signs of joint damage. There is no cure for JIA but remission little or no disease activity or symptoms is possible. Early aggressive treatment is key to getting the disease under control as quickly as possible.