Poor prognostic factors include,

- Persistent synovitis

- Early erosive disease

- Extra-articular findings (including subcutaneous rheumatoid nodules)

- Positive serum RF findings

- Positive serum anti-CCP autoantibodies

- Carriership of HLA-DR4 "Shared Epitope" alleles

- Family history of RA

- Poor functional status

- Socioeconomic factors

- Elevated acute phase response (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP])

- Increased clinical severity.

RA reduces lifespan on average from three to twelve years. According to the UK's National Rheumatoid Arthritis Society, Young age at onset, long disease duration, the concurrent presence of other health problems (called co-morbidity), and characteristics of severe RA—such as poor functional ability or overall health status, a lot of joint damage on x-rays, the need for hospitalisation or involvement of organs other than the joints—have been shown to associate with higher mortality". Positive responses to treatment may indicate a better prognosis. A 2005 study by the Mayo Clinic noted that RA sufferers suffer a doubled risk of heart disease, independent of other risk factors such as diabetes, alcohol abuse, and elevated cholesterol, blood pressure and body mass index. The mechanism by which RA causes this increased risk remains unknown; the presence of chronic inflammation has been proposed as a contributing factor. It is possible that the use of new biologic drug therapies extend the lifespan of people with RA and reduce the risk and progression of atherosclerosis. This is based on cohort and registry studies, and still remains hypothetical. It is still uncertain whether biologics improve vascular function in RA or not. There was an increase in total cholesterol and HDLc levels and no improvement of the atherogenic index.

FDG positron emission tomography (PET) may be useful to detect the condition early. Other imaging studies including MRI, CT scans, and X-rays may reveal inflammation and/or damaged cartilage facilitating diagnosis.

Patients presenting with acute episodes often have high levels of inflammatory markers such as erythrocyte sedimentation rate or C-reactive protein, ESR or CRP. Patients often have cartilage-specific antibodies present during acute relapsing polychondritis episodes. Antinuclear antibody reflexive panel, rheumatoid factor, and antiphospholipid antibodies are tests that may assist in the evaluation and diagnosis of autoimmune connective-tissue diseases.

Diagnosis of JIA is difficult because joint pain in children can be from many other causes. No single test can confirm the diagnosis, and most physicians use a combination of blood tests, X-rays, and clinical presentation to make an initial diagnosis of JIA. The blood tests measure antibodies and the rheumatoid factor. Unfortunately, the rheumatoid factor is not present in all children with JIA. Moreover, in some cases, the blood work is somewhat normal. X-rays are obtained to ensure that the joint pain is not from a fracture, cancer, infection, or congenital abnormality.

In most cases, fluid from the joint is aspirated and analyzed. This test often helps in making a diagnosis of JIA by ruling out other causes of joint pain.

New research shows that identifying what type of JIA a child has can help target treatment and lead to more positive outcomes. Identifying the specific biomarkers related to each type of JIA can help form more personalized treatment plans and decrease remission rates.

Children with JIA are more susceptible to cardiovascular disease, depression, sleep disturbance, anxiety and fatigue than healthy individuals. There is also limited information that suggests that children with JIA are at increased risk for malignancies when being treated with TNF blockers.

Prognosis is more positive when gene testing is undergone to identify what subtype of JIA is present in the child. Standardized treatment protocols are in place specific to each subtype of JIA. Treatment is more successful when targeted to the specific subtype of JIA.

When faced with monoarthritis, one of the main decisions to make is whether to perform a "joint aspirate" by inserting a needle into the affected joint and removing some fluid for microscopic analysis. This decision is largely taken on inflammatory markers in blood tests (e.g. CRP), fever and the clinical picture. The main use of aspiration is to detect bacteria and neutrophil granulocytes (in septic arthritis) and crystals (crystal arthropathies).

Ultrasonography and magnetic resonance imaging of the hands and/or feet have been proposed as useful diagnostic investigations in RS3PE.

Some studies linked RS3PE to HLA-B27 whereas others have not.

Polyarthritis is most often caused by an auto-immune disorder such as rheumatoid arthritis, amyloidosis, psoriatic arthritis, and lupus erythematosus but can also be caused by infection with an alphavirus such as chikungunya virus and Ross River virus. This condition is termed alphavirus polyarthritis syndrome. Sindbis virus, which is endemic in Northern Europe, Africa, the Middle East, and Australia, is the most widely distributed of the alphaviruses causing polyarthritis, though infection is usually mild or asymptomatic.

It may be associated with bilateral edema in lower limbs, pain and joint swelling. Sometimes there is previous history of inflammatory joint problems and bilateral edema of lower limbs.

Alphavirus Polyarthritis Syndrome has an incubation period of 3–21 days, depending on the specific virus, with either a gradual or sudden onset of fever, arthralgias, headache, and lymphadenitis and conjunctivitis in some forms. A maculopapular rash may present 4–8 days post symptom onset and may be accompanied by an increase in fever. Joint pains associated with this condition may recur for many months after initial illness for up to a year.

RS3PE responds excellently to low dose corticosteroids, with sustained and often complete remission. Non-steroidal anti-inflammatory drugs (NSAIDs) have also been used. Hydroxychloroquine has proven effective in some cases.

Occurs in 5-10% of patients who have psoriasis.Classic presentation involves the DIP(distal inerphalangeal joints).Morning stiffness is present.Deformity of involved joints,dactylitis and nail involvement are common.Well demarcated red plaques with silvery scaling - the classic lesions of psoriasis are seen on the dorsum of the hand.

In the presence of suspicious symptoms a number of test are helpful in the diagnosis:

- Muscle enzymes are often elevated, i.e. creatine kinase

- Anti-Jo-1 antibody testing

- Electromyography

- Muscle biopsy

- Pulmonary function testing

- Lung biopsy

In certain situations, testing of other antibodies, specific imaging (MRI, thoracic high resolution computed tomography), and swallowing evaluation may be needed.

Unfortunately, treatment for the anti-synthetase syndrome is limited, and usually involves immunosuppressive drugs such as glucocorticoids. For patients with pulmonary involvement, the most serious complication of this syndrome is pulmonary fibrosis and subsequent pulmonary hypertension.

Additional treatment with azathioprine and/or methotrexate may be required in advanced cases.

Prognosis is largely determined by the extent of pulmonary damage.

Adenocarcinoma of the bowel has been associated with coeliac disease.

Squamous carcinoma of the esophagus is more prevalent in coeliac disease. The increased prevalence may be secondary to GERD that results from chronic delayed gastric emptying. Other studies implicate the malabsorption of vitamin A and zinc as a result of multi-vitamin and mineral deficiencies seen in Coeliac disease.

Gonococcemia (also known as "Arthritis–dermatosis syndrome" and "Disseminated gonococcal infection") is a condition characterized by a hemorrhagic vesiculopustular eruption, bouts of fever, and arthralgia or actual arthritis of one or several joints.

It's characterized by a triad of symptoms: migratory polyarthritis, tenosynovitis, and dermatitis (pustular skin lesions).

Diagnosis is by a swab of the affected area for laboratory testing. A Gram stain is performed to show Gram-positive cocci in chains. Then, the organism is cultured on blood agar with an added bacitracin antibiotic disk to show beta-hemolytic colonies and sensitivity (zone of inhibition around the disk) for the antibiotic. Culture on agar not containing blood, and then performing the catalase test should show a negative reaction for all streptococci. "S. pyogenes" is CAMP and hippurate tests negative. Serological identification of the organism involves testing for the presence of group-A-specific polysaccharide in the bacterium's cell wall using the Phadebact test.

The rapid pyrrolidonyl arylamidase (PYR) test is used for the presumptive identification of group A beta-hemolytic streptococci. GBS gives a negative finding on this test.

Erythema marginatum is a type of erythema (redness of the skin or mucous membranes) involving pink rings on the torso and inner surfaces of the limbs which come and go for as long as several months. It is found primarily on extensor surfaces.

An association with bradykinin has been proposed in the case of hereditary angioedema.

It occurs in less than 5% of patients with rheumatic fever, but is considered a major Jones criterion when it does occur. The four other major criteria include carditis, polyarthritis, Sydenham's Chorea, and subcutaneous nodules. In this case, it is often associated with Group A streptococcal infection, otherwise known as "Streptococcus pyogenes" infection, which can be detected with an ASO titer.

It is an early feature of rheumatic fever and not pathognomonic of it. It may be associated with mild myocarditis (inflammation of heart muscle). It is also seen in conditions like allergic drug reactions, sepsis and glomerulonephritis.

It often occurs as a harbinger of attacks in hereditary angioedema. In this case it may occur several hours or up to a day before an attack.

Post-streptococcal glomerulonephritis (PSGN) is an uncommon complication of either a strep throat or a streptococcal skin infection. It is classified as a type III hypersensitivity reaction. Symptoms of PSGN develop within 10 days following a strep throat or 3 weeks following a GAS skin infection. PSGN involves inflammation of the kidney. Symptoms include pale skin, lethargy, loss of appetite, headache, and dull back pain. Clinical findings may include dark-colored urine, swelling of different parts of the body (edema), and high blood pressure. Treatment of PSGN consists of supportive care.

The easiest way to diagnose PDP is when pachydermia, finger clubbing and periostosis of the long bones are present. New bone formation under the periosteum can be detected by radiographs of long bones. In order diagnose PDP, often other diseases must be excluded. For example, to exclude secondary hypertrophic osteoarthropathy, any signs of cardiovascular, pulmonary, hepatic, intestinal and mediastinal diseases must be absent. MRI and ultrasound also have characterictic findings.

Skin biopsy is another way to diagnose PDP. However, it is not a very specific method, because other diseases share the same skin alterations with PDP, such as myxedema and hypothyroidism. In order to exclude these other diseases, hormonal studies are done. For example, thyrotropin and growth hormone levels should be examined to exclude thyroid acropachy and acrome. However, skin biopsy helps to diagnose PDP in patients without skin manifestations.

When clubbing is observed, it is helpful to check whether acroosteolysis of distal phalanges of fingers is present. This is useful to diagnose PDP, because the combination of clubbing and acroosteolysis is only found in PDP and Cheney’s syndrome.

Since elevated PGE2 levels are correlated with PDP, urinary PGE2 can be a useful biomarker for this disease. Additionally, HPGD mutation analyses are relatively cheap and simple and may prove to be useful in early investigation in patients with unexplained clubbing or children presenting PDP-like features. Early positive results can prevent expensive and longtime tests at identifying the pathology.

For the follow-up of PDP disease activity, bone formation markers such as TAP, BAP, BGP, carbodyterminal propeptide of type I procallagen or NTX can play an important role. Other biomarkers that can be considered are IL-6 and receptor activator of NF-κB ligand (RANKL), which are associated with increased bone resorption in some patients. However, further investigation is needed to confirm this use of disease monitoring.

Prostaglandin E2 may also be raised in patients with lung cancer and finger clubbing. This may be related to raised levels of cyclooxygenase-2, an enzyme involved in the metabolism of prostaglandins. A similar association has been noted in cystic fibrosis.

There is no effective treatment for this condition. It has been reported that clearance of lesions can be done with melphalan and cyclophosphamide alone or in combination with prednisone. Both isotretinoin and etretinate have also been shown to improve the conditions. All medications listed can cause adverse symptoms, with isotretinoin and etretinate particularly dangerous since they are both teratogens. Other attempted treatments include interferon-alpha, cyclosporine, PUVA photochemotherapy, electron-beam therapy, IVIg, and dermabrasion. However, the overall prognosis for the disease is poor. There are reported instances of remission of the disease when treated with a combination of Revlimid and Dexamethasone over a 24-month period.