A first-in-class treatment option for the management of psoriatic arthritis, apremilast is a small molecule phosphodiesterase-4 inhibitor approved for use by the FDA in 2014. By inhibiting PDE4, an enzyme which breaks down cyclic adenosine monophosphate, cAMP levels rise, resulting in the down-regulation of various pro-inflammatory factors including TNF-α, interleukin 17 and interleukin 23, as well as the up-regulation of anti-inflammatory factor interleukin 10.

It is given in tablet form and taken by mouth. Side effects include headaches, back pain, nausea, diarrhea, fatigue, nasopharyngitis and upper respiratory tract infections, as well as depression and weight loss.

Patented in 2014 and manufactured by Celgene, there is no current generic equivalent available on the market.

The most recent class of treatment is called biological response modifiers or biologics has been developed using recombinant DNA technology. Biologic medications are derived from living cells cultured in a laboratory. Unlike traditional DMARDS that affect the entire immune system, biologics target specific parts of the immune system. They are given by injection or intravenous (IV) infusion.

Biologics prescribed for psoriatic arthritis are TNF-α inhibitors, including infliximab, etanercept, golimumab, certolizumab pegol and adalimumab, as well as the IL-12/IL-23 inhibitor ustekinumab.

Biologics may increase the risk of minor and serious infections. More rarely, they may be associated with nervous system disorders, blood disorders or certain types of cancer.

The major types of medications used to treat ankylosing spondylitis are pain-relievers and drugs aimed at stopping or slowing the progression of the disease. All of these have potentially serious side effects. Pain-relieving drugs come in two major classes:

- The mainstay of therapy in all seronegative spondyloarthropathies are anti-inflammatory drugs, which include NSAIDs such as ibuprofen, phenylbutazone, diclofenac, indomethacin, naproxen and COX-2 inhibitors, which reduce inflammation and pain. Indomethacin is a drug of choice. 2012 research showed that those with AS and elevated levels of acute phase reactants seem to benefit most from continuous treatment with NSAIDs.

- Opioid painkillers

Medications used to treat the progression of the disease include the following:

- Disease-modifying antirheumatic drugs (DMARDs) such as sulfasalazine can be used in people with peripheral arthritis. For axial involvement, evidence does not support sulfasalazine. Other DMARDS, such as methotrexate, did not have enough evidence to prove their effect. Generally, systemic corticosteroids were not used due to lack of evidence. Local injection with corticosteroid can be used for certain people with peripheral arthritis.

- Tumor necrosis factor-alpha (TNFα) blockers (antagonists), such as the biologics etanercept, infliximab, golimumab and adalimumab, have shown good short-term effectiveness in the form of profound and sustained reduction in all clinical and laboratory measures of disease activity. Trials are ongoing to determine their long-term effectiveness and safety. The major drawback is the cost. An alternative may be the newer, orally-administered non-biologic apremilast, which inhibits TNF-α secretion, but a recent study did not find the drug useful for ankylosing spondylitis.

- Anti-interleukin-6 inhibitors such as tocilizumab, currently approved for the treatment of rheumatoid arthritis, and rituximab, a monoclonal antibody against CD20, are also undergoing trials.

- Interleukin-17A inhibitor secukinumab is an option for the treatment of active ankylosing spondylitis that has responded inadequately to (TNFα) blockers.

There is no cure for AS, although treatments and medications can reduce symptoms and pain.

JIA is best treated by a multidisciplinary team. The major emphasis of treatment for JIA is to help the child regain normal level of physical and social activities. This is accomplished with the use of physical therapy, pain management strategies, and social support. Another emphasis of treatment is to control inflammation and extra-articular symptoms quickly. Doing so should help to reduce joint damage and other symptoms, which will help reduce levels of permanent damage leading to disability.

Beneficial advances in drug treatment have been made over the last 20 years. Most children are treated with nonsteroidal anti-inflammatory drugs and intra-articular corticosteroid injections. Methotrexate, a disease-modifying antirheumatic drug (DMARD) is a powerful drug which helps suppress joint inflammation in the majority of JIA patients with polyarthritis (though less useful in systemic arthritis). Newer drugs have been developed recently, such as TNF alpha blockers, such as etanercept. No controlled evidence supports the use of alternative remedies such as specific dietary exclusions, homeopathic treatment, or acupuncture. However, an increased consumption of omega-3 fatty acids proved to be beneficial in two small studies.

Celecoxib has been found effective in one study.

Other aspects of managing JIA include physical and occupational therapy. Therapists can recommend the best exercise and also make protective equipment. Moreover, the child may require the use of special supports, ambulatory devices, or splints to help them ambulate and function normally.

Surgery is only used to treat the most severe cases of JIA. In all cases, surgery is used to remove scars and improve joint function.

Home remedies that may help JIA includes getting regular exercises to increase muscle strength and joint flexibility. Swimming is perhaps the best activity for all children with JIA. Stiffness and swelling can also be reduced with application of cold packs, but a warm bath or shower can also improve joint mobility.

In the future, genetic testing may be available allowing earlier detection of JIA. Early detection will help determine the severity of the disease in each child and help identify which therapies will be the most effective and beneficial treatment options.

The cause of JIA remains a mystery. However, the disorder is autoimmune — meaning that the body's own immune system starts to attack and destroy cells and tissues (particularly in the joints) for no apparent reason. The immune system is thought to be provoked by changes in the environment, in combination with mutations in many associated genes and/or other causes of differential expression of genes. Experimental studies have shown that certain mutated viruses may be able to trigger JIA. The disease appears to be more common in girls, and the disease is most common in Caucasians.

Associated factors that may worsen or have been linked to rheumatoid arthritis include:

- Genetic predisposition; When one family member has been diagnosed with rheumatoid arthritis or another autoimmune disorder, the chances are higher that other family members or siblings may also develop arthritis.

- Females are more likely to develop rheumatoid arthritis than males at all ages.

- A strong belief is held that psychological stress may worsen the symptoms of rheumatoid arthritis. However, when the emotional stress is under control, the arthritis symptoms do not always disappear, suggesting that the association is not straightforward.

- Though no distinct immune factor has been isolated as a cause of arthritis, some experts believe that the triggering factor may be something like a virus which then disappears from the body after permanent damage is done.

- Because rheumatoid arthritis is more common in women, perhaps sex hormones may play a role in causing or modulating arthritis. Unfortunately, neither sex hormone deficiency nor replacement has been shown to improve or worsen arthritis.

The cause of JIA, as the word "idiopathic" suggests, is unknown and an area of active research. Current understanding of JIA suggests that it arises in a genetically susceptible individual due to environmental factors.

Worldwide prevalence of spondyloarthropathy is approximately 1.9%.

Many individuals have mild symptoms, which recur infrequently, while others may have persistent problems that become debilitating or life-threatening.

There are no prospective randomized controlled trials studying therapies for relapsing polychondritis. Evidence for efficacy of treatments is based on case reports and series of small groups of patients.

For mild cases limited to joint pain or arthritis, oral nonsteroidal anti-inflammatory drugs (NSAIDs) may be used. Other treatments typically involve medications to suppress the immune system. Corticosteroids are frequently used for more serious disease. Steroid-sparing medications such as azathioprine or methotrexate may be used to minimize steroid doses and limit the side effects of steroids. For severe disease cyclophosphamide is often given in addition to high dose intravenous steroids.

Spondyloarthropathy or spondyloarthrosis refers to any joint disease of the vertebral column. As such, it is a class or category of diseases rather than a single, specific entity. It differs from spondylopathy, which is a disease of the vertebra itself. However, many conditions involve both spondylopathy and spondyloarthropathy.

Spondyloarthropathy with inflammation is called axial spondyloarthritis. In the broadest sense, the term spondyloarthropathy includes joint involvement of vertebral column from any type of joint disease, including rheumatoid arthritis and osteoarthritis, but the term is often used for a specific group of disorders with certain common features, the group often being termed specifically seronegative spondylarthropathies. They have an increased incidence of HLA-B27, as well as negative rheumatoid factor and ANA. Enthesopathy is also sometimes present in association with seronegative.

Non-vertebral signs and symptoms of degenerative or other not-directly-infected inflammation, in the manner of spondyloarthropathies, include asymmetric peripheral arthritis (which is distinct from rheumatoid arthritis), arthritis of the toe interphalangeal joints, sausage digits, Achilles tendinitis, plantar fasciitis, costochondritis, iritis, and mucocutaneous lesions. However, lower back pain is the most common clinical presentation of the causes of spondyloarthropoathies; this back pain is unique because it decreases with activity.

Oligoarthritis (from Greek "oligos" - 'few') is defined as arthritis affecting two to four joints during the first six months of disease.

With Behçet's disease as an intercurrent disease in pregnancy, the pregnancy does not have an adverse effect on the course of Behçet's disease and may possibly ameliorate its course. Still, there is a substantial variability in clinical course between patients and even for different pregnancies in the same patient. Also, the other way around, Behçet's disease confers an increased risk of pregnancy complications, miscarriage and Cesarean section.

Behçet's can cause male infertility, either as a result of the condition itself or of a side effect of concomitant medication such as Colchicine, which is known to lower sperm count.

Current treatment is aimed at easing the symptoms, reducing inflammation, and controlling the immune system. The quality of the evidence for treating the oral ulcers associated with Behçet's disease, however, is poor.

High-dose corticosteroid therapy is often used for severe disease manifestations. Anti-TNF therapy such as infliximab has shown promise in treating the uveitis associated with the disease. Another Anti-TNF agent, etanercept, may be useful in people with mainly skin and mucosal symptoms.

Interferon alpha-2a may also be an effective alternative treatment, particularly for the genital and oral ulcers as well as ocular lesions. Azathioprine, when used in combination with interferon alpha-2b also shows promise, and colchicine can be useful for treating some genital ulcers, erythema nodosum, and arthritis.

Thalidomide has also been used due to its immune-modifying effect. Dapsone and rebamipide have been shown, in small studies, to have beneficial results for mucocutaneous lesions.

Given its rarity, the optimal treatment for acute optic neuropathy in Behçet's disease has not been established. Early identification and treatment is essential. Response to ciclosporin, periocular triamcinolone, and IV methylprednisone followed by oral prednisone has been reported although relapses leading to irreversible visual loss may occur even with treatment. Immunosuppressants such as interferon alpha and tumour necrosis factor antagonists may improve though not completely reverse symptoms of ocular Behçet's disease, which may progress over time despite treatment. When symptoms are limited to the anterior chamber of the eye prognosis is improved. Posterior involvement, particularly optic nerve involvement, is a poor prognostic indicator. Secondary optic nerve atrophy is frequently irreversible. Lumbar puncture or surgical treatment may be required to prevent optic atrophy in cases of intracranial hypertension refractory to treatment with immunomodulators and steroids.

IVIG could be a treatment for severe or complicated cases.

In 1989, Brazilian researchers Professors Domingos Baggio (an entomologist from the Biomedical Sciences Institute of the University of São Paulo), Paulo Yasuda (a microbiologist from the same institute) and Natalino Hajime Yoshinari (a physician from the Rheumatology Department at University of São Paulo's Medical School) started research on Lyme disease in Brazil, by suggestion of Dr. Allen Steere. At that time, LD was almost unknown among Brazilian physicians.

The first cases were described in Brazil in 1992 in siblings from Cotia, São Paulo that developed symptoms as a migrating redness, general flu-like symptoms and arthritis after being bitten by ticks. Although the symptoms were similar to those presented by patients of Lyme disease, clinical and laboratorial results were considerably different. Ticks of the "Ixodes ricinus" complex were not found at the risk areas; bacteria from the "Borrelia burgdorferi" sensu lato complex —that cause Lyme disease— were not found in biological fluids and tissues of the siblings. Blood analysis of the patients on electron microscopy exhibited structures resembling microorganisms of the spirochaete phylum. For these reasons, the Brazilian zoonosis was considered a new disease and named Baggio–Yoshinari Syndrome (BYS), defined as: "Exotic and emerging Brazilian infectious disease, transmitted by ticks not belonging to the "Ixodes ricinus" complex, caused by latent spirochetes with atypical morphology, which originates LD-like symptoms, except for occurrence of relapsing episodes and auto-immune disorders".

The Baggio–Yoshinari syndrome (BYS), formerly known as the Brazilian Lyme-like disease and Brazilian human borreliosis, is a disease transmitted by the "Amblyomma cajennense" tick, but the organism that causes the infection is still unknown. Clinical features resemble those of Lyme disease (LD).

Biologic treatments such as the TNF inhibitors infliximab, adalimumab, and golimumab are commonly used to treat people with UC who are no longer responding to corticosteroids. Tofacitinib, vedolizumab, and etrolizumab can also produce good clinical remission and response rates in UC. Usually, these medications are only used if other options have been exhausted (i.e., the person has received and not responded favorably to high-dose corticosteroids and immunomodulators such as azathioprine and mesalazine).

Unlike aminosalicylates, biologics can cause serious side effects such as an increased risk of developing extra-intestinal cancers, heart failure; and weakening of the immune system, resulting in a decreased ability of the immune system to clear infections and reactivation of latent infections such as tuberculosis. For this reason, patients on these treatments are closely monitored and are often given tests for hepatitis and tuberculosis at least once a year.

Unlike Crohn's disease, ulcerative colitis has a lesser prevalence in smokers than non-smokers.

Studies using a transdermal nicotine patch have shown clinical and histological improvement.

In one double-blind, placebo-controlled study conducted in the United Kingdom, 48.6% of patients who used the nicotine patch, in conjunction with their standard treatment, showed complete resolution of symptoms. Another randomized, double-blind, placebo-controlled, single-center clinical trial conducted in the United States showed that 39% of patients who used the patch showed significant improvement, versus 9% of those given a placebo. Use of a transdermal nicotine patch without the addition of other standard treatments such as mesalazine has relapse occurrence rates similar to standard treatment without the use of nicotine.