In most cases sacroiliitis can be treated without surgery. Often patients will find relief through a combination of rest, heat / ice therapy and anti-inflammatory medication, like ibuprofen. Together these simple treatments help reduce inflammation and allow the body to deliver healing nutrients to the affected SI joints.

For more severe forms of sacroiliitis, sacroiliac joint injections might be recommended to help combat symptoms. If chosen, a physician will inject a numbing agent, usually lidocaine, and a steroid containing powerful anti-inflammatory medication into the joint using fluoroscopic guidance. These steroid injections can be delivered up to three or four times a year and should be accompanied with physical therapy to help rehabilitate the affected joint.

Surgery is often the last resort when dealing with sacroiliitis and is rarely required. However, it may be a viable option for patients who are suffering from severe pain that is unresponsive to nonsurgical treatments and is significantly impacting their quality of life. In these cases, a minimally invasive procedure known as Sacroiliac Joint Fusion can effectively stabilize the joint and increase its load-bearing capacity by fusing it together.

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.

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 main goal of treatment is to identify and eradicate the underlying infectious source with the appropriate antibiotics if still present. Otherwise, treatment is symptomatic for each problem. Nonspecific urethritis may be treated with a short course of tetracycline. Analgesics, particularly NSAIDs, are used. Steroids, sulfasalazine and immunosuppressants may be needed for patients with severe reactive symptoms that do not respond to any other treatment. Local corticosteroids are useful in the case of iritis.

Although a 2011 research article stated that disagreements between hand surgeons and rheumatologists remain regarding the indications, timing and effectiveness of rheumatoid hand surgery, arthritis mutilans may be successfully treated by iliac-bone graft and arthrodesis of the interphalangeal joints and the metacarpophalangeal joint in each finger.

The bone edema in arthitis mutilans can be treated with TNF inhibitors in the short term: a 2007 study found that the bone edema associated with psoriatic arthritis (of which arthitis mutilans is a subtype) responded to TNF inhibitors with "dramatic" improvement, but the study was not determinative of whether TNF inhibitors would prevent new bone formation, bone fusion, or osteolysis (bone resorption).

A common approach to treating a child with JIA typically involves a team of medical professionals including a rheumatologist, occupational therapist (OT), physical therapist (PT), nurse and social worker.

The role of the OT/PT is to help children participate as fully and independently as possible in their daily activities or "occupations", by preventing psychological and physical dependency. The aim is to maximize quality of life, and minimize disruption to the child’s and family’s life. OTs work with children, their families and schools, to come up with an individualized plan which is based on the child’s condition, limitations, strengths and goals. This is accomplished by ongoing assessments of a child’s abilities and social functioning. The plan may include the use of a variety of assistive devices, such as splints, that help a person perform tasks. The plan may also involve changes to the home, encouraging use of uninvolved joints, as well as providing the child and their family with support and education about the disease and strategies for managing it. OT interventions will be changed depending on the progression and remission of JIA, in order to promote age-appropriate self-sufficiency. Early OT involvement is essential. Interventions taught by an OT can help a child adapt and adjust to the challenges of JIA throughout the rest of their life.

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.

"Seronegative spondyloarthropathy" (or "seronegative spondyloarthritis") is a group of diseases involving the axial skeleton and having a negative serostatus.

"Seronegative" refers to the fact that these diseases are negative for rheumatoid factor, indicating a different pathophysiological mechanism of disease than what is commonly seen in rheumatoid arthritis.

Limited evidence suggests removal of the tonsils may benefit people with chronic plaque psoriasis, guttate psoriasis, and palmoplantar pustulosis.

Reactive arthritis may be self-limiting, frequently recurring, chronic or progressive. Most patients have severe symptoms lasting a few weeks to six months. 15 to 50 percent of cases involve recurrent bouts of arthritis. Chronic arthritis or sacroiliitis occurs in 15–30 percent of cases. Repeated attacks over many years are common, and patients sometimes end up with chronic and disabling arthritis, heart disease, amyloid deposits, ankylosing spondylitis, immunoglobulin A nephropathy, cardiac conduction abnormalities, or aortitis with aortic regurgitation. However, most people with reactive arthritis can expect to live normal life spans and maintain a near-normal lifestyle with modest adaptations to protect the involved organs.

Psoriasis resistant to topical treatment and phototherapy may be treated with systemic therapies including medications by mouth or injectable treatments. People undergoing systemic treatment must have regular blood and liver function tests to check for medication toxicities. Pregnancy must be avoided for most of these treatments. The majority of people experience a recurrence of psoriasis after systemic treatment is discontinued.

Non-biologic systemic treatments frequently used for psoriasis include methotrexate, ciclosporin, hydroxycarbamide, fumarates such as dimethyl fumarate, and retinoids. Methotrexate and ciclosporin are drugs that suppress the immune system; retinoids are synthetic forms of vitamin A. These agents are also regarded as first-line treatments for psoriatic erythroderma. Oral corticosteroids should not be used, for they can severely flare psoriasis upon their discontinuation.

Biologics are manufactured proteins that interrupt the immune process involved in psoriasis. Unlike generalised immunosuppressive drug therapies such as methotrexate, biologics target specific aspects of the immune system contributing to psoriasis. These medications are generally well-tolerated and limited long-term outcome data have demonstrated biologics to be safe for long-term use in moderate to severe plaque psoriasis. However, due to their immunosuppressive actions, biologics have been associated with a small increase in the risk for infection.

Guidelines regard biologics as third-line treatment for plaque psoriasis following inadequate response to topical treatment, phototherapy, and non-biologic systemic treatments. The safety of biologics during pregnancy has not been assessed. European guidelines recommend avoiding biologics if a pregnancy is planned; anti-TNF therapies such as infliximab are not recommended for use in chronic carriers of the hepatitis B virus or individuals infected with HIV.

Several monoclonal antibodies target cytokines, the molecules that cells use to send inflammatory signals to each other. TNF-α is one of the main executor inflammatory cytokines. Four monoclonal antibodies (MAbs) (infliximab, adalimumab, golimumab, and certolizumab pegol) and one recombinant TNF-α decoy receptor, etanercept, have been developed to inhibit TNF-α signaling. Additional monoclonal antibodies, such as ixekizumab, have been developed against pro-inflammatory cytokines and inhibit the inflammatory pathway at a different point than the anti-TNF-α antibodies. IL-12 and IL-23 share a common domain, p40, which is the target of the recently FDA-approved ustekinumab. In 2017 the US FDA approved guselkumab for plaque psoriasis.

Two drugs that target T cells are efalizumab and alefacept. Efalizumab is a monoclonal antibody that specifically targets the CD11a subunit of LFA-1. It also blocks the adhesion molecules on the endothelial cells that line blood vessels, which attract T cells. Efalizumab was voluntarily withdrawn from the European market in February 2009 and from the US market in June 2009 by the manufacturer due to the medication's association with cases of progressive multifocal leukoencephalopathy. Alefacept also blocks the molecules that dendritic cells use to communicate with T cells and even causes natural killer cells to kill T cells as a way of controlling inflammation. Apremilast may also be used.

Individuals with psoriasis may develop neutralizing antibodies against monoclonal antibodies. Neutralization occurs when an antidrug antibody prevents a monoclonal antibody such as infliximab from binding antigen in a laboratory test. Specifically, neutralization occurs when the antidrug antibody binds to infliximab's antigen binding site instead of TNF-α. When infliximab no longer binds tumor necrosis factor alpha, it no longer decreases inflammation, and psoriasis may worsen. Neutralizing antibodies have not been reported against etanercept, a biologic drug that is a fusion protein composed of two TNF-α receptors. The lack of neutralizing antibodies against etanercept is probably secondary to the innate presence of the TNF-α receptor, and the development of immune tolerance.

A number of treatments have some evidence for benefits include an exercise program. Paracetamol (acetaminophen) has not been found effective but is safe. NSAIDs are sometimes effective but should not be used after 30 weeks of pregnancy. There is tentative evidence for acupuncture.

Some pelvic joint trauma will not respond to conservative type treatments and orthopedic surgery might become the only option to stabilize the joints.

Ulcerative colitis can be treated with a number of medications, including 5-ASA drugs such as sulfasalazine and mesalazine. Corticosteroids such as prednisone can also be used due to their immunosuppressive and short-term healing properties, but because their risks outweigh their benefits, they are not used long-term in treatment. Immunosuppressive medications such as azathioprine and biological agents such as infliximab and adalimumab are given only if people cannot achieve remission with 5-ASA and corticosteroids. Such treatments are used less commonly due to their possible risk factors, including but not limited to increased risk of cancers in teenagers and adults, tuberculosis, and new or worsening heart failure (these side effects are rare). A formulation of budesonide was approved by the FDA for treatment of active ulcerative colitis in January 2013. The evidence on methotrexate does not show a benefit in producing remission in people with ulcerative colitis. Off-label use of drugs such as ciclosporin and tacrolimus has shown some benefits. Fexofenadine, an antihistamine drug used in treatment of allergies, has shown promise in a combination therapy in some studies. Opportunely, low gastrointestinal absorption (or high absorbed drug gastrointestinal secretion) of fexofenadine results in higher concentration at the site of inflammation. Thus, the drug may locally decrease histamine secretion by involved gastrointestinal mast cells and alleviate the inflammation.

Sulfasalazine has been a major agent in the therapy of mild to moderate ulcerative colitis for over 50 years. In 1977, Mastan S. Kalsi "et al." determined that 5-aminosalicylic acid (5-ASA and mesalazine) was the therapeutically active component in sulfasalazine. Since then, many 5-ASA compounds have been developed with the aim of maintaining efficacy but reducing the common side effects associated with the sulfapyridine moiety in sulfasalazine.

Management of wheat allergy consists of complete withdrawal of any food containing wheat and other gluten-containing cereals (gluten-free diet). Nevertheless, some patients can tolerate barley, rye or oats.

In people suffering less severe forms of wheat-dependent exercise induced anaphylaxis (WDEIA), may be enough completely avoiding wheat consumption before exercise and other cofactors that trigger disease symptoms, such as nonsteroidal anti-inflammatory drugs and alcohol.

Wheat is often a cryptic contaminant of many foods; more obvious items are bread crumbs, maltodextrin, bran, cereal extract, couscous, cracker meal, enriched flour, gluten, high-gluten flour, high-protein flour, seitan, semolina wheat, vital gluten, wheat bran, wheat germ, wheat gluten, wheat malt, wheat starch or whole wheat flour. Less obvious sources of wheat could be gelatinized starch, hydrolyzed vegetable protein, modified food starch, modified starch, natural flavoring, soy sauce, soy bean paste, hoisin sauce, starch, vegetable gum, specifically Beta-glucan, vegetable starch.

Triticeae gluten-free oats (free of wheat, rye or barley) may be a useful source of cereal fiber. Some wheat allergies allow the use of rye bread as a substitute. Rice flour is a commonly used alternative for those allergic to wheat. Wheat-free millet flour, buckwheat, flax seed meal, corn meal, quinoa flour, chia seed flour, tapioca starch or flour, and others can be used as substitutes.

Certain lifestyle changes can reduce symptoms, including dietary adjustments, elemental diet, proper hydration, and smoking cessation. Diets that include higher levels of fiber and fruit are associated with reduced risk, while diets rich in total fats, polyunsaturated fatty acids, meat, and omega-6 fatty acids may increase the risk of Crohn's. Smoking may increase Crohn's disease; stopping is recommended. Eating small meals frequently instead of big meals may also help with a low appetite. To manage symptoms have a balanced diet with proper portion control. Fatigue can be helped with regular exercise, a healthy diet, and enough sleep. A food diary may help with identifying foods that trigger symptoms. Some people should follow a low fiber diet to control acute symptoms especially if fibrous foods cause symptoms. Some find relief in eliminating casein (protein found in cow's milk) and gluten (protein found in wheat, rye and barley) from their diets. They may have specific dietary intolerances (not allergies).

Acute treatment uses medications to treat any infection (normally antibiotics) and to reduce inflammation (normally aminosalicylate anti-inflammatory drugs and corticosteroids). When symptoms are in remission, treatment enters maintenance, with a goal of avoiding the recurrence of symptoms. Prolonged use of corticosteroids has significant side-effects; as a result, they are, in general, not used for long-term treatment. Alternatives include aminosalicylates alone, though only a minority are able to maintain the treatment, and many require immunosuppressive drugs. It has been also suggested that antibiotics change the enteric flora, and their continuous use may pose the risk of overgrowth with pathogens such as "Clostridium difficile".

Medications used to treat the symptoms of Crohn's disease include 5-aminosalicylic acid (5-ASA) formulations, prednisone, immunomodulators such as azathioprine (given as the prodrug for 6-mercaptopurine), methotrexate, infliximab, adalimumab, certolizumab and natalizumab. Hydrocortisone should be used in severe attacks of Crohn's disease. Biological therapies (biopharmaceuticals) are medications used to avoid long-term steroid use, decrease inflammation, and treat people who have fistulas with abscesses. The monoclonal antibody ustekinumab appears to be a safe treatment option, and may help people with moderate to severe active Crohn's disease. The long term safety and effectiveness of monoclonal antibody treatment is not known. The monoclonal antibody briakinumab is not effective for people with active Crohn's disease.

The gradual loss of blood from the gastrointestinal tract, as well as chronic inflammation, often leads to anemia, and professional guidelines suggest routinely monitoring for this. Adequate disease control usually improves anemia of chronic disease, but iron deficiency may require treatment with iron supplements. Guidelines vary as to how iron should be administered. Besides other, problems include a limitation in possible daily resorption and an increased growth of intestinal bacteria. Some advise parenteral iron as first line as it works faster, has fewer gastrointestinal side effects, and is unaffected by inflammation reducing enteral absorption.

Other guidelines advise oral iron as first line with parenteral iron reserved for those that fail to adequately respond as oral iron is considerably cheaper. All agree that severe anemia (hemoglobin under 10g/dL) should be treated with parenteral iron. Blood transfusion should be reserved for those who are cardiovascularly unstable, due to its relatively poor safety profile, lack of long term efficacy, and cost.

Pelvic girdle pain (abbreviated PGP) is a pregnancy discomfort that causes pain, instability and limitation of mobility and functioning in any of the three pelvic joints. PGP has a long history of recognition, mentioned by Hippocrates and later described in medical literature by Snelling.

Antibiotics such as tetracyclines, rifampin, and the aminoglycosides streptomycin and gentamicin are effective against "Brucella" bacteria. However, the use of more than one antibiotic is needed for several weeks, because the bacteria incubate within cells.

Surveillance using serological tests, as well as tests on milk like the milk ring test, can be used for screening and play an important role in campaigns to eliminate the disease. Also, individual animal testing both for trade and for disease-control purposes is practiced. In endemic areas, vaccination is often used to reduce the incidence of infection. An animal vaccine is available that uses modified live bacteria. The World Organisation for Animal Health "Manual of Diagnostic Test and Vaccines for Terrestrial Animals" provides detailed guidance on the production of vaccines. As the disease is closer to being eliminated, a test and stamping out program is required to completely eliminate it.

The gold standard treatment for adults is daily intramuscular injections of streptomycin 1 g for 14 days and oral doxycycline 100 mg twice daily for 45 days (concurrently). Gentamicin 5 mg/kg by intramuscular injection once daily for seven days is an acceptable substitute when streptomycin is not available or contraindicated. Another widely used regimen is doxycycline plus rifampin twice daily for at least six weeks. This regimen has the advantage of oral administration. A triple therapy of doxycycline, with rifampin and co-trimoxazole, has been used successfully to treat neurobrucellosis.

Doxycycline is able to cross the blood–brain barrier, but requires the addition of two other drugs to prevent relapse. Ciprofloxacin and co-trimoxazole therapy is associated with an unacceptably high rate of relapse. In brucellic endocarditis, surgery is required for an optimal outcome. Even with optimal antibrucellic therapy, relapses still occur in 5 to 10% of patients with Malta fever.

The main way of preventing brucellosis is by using fastidious hygiene in producing raw milk products, or by pasteurizing all milk that is to be ingested by human beings, either in its unaltered form or as a derivate, such as cheese.

The mortality of the disease in 1909, as recorded in the British Army and Navy stationed in Malta, was 2%. The most frequent cause of death was endocarditis. Recent advances in antibiotics and surgery have been successful in preventing death due to endocarditis. Prevention of human brucellosis can be achieved by eradication of the disease in animals by vaccination and other veterinary control methods such as testing herds/flocks and slaughtering animals when infection is present. Currently, no effective vaccine is available for humans. Boiling milk before consumption, or before using it to produce other dairy products, is protective against transmission via ingestion. Changing traditional food habits of eating raw meat, liver, or bone marrow is necessary, but difficult to implement. Patients who have had brucellosis should probably be excluded indefinitely from donating blood or organs. Exposure of diagnostic laboratory personnel to "Brucella" organisms remains a problem in both endemic settings and when brucellosis is unknowingly imported by a patient. After appropriate risk assessment, staff with significant exposure should be offered postexposure prophylaxis and followed up serologically for six months. Recently published experience confirms that prolonged and frequent serological follow-up consumes significant resources without yielding much information, and is burdensome for the affected staff, who often fail to comply. The side effects of the usual recommended regimen of rifampicin and doxycycline for three weeks also reduce treatment adherence. As no evidence shows treatment with two drugs is superior to monotherapy, British guidelines now recommend doxycycline alone for three weeks and a less onerous follow-up protocol.