Reactive arthritis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Reactive arthritis (ReA) is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection. In fourth century B.C, Hippocrates was the first to associate the presence of arthritis and infection in the genitourinary tract. In 1818, Sir Benjamin Brodie, an English physician was the first to describe the triad of urethritis, arthritis, and conjunctivitis. It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. The exact mechanism by which infecting organism cause reactive arthritis is not fully understood. It is thought that microbial antigens are similar to certain body proteins (self proteins). When an immune response is mounted against the microbial proteins, the antibodies produced against microbial proteins also reacts with the self proteins of the body causing reactive arthritis.

Reactive arthritis (ReA) can be classified on the basis of previous gastrointestinal (GI) or genitourinary (GU) infection in to venereal or dysenteric ReA. Reactive arthritis should be distinguished from other HLA-B27 diseases causing arthritis of the peripheral skeleton, which present as arthralgia. The differentials include psoriatic arthritis, rheumatoid arthritis and ankylosing spondylitis. The incidence of reactive arthritis following a gastrointestinal or genitourinary infection is approximately 3-27 cases per 100,000 individuals worldwide. The prevalence of reactive arthritis is approximately 30-40 cases per 100,000 individuals worldwide. If left untreated, patients with reactive arthritis may progress to develop myalgias and joint pain especially in the lower extremities.

Reactive arthritis is diagnosed based on the clinical presentation with supporting laboratory evidence. The gold standard for diagnosis of reactive arthritis include spondyloarthritis and clear evidence of preceding infection by culture or polymerase chain reaction. The majority of cases (two-thirds) of reactive arthritis are self-limited and require only supportive care. Arthritis is the most common symptom and initially treated with NSAIDs. As the disease progresses or in case of no response, further management includes intra-articular and systemic steroids, DMARDs and finally TNF inhibitors. The role of antibiotics in reactive arthritis is not clear and their efficacy in reactive arthritis is not completely established. Surgical intervention is not recommended for the management of reactive arthritis. However, young adults who develop a chronic course may benefit from arthroscopic synovectomy. Patients with severe reactive arthritis with involvement of heart and vitreous chamber may require valve replacement surgery and vitrectomy respectively.

In fourth century B.C, Hippocrates was the first to associate the presence of arthritis and infection in the genitourinary tract. In 1818, Sir Benjamin Brodie, an English physician was the first to describe the triad of urethritis, arthritis, and conjunctivitis. In 1916, several reports from France & Germany showed association between diarrhea and post-infection arthritis.

Reactive arthritis (ReA) can be classified on the basis of previous gastrointestinal (GI) or genitourinary (GU) infection in to venereal or dysenteric ReA.

It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection. It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. The exact mechanism by which infecting organism cause reactive arthritis is not fully understood. It is thought that microbial antigens are similar to certain body proteins (self proteins). When an immune response is mounted against the microbial proteins, the antibodies produced against microbial proteins also reacts with the self proteins of the body causing reactive arthritis.

Common causes of reactive arthritis include infection with Chlamydia trachomatis, Neisseria gonorrhoeae, Salmonella enteritidis, Shigella flexneri, Campylobacter jejuni, Mycoplasma pneumoniae, Lymphogranuloma venereum, Mycobacterium tuberculosis, Clostridium difficile, and Streptococci viridans.

Reactive arthritis should be distinguished from other HLA-B27 diseases causing arthritis of the peripheral skeleton, which present as arthralgia. The differentials include psoriatic arthritis, rheumatoid arthritis and ankylosing spondylitis.

The incidence of reactive arthritis following a gastrointestinal or genitourinary infection is approximately 3-27 cases per 100,000 individuals worldwide. The prevalence of reactive arthritis is approximately 30-40 cases per 100,000 individuals worldwide. Reactive arthritis commonly affects young adults in the age group of 18-35 years of age. Men are more commonly affected with reactive arthritis than females with male to female ratio of approximately 4:1. There is no racial predilection to reactive arthritis.

Common risk factors in the development of reactive arthritis include abnormal joint structure (most important risk factor), male sex (four times more likely) rheumatoid arthritis, diabetes mellitus, malignancy, old age, use of systemic steroids, HIV infection, hemodialysis, previous joint surgery and injection drug abuse.

There is insufficient evidence to recommend routine screening for reactive arthritis.

If left untreated, patients with reactive arthritis may progress to develop myalgias and joint pain especially in the lower extremities. Over the course of time, patient develops urethritis and conjunctivitis. Complications of reactive arthritis are seen with chronic course and may include chronic arthritis with remitting relapsing course, urethral stricture, vitreous floaters, macular edema, cataracts or glaucoma, ankylosing spondylitis, and aortitis. Prognosis is generally good for patients with reactive arthritis. Patients who receive and respond to treatment generally have rapid reversal of symptoms. It is estimated that around 25% of patients may develop long term complication of arthropathy.

Reactive arthritis is diagnosed based on the clinical presentation with supporting laboratory evidence. The gold standard for diagnosis of reactive arthritis include spondyloarthritis and clear evidence of preceding infection by culture or polymerase chain reaction.

Obtaining history is an important aspect in making a diagnosis of reactive arthritis. The areas of focus should be on onset, duration, and progression of symptoms with special focus on past medical history and current medications. Previous history of gastrointestinal or genitourinary infections may predispose an individual to develop reactive arthritis. Symptoms start to appear after days to weeks of initial gastrointestinal or genitourinary infection. Common symptoms of reactive arthritis include urinary changes (increased frequency, dysuria/burning micturation and urgency), irritation and redness of eyes, and joint pain (arthralgia-commonly of lower limbs). Less common symptoms include inflammation of soft tissue, swollen toes, and skin rash. If symptoms are present for more than six months, it is termed as chronic reactive arthritis.

Physical examination of patients with reactive arthritis is usually remarkable for arthritis (lower extremity; weight bearing), conjunctivitis, and urethritis. As the duration and severity of reactive arthritis increases other signs include dactylitis (sausage-shaped fingers), enthesopathy, sacroiliitis, keratoderma blennorrhagicum, circinate balanitis, myocarditis, and pericarditis.

Laboratory findings consistent with the diagnosis of reactive arthritis include elevated erythrocyte sedimentation rate (ESR), elevated C-reactive protein (CRP), and elevated total leukocyte count (TLC) showing increased polymorphonuclear cells (PMNs). Synovial fluid or synovial membrane biopsy for detection of bacterial DNA by polymerase chain reaction (PCR) or immunofluorescence microscopy.

An x-ray may be helpful in the diagnosis of reactive arthritis. Reactive arthritis primarily involves the lower extremities and an x-ray of hip with sacroiliac joint, knees, ankles and feet may show juxta-articular osteoporosis, soft tissue swelling, bilateral asymmetric distribution uniform joint space loss, and bone proliferation.

MRI of the affected joints may be helpful in the diagnosis of reactive arthritis. Findings on MRI suggestive of reactive arthritis include bone edema, bone erosion and bony proliferation.

Ultrasound may be helpful in the diagnosis of reactive arthritis. Findings on an ultrasound suggestive of reactive arthritis include thickening of synovial sheath, synovial tendon and increased volume of synovial fluid.

There are no other diagnostic studies associated with reactive arthritis.

The majority of cases (two-thirds) of reactive arthritis are self-limited and require only supportive care. Arthritis is the most common symptom and initially treated with NSAIDs. As the disease progresses or in case of no response, further management includes intra-articular and systemic steroids, DMARDs and finally TNF inhibitors. The role of antibiotics in reactive arthritis is not clear and their efficacy in reactive arthritis is not completely established.

Surgical intervention is not recommended for the management of reactive arthritis. However, young adults who develop a chronic course may benefit from arthroscopic synovectomy. Patients with severe reactive arthritis with involvement of heart and vitreous chamber may require valve replacement surgery and vitrectomy respectively.

Effective measures for the primary prevention of reactive arthritis include early treatment of GI or GU infections, educating patients about association of GI and GU infection with reactive arthritis and use of barrier methods such as condoms can prevent spread of sexually transmitted disease.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

In fourth century B.C, Hippocrates was the first to associate the presence of arthritis and infection in the genitourinary tract. In 1818, Sir Benjamin Brodie, an English physician was the first to describe the triad of urethritis, arthritis, and conjunctivitis. In 1916, several reports from France & Germany showed association between diarrhea and post-infection arthritis.

• In fourth century B.C, Hippocrates was the first to associate the presence of arthritis and infection in the genitourinary tract.^[1]
• In late 1600s, the association of arthritis and dysentery or diarrhea was first identified.^[2]
• In 1818, Sir Benjamin Brodie, an English physician was the first to describe the triad of urethritis, arthritis, and conjunctivitis.^[3]
• In 1879, German born American physiologist Dr Neisser identified gonococcal arthritis and separated them from nongonococcal arthritis.^[4]
• In 1916, several reports from France & Germany showed association between diarrhea and post-infection arthritis.^[5]
• German scientist Hans Reiter coined the term Reiter’s syndrome. However, with the Nazi past and the allegations put on Hans Reiter; the Spondylitic Association of America, have strongly recommended that this syndrome should be called “reactive arthritis”. It was reported that Hans Reiter was responsible for involuntary sterilization, euthanasia, and medical experiments that killed thousands of concentration camp prisoners.^[6][7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Reactive arthritis (ReA) can be classified on the basis of previous gastrointestinal (GI) or genitourinary (GU) infection in to venereal or dysenteric ReA.

Reactive arthritis (ReA) can be classified on the basis of previous GI or GU infection in to venereal or dysenteric ReA.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection. It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. The exact mechanism by which infecting organism cause reactive arthritis is not fully understood. It is thought that microbial antigens are similar to certain body proteins (self proteins). When an immune response is mounted against the microbial proteins, the antibodies produced against microbial proteins also reacts with the self proteins of the body causing reactive arthritis.

It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections, which results in an autoimmune condition. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection.^[1][2][3]

• Reactive arthritis is associated with HLA-B27 (MHC class I molecule).
• It is estimated around 75% patients of reactive arthritis are positive for HLA-B27. Other alleles associated with reactive arthritis include HLA-B51 and HLA-DRB1.^[4]
• HLA B27 association with reactive arthritis can also be attributed to the fact that patients with family history of reactive arthritis tend to have a more severe form of disease.^[5]
• The exact mechanism by which infecting organism cause reactive arthritis is not fully understood. It is thought that microbial antigens are similar to certain body proteins (self proteins). When an immune response is mounted against the microbial proteins, the antibodies produced against microbial proteins also reacts with the self proteins of the body causing reactive arthritis.
  • HLA-B27 incorporated MHC class I molecule presents microbial antigens to CD8 cytotoxic T cells.
  • Antigen presenting cells (APCs) present microbial antigens to T helper cells which leads to their activation.
  • T helper cells then differentiates into TH1 cells and TH2 cells which leads to secretion of interleukins (IL-2, IL-3, IL-4, IL-6),TNF-alpha, TGF-β and Th17 cells.
  • Interleukins IL-3, IL-4, IL-6 leads to increased production of antibodies from plasma cells.
  • Th17 cells release IL-17 which is also a major pro-inflammatory cytokine.^[6]
  • Patients with defects in T cell regulatory function may lead to more severe inflammatory process and cytokine production.^[7]
  • The increased cytokine and antibody production leads to destruction of microbial proteins as well as self proteins causing an autoimmune reaction.
  • Furthermore, studies have shown the presence of T cells and intra-articular antibodies on synovial fluid analysis.

• Patients with HIV who later on develop reactive arthritis tend to have a more serious presentation.
• These patients present with severe generalised rash resembling psoriasis (pink color and scaly), severe arthritis and other AIDS related symptoms.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Common causes of reactive arthritis include infection with Chlamydia trachomatis, Neisseria gonorrhoeae, Salmonella enteritidis, Shigella flexneri, Campylobacter jejuni, Mycoplasma pneumoniae, Lymphogranuloma venereum, Mycobacterium tuberculosis, Clostridium difficile, and Streptococci viridans.

Common causes of reactive arthritis include infection with the following organisms:^{[1][2][3][4][5]}

• Chlamydia trachomatis
• Neisseria gonorrhoeae
• Salmonella enteritidis
• Shigella flexneri
• Yersinia enterocolitica
• Campylobacter jejuni
• Mycoplasma pneumoniae
• Lymphogranuloma venereum
• Mycobacterium tuberculosis
• Clostridium difficile
• Streptococci viridans

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Reactive arthritis should be distinguished from other HLA-B27 diseases causing arthritis of the peripheral skeleton, which present as arthralgia. The differentials include psoriatic arthritis, rheumatoid arthritis and ankylosing spondylitis.

Reactive arthritis should be distinguished from other diseases causing arthritis of the peripheral skeleton, which present as arthralgia. The differentials include:

Key:+ : Infrequently present, ++ : Frequently present, +++ : Always present, – : Absent

Reactive arthritis must be differentiated from other causes of rash and arthritis^[1][2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

The incidence of reactive arthritis following a gastrointestinal or genitourinary infection is approximately 3-27 cases per 100,000 individuals worldwide. The prevalence of reactive arthritis is approximately 30-40 cases per 100,000 individuals worldwide. Reactive arthritis commonly affects young adults in the age group of 18-35 years of age. Men are more commonly affected with reactive arthritis than females with male to female ratio of approximately 4:1. There is no racial predilection to reactive arthritis.

• The incidence of reactive arthritis following a gastrointestinal or genitourinary infection is approximately 3-27 cases per 100,000 individuals worldwide.^[1]
• The incidence rate of reactive arthritis varies with the underlying infection.^[2]
  • The incidence rate of reactive arthritis following Campylobacter infection is 900 per 100,000 cases.
  • The incidence rate of reactive arthritis following Salmonella and Shigella infection is 1200 per 100,000 cases.

• The prevalence of reactive arthritis is approximately 30-40 cases per 100,000 individuals worldwide.^[3][4][5]

• Patients of all age groups may develop reactive arthritis.
• Reactive arthritis commonly affects young adults in the age group of 18-35 years of age.

• There is no racial predilection to reactive arthritis.

• Reactive arthritis affects both men and women. However, men are more commonly affected than females.
• The male to female ratio is approximately 4:1.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Common risk factors in the development of reactive arthritis include abnormal joint structure (most important risk factor), male sex (four times more likely) rheumatoid arthritis, diabetes mellitus, malignancy, old age, use of systemic steroids, HIV infection, hemodialysis, previous joint surgery and injection drug abuse.

Common risk factors in the development of reactive arthritis include:^[1][2][3]

• HLA-B27
• Abnormal joint structure (important risk factor)
• Rheumatoid arthritis
• Diabetes mellitus
• Malignancy
• Old age
• Use of systemic steroids
• HIV infection
• Hemodialysis
• Previous joint surgery
• Injection drug abuse
• Male sex (four times more likely)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

There is insufficient evidence to recommend routine screening for reactive arthritis.

There is insufficient evidence to recommend routine screening for reactive arthritis.

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