AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Reactive arthritis is a systemic disorder of unknown etiology that is defined by the development of psoriatic plaques, balanitis, keratoderma, conjunctivitis, urethritis, arthritis, and spondylitis. This symptom complex usually follows an episode of either dysentery or urethritis.

The American Rheumatism Association criteria subcommittee defined this syndrome as 1 month of peripheral arthritis associated with urethritis, cervicitis, or both. The classic triad of the disease, namely urethritis, arthritis, and conjunctivitis, is present in only one third of the patients.

Stoll originally described this triad in 1776. In 1818, Brodie reported the triad in 5 patients. In 1916, 2 separate reports were published during World War I: Fiessinger and Leroy¹ detailed the findings in 4 patients (in French), and Reiter² documented the case of a single patient with this triad of symptoms (in German). In 1942, an article by Bauer and Engelman³ described the first known American patient with reactive arthritis; they called this disorder, a "syndrome of unknown etiology characterized by urethritis, conjunctivitis, and arthritis (so-called Reiter's disease)." Their work contained only one reference, Reiter's article, and stated erroneously, "First described by Reiter, it has been most commonly referred to as Reiter's disease." Thus, this eponym remains in use despite its historical inappropriateness and Hans Reiter's later activities as a National Socialist war criminal.^{4, 5, 6}

Reactive arthritis mostly affects young men. It is frequently associated with the human leukocyte antigen B27 (HLA-B27) haplotype and is classified with the seronegative spondyloarthropathies. Reactive arthritis is preferably viewed as a tetrad, with the addition of the mucocutaneous findings of balanitis and keratoderma blennorrhagicum to the classic triad. The complete and incomplete forms of reactive arthritis can be identified by the presence or absence of the full tetrad.

Young children tend to have the postdysenteric form, whereas adolescents and young men are most likely to acquire reactive arthritis after they have urethritis. Interpreting its mucocutaneous findings as pustular psoriasis and its seronegative arthritis as psoriatic arthritis, some believe that reactive arthritis is best classified as a type of psoriasis.⁷

The eMedicine Ophthalmology article Reactive Arthritis and Rheumatology article Reactive Arthritis may be helpful. Also of interest might be the Medscape CME course Psoriatic Arthritis: An Update From EULAR 2007 and the Medscape Arthritis Resource Center and Psoriasis Resource Center.

Pathophysiology

The etiology of reactive arthritis remains uncertain. Two forms are recognized: a sexually transmitted form and a dysenteric form. Because the urethritis is a possible primary event, research efforts have focused on the identification of a microorganism that could be responsible for activating this disease. The pathophysiologic mechanism is proposed to be the triggering of an autoimmune reaction by these microorganisms.

Mycoplasma (Ureaplasma) species, Neisseria gonorrhoeae, Chlamydia species, and several viruses are among the suspected causative pathogens. Some findings have indicated that Chlamydia species are the etiologic agents in reactive arthritis.⁸ The discovery of Chlamydia trachomatis organisms in an involved joint and the confirmation of an immune response against Chlamydia infection (as indicated by high titers of antichlamydial antibodies in serum) have provided additional support to this hypothesis. In situ hybridization has also been used to identify chlamydial infection in synovial tissue.⁹ Ureaplasma organisms can cause experimental and clinical nongonococcal urethritis. Synovial mononuclear cells from arthritic joints of patients with reactive arthritis react with Ureaplasma antigens; this organism has been isolated from a patient.

Reactive arthritis is also reported to occur after enteric bacterial infections, primarily those caused by parasites (Ascaris lumbricoides) and Shigella, Salmonella, Yersinia, Clostridium, and Campylobacter organisms. Impairment in the glycosaminoglycan defensive barrier was implicated in the development of reactive arthritis and reactive arthritides¹⁰; this impairment may facilitate the penetration of infectious agents that are capable of triggering the autoimmune response.

Genetic factors seem to be involved in the pathophysiology of reactive arthritis. The disease tends to cluster in certain families and almost exclusively affects males. HLA-B27 is found in 70-80% of patients with reactive arthritis. The presence of this HLA haplotype increases the risk of reactive arthritis by 25-fold. In approximately 20% of males who are HLA-B27 positive, reactive arthritis can develop after a triggering infection occurs. HLA-B27 probably shares some molecular characteristics with bacterial epitopes, and an autoimmune cross-reaction is believed to take part in the pathogenesis.

The most accepted theory about the pathophysiology of reactive arthritis involves initial activation by a microbial antigen, followed by an autoimmune reaction that involves the skin, eyes, and joints.

Frequency

United States

Reactive arthritis is a rare entity. Its frequency in the general population is difficult to assess. Its prevalence may be relatively high among patients with AIDS, especially men who are HLA-B27 seropositive. Reactive arthritis develops in almost 75% of HIV-positive men with HLA-B27.

A population-based study assessed reactive arthritis following culture-confirmed infections with bacterial enteric pathogens in Minnesota and Oregon.¹¹ The estimated incidence following culture-confirmed Campylobacter, Escherichia coli O157, Salmonella, Shigella, and Yersinia infections in Oregon was 0.6-3.1 cases per 100,000 population.

International

In the United Kingdom, the incidence of reactive arthritis after urethritis is about 0.8%. Nearly 2% of Finnish males had reactive arthritis after nongonococcal urethritis; the incidence of HLA-B27 is higher among the Finnish population. Reactive arthritis develops in almost 75% of HIV-positive men with HLA-B27. Its incidence is high among patients with AIDS, and HIV testing is mandatory in patients in whom reactive arthritis is newly diagnosed, even if they do not have risk factors.

Mortality/Morbidity

Reactive arthritis can dramatically alter the patient's life because arthritis and other findings may produce considerable morbidity.

Race

Reactive arthritis affects persons of all races.

Sex

• Reactive arthritis usually affects young men.
• Reactive arthritis is uncommon in women, who represent 2-10% of patients in published series.
• A possible prostatic focus of persistent infection is postulated to explain the male predominance of reactive arthritis.

Age

• Reactive arthritis is most common in young men.
• Reactive arthritis is uncommon in children. When it occurs in children, the enteric form of the disease is predominant.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

A vast majority of cases of reactive arthritis are oligosymptomatic, and conjunctivitis or urethritis are present weeks before the patient's first visit, so they must be found by means of a correct anamnesis.

• Urethritis
• • An estimated 0.5-1% of cases of urethritis evolve into reactive arthritis. Urethritis develops acutely 1-2 weeks after infection through sexual contact, and is similar to gonococcal urethritis. A purulent or hemopurulent exudate appears, and the patient complains of dysuria.
  • Balanitis and vulvitis are rare in children; when they occur, they are suggestive of reactive arthritis.¹²
  • In men, urethritis is less painful and produces less purulent discharge than acute gonorrhea, and can go unnoticed. Findings from microscopic examination and cultures can be used to rule out N gonorrhoeae infection. Co-infection with both Chlamydia and Neisseria organisms is possible and common in some areas.
  • In women, urethritis and cervicitis may be mild, with dysuria or slight vaginal discharge, or asymptomatic, which makes diagnosis difficult.
  • Often, the initial urethritis is treated with antibiotics (especially wide-spectrum tetracyclines or macrolides) when findings suggest gonorrhea.
  • Despite an apparent early cure, the manifestations of the disease appear several weeks later, and the patient may not relate them to a prior episode of urethritis.
• Diarrhea: In enteric cases, diarrhea and dysenteric syndrome (usually mild) is followed by the clinical triad, which includes urethritis, in 1-4 weeks.
• General involvement
  • A syndrome, with malaise, low-grade fever, and generalized myalgia or headache can be present.
  • Pericarditis, aortic disease with aortic incompetence, auriculoventricular blockade, optical neuritis, pleuritis, pulmonary infiltrates, thrombophlebitis, and amyloidosis are rarely described in reactive arthritis.

Physical

• Immunoglobulin A (IgA) nephropathy: This is the most common type of primary glomerulonephritis worldwide and is reported in association with reactive arthritis.¹³
• Manifestations of the urogenital system
• • Circinate balanitis (see Media File 1) is characteristic. Circinate balanitis is defined by circinate or gyrate white plaques that grow centrifugally and eventually cover the entire surface of the glans penis. The penile shaft and scrotum can be involved. The lesions become rapidly keratotic in a circumcised penis.
  • Circinate vulvitis is reported in women.
  • Prostatitis, cystitis, and pyelonephritis are rare but possible urogenital manifestations of reactive arthritis.
  • Bartholinitis can be present in women.
  • Proctitis caused by Chlamydia species can occur in both sexes after anal intercourse.
• Conjunctivitis
• • Eye involvement is common.
  • Conjunctivitis appears in approximately 50% of patients with reactive arthritis.
  • Conjunctivitis is often bilateral, and it may be overlooked because of its transitory course.
  • An intense red, velvetlike conjunctival injection characterizes the conjunctivitis.
  • Edema and a purulent discharge are not rare in reactive arthritis–associated conjunctivitis.
• Other ocular manifestations
• • Iritis, iridocyclitis, and uveitis are seldom reported.
  • Iritis is more common in late recurrent episodes, and it only occurs in 3-8% of patients in the first attack.
  • At clinical examination, redness, pain, impaired vision, and exudation with hypopyon can suggest iritis.
  • Recurrent episodes can lead to pupillary synechia and glaucoma.
  • Keratitis rarely is reported.
• Arthritis
• • Articular involvement often is the key symptom of the syndrome. It is common and occurs in approximately 95% of patients.
  • The knee and tarsal joints (which support more weight than other joints) and the sacroiliac region are preferentially involved.
  • Clinically, the articular involvement resembles rheumatoid arthritis, but it is asymmetrical and commonly involves a single joint.
  • Articular swelling; intense pain; and involvement of soft tissue, fascia, and tendons occur.
  • Muscular atrophy can develop in symptomatic cases.
• • Enthesopathy (ie, inflammation at the tendinous insertion into bone) is common in reactive arthritis and in other seronegative arthritides (eg, plantar fasciitis, digital periostitis, Achilles tendinitis).
  • Sacroiliitis is commonly asymptomatic and self-limiting.
  • Early morning pain and stiffness are usually the most common manifestations.
  • Chronic spondylitis indistinguishable from ankylosing spondylitis is described in patients with reactive arthritis.
• Cutaneous involvement
• • Psoriasiform cutaneous lesions can develop weeks after urethritis in 10% of the patients. The palms and soles (see Media File 2) are most commonly involved with keratotic papules, plaques, and pustules that resemble those of pustular psoriasis.
  • In some patients, typical keratoderma blenorrhagica develops 1-2 months after the onset of arthritis, with keratotic papules and plaques that are painful under pressure; sometimes, these can be disabling.
  • Distal involvement with painful and erosive lesions in the tips of the fingers (see Media File 3) and toes, with pustules and subungual pustular collections, also occurs.
  • Nail dystrophy is present in 20-30% of patients and often results in nail shedding.
  • Erythroderma is described as a rare complication of reactive arthritis.
• Mucosal lesions
• • Erythematous macules and plaques, diffuse erythema, erosions, and bleeding can appear on the oral and pharyngeal mucosae.
  • Circinate lesions on the tongue resemble geographic tongue (see Media File 4).
  • Involvement of the enteric mucosa can result in enteritis and diarrhea.
• Reactive arthritis in association with HIV infection^{14, 15}
• • Reactive arthritis is particularly common in the context of HIV infection.
  • Patients who are HIV positive are prone to have severe psoriasiform dermatitis, which commonly involves the flexures, scalp, palms, and soles.
  • Frequently, psoriasiform dermatitis is associated with arthritis that involves the distal joints with a destructive pattern.
  • The disturbances of immune homeostasis in AIDS could account for this peculiar expression of psoriasis in these patients.
  • The existing immunodepression in patients with AIDS poses special management problems.

Causes

The etiology of reactive arthritis remains uncertain. However, 2 forms are recognized: a sexually transmitted form and a dysenteric form.

• Because urethritis is a possible primary event, research efforts have focused on identification of a microorganism that could be responsible for activating this disease.
• The pathophysiologic mechanism is thought to be a triggering of an autoimmune reaction by the microorganisms.
• Mycoplasma (Ureaplasma) species, N gonorrhoeae, Chlamydia species, and several viruses are among the suspected causative pathogens.
• Reactive arthritis triggered by adalimumab (Humira) and leflunomide (Arava) in a patient with ankylosing spondyloarthropathy and Crohn disease was recently described.¹⁶

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Gonorrhea and other types of infectious urethritis must be ruled out by means of microbiologic cultures of the urethral exudate.

Gonococcal arthritis does not involve the spine.

Rheumatoid and psoriatic arthritis, and ankylosing spondylitis must be differentiated from arthritis in reactive arthritis.

Septic arthritis and pyogenic arthritis also can mimic reactive arthritis.

Oligoarticular and asymmetrical involvement, together with the clinical course, may contribute to the diagnostic suspicion.

Other seronegative arthritides can be present. Differentiating these from reactive arthritis is academic because they share a common pathophysiologic pathway and similar treatment.

Rheumatic fever and serum sickness are characterized by a course that is more acute than that of reactive arthritis.

Cutaneous lesions of reactive arthritis can mimic the following, but the characteristic clinical picture must raise a suspicion of reactive arthritis: Norwegian scabies, mycosis fungoides, subcorneal pustulosis of Sneddon-Wilkinson, atopic dermatitis, acute exanthematic pustulosis, and other causes of erythroderma.

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• No laboratory or imaging finding is diagnostic of reactive arthritis. The diagnosis is based on clinical data.
• Although a positive HLA-B27 result is not specific of the disease, haplotyping can be used to diagnose reactive arthritis.
• Microbiologic examination of smears, immunofluorescence results, and cultures of the urethral secretion must be considered.
• Microbiologic studies of urine and stool are less helpful; nevertheless, in the dysenteric form, stool culture for enteric pathogens (eg, Salmonella, Shigella, and Yersinia species) should be considered.
• Aspirates of joint fluid usually are sterile.
• A Japanese man with reactive arthritis was negative for HLA-B27 and other HLA-B27 cross-reactive major histocompatibility complex (MHC) class I antigens, but he was positive for human leukocyte antigen B51 (HLA-B51).¹⁷
• • The laboratory examination findings showed significant elevation of serum levels of immunoglobulin G (IgG) and IgA antichlamydial antibodies.
  • A combination of Chlamydia infection and HLA-B51 presence was suggested to play a role in the pathogenesis of reactive arthritis in this patient.

Imaging Studies

• Radiologic signs are present in only 40% of the cases. These signs can be completely absent regardless of the severity.
• Whole-body scintigraphy is a sensible diagnostic tool for use in screening for enthesopathy and arthropathy.¹⁸

Other Tests

• The incidence of reactive arthritis is high among patients with AIDS, and HIV testing is mandatory in patients in whom reactive arthritis is newly diagnosed, even if they do not have the risk factors.

Histologic Findings

Histopathologic changes are not different from the histopathologic picture of a psoriasis vulgaris. Acanthosis, with elongation of the rete ridges, psoriasiform hyperplasia, subcorneal abscesses, and spongiform pustules, are observed. The upper dermis shows a mixed inflammatory infiltrate with neutrophils.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

No curative treatment for reactive arthritis exists. Almost two thirds of patients have a self-limited course and need no treatment other than symptomatic and supportive care. However, reactive arthritis may be associated with chronic recurrent ocular inflammation that mandates systemic therapy (including immunosuppressive treatment) to control the ocular inflammation and to prevent progressive visual loss.¹⁹

• Urethritis usually is treated with tetracyclines or macrolides because of the frequency of coexisting infections. The treatment of urethritis has not been shown to modify the course of the disease, but, in the absence of contraindications, treatment is commonly recommended. The antibiotic treatment of enteritis is even more controversial.
• Arthritis in reactive arthritis is amenable to successful treatment with nonsteroidal anti-inflammatory drugs (eg, indomethacin). Occasionally, intra-articular injections of corticosteroids are prescribed. Treatment with methotrexate, azathioprine, gold salts, and penicillamine is proposed in severe cases of reactive arthritis.
• Cutaneous lesions can be treated as those of psoriasis vulgaris. The author recommends beginning with topical 0.1% triamcinolone cream 3 times per day for adults and 2.5% hydrocortisone cream twice per day for children. A topical keratolytic, such as 10% salicylic acid ointment, can be added if needed. Topical salicylic acid and hydrocortisone with oral aspirin has also been suggested.¹²
• Systemic therapy, if required, consists of the administration of oral acitretin and/or PUVA, methotrexate, or cyclosporine.
• The treatment of reactive arthritis in the setting of HIV infection poses special problems. However, potentially immunosuppressive therapies (eg, cyclosporine, methotrexate, PUVA) have been used in some cases, with variable success and a relative scarcity of severe complications.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Antibiotics

Antibiotics may be used to treat antibacterial and anti-inflammatory effects, as well for possible coexistent infection.

Drug Category: Vitamins

These agents are essential for normal DNA synthesis and metabolism of proteins, carbohydrates, and fats.

Drug Category: Nonsteroidal anti-inflammatory drugs

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Drug Category: Antineoplastic agents

These agents have antiproliferative and immunosuppressive effects.

Drug Category: Antimalarials

Derivatives of 4-aminoquinoline are active against a variety of autoimmune disorders. Use with caution because hydroxychloroquine has a known risk of exacerbating psoriasis. These agents should probably be used only in conjunction with rheumatologic evaluation because it is used for the arthritis and not the skin involvement.

Drug Category: Retinoids

Retinoids decrease the cohesiveness of abnormal hyperproliferative keratinocytes and may reduce the potential for malignant degeneration. They also modulate keratinocyte differentiation.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Careful monitoring of this systemic disease is indicated.

Complications

• Erythroderma is described as a rare complication of reactive arthritis.
• In severe cases, functional impairment may be severe, and a chronic and prolonged clinical course is followed by sequelae (eg, urethral stenosis, chronic arthritis, ocular impairment).
• In some patients, arthropathic psoriasis develops.

Prognosis

• The course of reactive arthritis is prolonged. Acute exacerbations and remissions may occur for weeks to months (seldom years), and spontaneous healing may occur with the possibility of recurrences.
• An estimated recurrence rate of 15% per patient-year is reported.
• A fatal outcome is seldom reported, but death can occur, and it is usually related to the adverse effects of treatment.

Patient Education

• Patients should be educated about the many facets of this disorder.
• For excellent patient education resources, visit eMedicine's Arthritis Center, Sexually Transmitted Diseases Center, and Bacterial and Viral Infections Center. Also, see eMedicine's patient education articles Knee Pain, Chlamydia, Gonorrhea, and Psoriatic Arthritis.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• A patient with new-onset reactive arthritis must be evaluated for HIV. Such patients are at risk for severe psoriasiform dermatitis, which commonly involves the flexures, scalp, palms, and soles. Frequently, psoriasiform dermatitis is associated with arthritis that involves the distal joints in a destructive pattern.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Circinate balanitis in a patient with reactive arthritis.
	View Full Size Image
Media type:  Photo

Media file 2:  Plaques on the soles of a patient with reactive arthritis.
	View Full Size Image
Media type:  Photo

Media file 3:  Painful erosions on the fingers in a patient with reactive arthritis.
	View Full Size Image
Media type:  Photo

Media file 4:  Plaques and erosions of the tongue in a patient with reactive arthritis.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

1. Fiessinger N, Leroy E. Contribution a l etude d'une epidemie de dysenterie dans la somme. Bull Soc Med Hop. 1916;40:2030-2069.
2. Reiter H. Spirochateninfektion (Spirochaetosis arthritica). Deutsche Medizinische Wochenschrift. 1916;42:1535-6.
3. Bauer W, Engelman EP. A syndrome of unknown etiology characterized by urethritis, conjunctivitis, and arthritis (so-called Reiter's disease). Trans Assoc Am Physicians. 1942;57:307-313.
4. Panush RS, Wallace DJ, Dorff RE, Engleman EP. Retraction of the suggestion to use the term "Reiter's syndrome" sixty-five years later: the legacy of Reiter, a war criminal, should not be eponymic honor but rather condemnation. Arthritis Rheum. Feb 2007;56(2):693-4. [Medline].
5. Wallace DJ, Weismann M. Should a war criminal be rewarded with eponymous distinction?. J Clin Rheumatol. 2000;6:49-54.
6. Weyers W. The fame and infamy of Hans Reiter. Dermatopathol Pract Concept. 2000;6:340-343.
7. Mahmood A, Ackerman AB. Reiter's syndrome is psoriasis!. Dermatopathol Pract Concept. 2000;6:337-339.
8. Kousa M, Saikku P, Richmond S, Lassus A. Frequent association of chlamydial infection with Reiter's syndrome. Sex Transm Dis. Apr-Jun 1978;5(2):57-61. [Medline].
9. Berlau J, Junker U, Groh A, Straube E. In situ hybridisation and direct fluorescence antibodies for the detection of Chlamydia trachomatis in synovial tissue from patients with reactive arthritis. J Clin Pathol. Nov 1998;51(11):803-6. [Medline].
10. Russell AL. Glycoaminoglycan (GAG) deficiency in protective barrier as an underlying, primary cause of ulcerative colitis, Crohn's disease interstitial cystitis and possibly Reiter's syndrome. Med Hypotheses. Apr 1999;52(4):297-301. [Medline].
11. Townes JM, Deodhar AA, Laine ES, Smith K, Krug HE, Barkhuizen A, et al. Reactive arthritis following culture-confirmed infections with bacterial enteric pathogens in Minnesota and Oregon: a population-based study. Ann Rheum Dis. Feb 13 2008;[Medline].
12. Arora S, Arora G. Reiter's disease in a six-year-old girl. Indian J Dermatol Venereol Leprol. Jul-Aug 2005;71(4):285-6. [Medline].
13. Satko SG, Iskandar SS, Appel RG. IgA nephropathy and Reiter's syndrome. Report of two cases and review of the literature. Nephron. Feb 2000;84(2):177-82. [Medline].
14. Lin RY. Reiter's syndrome and human immunodeficiency virus infection. Dermatologica. 1988;176(1):39-42. [Medline].
15. Romani J, Puig L, Baselga E, De Moragas JM. Reiter's syndrome-like pattern in AIDS-associated psoriasiform dermatitis. Int J Dermatol. Jul 1996;35(7):484-8. [Medline].
16. Thielen AM, Barde C, Janer V, Borradori L, Saurat JH. Reiter syndrome triggered by adalimumab (Humira) and leflunomide (Arava) in a patient with ankylosing spondylarthropathy and Crohn disease. Br J Dermatol. Jan 2007;156(1):188-9. [Medline].
17. Shimamoto Y, Sugiyama H, Hirohata S. Reiter's syndrome associated with HLA-B51. Intern Med. Feb 2000;39(2):182-4. [Medline].
18. Kim SH, Chung SK, Bahk YW, Park YH, Lee SY, Sohn HS. Whole-body and pinhole bone scintigraphic manifestations of Reiter's syndrome: distribution patterns and early and characteristic signs. Eur J Nucl Med. Feb 1999;26(2):163-70. [Medline].
19. Kiss S, Letko E, Qamruddin S, Baltatzis S, Foster CS. Long-term progression, prognosis, and treatment of patients with recurrent ocular manifestations of Reiter's syndrome. Ophthalmology. Sep 2003;110(9):1764-9. [Medline].
20. Amor B. Reiter's syndrome. Diagnosis and clinical features. Rheum Dis Clin North Am. Nov 1998;24(4):677-95, vii. [Medline].
21. Barth WF, Segal K. Reactive arthritis (Reiter's syndrome). Am Fam Physician. Aug 1999;60(2):499-503, 507. [Medline].
22. Carter JD, Gerard HC, Hudson AP. Psoriasiform lesions induced by TNF antagonists: a skin-deep medical conundrum. Ann Rheum Dis. Feb 25 2008;[Medline].
23. Goyal NN, Dhurat RS, Jerajani HR. Carbamazepine in Reiter's syndrome. Sex Transm Infect. Jun 2000;76(3):220. [Medline].
24. Kim YA, Bagley MP, Thomas I. Incomplete Reiter's syndrome in a black patient showing HLA B 27. Cutis. Apr 1991;47(4):253-4. [Medline].
25. Reiter H. Vorschlage zur Neugestaltung des Hygieneunterrichts und zur Sicherung des Nachwuchses auf dem Gebiet der Hygiene. Munch Med Wschr. 1938;85:16-19.
26. Zivony D, Nocton J, Wortmann D, Esterly N. Juvenile Reiter's syndrome: a report of four cases. J Am Acad Dermatol. Jan 1998;38(1):32-7. [Medline].

Article Last Updated: Apr 21, 2008