Indian Journal of Paediatric Dermatology

: 2018  |  Volume : 19  |  Issue : 2  |  Page : 154--156

Reiter's disease in a 8-year-old boy

Rohit Kapoor1, Syed Md Azad1, Anwesha Mukherjee1, Sandipan Dhar2,  
1 Department of Paediatric Medicine, Institute of Child Health, Kolkata, West Bengal, India
2 Department of Pediatric Dermatology, Institute of Child Health, Kolkata, West Bengal, India

Correspondence Address:
Rohit Kapoor
Students Hostel, Institute of Child Health, 11, Biresh Guha Street, Kolkata - 700 017, West Bengal


An 8-year-old male child presented with complaints of pain abdomen and appearance of rashes all over the body, with pain and swelling of the left knee joint. The child was a known case of developmental delay with seizure disorder, and the rashes had appeared just after starting oral valproate. On examination, the child appeared well except for the rashes and local swelling with decreased range of motion in the left knee joint. Redness around the urethral meatus was also noted. Skin biopsy revealed features suggestive of reactive arthritis. The child responded well to nonsteroidal anti-inflammatory drugs.

How to cite this article:
Kapoor R, Azad SM, Mukherjee A, Dhar S. Reiter's disease in a 8-year-old boy.Indian J Paediatr Dermatol 2018;19:154-156

How to cite this URL:
Kapoor R, Azad SM, Mukherjee A, Dhar S. Reiter's disease in a 8-year-old boy. Indian J Paediatr Dermatol [serial online] 2018 [cited 2021 Jan 16 ];19:154-156
Available from:

Full Text


Reiter's disease is an autoimmune condition that develops in response to an infection. It has been associated with gastrointestinal (GI) infections with Shigella, Salmonella, Campylobacter, and other organisms, as well as with genitourinary (GU) infections (especially with Chlamydia trachomatis). The classic triad of ReA symptoms includes noninfectious urethritis, arthritis, and conjunctivitis; however, all these symptoms are found only in one-third of the patients.[1]

 Case Report

An 8-year-old boy, a known case of developmental delay with seizure disorder, presented with complaints of pain abdomen for the past 2 weeks, rashes all over the body for the past 1 week, and swelling of the left knee joint for the past 1 week. The pain abdomen was diffuse and cramping in nature and was not associated with loose stools, vomiting, or fever. The child developed rashes all over the body starting from the truncal area 1 week after the onset of the pain. The rashes were sharply demarcated papules and rounded plaques covered by silvery scale [Figure 1] and [Figure 2]. The child was started on oral valproate just before the appearance of the rash. There were also pain and swelling in the left knee joint along with the appearance of the rash. On examination, vitals were stable and rashes were present all over the body, which were identical to psoriatic rash. Auspitz sign was present [Figure 3]. There was obvious swelling in the knee joint with tenderness, increase in local temperature, and decreased range of motion [Figure 4]. Redness in the urethral area was also noted [Figure 5]. Laboratory investigations showed a total leukocyte count of 7800 with 72% neutrophils, C-reactive protein was 12 (normal <6), and erythrocyte sedimentation rate was 92. Urine routine examination showed 15–20 pus cells with no red blood cell and urine culture was negative. Ultrasonography of the left knee joint showed periarticular collection. Ophthalmological examination revealed no significant abnormality. The child was initially started on intravenous antibiotics which were later stopped after the skin biopsy report. Skin biopsy showed ruptured vesiculopustules in the epidermis with adjacent spongiosis and elongated rete ridges, suggestive of ReA [Figure 6]. The child was then started on naproxen to which he responded quite well. Human leukocyte antigen (HLA) B27 was done which came out to be positive.{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}{Figure 6}


The name Reiter's syndrome was popularized in English texts by Bauer and Engelman in 1942, who thought that Reiter was the first to describe it.[2],[3] At the same time of the disease's description by Reiter in 1916, two French doctors, Fiessinger and Leroy, attribute a case of ReA to Shigella infection. In 1818, Brodie published a case of Reiter's syndrome after venereal infection, followed by Stoll, who described a case of the disease in 1869.[2],[3]

ReA is an immune-mediated seronegative arthritis that belongs to the group of spondyloarthropathies and develops after a GI or GU system infection. The condition is considered to be characterized by a triad of symptoms (conjunctivitis, arthritis, and urethritis) although a constellation of other manifestations may also be present. ReA is characterized by psoriasiform dermatological manifestations that may resemble those of pustular psoriasis and, similar to guttate psoriasis, is a postinfectious entity. ReA, Reiter's syndrome, and other spondyloarthropathies (ankylosing spondylitis, psoriatic arthritis, and arthritis associated with inflammatory bowel disease) are associated with the immunogenetic marker HLA-B27.[4],[5] It is well known that psoriasis not only affects the skin but also is an autoimmune disease causing increase in inflammatory markers.

The mechanism by which the organisms causing infection in the urogenital or GI tract lead to Reiter's syndrome in some individuals is not clear. One hypothesis is cross-reactivity, in which antibodies developed against the inciting infection also have affinity for HLA-B27.[6] Another hypothesis involves cytokines. One study found decreased interleukin-2 production in HLA-B27 and B7-positive patients who developed ReA after Salmonella infection, suggesting that impaired cellular immunity against the inciting organism may correlate with the development of the disease.[7]

Cutaneous involvement includes psoriasiform lesions, named keratoderma blenorrhagicum (in about 10%), painful and erosive lesions on the tips of the fingers and toes, nail dystrophy (20%–30%), and erythroderma as a rare complication. Erythematous macules and plaques, diffuse erythema, erosions, and bleeding can appear on the oral and pharyngeal mucosae. Lesions on glans penis, termed circinate balanitis (up to 50%), are common and consist of vesicles that rupture to form painless superficial erosions. Keratoderma blenorrhagicum is the characteristic cutaneous manifestation of the disease although it occurs in only about 10% of patients. It usually appears 1–2 months after the onset of arthritis.

The clinical and histological features of Reiter's disease skin lesions are psoriasiform and fall within a spectrum of changes seen in idiopathic psoriasis. Nevertheless, the overall pattern, course, and distribution of the eruption in Reiter's disease are usually distinctive.[1]

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Wu IB, Schwartz RA. Reiter's syndrome: The classic triad and more. J Am Acad Dermatol 2008;59:113-21.
2Kingsley GH. Reactive arthritis: A paradigm for inflammatory arthritis. Clin Exp Rheumatol 1993;11 Suppl 8:S29-36.
3Aribandi AK, Demuren OA. Reiter Syndrome, Musculoskeletal, Juli – Article on eMedicine; 2006. Available from: [Last accessded on 2017 May 8].
4Håkansson U, Eitrem R, Löw B, Winblad S. HLA-antigen b27 in cases with joint affections in an outbreak of salmonellosis. Scand J Infect Dis 1976;8:245-8.
5Schwartz RA, Romann J. Juli, Reactive arthritis – Article on eMedicine; 2006.
6Eapen BR. A new insight into the pathogenesis of Reiter's syndrome using bioinformatics tools. Int J Dermatol 2003;42:242-3.
7Inman RD, Chiu B, Johnston ME, Vas S, Falk J. HLA class I-related impairment in IL-2 production and lymphocyte response to microbial antigens in reactive arthritis. J Immunol 1989;142:4256-60.