Reiters Disease

Reiter's disease is a sterile arthritis associated in most cases with a distant infection causing enteritis or urethritis. Reiter's disease predominantly affects young men and consists of the triad of urethritis, arthritis, and conjunctivitis. Although as a rule the arthritis occurs in attacks and is followed by recovery, it progresses in some cases to cause permanent damage to the affected joints . Cutaneous lesions occur in about half of affected patients. Lesions have a predilection for glans penis {balanitis circinata}, palms and soles {keratoderma blennorrhagicum}, and the subungual regions .

In uncircumcised men, balanitis circinata presents as superficial crusted erosions forming a serpiginous pattern. In circumcised men the condition presents as erythematous hyperkeratotic and coalescent papules on the glans. Lesions on the palms and soles are erythematous, mollusk-like plaques with central keratotic excrescences. Pustular lesions may also develop. The subungual lesions consist of hyperkeratosis with opacification of the nail plate, and eventual shedding of the nail plate may occur. The prevalence of Reiter's disease in HIV-infected individuals is less than 1 %; however, the disease appears to be more severe in immunocompromised patients .

Histopathology.

 Early pustular lesions on the palms or soles show a spongiform macropustule in the upper epidermis . In addition, oneobserves parakeratosis and elongation of the rete ridges 

As the lesions age, the parakeratotic cornified layer thickens considerably, which correlates with the keratotic excrescences seen clinically. The parakeratotic cornified layer is intermingled with the pyknotic nuclei of neutrophils. In old lesions, spongiform pustules are no longer seen, and the histologic picture shows acanthosis and orthokeratosis with only a few areas of parakeratosis, but occasionally the histologic picture resembles that of psoriasis .

Pathogenesis. Most cases of Reiter's disease are probably caused by microorganisms that infect the urogenital or gastrointestinal systems, such as Chlamydia trachoma tis, Ureaplasma urealyticum, and Shigella, Salmonella, Campylobacter, Cyclospora, and Yersinia species. Chlamydia trachomatis has been cultured from urethral samples in nearly half of the patients and is believed to be capable of triggering Reiter's syndrome in susceptible men {178}. Although joint cultures are negative for bacteria in Reiter's disease, hybridization studies have detected chlamydial RNA in synovial specimens . The occurrence of Reiter's syndrome after bacille Calmette-Guerin immunotherapy for bladder cancer has been reported . Eighty percent of Reiter's disease patients are HLA-

827 positive ; however, the precise role of this major histocompatibility class I antigen in the development of this disease is unclear.

A close relationship to psoriasis has been assumed for the cutaneous lesions because of their clinical resemblance to psoriasis and the presence of spongiform pustules . Similarly, the arthritis of Reiter's disease resembles that of psoriasis not only clinically but also by the absence of rheumatoid factor .

Differential Diagnosis. The early spongiform pustule seen in Reiter's disease is indistinguishable from the spongiform pustule seen in pustular psoriasis. Slightly older lesions often can be identified as representing Reiter's disease, in contrast to psoriasis, by the presence of a markedly thickened cornified layer.