A 42-year-old white homosexual man presented to our clinic in April, 2008, with a 12-day history of right knee and back pain, conjunctivitis, and proctitis. 10 days earlier, after a normal radiograph, an arthrocentesis of his right knee had been done; 40 mL of clear synovial fl uid was aspirated and corticosteroids were injected locally. There was no history of recent injury, febrile illness, or rheumatological conditions. He reported anonymous unprotected receptive anal sex 1 month earlier. Since 2000, he had had three episodes of uncomplicated urethritis, secondary syphilis, HIV, and an episode of primary syphilis (rapid plasma reagin [RPR] 1/32 in August, 2007). He had been taking antiretrovirals since October, 2007, with a CD4 count of 300 per μL (31%) and undetectable viral load in March, 2008. On examination, his right knee was cool, swollen, and painful, and he had a right non-purulent conjunctivitis. Proctoscopy showed a hyperaemic mucosa with superfi cial ulcers and a mucopurulent exudate (fi gure A); gram stain showed more than 40 leucocytes per high-power fi eld (magnifi cation ×1000) without diplococci. Making a presumptive diagnosis of lymphogranuloma venereum and sexually acquired reactive arthritis (SARA), we gave our patient 100 mg doxycycline twice daily for 21 days and non-steroidal anti-infl ammatory drugs (NSAIDs). He returned 4 days later because of diffi culty walking (he was using crutches), fever (38·5°C), and a painful and swollen right elbow and left knee (fi gure B). Arthrocentesis of his left knee was done and 45 mL of synovial fl uid was aspirated. Laboratory test results showed RPR 1/8 and TPHA 1/2560; rectal and conjunctival infection with Neisseria gonorrhoeae and conjunctival infection with chlamydia were ruled out. Rectal lymphogranuloma venereum was diagnosed using real-time PCR. On day 10 his general condition improved, he had no fever or conjunctivitis, and proctitis was improving, although he was still using crutches. Cultures from synovial fl uid were negative, haematological and other blood tests were normal, HLA-B27 was negative, although C-reactive protein was mildly raised at 13·79 mg/L. On day 12, he had another arthrocentesis of his right knee with aspiration of 112 mL of serous fl uid, and he was prescribed prednisone 5 mg three times daily. By day 39, on tapered prednisone, he felt “80%” better and proctoscopy showed no rectal infl ammation. PCR for the lymphogranuloma venereum-causing organism was negative on day 46. When last seen in August, 2008, the patient was well. SARA is a spondyloarthritis and an important cause of lower limb oligoarthritis, predominantly aff ecting young adults. It consists of sterile axial or peripheral articular infl ammation, enthesitis, and extra-articular manifestations. Reactive arthritis is precipitated by an infection localised in the genitourinary or gastrointestinal tract and susceptibility may be related with the HLA-B27 gene. The bacteria principally involved are chlamydia, salmonella, shigella, campylobacter, and yersinia species. Diagnosis is a two-stage process requiring demonstration of a temporal link with a recognised trigger infection. The standard therapy is NSAIDs and steroids. Lymphogranuloma venereum is a systemic sexually transmitted infection caused by the L serovars of Chlamydia trachomatis. Since 2003, outbreaks of rectal lymphogranuloma venereum have occurred in Europe aff ecting mostly core groups of HIV-positive homosexual men, although arthritis rarely accompanies infection. We have diagnosed 35 cases of lymphogranuloma venereum as of October, 2008. Lymphogranuloma venereum in Europe is unknown by many physicians not working in genitourinary medicine and is frequently diagnosed late in patients with proctitis. Therefore, because of increasing cases, physicians should be aware that lymphogranuloma venereum can also be a cause of SARA.