Effectiveness of ustekinumab in patients with psoriatic arthritis in a real-world, multicenter study.

OBJECTIVE: To assess the effectiveness and survival of ustekinumab (UST) among patients with psoriatic arthritis (PsA) treated under routine clinical care. METHODS: Multicenter study. Epidemiological and clinical data was collected through electronic medical records of all patients with PsA who started UST in 15 hospitals of Spain. RESULTS: Two hundred and one patients were included, 130 (64.7%) with 45 mg and 71 (35.3%) with 90 mg. One hundred and thirty one patients (65.2%) had previously received another biological therapy. The median baseline DAS 28 ESR was 3.99, and Psoriasis Area and Severity Index (PASI) was 3. Overall, there was a significant decrease in DAS66/68 CRP, swollen joint count (SJC), tender joint count (TJC), and PASI in the first month of treatment, with earlier improvement in skin (PASI) than joints outcomes. Survival was numerically lower in patients with UST 45 mg (58.1%) than 90 mg (76.1%), although significant differences were not found (p = 0.147). When comparing naïve and < 1 TNF blocker versus > 2 TNF blocker-experienced patients, a significantly earlier response was seen in the former group regarding SJC (p = 0.029) at 1 month. Fifty-one patients (25.3%) stopped UST due to joint inefficacy and 4 patients due to adverse events (1.9%). Drug survival was significantly better in patients with fewer lines of previous biological agents (p = 0.003 for < 1 TNF blocker versus > 2 TNF blocker users). CONCLUSIONS: UST was effective in PsA patients in a routine clinical care setting. Patients with UST 90 mg and fewer lines of previous biologics achieved better and faster responses. Key Points • Largest cohort of patients with PsA in treatment with UST with specific rheumatological indication. • First cohort of patients with PsA comparing effectiveness of UST according to 45/90 mg dose.

Necrotizing fasciitis and myositis caused by streptococcal flesh-eating bacteria.

Three types of group A streptococcal infections are particularly feared: necrotizing fasciitis, myositis, and streptococcal toxic shock syndrome (TSS). We present 3 cases of necrotizing fasciitis due to Streptococcus pyogenes, one in an immunocompromised patient who had received kidney transplant and 2 healthy patients. Mean age of patients was 52 years (range, 42-67 years), and all 3 were male. One spontaneous case in absence of any obvious portal of entry is reported. The clinical course was initially indolent but quickly destructive. All patients required emergency surgical debridement and intravenous antibiotics. In 2 cases, intravenous immunoglobulin therapy was added. Differential diagnoses include septic arthritis, cellulitis, gout, other causes of tenosynovitis, erysipelas, and deep vein thrombosis.Blood and soft-tissue cultures should be obtained to identify the bacteria, and emergency computed tomography or magnetic resonance imaging scan should be performed to confirm the diagnosis and define the extension of the necrosis. Aggressive surgical debridement in the first 24 to 48 hours and antibiotic treatment, including penicillin and clindamycin, are the cornerstones in the management of these infections. Adjuvant intravenous immunoglobulin therapy might be useful in case of TSS. Diagnostic and treatment delays are the main causes of mortality in these infections.

Role of technetium-99m diphosphonate and gallium-67 citrate bone scanning in the early diagnosis of infectious spondylodiscitis. A comparative study.

A comparative study of the parts played by technetium-99m diphosphonate and gallium-67 citrate bone scanning in the early diagnosis of infectious spondylodiscitis is presented. Nineteen patients were included in the study. All patients (11 men aged 19-70 years and eight women aged 18-72 years) had a history of back pain varying in duration from one to 15 weeks. A 99mTc diphosphonate bone scan was positive in 17 patients. The two patients with negative results had less than two weeks of back pain. The 67Ga citrate bone scan showed uptake in all patients.

Infectious arthritis in patients with rheumatoid arthritis.

Eleven cases of infectious arthritis occurring in patients with rheumatoid arthritis are reported. Staphylococcus aureus was the causative organism in eight patients. Streptococcus anginosus and Streptococcus agalactiae in one patient each, and Mycobacterium tuberculosis in two patients. The mean duration of symptoms before diagnosis was 16 days in patients with pyogenic arthritis. The diagnosis of joint infection caused by Mycobacterium tuberculosis was especially delayed (57 days). Four patients died; they were found to have a longer time to diagnosis and two of them had multiple joint infection. Although Staphylococcus aureus is the microorganism most often affecting patients with rheumatoid arthritis, infection caused by Mycobacterium tuberculosis must also be considered in such patients.

Pyogenic arthritis caused by Streptococcus milleri in a nonimmunocompromised host.

We describe a case of pyogenic arthritis caused by S. milleri (S. anginosus) in a non-immunocompromised host. No other septic focus was found. S. milleri is now widely recognized as an important cause of pyogenic infection, though it eluded suspicion for many years. The rarity of reports of articular infections by S. milleri might be due to problems associated with its recognition.

Munchausen's syndrome simulating reflex sympathetic dystrophy.

A 15 year old girl who had pain, oedema of her left hand, and fever of four months' duration is described. Marked demineralisation of her hand was shown by radiography, and increased articular uptake by technetium-99m bone scan. All these changes were indistinguishable from reflex sympathetic dystrophy. After two admissions to hospital and multiple explorations we discovered that she had induced her symptoms herself and a diagnosis of Munchausen's syndrome was made. As far as we know this presentation has not been previously reported and might help to explain the physiopathology of some signs of reflex sympathetic dystrophy.