Outcome Assessments for the Rheumatoid Hand.

Rheumatoid arthritis profoundly affects hand function and quality of life. Standardized outcome measures are lacking, hindering comparison between studies. Clinical assessment traditionally relies on performance-based tests like range of motion, grip, and the Jebsen-Taylor Hand Function Test, crucial for evaluating treatment effects, especially surgery.

Surgery, Needle Fasciotomy, or Collagenase Injection for Dupuytren Contracture : A Randomized Controlled Trial.

Background: Surgery, needle fasciotomy, and collagenase injection are used to treat Dupuytren contracture. The treatment decision requires balancing initial morbidity and costs of surgery against its potential long-term benefits over needle fasciotomy and collagenase.

Objective: To compare the effectiveness of surgery, needle fasciotomy, and collagenase injection at 3 months and 2 years (secondary time points of the trial).

Proximal ROw carpectOmy versus four-corner Fusion (PROOF-trial) for osteoarthritis of the wrist: study protocol for multi-institutional double-blinded randomized controlled trial.

Background: Scapholunate advanced collapse (SLAC) and scaphoid non-union advanced collapse (SNAC) are common types of wrist osteoarthritis (OA). Non-operative treatment consists of pain medication, splinting, and avoiding activities that induce pain. However, in case a course of conservative treatment is unsuccessful, operative treatment is needed.

Minimal important difference and patient acceptable symptom state for the Numerical Rating Scale (NRS) for pain and the Patient-Rated Wrist/Hand Evaluation (PRWHE) for patients with osteoarthritis at the base of thumb.

Background: The Numerical Rating Scale (NRS) and Patient-rated wrist/hand evaluation (PRWHE) are patient-reported outcomes frequently used for evaluating pain and function of the wrist and hand. The aim of this study was to determine thresholds for minimal important difference (MID) and patient acceptable symptom state (PASS) for NRS pain and PRWHE instruments in patients with base of thumb osteoarthritis.

Methods: Fifty-two patients with symptomatic base of thumb osteoarthritis wore a splint for six weeks before undergoing trapeziectomy.

Platelet-rich plasma versus corticosteroid injection for treatment of trigger finger: study protocol for a prospective randomized triple-blind placebo-controlled trial.

Background: Trigger finger is a common hand disorder that limits finger range of motion and causes pain and snapping of the affected finger. Trigger finger is caused by an imbalance of the tendon sheath and the flexor tendon. The initial treatment is generally a local corticosteroid injection around the first annular (A1) pulley.

Low TNF-induced NF-kappaB and p38 phosphorylation levels in leucocytes in tumour necrosis factor receptor-associated periodic syndrome.

Objective: TNF receptor-associated periodic syndrome (TRAPS) is a systemic autoinflammatory disorder caused by mutations in the type 1 TNF receptor (TNFRSF1A) gene. Because the pathomechanism of TRAPS may involve aberrant TNF-mediated intracellular signalling, we examined phosphorylation levels of nuclear factor kappaB (NF-kappaB) and p38 in response to TNF in 10 patients with three different TNFRSF1A mutations (C73R, C88Y and F112I).

Methods: Phosphorylation levels of NF-kappaB p65 and p38 were determined in fresh leucocytes stimulated with TNF (0-100 ng/ml) for 2.

Abnormal tumor necrosis factor receptor I cell surface expression and NF-kappaB activation in tumor necrosis factor receptor-associated periodic syndrome.

Objective: Tumor necrosis factor receptor-associated periodic syndrome (TRAPS) is an autosomal-dominant autoinflammatory condition caused by mutations in the TNFRSF1A gene. The cellular mechanisms by which mutations in this gene trigger inflammation are currently unclear. Because NF-kappaB is the major intracellular signaling component inducing secretion of proinflammatory cytokines, we sought to determine whether differences in the clinical phenotype of patients with TRAPS may be attributable to variable effects of TNFRSF1A mutations on TNFRI expression, localization, or NF-kappaB activity.