Background: The assessment of disease activity in patients with ankylosing spondylitis (AS) continues to be a chal- lenging issue. The currently available markers like C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) show poor correlation with clinical disease activity. There is a need for good biomarkers to assess disease activity. We explored serum nitrite, a stable end product of metabolism of NO, which is known to rise in inflammation, as a potential biomarker of disease activity in AS. Objectives: To compare the levels of serum nitrite between patients with AS and healthy controls and to correlate levels of serum nitrite with disease activity in four assessment in ankylosing spondylitis (ASAS) domains. Methods: Fifty patients satisfying modified New York criteria for AS were recruited for the study. Patients were assessed in the following ASAS domains: physical function (BASFI), pain (VAS, 0-100), patient global assessment (VAS, -100) and inflammation (mean of the two morning stiffness related BASDAI scores). Eighty-seven healthy controls were also included for comparison. Blood samples (12 hours fasting) were obtained and stored for serum nitrite level estimation, which was done by Ding's method. The median levels of serum nitrite were compared between the two groups. Correlation of serum nitrite levels was sought with individual domains of disease activity. Results: The median serum nitrite levels in patients with AS were markedly elevated as compared to those in con- trols (39 μmol/L [IQR 27-50] vs. 4.75 μmol/L [2.53-12], P = 0.001 (Mann-Whitney U test). There was only one patient whose serum nitrite level overlapped with that of controls. Clinical assessment of disease activity (individual ASAS domains-physical function (BASFI), pain, patient global assessment and inflammation (mean of the two morning stiffness) did not show a good correlation with serum nitrite levels. Conclusions: Serum nitrite level was increased eight folds in patients with AS when compared with controls. Thus its measurement holds promise in differentiating between inflammatory and mechanical low back pain. However, there was no variation across a range of levels of disease activity making it unsuitable as a biomarker to monitor disease activity in AS.

Objective: Rheumatoid factor (RF) positivity has been associated with an unfavourable outcome in rheumatoid arthritis (RA). Our study aimed to find a baseline RF cut-off level that would determine the response to standard disease modifying anti-rheumatic drug (DMARD) combination treatment. Patients and methods: We studied 233 seropositive (RF levels ≥ 20 IU/mL at presentation) RA patients over a period of up to 5 years. Disease activity was assessed at each patient-encounter using disease activity score on 28 joints (DAS28). Treatment consisted of weekly methotrexate, daily hydroxychloroquine and low dose oral methlypred- nisolone as an adjunct. Sulfasalazine or leflunomide were added to the ongoing regimen if satisfactory response was not achieved by 3 months of treatment. Individual response of patients to treatment was graded using the fol- lowing DAS28 cut-off values: < 3 as low disease activity (satisfactory response), ≥ 3 as moderate and ≥ 5.1 as high (unsatisfactory response). Results: By analyzing all possible 2 × 2 contingency tables based on the different values of RF in the data set, using Fisher's exact test of association between RF levels and DAS28 values, a cut-off level for RF of 70 IU/mL gave the optimal discrimination between 'low' versus 'moderate or high' disease activity in the follow-up. Conclusion: A baseline RF cut-off value of 70 IU/mL appears to predict a 'satisfactory' versus 'unsatisfactory' response to standard DMARD-combination therapy in RA over time.

Late onset rheumatoid arthritis (LORA) is a distinct subset of rheumatoid arthritis with age of onset over 60. It differs from young onset disease (YORA) by a more equal sex distribution, a higher frequency of abrupt disease onset, more large joint complaints and lesser extraarticular features. Different immunogenetic associations have been described. Disease modifying drugs and low doses of prednisone are the mainstream of therapy. Biologicals are increasingly being used with better efficacy and tolerability in recent studies.

Nuclear medicine is a evolving speciality with a promising role in rheumatic disorders. A number of radiopharmaceu- ticals and nuclear scintigrahic procedures are available for evaluation of inflammatory and non inflammatory joint diseases. This review focuses on the current application of nuclear medicine in joint diseases.