Calprotectin, a sensitive marker of inflammation, is robustly assessed in plasma from patients with early or established rheumatoid arthritis by use of different laboratory methods.

Calprotectin (S100A8/S100A9, MRP8/MRP14) is a major leukocyte protein found to be more sensitive than C-Reactive Protein (CRP) and Erythrocyte Sedimentation Rate (ESR) as a marker of inflammation in patients with rheumatoid arthritis (RA). The present objective was to explore the robustness of calprotectin assessments by comparing two different laboratory methods assessing calprotectin in plasma samples from patients with early or established RA. A total of 212 patients with early RA (mean (SD) age 52(13.3) years, disease duration 0.6(0.5) years) and 177 patients with established RA (mean (SD) age 52.9(13.0) years, disease duration 10.0(8.8) years) were assessed by clinical, laboratory, and ultrasound examinations. Frozen plasma samples (-80 °C) were analysed for calprotectin levels at baseline, 1, 2, 3, 6 and 12 months by use of either enzyme-linked immunosorbent assay (ELISA) or fluoroenzyme immunoassay (FEIA). The ELISA technique used kits from Calpro AS and the FEIA technology was assessed on an automated Thermo Fisher Scientific instrument. The results showed high correlations between the two methods at baseline and during follow-up, with Spearman correlation at baseline 0.93 (p < 0.001) in the early and 0.96 (p < 0.001) in the established RA cohorts. The correlations between each of the two calprotectin assessments and clinical examinations had similar range. Calprotectin correlated well with clinical examinations, with at least as high correlations as CRP and ESR. The present study showed similar results for the two analytical methods, supporting the robustness of calprotectin analyses, and suggest calprotectin in plasma to be included in the assessments offered by clinical routine laboratories.

A 35-year-old woman with influenza A-associated thrombotic thrombocytopenic purpura.

A previously healthy 35-year-old woman presented with severe thrombotic thrombocytopenic purpura (TTP) affecting several organs and concomitant influenza A infection. On admission to hospital, haemoglobin was 5.4 g/dl, platelet count 6 × 10/l, Schistocyte count in peripheral blood 5%, and throat swab positive for influenza A RNA. The patient was treated with antiviral medication and transfusions of fresh frozen plasma before plasma exchange therapy with excellent response. Plasmaphereses were attenuated after 5 days, resulting in TTP relapse 3 days later. A disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) protein was very low (<0.04 U/l) and anti-ADAMTS13 elevated (>2 U/l), consistent with acquired TTP. Platelet counts normalized after five additional plasma exchanges and oral corticosteroids. Antinuclear antibodies and subgroup anti-Ro/Sjögren's syndrome A antigen (SSA) were detected in serum and have remained borderline-elevated, although evaluation during TTP, recovery and follow-up have lacked clinical manifestations of connective tissue disease. Influenza A infection induced production of ADAMTS13 inhibitor, which resulted in TTP in a patient with circulating antinuclear antibodies, lacking other manifestations of connective tissue disease.

Minimal change in HSV-2 seroreactivity: a cross-sectional Swedish population study.

The prevalence of antibodies to herpes simplex virus type 2 (HSV-2) was determined in sera collected from 2 Swedish cross-sectional populations during 1990/91 and 1996/97. A glycoprotein G2 (gG-2) peptide ELISA was used to analyse 2899 sera from adults. We found a prevalence of 13.0% in 18-70-y-olds in 1990/91 and 16.4% in 31-55-y-olds in 1996/97. Seropositivity to HSV-2 was somewhat higher in women than in men; 14.4% compared to 11.6% in 1990/91 and 18.9% compared to 13.6% in 1996/97. Overall there was a significant difference in female prevalence of HSV-2 compared to prevalence in males of the same age groups (p=0.013). Total antibody prevalence to HSV-1 of 88% in HSV-2 negative individuals above 18 y of age was found. HSV-2 positive individuals were found seropositive to HSV-1 in approximately 95% of the cases. 12% were negative for both HSV-1 and HSV-2 antibodies. In addition, there was no serological sign that the reported increase of HSV-1 as an early sexual disease had reduced the frequency of HSV-2 seropositivity in the sexually most active age groups. In conclusion, our investigation has shown no significant increase of HSV-2 seroprevalence in randomly selected Swedish subjects during the defined time period.