Autoantibodies Appear Early in Sjögren Syndrome
A quintet of autoantibodies seem to turn up nearly two decades before symptom onset in primary Sjögren Syndrome. Also, yet more on bacteria as triggers of RA.
Last week's articles on rheumatology topics in the major non-rheumatology journals.Autoantibodies Present Before Symptom Onset in Primary Sjgren SyndromeJAMA, November 6, 2013
Patients with primary Sjgren Syndrome (pSS) had autoantibodies long before symptoms appeared.
Since 1984, 360 patients have been diagnosed with pSS at Malm hospital in Sweden. Among the 44 of these patients who previously contributed serum samples to a biobank for unrelated reasons, 29 (66%) had detectible autoantibodies in their earliest serum samples – as early as 18 years before symptom onset.
The antibodies were antinuclear antibodies, rheumatoid factor, anti-Ro60/SSA, anti-Ro52/SSA, and anti-La/SSB.
Editorial: Idiopathic pulmonary fibrosisBMJ, November 7, 2013
Idiopathic pulmonary fibrosis - pirfenidone (TA282)
NICE Technology appraisals, April 2013
The UK's National Institute for Health and Care Excellence (NICE) has approved pirfenidone for mild to moderate idiopathic pulmonary fibrosis, which can co-occur with rheumatoid arthritis.
A Cochrane review found that pirfenidone reduces the risk of disease progression by 30%, although it has no effect on mortality. The orally administered drug is antifibrotic, anti-inflammatory, and antioxidant.
Pirfenidone is available in Europe, but not in the US, where a phase III trial for approval is underway.
Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritiseLife, November 5, 2013
The intestinal bacterium Prevotella corpri (P. corpri) was found in the intestines of 75% of patients with newly diagnosed rheumatoid arthritis (RA), but in only 37% of patients with psoriatic arthritis or established RA compared with 21% of healthy controls.
Researchers sequenced the 16S ribosomal RNA, which is used to identify bacteria, from the stool samples of 114 patients and controls.
In mouse models, P. corpri displaces normal Bacteroides species, activates Th17 cells, and causes inflammation.
However, these results don’t demonstrate that P. corpri causes RA in humans. RA may favor the growth of P. corpri, or a third factor may promote RA and P. corpri.
