EULAR 2006

EULAR 2006 Odds and ends (posters):

ESPOIR cohort: predicting the evolution of undifferentiated Inflammatory arthritis into RA. Multiple regression analysis gave the following odds ratios: Symmetrical onset 2.5; morning stiffness >60 minutes 1.7; synovitis >6 4.1; RF+ 2.2; anti-CCP+ 5.6. (Abstract THU0103). This does highlight the importance of anti-CCP. I hope we can get it soon.

Use of MTX (10-20mg/week) in Chronic pyrophosphate arthropathy. Tiny uncontrolled study of five patients but all reported as significantly improved. (THU0468)

Use of questionnaires to ask about recent medical and demographic events to improve efficiency in clinics (by T Pincus THU0130). I wonder if we should add something like this to our own clinic questionnaires?

Anti-CCP antibodies may predict which patients with palindromic rheumatism will evolve into RA (FRI0044). But what good that will do remains to be seen.

Patients on adalimumab seem to respond normally to immunisation against pneumococci and influenza (FRI0064). Which is I suppose useful.

Etanercept reported as effective in refractory PMR (series of 3, uncontrolled study) FRI0267. Significant changes in pain scores and HAQ of the order of 50%, but it only seemed to achieve a reduction in prednisolone of 5-7.5mg.

Two case reports of successful treatment of chronic tophaceous gout with infliximab. (FRI0491, FRI0496). Hmmm?

A Dutch study showed acute gout was more common in the Spring (FRI0495). I will mull over how that will change my practice.

A survey of UK rheumatologists (which included me!) showed that the BNF colchicine regime was used by only a minority. More than half used colchicine bd or tds.(FRI0498)

I have put the abstract numbers in, since you can get the abstracts online from the eular website http://www.eular.org

So what questions are raised by this meeting?



1. Can we be any better at predicting which patients with undifferentiated inflammatory arthritis will develop damaging arthritis?

Possibly, we know that anti-CCP positive patients with UIA are more likely to develop RA: 21% of UIA are CCP+, of those 93% develop RA, but 25% of CCP- also develop RA. In one talk this meeting it was suggested that a clinical prediction rule using 9 variables (including CCP) was able to assign patients such that only 6% of those predicted not to develop RA actually did go on to RA. This needs to be tested prospectively but if it does hold true, we need to consider if delaying treatment in this 6% with RA is acceptable. Clearly some members of the audience did not think it was. I will continue to treat all UIA/PISA with DMARDs for the time being.

I do wonder though if it might be feasible to use anti-CCP status to inform decisions about withdrawing DMARDs in that group which enters remission. They have either really gone into remission or are held in remission by treatment. It would seem reasonable to give greater consideration to stopping DMARDs in the CCP negative cases...but I do not think there is evidence to support this.

2. Which DMARD to use in early inflammatory arthritis?
The easy answer is...one that works. But which to try first? If monotherapy is used it looks as if it should be with more intensive follow-up and tight control of synovitis (IM/IA steroids?). I tend to use MTX but the TICORA study did well with SASP as the initial drug.

MJM

EULAR 2006

Today has been a busy day at the conference, and my internet time is running out...so this will have to be quick, key points only.

The question was raised again as to whether Anti-CCP positive/negative Rheumatoid disease is different. One postulation is that proteins become citrillunated (by smoking for example) and subjects with the shared epitope variants of DR4 then develop anti-CCP antibodies. The Prompt study from yesterday showed that MTX had no impact on the evolution of anti-CCP negative undifferentiated arthritis to RA, but in anti-ccp positive UA MTX significantly reduced the evolution to RA. Treatment with anti-BLys antibodies was also less effective in CCP negative RA.

Much talk about the best use of DMARDs...use early in adequate doses (dare I say aggressive doses?), monitor frequently and adjust to control disease (as in the TICORA study). Consider checking anti-CCP status in RF negative inflammatory arthrtis.

Treatment of refractory RA (ie failed MTX and one anti-TNF)
Optimise DMARD: dose to 25mg/week, change PO to SubCut, use a split dose (more on that later)
Optimise Anti-TNF: dose, frequency
Switch TNF: more useful for secondary failures (ie worked initially) than primary failures
Use another biologic: Abatacept, Rituximab.

Just a short note for now since my internet connection is about to run out of money.










PS split dose MTX: taking some in the evening and some next morning may improve bioavailability of higher doses (above 15mg) but the evidence is limited. Worth a try if all else fails though.

MJM

History of Thiamine

Why Vitamin B is so named.




MP3 File

The structure of Thiamine



Bondol. A small bird which contributed to a Nobel prize.




Further reading on beriberi.

Wardround 2vi6

This week’s two minute tutorials were themed around diabetes:

Diagnosis and investigation (JCM)
Presentations (CC)
Complications (EB)
Oral hypoglycaemics (JA)
Diet (RS)
Insulin ℞ (VA)

Well researched talks overall, and several well timed to the two minutes. I was surprised by the fact that by 55 years of age 35% of patients with T1DM would have died from MI. Nice touch by VA to have used the diabetes specialist nurses as a source. If you want to read a quick (<15 minutes ) review of DM try these documents:

http://www.emedicine.com/emerg/topic133.htm
http://www.emedicine.com/emerg/topic134.htm

For next week the topic is renal:

Assessment of renal function (JCM)
Causes of acute renal failure (VA)
Management of ARF other than dialysis (EB)
Dialysis in ARF (CC)
Complications of CRF (PS)

Remember, two minutes only, so keep it concise and precise. Quote your sources.

The reading last week was A Mysterious Death. Oldach DW et al. NEJM 1998; 338(24):1763-1769. This is a case discussion of the death of Alexander the Great. The systematic approach to differential diagnosis is instructive, and the paper should act as a trigger to revise the features of those diseases mentioned. Perhaps if we do this paper again it would be useful to combine it with the two minute talks to revise the features of the major diagnoses discussed? Comments please?

For next time the reading is: Spellbinding and spellbreaking in convalescence. George Day. Lancet 1961; 279 (7222):211-213. Log on to the NHS Scotland elibrary with your Athens password and choose the Lancet. You will be offered several sources, choose the Sciencedirect Lancet site. If you have trouble (you shouldn’t) come and find me...I have a hard copy.

MJM