This is my personal, highly selective take on articles in the August Arthritis & Rheumatism. Login is required if you want to read the actual articles – I frequently have trouble loggin on to their site anyway.

There is an article about TNF antagonists in pregnancy with an accompanying editorial by Jane Salmon & Deborah Alpert. The gist is that 23 British women were exposed to TNFs during pregnancy and had outcomes that were about the same as those in ‘normal’ pregnancies. Most women discontinued the TNF, but one took etanercept throughout pregnancy. There were a few complications, but the authors didn’t think they differed from outcomes in the general population. Salmon & Alpert comment that there’s lots we don’t know so use caution. Duh! But the authors do make a legitimate case for being able to tell patients not to panic if they do get pregnant on a TNF.

Another article about TNFs – this time the risk of serious infection in those taking a TNF compared to those on a DMARD. Its an observational study, again done in Britain, using a cohort of RA patients on TNF and another cohort of RA patients not yet on TNFs. Nice data set since all TNF users have to be registered in the database. In general the comparison group was less sick than the exposed group. In unadjusted analysis, the TNF group had higher rates of serious infection, but this pretty much disappeared after adjustment for comorbidities, and disease severity. No differences between individual TNFs. There was a significantly elevated risk of skin and soft tissue infection in TNF users compared to comparison – incidence rate ratio 4.3. I’m not sure what to make of that. The confidence interval was pretty wide (1 to 17) which means it’s not a very precise result. Is it a true effect or is it the random positive result you see among a bunch of negative results?

But generally not a lot of evidence here for an elevated risk of serious infection, which, again, is reassuring.

A dose escalation trial of another anti-TNF: anti-CCL2/MCP-1 monoclonal antibody (ABN912). (Phew! What a name!). Stone cold negative study. Won’t be seeing that one on the market any time in the near future!

Hmmm … skipping over lots of basic science stuff …

Change in joint space width: cartilage or meniscus? Maybe it’s not all cartilage loss in OA after all. It seems the meniscus plays a pretty large role too.

An article on mortality in catastrophic antiphospholipid syndrome (CAPS) – it’s high. 45% of patients in the registry died. Roughly 30% of those died of stroke. The only risk factor associated with mortality identified was the presence of lupus. It’s very hard to figure out what the best treatment is in an observational study like this, but for what it’s worth, those who received steroids, anti-coagulants, and plasma exchange had the best rate of recovery (about 78%).

New classification criteria for psoriatic arthritis from the CASPAR study group. These are, of course, research not diagnostic criteria:

To meet the CASPAR (Classification criteria for Psoriatic Arthritis) criteria, a patient must have inflammatory articular disease (joint, spine, or entheseal) with 3 points from the following 5 categories:

1. Evidence of current psoriasis, a personal history of psoriasis, or a family history of psoriasis.

Current psoriasis is defined as psoriatic skin or scalp disease present today as judged by a rheumatologist or dermatologist.

A personal history of psoriasis is defined as a history of psoriasis that may be obtained from a patient, family physician, dermatologist, rheumatologist, or other qualified health care provider.

A family history of psoriasis is defined as a history of psoriasis in a first- or second-degree relative according to patient report.

2. Typical psoriatic nail dystrophy including onycholysis, pitting, and hyperkeratosis observed on current physical examination.

3. A negative test result for the presence of rheumatoid factor by any method except latex but preferably by enzyme-linked immunosorbent assay or nephelometry, according to the local laboratory reference range.

4. Either current dactylitis, defined as swelling of an entire digit, or a history of dactylitis recorded by a rheumatologist.

5. Radiographic evidence of juxtaarticular new bone formation, appearing as ill-defined ossification near joint margins (but excluding osteophyte formation) on plain radiographs of the hand or foot.

AHA! Here’s an article that’s right up my alley: Gout and the risk of acute myocardial infarction.

Subjects were men at high risk of coronary heart disease, but without diabetes or prior heart disease. An elevated urate level was considered to be >= 7.0 mg/dl. Definition of gout was self reported gout with sustained hyperuricemia (elevated urate level). Primary outcome was acute MI (myocardial infarction – a heart attack). 5337 men were hyperuricemic out of 12,866. 1123 reported gout. No difference in groups with relation to baseline coronary risk, but those with gout were more likely to use alcohol and diuretics (a blood pressure pill – both alcohol and this class of medication are well known gout risk factors).

Results: those with gout had an elevated risk of MI. After adjustment for all kinds of stuff (most of which appears appropriate and sufficient to me), those with gout had 1.26 the odds of an MI (just to be technical for a second, this is probably really a risk ratio – I’ll have to check on that), and those with elevated uric acid had 1.11 the odds. The risk of MI was 4% higher for each each elevation of 1 mg/dl of urate.

Overall, these are pretty small risks. I know a few epidemiologist who would say that they may mean nothing. And there are potential unknown condounders that could account for this as well. Maybe uric acid is associated with … I don’t know, anything, and that’s what we’re seeing. On the other hand, it may be a valid finding. But it’s hard to be sure with a risk ratio this small.

Anyway, that finishes up the A&R Roundup for this month! Tune back in and see if there’s another one next month!

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