I understand. But it does not sound as though someone has to have all of the signs, such as the skin signs, to be diagnosed.
I guess my point is that a particular syndrome might be very tightly defined by some clinicians, excluding people who don't have a particular sign that the clinician believes is characteristic. But the people excluded might still have a collection of odd signs and symptoms following an infection. If conditions like Reiters can be defined by such an eclectic combination of symptoms, it's surprising that there is such closed mindedness about the possibility of other collections of symptoms being the product of another combination of a particular infection, the genes of the host and chance.
That is right. All you need is one diagnostic sign. Maybe keratoderma or maybe a nail dystrophy. If the signs are less unique in pattern then the diagnosis becomes more a matter of probability but that is standard in medicine, we often work with probables as much as definite.
I think it is reasonable to be confident that we are identifying a specific Reiter process when we see the unique rash or nail abnormality, just as it is reasonable to identify a plant if you just have a very typical flower or leaf.
We don't exclude the people who don't have the rash or nails, we just widen the range of possibilities that need considering. So someone with a single knee synovitis at the age of 20 is quite likely to have the Reiter's process but also reasonably likely to have RA. We manage them as if they might have both.
There are times when the distinction does not matter - if wanting to offer a TNF inhibitor, which works for both. If rituximab is an option then it is important to weigh up as carefully as possible the likelihood of one or the other because Reiter's is not B cell related.
If people had odd collections of symptoms and signs I would follow them as having uncertain diagnosis but offer them anything that was a reasonable risk/benefit choice for the possible diagnostic options - and that would include generalised diagnoses like inflammatory synovitis not otherwise specified. I don't recall closed mindedness amongst my colleagues on this. We all thought we were inching our way forward in semidarkness trying to understand how to categorise in a way that optimised treatment. We all recognised OOTT - one of those things - the illness that did not fit but still needed managing. I got a lot of such cases referred to me in the hope that I might think rituximab would work when the physician had run out of ideas.
And colleagues were always keen to be the first to get on to some new proposed syndrome of a new pattern of association like post-parvovirus arthropathy or Lyme. People were constantly speculating on new micro-syndromes they thought they had picked out.
I realise that I was working in an academic department and one with a number of leading people in the field going through but I don't actually think we were so unusual. In fact the department had so many trainees in the 1980s (12 registrars and 12 senior registrars where most departments had none) that a good proportion of rheumatologists in the UK were trained there.
I actually think the problem here is something a bit different. The way we manage people is probably more dependent on the evidence for a local process that we think we can alter than on a diagnosis. If people have synovitis, which is evidenced by clear physical signs, then we know that we may well help that with steroid injections or TNF inhibitors. But where there is joint pain and no signs of synovitis it is more difficult. Even if I diagnosed Reiter's I would not want to inject steroid into a joint if there was no evidence of inflammation or use a TNF inhibitor.
Other physicians often explain what they do in a different way from me - which is probably why I was invited to give lectures on my slightly unusual ideas about diagnostic categories. But I think this has more to do with the way people talk than how they actually act. There was much less disagreement amongst us what we would do in particular situations.
Of course the bottom line in all this is the raw deal that the person with a problem that we do not know how to fix gets. So pain without synovitis gets a raw deal. The BPS people think they can conjure up some stories to wade in. People like me who need some biological clue to work from are stuck, so I never got anywhere with problems of that sort. As I have said before, I think this is probably the biggest reason why PWME get a raw deal.
