The blurb from the Amazon page (no doubt available from all good bookshops and online retailers as well). "Written by the world's leading immunologist Professor Danny Altmann and expert patient Gez Medinger, The Long Covid Handbook translates cutting-edge science, patient-led research and practical guidance with clarity. This book will equip you with expert information and advice on: - Long Covid's 200 symptoms, which include fatigue, brain fog, breathlessness and more - Tips for recovery - Which treatments are most effective and why - Who is most susceptible to the condition and why - What we can learn about Long Covid from other chronic illnesses - The impact on mental health This is the essential guide for anyone living with the condition, as well as clinicians seeking to better understand this little-understood illness." Code: https://smile.amazon.co.uk/Long-Covid-Handbook-Gez-Medinger/dp/1529900123/
Some screenshots from the Amazon preview where the text mentions ME/CFS, or is otherwise of likely interest to members.
Hmm. The page on autoimmunity is wrong. Reactive arthritis is not autoimmunity and nor is there a whole subsection of medicine devoted to post-infectious autoimmunity. This is about as bad as it could be I'm afraid.
The bit classifying rheumatoid arthritis, Fibromyalgia and Ehlers-Danlos under connective tissue disease is just laughable. 'Connective Tissue Disease' has always had two completely unrelated meanings - one for autoimmunity and one for inherited tissue matrix problems. This is so dumb it is hard to believe. I am wondering who the 'I' is in these texts since there are two authors.
Evening Standard covering the book launch https://www.standard.co.uk/futurelo...dbook-burden-nhs-ons-immunology-b1034055.html
Reading those few pages doesn't fill me with confidence either. All that stuff about type A personalities and past trauma sounds ominous. Can't tell from just the bit shown where they go with that.
What is Reactive arthritis if not autoimmunity? I thought at least some cases are in remission of the initial infection, yet the inflammation persists - so it cannot merely be a bystander effect. Secondly, some autoimmune conditions are clearly associated with infection, eg GBS. Does this not warrant a "whole subsection"?
Somewhat sheepishly, I always thought reactive arthritis was autoimmune (i.e. T cell-mediated cross reactivity between pathogen and synovium). Have I missed the fundamentals or is it more of a nuance in definition? (I think the whole subsection comment probably refers to how it's still organ/system-specialty based, eg rheumatic valve disease would be principally looked after by cardiology/cardiac surgery with assist from ID, rather than rheumatology).
Nobody ever found an adaptive autoimmune response in reactive arthritis or any reason to think there was one. The meme about cross-reactivity with synovial made me groan when I was doing my doctorate in 1980. It is still around. It never made any sense. What we now know about the seronegative arthropathies is that they are partly due to genetic weighting in MHC Class I (B27, B7, Cw6). The pathology is of T cell activation but not antigen driven - the distributions are wrong. Paul Bowness, Jim Archer and I wrote an Immunology Today review around 2000 pointing out that the distribution is partly subset trafficking related and partly mechanically related - quite likely mediated through the effect of mechanical stimulus on local TGF beta adsorption on to fibrillin. Everything makes it look like a non-specific CD8 T cell hyperactivity state. That might fit into 'innate autoimmunity' but since we have no reason to think any specific self component is targeted the now standard term 'auto inflammatory' is much better. Guillain Barre is maybe the one post-infective state that looks as if it might genuinely be autoimmune. I have doubts about Willison's invocation of campylobacter(?) cross reaction though. Rheumatic fever never was, as far as I can see. The eminent German pathologist Wegener pointed out to me years ago that it has the features of an immune complex syndrome, not a tissue-antigen specific mechanism. It is possible that short term production of something like anti-complement antibodies in involved but last time I searched the literature there was nothing very convincing.
Amazing. I suspected your answer would indicate I had the fundamentals all wrong, even while I hoped it was just something more subtle! That's quite a broad lecture in a few succinct paragraphs. Thank you.
The bit about trauma, type A personality can be read here. In my opinion it's pseudoscience. Not very helpful...
Volume 401, Issue 10378, 4–10 March 2023, Pages 723-724 Healing Long Covid: a marathon not a sprint Gez Medinger, Danny Altmann, The Long Covid Handbook, Cornerstone Press (2022), p. 336, £14·99, ISBN: 9781529900125 Nisreen A Alwan School of Primary Care, Population Science and Medical Education, University Hospital Southampton NHS Foundation Trust, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK Available online 2 March 2023, Version of Record 2 March 2023. https://www.sciencedirect.com/science/article/abs/pii/S0140673623004087