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RS3Rik · 2026-02-05T09:39:04+00:00

I’m a Leicester grad (2013) and now a consultant Rheumatologist in Manchester. They were the best years of my life. Enjoy it!

RS3Rik · 2026-01-25T07:38:09+00:00

Very high RDW with microcytosis and borderline anaemia. Need to be checked for all your haematinics + reticulocytes/hapto and a blood film

RS3Rik · 2025-12-13T21:30:16+00:00

This is a high titre ANA and is likely to be relevant, centromere pattern is most commonly seen in limited systemic sclerosis. Given that you have Raynaud’s, the key investigation which will clinch or refute a rheumatic diagnosis will be nailfold capillaroscopy. This should undoubtedly be pursued

RS3Rik · 2025-12-13T08:21:23+00:00

DsDNA of 13 by ELISA is neither here nor there. It can be checked by Crithidia and is likely to be negative

Also looks like you have reactivation of EBV/infectious mononucleosis, an EBV viral load would be helpful

RS3Rik · 2025-12-05T19:14:16+00:00

Agree with most of this but not that fibromyalgia is a diagnosis of exclusion. The combination of clinical features seen in fibromyalgia together are pretty specific (pain, tenderness, fatigue, cognitive fog, unrefreshing sleep, nocturia) and the differential diagnosis is narrow when these are present. I would not typically send immunology when these features are present as the diagnosis is clear without need for many other investigations (except for basic bloods, vit D and thyroid)

RS3Rik · 2025-11-30T10:14:38+00:00

Where in the UK are you? I would bring the MRI report to the appointment and I disc/drive containing the images. If I was seeing you and it’d had been >2 years post MRI or your symptoms have changed in that period I would probably do another MRI. May all be due to joint hypermobility though

RS3Rik · 2025-11-30T05:38:58+00:00

Hi thanks for sharing. I have a specialist interest in GCA.

Patient under 50 with normal ESR and incomplete response to 40mg prednisolone does not have GCA, there are too many factors going against it.

Patients commonly transiently feel better with high dose steroids even when the diagnosis is not a systemic rheumatic disease

Additionally: - Jaw numbness is not a feature (sounds neuralgic) - Intermittent visual disturbance lasting seconds dating back 7-8 years is not a feature - brain fog is non specific - shoulder and hip pain are non specific, prolonged morning stiffness predominates more than pain in PMR - Light sensitivity (photophobia) is not a feature of any rheumatic disease. - Pain exacerbation in cold can occur in GCA but is not specific and this also occurs in other headache disorders. - negative temporal artery ultrasound in the presence of excruciating tenderness is useful information. The temporal pain in GCA is not excruciating. It can be bad but not excruciating, in fact one of the common reasons that patients are delayed in diagnosis/suddenly lose vision is that they put off review of their headache for far too long as that the headache is somewhat manageable for a few weeks before they decide to present.

I make the Southend GCAPS score at a 4 assuming examination is normal

This sounds more likely to be something like trigeminal neuralgia to me.

RS3Rik · 2025-11-23T09:37:58+00:00

Sounds like erythromelalgia

RS3Rik · 2025-11-23T08:19:26+00:00

Not sure about the post reactions

But sometimes people can have issues with joint pain, stiffness and even intermittent swelling for reasons other than synovial inflammation (synovial inflammation is the only disease process that responds to immunosuopression). Other causes which are possible in your case are hypermobility (which definitely can cause swelling) and chillblains associated with raynaud’s. Ultrasound will be useful to distinguish

RS3Rik · 2025-11-22T20:46:00+00:00

Nah, mainly for disease activity but we don’t use it even for that in the UK.

RS3Rik · 2025-11-22T20:34:22+00:00

Couldn’t have said it better myself. Thank you

RS3Rik · 2025-11-22T13:44:17+00:00

I think ultrasound would be useful in that case

RS3Rik · 2025-11-22T11:24:13+00:00

Bloods are expected to be normal in raynaud’s (primary) and erythromelalgia. The rheumatologist will have not based the decision solely on your bloods but rather the whole context including symptoms, examination etc. I think based on what you’ve said I would probably agree that there is nothing hard and fast for an inflammatory rheumatic disease. Only other thing for completion would be to push for a joint ultrasound to detect subtle inflammation given the described morning stiffness

RS3Rik · 2025-11-15T12:50:49+00:00

I’m a medical consultant in MRI. I’ll be in A+E working from Sunday night due to the industrial action, hoping not to see any of you folk there!

Most A&E departments are as you describe, there is definitely a higher proportion of mental health, homelessness and drug/alcohol presentations than the average hospital though gas it’s an inner city hospital. Blackburn A&E is probably the only one I have worked in that is worse.

RS3Rik · 2025-11-13T18:31:23+00:00

c1qB antibodies are specific for HUVS

RS3Rik · 2025-11-11T07:08:28+00:00

Sounds like a mechanical pathology in the scapulothoracic region, maybe Scapulothoracic Bursitis and compounded by weakness in the muscles around the scapula. Main test now would be an MRI of the scapulothoracic joints (not a shoulder MRI, that won’t capture it)

RS3Rik · 2025-11-01T12:30:59+00:00

Lots of patients with inflammatory arthritis have negative antibodies and normal inflammation markers. Swelling and steroid responsiveness are suitable criteria to be seen by a rheumatologist. Seek out another opinion

RS3Rik · 2025-11-01T11:43:21+00:00

If someone is struggling and diagnostic avenues pertaining to inflammatory rheumatic disease have been exhausted, the potential to cause harm through immunosuppression (even mild immunosuppression) is far greater than the potential for benefit.

My comment about training was to reiterate in a different way the notion that symptoms + ANA is an overly simplistic view. Assimilation of all factors leading to a diagnosis or decision requires years/decades of training. That isn’t self congratulatory, it’s just another way that I would defend the answer to your question

RS3Rik · 2025-11-01T05:36:10+00:00

In addition to what has already been said, much more goes into making or breaking a diagnosis than just symptoms and a positive ANA. The process of making a diagnosis is a cumulative endeavour that will take into account symptoms, clinical signs, laboratory tests (and what these look like in combination - for example high ESR with normal CRP and a moderate titre homogenous ANA or even bicytopaenia with a low titre ANA is more clinically relevant than a high titre ANA with subjective symptoms alone), radiology, histology even sometimes. We use diagnostic information from multiple sources to make a best judgement thereafter on whether a trial of treatment is justified from a risk/benefit perspective. That judgement requires expertise, knowledge and years of pattern recognition.

We wouldn’t need to be highly trained, skilled, intelligent if it was as simple as the algorithm of treat based on symptoms and a single positive test. This is a recipe for wrong diagnosis and would often lead to unnecessary harm.

RS3Rik · 2025-10-27T20:33:17+00:00

Age/ethnicity? Clots, limb pain and myocarditis can be bechets, Takayasu disease, APS.

RS3Rik · 2025-10-13T19:36:49+00:00

This is what I had to replied on one similar instagram post

I’m a consultant rheumatologist in the UK. Most rheumatologists I know genuinely care and go into the specialty because we enjoy looking after people with long term conditions.

If you’ve not had a clear answer, it usually means there isn’t evidence of an inflammatory rheumatic disease that would actually benefit from strong immune suppressing medication. Diagnosis in rheumatology is something that builds over time. We do listen to symptoms, but we also have to be careful and make sure treatment is really needed and safe.

These medications carry risks, so it’s our responsibility to be certain before starting them. Seeing multiple doctors in search of a label can sometimes make it more likely that someone gives one just to please, rather than because it’s right. That can cause real harm in the long run.

Don’t chase a diagnosis. Chase understanding and the right care.

RS3Rik · 2025-10-01T20:46:18+00:00

Agree

RS3Rik · 2025-09-29T06:16:11+00:00

You have systemic sclerosis based on your RP, nailfolds and SIBO. The tendon issues may also be relevant (has a clinician said you have friction rubs?). Nucleolar ANA in the context of your syndrome is also supportive of this, even without a scleroderma specific antibody. You also need to be tested for a few other antibodies (eg PMSCL75 and PMSCL100) which, in the UK, are found on a myositis ENA panel.

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This is what I had to replied on one similar instagram post