ElaineD, you could discuss the option of having your serum levels of TNF tested with your immunologist.

TNF is an inflammatory cytokine, mainly made by activated macrophages, which are recruited to sites of tissue inflammation.

TNF is associated with the tissue damage in a number of diseases with an inflammatory component (rheumatoid arthritis, ankylosing spondylitis and inflammatory bowel disease among others.

If your TNF levels are abnormally high, this can be treated with humanised monoclonal antibodies specific for it (infliximab is an example) or with what is in effect a soluble form of a TNF receptor (etanercept).

Depending on the results of the tests, your immunologist should be able to discuss these treatment options with you.

Thanks for this fascinating thread. I'm afraid some of the science mentioned defeats me, but I did want to chip in by saying that I believe Psoriasis is now thought to be an autoinflammatory disease rather than an autoimmune disease? Or perhaps this only applies to Spondyloarthritis rather than to Psoriasis as a skin disease on its own? I think this means that treatment options are somewhat different for the Spondyloarthritis family to those who have autoimmune types of inflammatory arthritis or immune mediated neuropathies.

I have several friends who suffer from Psoriatic Arthritis and Ankilosyng Spondilitis and they also have degrees of peripheral neuropathy and other symptoms that they share with mine. Obviously PsA involves arthritis but it doesn't always involve having Psoriasis. Spondyloarthritis's usually respond well to steroids and NSAIDs, commonly affect the lower back and are usually seronegative - often not even showing up in inflammatory markers either.

Regarding the nail bed testing - I went to a talk about primary and secondary Raynauds at a EULAR congress a few years ago and secondary Raynauds is strongly associated with Scleroderma where about 20% of Lupus sufferers and 12% of RA sufferers also have secondary Raynauds with capillaries that show up when the nailfold/ nail bed is microscopically examined apparently. So perhaps this relatively simple and non invasive test should be run routinely to determine whether small fibre neuropathy indicates whether the cause is a connective tissue disease or not?

My SFN has been quiet for months apart from in my gums, lips and up the left side of my face into my left eye. I could still feel the tingle but my gait improved a lot and it stopped waking me during the night with the terrible pain we all know so well. . This improvement preceded the start of T3 for hypothyroidism but this thyroid med appears to have boosted my circulation and improved my hair, skin and energy levels. I'm also taking Methyl B12 as an OTC add on and this might be helping too although I have to say that it didn't when I took it a few years ago.

Now it is suddenly back and affecting my arms and legs again in equal measure. With these flare ups I seem to suffer from constipation too. No one will commit to a diagnosis apart from falling back on the original one of seronegative RA from when my joints were inflammed and very painful. However, unless or until it returns to my joints I will not be offered further immunesuppressants or steroids - let alone IVIG which I would really be keen to try. I'm told I'm lucky that my joints are presently unaffected and that this only affects my small nerve fibres so far. I think luck is all relative and if these doctors had to learn to live with this degree of uncertainty plus a measure of numbness they might not consider themselves to be that fortunate!

Hi Kiwi,

The TNF inhibitors you mention (etanercept, infliximab) are known to enduce neuropathy. It is truly a crapper of a predicament as I think the inhibition of TNF could actually help where cytokines are the cause of nerve damage. But the risk is very real.

I think with immune deficiency issues it might be dangerous to use these drugs as they further dampen down the immune system.

It's all good fun!

From Wikipedia:

Causes[edit]
There are many possible causes of small fiber neuropathy. The most common cause is diabetes or glucose intolerance.[8] Other possible causes include hypothyroidism, Sjögren's syndrome, Lupus, vasculitis, sarcoidosis, nutritional deficiency, Celiac disease, Lyme disease, HIV, Fabry disease, amyloidosis and alcoholism.[9] A 2008 study reported that in approximately 40% of patients no cause could be determined after initial evaluation.[10] When no cause can be identified, the neuropathy is called idiopathic. A recent study revealed dysfunction of a particular sodium channel (Nav1.7) in a significant portion of the patient population with an idiopathic small fiber neuropathy.[11]

Recently several studies have suggested an association between autonomic small fiber neuropathy and postural orthostatic tachycardia syndrome.[12] Other notable studies have shown a link between erythromelalgia,[13] and fibromyalgia[14]

Small fiber peripheral neuropathy - Wikipedia, the free encyclopedia

Hugs, ElaineD