An IgA PDNer thinking forum aloud.
I have been following this thread since Allaug started it way back in May 2006! As an IgA PDN sufferer for almost 15 years I have felt to be a sort of intruder but the discussion about T cells and B cells has come together for me as my experience has taken a sharp downhill turn in the past year.
Allaug has graciously stated that she had learned from me and my website but I have been learning from her and all of you. Here is my thinking aloud. >
From my own PDN website. “Paraprotein or monoclonal gammopathy is the presence in the blood/serum of an abnormal amount of any single type of protein/antibody/immunoglobulin.
WHAT CAUSES THE PARAPROTEIN? The anti-body producing plasma cells in the bone marrow or lymphoid organs have gone out of control. They have expanded to form benign or malignant tumours. These are, so to speak, locked in an “on” position and secrete or spew out clones of the same, single antibody (or immunoglobulin). This process is known as Monoclonal Gammopathy.”
As a matter of information I had gall bladder surgery by keyhole process in mid-February 1993 and in May a small calcaneal spur removal on my left heel. On the time scale of the monoclonal gammopathy and neuropathy occurring I have sometimes wondered.
As has been said on this thread when discussing anti-MAG IgM PDN/MGUS this cloning results from one single damaged B-cell getting out of control and the cloning to create a proliferation of monoclonal antibodies over the years – in my case of IgA antibodies and since mid-June 1993. Although the pathogenesis (what happened) is not clear about IgA PDN/MGUS neuropathy it seems possible or even probable that there was an immune reaction to an antigen, possibly a bacteria, targeted by IgA rather than IgG and my peripheral nerve myelin was attacked. The havoc was limited to my feet and mainly to the sensory nerves, but over 14+ years pain has increased, greatly in very recent years, and walking has become disabled in the past 8 months being severely limited by the muscles cramping much more than previously as the motor nerves are sending chaotic messages to my feet.
As I have indicated on another recent thread there is a relationship between my IgA PDN and anti-MAG PDN/MGUS associated demyelinating neuropathy.
Some IgA PDN/MGUS associated demyelinating neuropathy sufferers ‘can show features similar to anti-MAG IgM patients’. (Cocito et al 2003.)
A joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society reported in ‘Guidelines on management of paraproteinaemic demyelinating neuropathies’ that “a minority of patients with IgG or IgA PDN have the DADS clinical phenotype (observable characteristics) and associated electrophysiological features”.
Most patients with IgM PDN have DADS clinical phenotype most strongly associated with anti-MAG antibodies. The phenotype is distal (away from the centre point of attachment), acquired demyelinating symmetrical. It is chronic, slowly progressive, symmetric, predominantly sensory involvement, relatively mild or no weakness, ataxia and often tremor.
That description is closely similar to my IgA PDN clinical and my experienced characteristics. Mainly sensory, mild or little weakness, symmetric, slowly progressive. No tremor initially but I have some now, but that could be age related – now 80+ compared with 65 at onset.
I am in mid-spell of the half life of IVIg after 5 days infusions 3 weeks ago. No significant change yet. IVIg targets the T-cells? So perhaps I need treatment targetting the rogue b-cells? It has been helpful to some of you be you anti-MAG IgM or CIDP in some cases.
Your comments please.:confused: