Norb and Threads
I agree with what Norb says…that the biology of the immune system is certainly not black and white as suggested in the literature. The existance of plasma cells with CD20 and of B cells producing antibodies is understandable as explained by Threads, and, in my view, goes a long way towards explaining the variablility of results from treatment with Rituxan.
Consequently, rather than considering different types of IgM MGUS as I had suggested in an earlier posting (which would likely be too black and white), the disease is probably more of a progression with overlap between the sources of anti-MAG.
Norb…while looking for a definition of the units of measurement of anti-MAG titers, I came across the following paper. Had you seen it before? Is it worth trying to get a copy?
[B]Polyneuropathy associated with anti-MAG IgM antibodies[/B]
By: Mazen Dimachkie
Dr. Dimachkie has received honoraria from Merck and Pfizer for serving as a guest speaker.
Historical note and nomenclature
Anti-myelin associated glycoprotein antibodies were first described in 1980 in a patient with neuropathy and IgM monoclonal gammopathy (Latov et al 1980; Braun et al 1982). More than 200 patients with this syndrome subsequently have been described. Several studies have delineated the clinical, laboratory, electrodiagnostic, immunologic, pathologic, and therapeutic aspects of this condition (Latov et al 1988; Nobile-Orazio et al 1989; Ellie et al 1996; Chassande et al 1998; Nobile-Orazio et al 2000; Eurelings et al 2001; Gorson et al 2001).
Patients typically have an insidiously progressive, distal and symmetrical, sensory or sensorimotor neuropathy. The disorder usually afflicts men over the age of 60 years. Initial features include acral numbness, paresthesias, reduced proprioception, and Romberg sign. Sensory ataxia occurs in half of the cases and often is the most disabling symptom (Chassande et al 1998; Nobile-Orazio et al 1994; Nobile-Orazio et al 2000; Gorson et al 2001). Neuropathic pain is rarely a presenting feature but develops in a minority of patients as the condition advances (Gorson et al 2001). Sensory disturbances invariably begin in the feet in a stocking distribution and frequently involve all modalities, but vibration sensation and proprioception are preferentially affected. Strength is usually normal or only mildly affected at the outset, although as many as 50% of patients develop substantial weakness (Ellie et al 1996; van den Berg et al 1996; Gorson et al 2001). Deep tendon reflexes are absent or diminished (Ellie et al 1996). An intention tremor is common, may occur at any stage of the illness, and frequently becomes a disabling feature (Nobile-Orazio 1994; Pedersen et al 1997; Chassande et al 1998; Nobile-Orazio et al 2000). Cranial nerves and autonomic functions are rarely affected. A minority of patients have a fulminant, predominantly motor neuropathy with rapid progression, profound weakness, and fatal outcome (Antoine et al 1993; Van den Berg et al 1996).
I am still waiting to hear back from my neurologist about an anti-MAG test, and a visit to the hematologist. So no news on that front. Fingers are crossed.
Norb…you mention that you see no change in symptoms. Do you think that there has been a termination in the worsening of the symtoms? I hope so.