Transverse Myelitis - ANTI-RO (SSA-RO52)

[Mike Bartolatz]

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Transverse Myelitis Association
Journal Volume 1 - January 2006

Article 7 The Presence of Anti-Ro (SSA) Autoantibodies in Recurrent Transverse Myelitis
Chitra Krishnan, M.H.S.
Research Associate
Johns Hopkins Transverse Myelitis Center

This article was originally published in NEUROLOGY 2004; 62:147–149. Copyright © 2004 by AAN Enterprises, Inc. 147

Hopkins researchers report an association between recurrent Tranvserse Myelitis (TM) and anti-Ro autoantibodies. The association of this unique clinical phenotype (visible characteristics that result from a combination of genetic and environmental factors) and a specific autoantibody provides circumstantial evidence that an autoimmune process has pathologic (possible explanation of the cause) importance in recurrent TM.

Transverse myelitis (TM) is a rare inflammatory disorder of the spinal cord that can be idiopathic or associated with a specific disease such as systemic lupus erythematosus (SLE), Sjögren syndrome, and antiphospholipid antibody syndrome. Typically TM is monophasic; however, some patients develop recurrent TM without any identifiable associated disease. The study reported an association between anti-Ro antibodies and recurrent TM, which suggests that the mechanism of spinal cord injury may be autoimmune in nature. In this retrospective case-control study, antibodies to 52-kd Ro were demonstrated in 77% of recurrent cases (10/13) compared with only 33% of control subjects (4/12).

In this study, recurrence was defined as more than one episode of TM separated in time with intervening improvement both clinically and radiologically. Patients were excluded if they had evidence of multiple sclerosis (defined as demyelinating lesions on MRI of the brain at presentation or in follow-up). All control cases were diagnosed as either idiopathic monophasic TM (five), idiopathic monophasic myelopathy (four), recurrent transverse myelopathy (one), or disease-associated TM (two). They were also evaluated during intercritical periods at the center.

Anti-Ro (SSA) is the name of an autoantibody in the blood. An autoantibody is a protein that binds to your own tissue/cells. Normal people do not have autoantibodies. The B lymphocytes that make antibodies make them only to foreign substances, like viruses or bacteria, in order to eradicate the infection. In people with an autoimmune disorder, the B lymphocytes make antibodies to self tissue/cells. NMO-IgG is an example of an autoantibody (associated with Neuromyelitis Optica or Devic’s disease). ANA is another example of an autoantibody. SSA is a particular autoantibody that is highly associated with (but is not specific for) Sjogren's syndrome.

An autoantibody can be directly harmful to a cell or tissue, or more commonly is not directly harmful, but is the flag that denotes a person has a deranged immune system. So, our hypothesis was that if you have the presence of an autoantibody in your blood, that you have an 'autoimmune' immune system and therefore would be more likely to have recurrent disease. Further, that people with monophasic TM had a one-time trick of the immune system but did not have time to develop autoantibodies by the time the immune system corrected itself.

Interestingly, while some patients with SSA do have full-blown Sjogren's syndrome, many of our recurrent TM SSA+ patients (positive for the presence of SSA) do not have the full syndrome (dry eyes, dry mouth, artificial tears – symptoms of Sjogren's syndrome). The ramifications are that if a person has TM and SSA, we watch them more closely for recurrent disease.

Further, anti-Ro antibodies are postulated to directly cause injury to the fetal heart tissue, leading to congenital heart block of the newborn. As with other autoimmune phenomena, these antibodies may be directly pathogenic or may be a marker of the key pathogenic event that results in the specific phenotype, in this case, spinal cord inflammation.

Therefore, patients with idiopathic recurrent TM represent a unique clinical phenotype and that the pathogenesis (the cause, development, and effects of a disease) is immunologic in nature and may associate with anti-Ro antibodies.

There are several possible clinical and pathologic implications of the association of anti-Ro antibody and recurrent TM. First, the presence of these antibodies in patients who present with their first episode of TM may be predictive of recurrence. Second, patients with idiopathic TM may have an incomplete expression of a connective tissue disorder. Last, patients with autoantibodies may respond to immunosuppressive therapy, including maintenance therapy to prevent recurrences of TM.

The strengths of this retrospective analysis include a case-control design with a large number of patients with this rare disease. A prospective study of a larger population with recurrent TM is now underway at our center to better define the associated serologic and clinical features of these patients.

Orginal Research Paper:

L.K. Hummers, MD; C. Krishnan, MHS; L. Casciola–Rosen, PhD; A. Rosen, MBChB; S. Morris, MS; J.A. Mahoney, PhD; D.A. Kerr, MD, PhD; and F.M. Wigley, MD. 2004. Recurrent transverse myelitis associates with anti-Ro (SSA) autoantibodies. Neurology; 62: 147-149.

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