Human T-cell lymphotropic virus type-I associated myelopathy complicated by optic neuritis.

A 48-year-old Japanese woman from Kyushu was admitted to the Nippon Medical School First Hospital with complaints of numbness in both legs, gait disturbance, and urinary problems. On examination, her lower extremities were spastic with increased reflexes and positive Babinski sign. Sensation was absent below the T4 spinal level. The cerebrospinal fluid contained HTLV-I antibodies and she was diagnosed with HTLV-I associated myelopathy. Her symptoms were resolved with prednisolone, but six months later a visual disturbance of the left eye edema developed. Orbital CT scans showed that left optic nerve was edematous. T2 enhanced MRI revealed a high intensity lesion of the left optic nerve. ERG was normal and no VEP was detected in response to flashing stimulation to the left eye. The HTLV-I antigen titer of CBF was very high. Her optic neuritis improved following oral administration of prednisolone and retrobulbar injections of dexamethasone. This is the first case report of HTLV-I associated myelopathy complicated by optic neuritis.

Determination of complement breakdown fragments C3d and its subfragments in health and disease.

The breakdown products of the third component of complement in approximately 400 samples were measured by rocket immunoelectrophoresis and two-dimensional electrophoresis using the method of Brandslund et al [3]. It was confirmed that the measurement of the C3d level provides useful information on increased C3 consumption irrespective of the synthetic rate. Furthermore, three subfragments with C3d but without C3c antigenicity were distinguished, which were designated as C3d1, C3d2, and C3d3. The subfragment C3d3 which migrated to the most anodal side was a predominant component in the plasma from patients with autoimmune diseases. Little C3d3 subfragment was detected in normal plasma and in normal sera incubated in vitro for 24 hr. Even in the normal sera converted completely in vitro which contained little intact C3, only a limited amount of C3d3 was detected. In the plasma from postsurgical patients in whom activation of the complement system was considered to be in an acute phase, C3d3 was detected, but the C3d2 level was higher than the C3d3 level. In the plasma from patients with systemic lupus erythematosus having the normal C3d level, C3d3 was a major fragment. It is predicted that the preponderant presence of C3d3 in plasma could be the result of chronic continuous complement activation by immune complexes.