POLYNEUROPATHIES ASSOCIATED WITH HIGH-TITER ANTISULPHATIDE ANTIBODIES- CHARACTERISTICS OF PATIENTS WITH AND WITHOUT SERUM MONOCLONAL PROTEINS

Objectives-Previous studies of small numbers of patients have shown th at antisulphatide autoantibodies are associated with polyneuropathies having a prominent sensory component. However, clinical and electrodia gnostic features are variable. The range of clinical and electrodiagno stic findings in 19 patients with polyneuropathies and high titre (> 4 500) serum IgM antisulphatide antibodies is described, together with t esting for serum monoclonal (M) proteins. Methods-About 20 000 serum s amples that were referred to the clinical laboratory from 1990 to the end of 1994 were screened by enzyme linked immunosorbent assay (ELISA) for specific high titre antisulphatide antibodies. The clinical and e lectrodiagnostic data in 23 patients with positive results were review ed. IgM binding to peripheral nerve structures was also evaluated in t hese patients. Results-Nineteen patients had predominantly distal, sym metric pansensory loss. Patients with IgM antisulphatide antibodies an d no serum M protein usually had clinical syndromes that included: (I) neuropathic pain or dysaesthesiae, (2) no functionally significant we akness, and (3) an axonal neuropathy on electrodiagnostic testing. On immunocytochemical studies serum IgM from the patients without M prote ins usually (nine of 10; 90%) bound to peripheral nerve axons, but nev er to myelin. Patients with antisulphatide antibodies and a serum M pr otein, usually IgM, were more likely than patients without a serum M p rotein, to have syndromes with: (1) no pain or dysaesthesiae, (2) moto r abnormalities, and (3) a demyelinating polyneuropathy by electrodiag nostic criteria. In immunocytochemical studies serum IgM most often bo und to either peripheral nerve myelin or endoneurial structures. Concl usion-Patients with polyneuropathy and high titre serum IgM antisulpha tide antibodies can be classified into subgroups according to the pres ence or absence of a serum M protein. Patients without an M protein ar e more likely to have pure sensory syndromes, pain, an axonal neuropat hy, and serum IgM binding to axons. Patients with a serum M protein co mmonly had syndromes with prominent motor involvement, no pain, and a demyelinating neuropathy.