OBJECTIVE: We investigated the presence of antisulfatide and antiphospholipid antibodies and the relationship between these antibodies and the results of quantitative tests of nerve function in NIDDM patients with diabetic neuropathy. RESEARCH DESIGN AND METHODS: Antisulfatide and antiphospholipid antibodies were measured in serum samples obtained from 68 NIDDM patients with diabetic neuropathy by an enzyme-linked immunosorbent assay (ELISA). Each patient was classified into one of three groups based on the combined neuropathy score (determined by the symptom score, the results of autonomic nerve function tests, and the vibration perception test), as follows: mild (n = 26), moderate (n = 22), and severe (n = 20). Nerve conduction studies were performed in a subgroup of 37 patients. RESULTS: The antisulfatide antibody was detected in 1 (4%) of 26 patients in the mild group, 4 (18%) of 22 patients in the moderate group, and 8 (40%) of 20 patients in the severe group (P < 0.01 vs. mild group). The antiphospholipid antibody was detected in none of the patients in the mild group, 8 (36%) of 22 patients in the moderate group (P < 0.001 vs. mild group), and 6 (30%) of 20 patients in the severe group (P < 0.01 vs. mild group). The threshold amplitude, determined by the vibration perception test, was significantly higher in antibody-positive patients than in antibody-negative patients: antisulfatide antibody, 55.9 +/- 46.8 microns (n = 13) vs. 22.9 +/- 13.7 microns (n = 55), P < 0.001; antiphospholipid antibody, 47.2 +/- 32.5 microns (n = 14) vs. 24.5 +/- 23.2 microns (n = 54), P < 0.01. The conduction velocity of the sural nerve was slower in the antisulfatide antibody-positive group (37.9 +/- 11.1 m/s, n = 12) than in the antisulfatide antibody-negative group (45.2 +/- 6.0 m/s, n = 19) (P < 0.05). CONCLUSIONS: These results suggest that autoimmune nerve destruction may be involved in diabetic neuropathy in NIDDM patients.
OBJECTIVE: We investigated the presence of antisulfatide and antiphospholipid antibodies and the relationship between these antibodies and the results of quantitative tests of nerve function in NIDDMpatients with diabetic neuropathy. RESEARCH DESIGN AND METHODS: Antisulfatide and antiphospholipid antibodies were measured in serum samples obtained from 68 NIDDMpatients with diabetic neuropathy by an enzyme-linked immunosorbent assay (ELISA). Each patient was classified into one of three groups based on the combined neuropathy score (determined by the symptom score, the results of autonomic nerve function tests, and the vibration perception test), as follows: mild (n = 26), moderate (n = 22), and severe (n = 20). Nerve conduction studies were performed in a subgroup of 37 patients. RESULTS: The antisulfatide antibody was detected in 1 (4%) of 26 patients in the mild group, 4 (18%) of 22 patients in the moderate group, and 8 (40%) of 20 patients in the severe group (P < 0.01 vs. mild group). The antiphospholipid antibody was detected in none of the patients in the mild group, 8 (36%) of 22 patients in the moderate group (P < 0.001 vs. mild group), and 6 (30%) of 20 patients in the severe group (P < 0.01 vs. mild group). The threshold amplitude, determined by the vibration perception test, was significantly higher in antibody-positive patients than in antibody-negative patients: antisulfatide antibody, 55.9 +/- 46.8 microns (n = 13) vs. 22.9 +/- 13.7 microns (n = 55), P < 0.001; antiphospholipid antibody, 47.2 +/- 32.5 microns (n = 14) vs. 24.5 +/- 23.2 microns (n = 54), P < 0.01. The conduction velocity of the sural nerve was slower in the antisulfatide antibody-positive group (37.9 +/- 11.1 m/s, n = 12) than in the antisulfatide antibody-negative group (45.2 +/- 6.0 m/s, n = 19) (P < 0.05). CONCLUSIONS: These results suggest that autoimmune nerve destruction may be involved in diabetic neuropathy in NIDDMpatients.
Authors: Jasper M Morrow; Shirley D'Sa; Rupert A Page; Mahir Al Hilali; Michael P Lunn; Mary M Reilly Journal: J Neurol Date: 2011-09-02 Impact factor: 4.849
Authors: P Gargiulo; J Goldberg; B Romani; R Schiaffini; P Ciampalini; W P Faulk; J A McIntyre Journal: Clin Exp Immunol Date: 1999-10 Impact factor: 4.330