title: Serum autoantibodies against sulfatide and phospholipid in NIDDM patients with diabetic neuropathy.
abstract: 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.
  
  
  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.
authors.affiliation: Osaka General Hospital of West Japan Railway Company, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Shigeta
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: K
authors.initials: K
authors.lastname: Nakano
authors.forename: H
authors.initials: H
authors.lastname: Obayashi
authors.forename: R
authors.initials: R
authors.lastname: Takemura
authors.forename: M
authors.initials: M
authors.lastname: Fukui
authors.forename: M
authors.initials: M
authors.lastname: Fujii
authors.forename: K
authors.initials: K
authors.lastname: Yoshimori
authors.forename: G
authors.initials: G
authors.lastname: Hasegawa
authors.forename: N
authors.initials: N
authors.lastname: Nakamura
authors.forename: Y
authors.initials: Y
authors.lastname: Kitagawa
authors.forename: M
authors.initials: M
authors.lastname: Kondo
mesh_terms: D000368:Aged; D017152:Antibodies, Antiphospholipid / Q000097:blood* / Q000276:immunology; D001323:Autoantibodies / Q000097:blood* / Q000276:immunology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000276:immunology*; D003929:Diabetic Neuropathies / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009431:Neural Conduction / Q000276:immunology / Q000502:physiology*; D010743:Phospholipids / Q000276:immunology; D013433:Sulfoglycosphingolipids / Q000097:blood / Q000276:immunology*
chemical_list: D017152:Antibodies, Antiphospholipid; D001323:Autoantibodies; D010743:Phospholipids; D013433:Sulfoglycosphingolipids