Diabetes associated with Guillain-Barre syndrome.
Transient diabetes is not recognized as one of the known metabolic complications of acute inflammatory polyradiculopathy or Guillain-Barré syndrome (GBS). Four patients are described who developed this disorder during the paralytic phase of their illness and one who was hyperinsulinaemic but not hyperglycaemic. The mean age of the patients was 34.4 yr. No patient received steroids and three were ventilated. The mean cerebrospinal fluid protein concentration was 1.6 g/l. Two patients required short term insulin therapy. Four had intravenous glucose tolerance tests performed acutely (AP) and after one month (1 M). Three had a repeat study after long term follow-up. One subject had increased his Body Mass Index from 23.8-26.8 and therefore his IVGTT reflected insulin resistance. The other three patients had elevated basal glucose during GBS and similar first phase glucose response to IVGTT. The mean fasting glucose was 6.9 mmol/l (AP), 3.9 mmol/l (1 M) and 4.4 mmol/l at 6 yr. The mean fasting insulin was 114.9 pM/l (AP), 114.9 pM/l (1 M) and 25.9 pM/l (6 yr). The mean fasting C-peptide was 1.3 nmol/l (AP), 1.0 nmol/l (1 M) and 0.5 nmol/l (6 yr). Homeostatic modelling of the paired insulin and C-peptide data show a trend consistent with the hypothesis that insulin resistance is the dominant feature of impaired glucose tolerance in Guillain-Barre syndrome.
Flax
H
H
Diabetes Research Laboratories, Radcliffe Infirmary, Oxford, UK.
Matthews
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DR
D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D003920:Diabetes Mellitus / Q000097:blood / Q000209:etiology*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D011129:Polyradiculoneuropathy / Q000097:blood / Q000150:complications*
D001786:Blood Glucose; D007328:Insulin