A-23-year-old woman with
systemic lupus erythematosus (SLE) and on
hemodialysis for 5 years was admitted to the hospital because of severe general
fatigue. On admission, laboratory findings showed that fasting plasma
glucose levels ranged from 25 â 45 mg/dl, a test for
antinuclear antibody (ANA) was positive (1 : 320, with a discrete-speckled pattern), serum C3 and
C4 complement and CH50 level were remarkably depressed (22.5 mg/dl, < 5.1 mg/dl, < 13 U/ml, respectively), and
insulin receptor antibodies were present (89.3% inhibition of 125I-
insulin binding to cultured human lymphocytes by a binding inhibition assay). She also showed
acanthosis nigricans. The patient was diagnosed to suffer from a Type
B insulin resistance syndrome. The patient's serum
insulin and
C-peptide levels were markedly elevated during
hypoglycemia without
insulinoma (2,313.8 microU/ml, 55 ng/ml, respectively). Interestingly, not only
postprandial hyperglycemia but also
fasting hypoglycemia was observed. Treatment with
steroid pulse and subsequent high dose of
prednisolone resulted in restoration of euglycemia associated with disappearance of
insulin receptor antibodies and improvement of both serum hypocomplementemia and the high titer of ANA. Later, the patient's course was complicated by
hemorrhagic shock due to
duodenal ulcer and she died of subsequent
pneumocystis carinii pneumonia. The presented patient developed a Type
B insulin resistance syndrome induced by increased activity of SLE after she had been treated with
hemodialysis for 5 years. This is the first reported case with such a history and constellation. It is recommended that SLE patients on dialysis are carefully followed-up by clinical and serological monitoring. Type
B insulin resistance syndrome must be considered in the differential diagnosis of
hypoglycemia in SLE patients on dialysis.