Abstract
Background A 55-year-old woman with vitiligo, hypothyroidism, interstitial lung disease and diabetes mellitus developed severe insulin resistance during a hospital admission for respiratory failure. Before hospitalization, her HbA1c level was 8.1% on ∼100 U/day of insulin. Her interstitial lung disease had been treated with glucocorticoids, but after their withdrawal her insulin requirements had increased dramatically. She remained hyperglycemic (blood glucose levels 16.7–27.8 mmol/l), despite intravenous insulin at doses as high as 30,000 U/day.
Investigations The patient's serum creatinine level was 301 µmol/l and her liver function tests were normal. A mildly elevated white cell count was present. The patient was diagnosed with pneumonia due to Pseudomonas aeruginosa. When the patient's plasma glucose level was 22.5 mmol/l, her plasma C-peptide level was 0.9 nmol/l and her serum insulin level was 294 pmol/l. At that time the patient was on 2,600 U/day of intravenous insulin aspart. Anti-insulin and anti-islet-cell antibodies were not detected, but anti-insulin-receptor antibodies were found.
Diagnosis Type B insulin resistance syndrome.
Management The patient's insulin resistance responded to glucocorticoids and plasmapheresis. After the patient was treated with prednisone (60 mg/day), her insulin requirements decreased within 1 week to pre-admission doses. When steroids were subsequently discontinued, glycemic control deteriorated once again. Plasmapheresis was initiated, inducing a striking acute decline in insulin needs. On a maintenance dose of 10 mg prednisone/day, glucose control improved (HbA1c 5.8%) with an average of 60 U of isophane insulin twice daily.
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Acknowledgements
RN Kulkarni is supported by NIH grants RO1 DK67536 and P30DK 36836.
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Page, K., Dejardin, S., Kahn, C. et al. A patient with type B insulin resistance syndrome, responsive to immune therapy. Nat Rev Endocrinol 3, 835–840 (2007). https://doi.org/10.1038/ncpendmet0693
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DOI: https://doi.org/10.1038/ncpendmet0693
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