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A patient with type B insulin resistance syndrome, responsive to immune therapy

Nature Clinical Practice Endocrinology & Metabolism volume 3, pages 835–840 (2007)Cite this article

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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Figure 1: Changes in insulin requirements and blood glucose over time.

References

  1. Langouche L et al. (2007) Therapy Insight: the effect of tight glycemic control in acute illness. Nat Clin Pract Endocrinol Metab 3: 270–278

    Article  Google Scholar 

  2. Soop M et al. (2007) Stress-induced insulin resistance: recent developments. Curr Opin Clin Nutr Metab Care 10: 181–186

    Article  CAS  Google Scholar 

  3. Luna B and Feinglos M (2001) Drug-induced hyperglycemia. JAMA 286: 1945–1948

    Article  CAS  Google Scholar 

  4. Park-Wyllie L et al. (2006) Outpatient gatifloxacin therapy and dysglycemia in older adults. N Engl J Med 354: 1352–1361

    Article  CAS  Google Scholar 

  5. Yip C and Lee AJ (2006) Gatifloxacin-induced hyperglycemia: a case report and summary of the current literature. Clin Ther 28: 1857–1866

    Article  CAS  Google Scholar 

  6. Newcomer JW (2005) Second-generation (atypical antipsychotics) and metabolic effects. A comprehensive literature review. CNS Drugs 19: 1–93

    Article  CAS  Google Scholar 

  7. Kahn CR et al. (1976) The syndromes of insulin resistance and acanthosis nigricans. N Engl J Med 294: 739–745

    Article  CAS  Google Scholar 

  8. Arioglu E et al. (2002) Clinical course of the syndrome of autoantibodies to the insulin receptor (Type B insulin resistance): a 28-year perspective. Medicine 81: 87–100

    Article  CAS  Google Scholar 

  9. Taylor S et al. (1989) Syndromes of autoimmunity and hypoglycemia. Endocrinol Metab Clin North Am 18: 123–143

    Article  CAS  Google Scholar 

  10. Bao S et al. (2007) Type B insulin resistance syndrome associated with systemic lupus erythematosus. Endocr Pract 13: 51–54

    Article  Google Scholar 

  11. Magsino C and Spencer J (1999) Insulin receptor antibodies and insulin resistance. South Med J 92: 717–719

    Article  Google Scholar 

  12. Eriksson J et al. (1998) Successful treatment with plasmapheresis, cyclophosphamide, and cyclosporin A in type B syndrome of insulin resistance. Diabetes Care 21: 1217–1220

    Article  CAS  Google Scholar 

  13. Kawanishi Y et al. (1976) Successful immunosuppressive therapy in insulin resistant diabetes caused by anti-insulin receptor autoantibodies. J Clin Endocrinol Metab 44: 15–20

    Article  Google Scholar 

  14. Coll A et al. (2004) Rituximab therapy for the type B syndrome of insulin resistance. N Engl J Med 350: 310–311

    Article  CAS  Google Scholar 

  15. Gehi A et al. (2003) Treatment of systemic lupus erythematosus-associated type B insulin resistance syndrome with cyclophosphamide and mycophenolate mofetil. Arthritis Rheum 48: 1067–1070

    Article  Google Scholar 

  16. Fareau GG et al. (2007) Regression of acanthosis nigricans correlates with disappearance of anti-insulin receptor autoantibodies and achievement of euglycemia in type B insulin resistance syndrome. Metabolism 56: 670–675

    Article  CAS  Google Scholar 

  17. Flier JS et al. (1977) Autoantibodies to the Insulin Receptor. Effect on the insulin receptor interaction in IM-9 lymphocytes. J Clin Invest 60: 784–794

    Article  CAS  Google Scholar 

  18. Flier JS et al. (1976) Characterization of antibodies to the insulin receptor: a cause of insulin-resistant diabetes in man. J Clin Invest 58: 1442–1449

    Article  CAS  Google Scholar 

Download references

Acknowledgements

RN Kulkarni is supported by NIH grants RO1 DK67536 and P30DK 36836.

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Authors and Affiliations

  1. KA Page is a Clinical Endocrinology Fellow, KC Herold is a Professor of Immunology and SE Inzucchi is a Professor of Medicine, at the Yale School of Medicine, New Haven, CT, USA.,

    Kathleen A Page, Kevan C Herold & Silvio E Inzucchi

  2. S Dejardin is a Research Associate at the Joslin Diabetes Center, Boston, MA, USA.,

    Stephanie Dejardin

  3. CR Kahn is a Mary K Iacocca Professor of Medicine and RN Kulkarni is an Assistant Professor of Medicine, both at the Harvard School of Medicine, Boston, MA, USA.,

    C Ronald Kahn & Rohit N Kulkarni

Authors
  1. Kathleen A Page
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  2. Stephanie Dejardin
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Correspondence to Kathleen A Page.

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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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