title: A patient with type B insulin resistance syndrome, responsive to immune therapy.
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 HbA(1c) level was 8.1% on approximately 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.
  
  
  METHODS
  The patient's serum creatinine level was 301 micromol/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.
  
  
  METHODS
  Type B insulin resistance syndrome.
  
  
  RESULTS
  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 (HbA(1c) 5.8%) with an average of 60 U of isophane insulin twice daily.
authors.affiliation: Section of Endocrinology, Department of Internal Medicine, Yale School of Medicine, New Haven, CT 06520-8020, USA. kathleen.page@yale.edu
authors.forename: Kathleen A
authors.initials: KA
authors.lastname: Page
authors.forename: Stephanie
authors.initials: S
authors.lastname: Dejardin
authors.forename: C Ronald
authors.initials: CR
authors.lastname: Kahn
authors.forename: Rohit N
authors.initials: RN
authors.lastname: Kulkarni
authors.forename: Kevan C
authors.initials: KC
authors.lastname: Herold
authors.forename: Silvio E
authors.initials: SE
authors.lastname: Inzucchi
mesh_terms: D001323:Autoantibodies / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D003131:Combined Modality Therapy; D003404:Creatinine / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000276:immunology / Q000628:therapy*; D003937:Diagnosis, Differential; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000627:therapeutic use; D007328:Insulin / Q000008:administration & dosage / Q000097:blood / Q000627:therapeutic use; D007333:Insulin Resistance; D008875:Middle Aged; D010956:Plasmapheresis / Q000379:methods; D011241:Prednisone / Q000008:administration & dosage / Q000627:therapeutic use; D011972:Receptor, Insulin / Q000276:immunology; D013577:Syndrome
chemical_list: D001323:Autoantibodies; D001786:Blood Glucose; D003404:Creatinine; D005938:Glucocorticoids; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D011241:Prednisone; D011972:Receptor, Insulin