Endocrinol Metab.  2011 Dec;26(4):360-363. 10.3803/EnM.2011.26.4.360.

A Case of the Type B Insulin Resistance Syndrome with Chronic Hepatitis B

• Choi HS
• Choi BH
• Jeong SH
• Choi SH
• Shin DS
• Kim SH
• Eom YS
• Lee S
• Kim YS
• Park IB
• Lee KY

• KMID: 2169270
• DOI: http://doi.org/10.3803/EnM.2011.26.4.360

Abstract

Type B insulin resistance syndrome is rare autoimmune disease that is characterized by various abnormalities of glycemic homeostasis, from hyperglycemia caused by extreme insulin resistance to fasting hypoglycemia. It can combine with other autoimmune diseases, most commonly systemic lupus erythematosus. It usually occurs in women and accompanies acanthosis nigricans, hyperandrogenism, and, in many cases, ovary dysfunction. The diagnosis of type B insulin resistance syndrome is based largely on the presence of insulin receptor autoantibodies and hyperglycemia, or hypoglycemia and hyperinsulinemia. In some cases, patients with the type B insulin resistance have been successfully treated with immunosuppressive therapy and plasmapheresis. We experienced type B insulin resistance syndrome in a patient with chronic hepatitis B and used only plasmapheresis for treatment. The immunosuppressive therapy was omitted due to the state of activation of chronic hepatitis B. We present this case with a review of relevant literature.

Keyword

Insulin receptor antibody; Plasmapheresis; Type B insulin resistance syndrome

MeSH Terms

Acanthosis Nigricans
Autoantibodies
Autoimmune Diseases
Female
Hepatitis B, Chronic
Hepatitis, Chronic
Homeostasis
Humans
Hyperandrogenism
Hyperglycemia
Hyperinsulinism
Hypoglycemia
Insulin
Insulin Resistance
Lupus Erythematosus, Systemic
Ovary
Plasmapheresis
Receptor, Insulin
Autoantibodies
Insulin
Receptor, Insulin

Figure

• 

  Fig. 1 Serum glucose change during plasmapheresis. X axis indicates days, we started plasmapheresis on day 1 and performed plasmapheresis nine times more during 2 weeks. Square spots is the day that plasmapheresis was done. Y axis indicates serum glucose level (mg/dL). After first and eighth plasmpheresis, rapid decrease of serum glucose level is showed. But hyperglycemia was developed subsequently. Eventually serum glucose was not controlled.

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