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Insulin Receptor Autoantibodies in Sepsis
[ill]udy A. Spitzer, PhD;
Paul R. Hastings, MD;
[ill]tephen H. Leech, MB, ChB, PhD, FRCP(C)
Arch Intern Med. 1984;144(10):2019-2022.
Abstract
• This study was undertaken to investigate possible factors [ill]ontributing to altered glucose homeostasis in a patient with a [ill]story of total pancreatectomy and intermittent sepsis. Blood [ill]as drawn when the patient had received no exogenous [ill]sulin for the previous 24 hours, had a serum insulin level of [ill]3 µU/mL, and gave an inappropriately low glucose response [ill]large amounts of infused glucose. The IgG fraction prepared [ill]om this serum stimulated glucose oxidation in vitro and [ill]hibited binding of insulin labeled with I 125 to isolated rat [ill]dipocytes, thus fulfilling some of the criteria for autoan[ill]bodies to the insulin receptor. The results are compatible with [ill]e hypothesis that insulin-receptor autoantibodies may have [ill]eveloped as a result of perturbation of this patient's immune [ill]tatus promoted by intermittent septic episodes and that, [ill]eterminally, as these antibodies converted in vivo to their in [ill]tro—type behavior, they may have been partially responsible [ill]or the severe disturbances of glucose homeostasis.
(Arch Intern Med 1984;144:2019-2022)
Author Affiliations
From the Departments of Physiology (Dr Spitzer), Medicine (Drs Spitzer [ill]d Leech), and Surgery (Dr Hastings), Louisiana State University Medical [ill]enter, New Orleans.
Footnotes
Accepted for publication March 15, 1984.
Read before the annual meeting of the Southern Section, American [ill]deration for Clinical Research, New Orleans, Jan 14, 1982.
Reprint requests to Louisiana State University Medical Center, 1901 [ill]erdido St, New Orleans, LA 70112 (Dr Spitzer).
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