Rapid Normalization of High Glutamic Acid Decarboxylase Autoantibody Titers and Preserved Endogenous Insulin Secretion in a Patient with Diabetes Mellitus: A Case Report and Literature Review

Nobumasa Ohara; Masanori Kaneko; Tatsuo Furukawa; Tadashi Koike; Hirohito Sone; Shoichiro Tanaka; Kenzo Kaneko; Kyuzi Kamoi

doi:10.2169/internalmedicine.55.5398

CASE REPORTS

Rapid Normalization of High Glutamic Acid Decarboxylase Autoantibody Titers and Preserved Endogenous Insulin Secretion in a Patient with Diabetes Mellitus: A Case Report and Literature Review

Nobumasa Ohara, Masanori Kaneko, Tatsuo Furukawa, Tadashi Koike, Hirohito Sone, Shoichiro Tanaka, Kenzo Kaneko, Kyuzi Kamoi

Author information

Nobumasa Ohara
Department of Endocrinology and Metabolism, Nagaoka Red Cross Hospital, Japan
Department of Hematology, Endocrinology and Metabolism, Niigata University Faculty of Medicine, Japan
Masanori Kaneko
Department of Endocrinology and Metabolism, Nagaoka Red Cross Hospital, Japan
Department of Hematology, Endocrinology and Metabolism, Niigata University Faculty of Medicine, Japan
Tatsuo Furukawa
Department of Hematology, Nagaoka Red Cross Hospital, Japan
Tadashi Koike
Department of Hematology, Nagaoka Red Cross Hospital, Japan
Hirohito Sone
Department of Hematology, Endocrinology and Metabolism, Niigata University Faculty of Medicine, Japan
Shoichiro Tanaka
Third Department of Internal Medicine, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Japan
Kenzo Kaneko
Department of Endocrinology and Metabolism, Nagaoka Red Cross Hospital, Japan
Kyuzi Kamoi
Center of Diabetes, Endocrinology and Metabolism, Joetsu General Hospital, Japan

Keywords: diabetes mellitus, glutamic acid decarboxylase autoantibody, C-peptide, human leukocyte antigen, insulin therapy

JOURNAL OPEN ACCESS

2016 Volume 55 Issue 5 Pages 485-489

DOI https://doi.org/10.2169/internalmedicine.55.5398

Details

Abstract

A 59-year-old Japanese woman developed diabetes mellitus without ketoacidosis in the presence of glutamic acid decarboxylase autoantibody (GADA) (24.7 U/mL). After the amelioration of her hyperglycemia, the patient had a relatively preserved serum C-peptide level. Her endogenous insulin secretion capacity remained almost unchanged during 5 years of insulin therapy. The patient's GADA titers normalized within 15 months. The islet-related autoantibodies, including GADA, are believed to be produced following the autoimmune destruction of pancreatic beta cells and are predictive markers of type 1 diabetes mellitus. Therefore, the transient appearance of GADA in our patient may have reflected pancreatic autoimmune processes that terminated without progression to insulin deficiency.

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