A patient with rapid metabolic deterioration mimicking the onset of fulminant type 1 diabetes during treatment for autoimmune type 1 diabetes

Junpei Yamamoto, Keizo Kaneko, Kei Takahashi, Chihiro Satake, Uiko Tsunoda, Hiroko Kohno, Shojiro Sawada, Yutaka Hasegawa, Kenji Uno, Junta Imai, Tetsuya Yamada, Yasushi Ishigaki, Yoshitomo Oka, Hideki Katagiri

Research output: Contribution to journalArticlepeer-review

Abstract

A 55-year-old man, recognized as having impaired glucose tolerance three years earlier, presented with an HbA1c (JDS) of 11 %. Sulfonylurea plus α-glucosidase inhioitor treatment was started, resulting in a decrease in HbA1c to 6.6 % two months later. However, since GAD (glutamic acid decarboxylase) antibodies were positive, he was diagnosed as having autoimmune type 1 diabetes and his treatment regimen was switched to intensive insulin therapy. Ten U/day of insulin effectively controlled his metabolic state for about 40 days: preprandial SMBG (self-monitoring of blood glucose) levels were approximately 100 mg/dl. However, despite the absence of known triggers including dietary conditions, he developed sudden abdominal fullness, thirst and polyuria and preprandial SMBG levels rose rapidly to more than 300 mg/dl for ten days. On admission, though he had already started insulin therapy, clinical findings met the diagnostic criteria for fulminant type 1 diabetes. At the time of discharge, 36 U/day of insulin were needed for glycemic control. In this case, SMBG enabled us to demonstrate rapid metabolic deterioration, mimicking the onset of fulminant type 1 diabetes, despite good control of autoimmune type 1 diabetes.

Original languageEnglish
Pages (from-to)122-128
Number of pages7
JournalJournal of the Japan Diabetes Society
Volume55
Issue number2
Publication statusPublished - 2012 Feb 1

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Fingerprint Dive into the research topics of 'A patient with rapid metabolic deterioration mimicking the onset of fulminant type 1 diabetes during treatment for autoimmune type 1 diabetes'. Together they form a unique fingerprint.

Cite this