title: Glucose variability before and after treatment of a patient with Graves' disease complicated by diabetes mellitus: assessment by continuous glucose monitoring.
abstract: A 48-year-old woman was diagnosed and treated for Graves' disease (GD) in 1999 but she discontinued treatment at her own discretion. In 2011, she was admitted to a local hospital for management of thyrotoxic crisis. Treatment with propylthiouracil, iodide potassium (KI), and prednisolone (PSL) was started, which resulted in improvement of the general condition. PSL and KI were discontinued before she was transferred to our hospital. At the local hospital, fasting plasma glucose (FPG) was 212 mg/dL and hemoglobin A1c concentration was 11.2%; intensive insulin therapy had been instituted. Upon admission to our hospital, FPG level was 122 mg/dL, but insulin secretion was compromised, suggesting aggravation of thyroid function and deterioration of glycemic control. The FPG level increased to 173 mg/dL; continuous glucose monitoring (CGM) identified dawn phenomenon at approximately 0400 h. Resumption of KI resulted in improvement of FPG and disappearance of the dawn phenomenon, as assessed by CGM. These results indicate that in patients with compromised insulin secretion, hyperthyroidism can induce elevation of not only postprandial blood glucose, but also FPG level due to the dawn phenomenon and that the dawn phenomenon can be alleviated with improvement in thyroid function. To our knowledge, no studies have assessed glucose variability by CGM before and after treatment of Graves' disease. The observations made in this case shed light on the understanding of abnormal glucose metabolism associated with Graves' disease.
authors.affiliation: First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushyu 807-8555, Japan.
authors.forename: Keiichi
authors.initials: K
authors.lastname: Torimoto
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Okada
authors.forename: Tadashi
authors.initials: T
authors.lastname: Arao
authors.forename: Hiroko
authors.initials: H
authors.lastname: Mori
authors.forename: Sunao
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Manabu
authors.initials: M
authors.lastname: Narisawa
authors.forename: Akira
authors.initials: A
authors.lastname: Kurozumi
authors.forename: Yoshiya
authors.initials: Y
authors.lastname: Tanaka
mesh_terms: D013956:Antithyroid Agents / Q000627:therapeutic use; D001786:Blood Glucose / Q000032:analysis*; D057210:Delayed Diagnosis; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy; D016903:Drug Monitoring; D004359:Drug Therapy, Combination; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006111:Graves Disease / Q000097:blood / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000378:metabolism; D061267:Insulin Aspart / Q000627:therapeutic use; D000069036:Insulin Glargine; D000078790:Insulin Secretion; D049528:Insulin, Long-Acting / Q000627:therapeutic use; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism; D008875:Middle Aged; D018670:Monitoring, Ambulatory; D011193:Potassium Iodide; D011441:Propylthiouracil / Q000627:therapeutic use; D013958:Thyroid Crisis / Q000209:etiology; D013961:Thyroid Gland / Q000187:drug effects* / Q000503:physiopathology; D016896:Treatment Outcome
chemical_list: D013956:Antithyroid Agents; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D061267:Insulin Aspart; D000069036:Insulin Glargine; D049528:Insulin, Long-Acting; D011193:Potassium Iodide; D011441:Propylthiouracil