Fulminating Onset Type 1 Diabetes with Positivity for Anti-GAD Antibody and Elevated Pancreatic Exocrine Enzyme Concentrations

Kahara, Toshio; Takamura, Toshinari; Ando, Hitoshi; Sakurai, Masaru; Ota, Tsuguhito; Misaki, T; Oba, Sakae; Iguchi, Masaharu; Komori, Kazutoshi; Kobayashi, Kenichi

doi:10.2169/internalmedicine.42.517

Cited by 7 publications

(5 citation statements)

References 13 publications

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“…However, high serum pancreatic enzyme levels cannot rule out the presence of autoimmune type 1 diabetes, as it has been shown that 10% of newly diagnosed type 1 diabetic patients in Belgium and a Japanese patient diagnosed with fulminant-onset type 1 diabetes had elevated pancreatic exocrine enzyme concentrations along with clear signs of autoimmune abnormalities (i.e., GAD autoantibodies, etc.) (21,22).…”

Section: Type 1 Diabetes: a Chronic Inflammatory Disease Of The Isletsmentioning

confidence: 99%

The Heterogeneity of Diabetes

2007

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Diabetes is an emblematic example of a heterogeneous disease. Systemic inflammation has emerged as a prominent factor in the type 2 diabetes pathoetiology, but it remains ill-defined in type 1 diabetes. There is a wide spectrum of associations between inflammatory responses and diabetic syndromes. At one end of this spectrum, there is type 1 diabetes for which there is convincing evidence that chronic inflammation of pancreatic islets is a central aspect of disease pathogenesis. At the opposite end, is type 2 diabetes that is clearly associated with systemic inflammation, which could be either the cause or simply mark the underlying pathology. Accumulating evidence has substantiated that a subgroup of adult patients clinically diagnosed with type 2 diabetes exhibit autoantibody responses to islet autoantigens. The presence of these immunologic abnormalities is associated with a severe insulin secretory defect and the absence of signs of systemic inflammation as documented by plasma C-reactive protein and fibrinogen levels that are comparable with those of control populations. Islet autoantibody evaluation should be part of the diagnostic assessment for clinically diagnosed type 2 diabetes not only because it might predict the rate of progression to insulin requirement in adult populations but also to identify a pathogenically distinct disease phenotype characterized by the absence of systemic inflammation and its related disorders. A more appropriate characterization of this subgroup of clinically diagnosed type 2 diabetes, diabetes of autoimmune pathogenesis, will promote future research into the etiology, natural history, and treatment.

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Section: Type 1 Diabetes: a Chronic Inflammatory Disease Of The Isletsmentioning

confidence: 99%

The Heterogeneity of Diabetes

2007

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“…here we report a 63-year-old case of abrupt onset autoimmune type 1 diabetes, mimicking FT1DM. in addition to the above mentioned two autoimmune cases [6,7], the present case draws an attention in terms of differential diagnosis between typical FT1DM and this rapidly progressive form of autoimmune type 1 diabetes. …”

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confidence: 76%

“…although FT1DM is basically classified into type 1B diabetes as indicated by absence of islet-related autoantibodies, two atypical cases showing the mixed characteristics of FT1DM and autoimmune type 1 diabetes (i.e. anti-GaD antibody positivity) have been reported [6,7].…”

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confidence: 99%

A Case of Abrupt Onset Autoimmune Type 1 Diabetes Mimicking Fulminant Type 1 Diabetes

et al. 2009

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Abstract.A 63-year-old male was admitted to our hospital with diabetic ketoacidosis. He had flu-like symptoms 10 days before admission and developed thirst, polyuria and anorexia with 9 kg of body weight loss in a week. Plasma glucose level on admission was 983 mg/dL and hba1c was 7.5%. Despite high levels of serum pancreatic enzymes, lack of severe abdominal pain and no morphological change of pancreas in the abdominal CT scan eliminated the complication of classical acute pancreatitis. These findings suggested the diagnosis of fulminant type 1 diabetes. However, urinary and plasma C-peptide levels showed that insulin secretion was not completely depleted at onset. Furthermore, an examination of isletrelated antibodies revealed the presence of high titer anti-GaD antibody. his hLa typing showed that DRb1*0901-DQb1*0303 and a24 were present. he has been doing well with continuation of insulin therapy. Over two years after onset, his plasma C-peptide level was gradually lowered, and anti-GaD antibody was still positive. Taken together, this is a rare case of abrupt onset autoimmune type 1 diabetes with transient but apparent exocrine pancreatic impairment at onset. Similar cases should be accumulated to clarify pathophysiological similarities and/or differences between fulminant type 1 diabetes and abrupt onset autoimmune type 1 diabetes. (FT1DM) is a novel clinical entity which is characterized by an extremely abrupt onset of the disease and remarkably acute destruction of pancreatic beta cells with urinary C-peptide secretion less than 10 µg/day: however, more than 90% of FT1DM patients were adolescent or adult [3][4][5]. although FT1DM is basically classified into type 1B diabetes as indicated by absence of islet-related autoantibodies, two atypical cases showing the mixed characteristics of FT1DM and autoimmune type 1 diabetes (i.e. anti-GaD antibody positivity) have been reported [6,7]. here we report a 63-year-old case of abrupt onset autoimmune type 1 diabetes, mimicking FT1DM. in addition to the above mentioned two autoimmune cases [6,7], the present case draws an attention in terms of differential diagnosis between typical FT1DM and this rapidly progressive form of autoimmune type 1 diabetes. Case Reporta 63-year-old male was admitted to our hospital with diabetic ketoacidosis on December 23 in 2006. his medical history revealed that he had been suffering from hypertension and angina pectoris for 7 years, but there was no sign of diabetes. The hba1c level in June, 2006 was 5.5%, while fasting plasma glu-

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“…Several reports have remarkably demonstrated cases of the onset of fulminant type 1 diabetes with a presence of GAD Ab during ICI therapy. 4 , 11 , 12 , 13 Previous reports suggest that the destruction of β-cells due to ICI therapy could cause a rapid release of the intracellular GAD antigen with the consequent development of GAD Abs. 14 , 15 Alternatively, there is insufficient evidence to conclude that the presence of GAD Abs at baseline is a risk factor for type 1 diabetes in patients treated with ICI therapy.…”

Section: Discussionmentioning

confidence: 99%