Rapid Loss of Insulin Secretion in a Patient With Fulminant Type 1 Diabetes Mellitus and Carbamazepine Hypersensitivity Syndrome

Sekine, Nobuo

doi:10.1001/jama.285.9.1153

Cited by 103 publications

(74 citation statements)

References 5 publications

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“…Flu-like symptoms suggesting the pre-existence of a viral infection were observed in 71.7% of fulminant diabetic patients, in contrast to in only 26.9% of Type 1A diabetic patients [5]. Cases of human herpesvirus 6 [8] and Echovirus [9] were reported to precede infection before the onset of fulminant Type 1 diabetes.…”

Section: Discussionmentioning

confidence: 95%

“…Case reports have described pancreatic insulitis in an autopsy case, and later detection of antibodies after the onset of fulminant Type 1 diabetes [6,7]. On the other hand, the involvement of viral infections has also been suggested because of the abrupt onset [8,9]. However, the common aetiology of fulminant Type 1 diabetes has not yet been clarified.…”

Section: Introductionmentioning

confidence: 99%

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T lymphocyte response against pancreatic beta cell antigens in fulminant Type 1 diabetes

et al. 2004

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Aims/hypothesis. Fulminant Type 1 diabetes is a novel subtype of Type 1 diabetes that involves the abrupt onset of insulin-deficient hyperglycaemia. This subtype appears to be non-autoimmune because of the absence of diabetes-related autoantibodies in the serum, and of insulitis in pancreatic biopsy specimens. The pathogenesis of the disease is still unknown. In this study, we investigated whether T cell autoimmune responses are involved in fulminant Type 1 diabetes. Methods. Cellular immune responses to beta cell autoantigens were studied by enzyme-linked immunospot (ELISPOT) assay in 13 fulminant Type 1 diabetic patients and 49 autoantibody-positive autoimmune Type 1 diabetic patients. Results were compared with those of 18 Type 2 diabetic patients, six secondary diabetic patients (diabetes due to chronic pancreatitis) and 35 healthy controls. Results. Nine of 13 (69.2%) GAD-reactive Th1 cells, and three of 12 (25%) insulin-B9-23-reactive Th1 cells were identified in fulminant Type 1 diabetic patients by ELISPOT, as in autoantibody-positive Type 1 diabetic patients. Four fulminant Type 1 diabetic patients possessed the highly diabetes-resistant allele DR2, three of whom had GAD-reactive Th1 cells in the periphery. Conclusions/interpretation. Peripheral immune reaction was observed in 69.2% of fulminant Type 1 diabetic patients, indicating that autoreactive T cells might contribute, at least in part, to the development of fulminant Type 1 diabetes.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

T lymphocyte response against pancreatic beta cell antigens in fulminant Type 1 diabetes

et al. 2004

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“…The underlying pathogenesis remains unclear, although the high frequency of 'flu-like' symptoms just before the onset of fulminant type 1 diabetes suggest that it might be associated with viral infection. Two case reports have described fulminant type 1 diabetes developing after the reactivation of human herpes virus-6 or infection with the herpes simplex virus [82,83]. Elevation of IgA antibodies to enterovirus has also been observed in patients with fulminant type 1 diabetes [84], suggesting that recurrent enterovirus infection may be one of the triggers for the development of fulminant type 1 diabetes.…”

Section: Resultsmentioning

confidence: 99%

Type 1 diabetes in Japan

2006

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“…Patients with drug-induced hypersensitivity syndrome (DIHS) exhibit severe drug-induced rashes accompanied by fever and organ dysfunction 2-6 weeks after the oral intake of certain kinds of medications (1)(2)(3)(4). It is thought that the complication rate of lung injury in DIHS patients is approximately 5% (5).…”

Section: Introductionmentioning

confidence: 99%

“…It is thought that the complication rate of lung injury in DIHS patients is approximately 5% (5). In most previous report, chest computed tomography (CT) demonstrated infiltrative shadows (1)(2)(3)(4), and only one reported case involved centrilobular nodular shadows (6). Importantly, no reports have investigated the pulmonary lesions of patients with DIHS pathologically.…”

Section: Introductionmentioning

confidence: 99%

Drug-induced Hypersensitivity Syndrome Accompanied by Pulmonary Lesions Exhibiting Centrilobular Nodular Shadows

et al. 2016

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A 51-year-old woman diagnosed with Crohn's disease developed drug-induced hypersensitivity syndrome (DIHS) 12 and six weeks after starting the oral intake of mesalazine and trimethoprim/sulfamethoxazole, respectively. Chest CT showed centrilobular nodular shadows and a transbronchial lung biopsy (TBLB) revealed infiltration of inflammatory cells predominantly in the small pulmonary artery walls and bronchiolar walls. Regarding pulmonary lesions of DIHS, infiltrative shadows have sometimes been reported, whereas nodular shadows have rarely been documented. This is a valuable case report for considering the mechanism underlying the development of pulmonary lesions in case of DIHS.

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Rapid Loss of Insulin Secretion in a Patient With Fulminant Type 1 Diabetes Mellitus and Carbamazepine Hypersensitivity Syndrome

Cited by 103 publications

References 5 publications

T lymphocyte response against pancreatic beta cell antigens in fulminant Type 1 diabetes

T lymphocyte response against pancreatic beta cell antigens in fulminant Type 1 diabetes

Type 1 diabetes in Japan

Drug-induced Hypersensitivity Syndrome Accompanied by Pulmonary Lesions Exhibiting Centrilobular Nodular Shadows

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