A case of fulminant Type 1 diabetes associated with mexiletine hypersensitivity syndrome

Seino, Yutaka; Yamauchi, Mika; Hirai, Chihiro; Okumura, Atsuko; Kondo, Kunïkazu; Yamamoto, Masahiro; Okazaki, Yuki

doi:10.1111/j.1464-5491.2004.01307.x

Cited by 28 publications

(12 citation statements)

References 8 publications

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“…IgA antibody titers to enterovirus were significantly higher in fulminant type 1 diabetes, but there was no elevation in anti-coxsackie A2-10 or coxsackie B1-6 virus serotype-specific neutralizing antibodies in paired sera of 20 recent-onset fulminant type 1 diabetic patients in a nationwide survey (unpublished observation). This was also the case in human herpes virus (HHV)-6, although 6 patients were reported to suffer from fulminant type 1 diabetes after infection with or reactivation of this virus [11,14,[23][24][25][26]. Titers of other viruses, HHV-7, cytomegalovirus, Epstein-Barr virus and rotavirus, were not elevated either in paired sera of 20 recent-onset fulminant type 1 diabetic patients (unpublished observation).…”

Section: Virus-primary Candidate?mentioning

confidence: 97%

“…Symptoms associated with gastrointestinal infection, such as diarrhea (5.5%) or lower abdominal pain (11.0%), were also reported. Indeed, some cases of fulminant type 1 diabetes were reported, in which the onset of diabetes was accompanied by the reactivation of human herpes virus-6 [11,14,[23][24][25][26] and infection with herpes simplex virus [27] or coxsackie B3 virus [28][29].…”

Section: Virus-primary Candidate?mentioning

confidence: 99%

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Pathogenesis of Fulminant Type 1 Diabetes

Imagawa¹,

Hanafusa²

2006

Rev Diabetic Stud

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■ AbstractFulminant type 1 diabetes is a new subtype of type 1 diabetes. The term was established in 2000. It is a syndrome characterized by a markedly rapid and almost complete destruction of pancreatic β-cells. Several lines of evidence suggest that both genetic factors, such as human leukocyte antigen (HLA), and environmental factors, such as viral infection, contribute to the development of this disease. It is also suggested that autoimmune processes contribute less critically to fulminant type 1 diabetes than to classic type 1A diabetes. Based on the findings made to date, both viral infection and the subsequent immune reaction in genetically susceptible individuals cause β-cell destruction and lead to fulminant type 1 diabetes.

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Section: Virus-primary Candidate?mentioning

confidence: 97%

Section: Virus-primary Candidate?mentioning

confidence: 99%

Pathogenesis of Fulminant Type 1 Diabetes

Imagawa¹,

Hanafusa²

2006

Rev Diabetic Stud

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“…Interestingly, 4 years before onset of KFD, he had had an episode of drug-induced hypersensitivity syndrome (DIHS), which is a life-threatening multiorgan reaction induced by a limited number of drugs (including anticonvulsants, such as carbamazepine, phenytoin, and allopurinol [3,4,5,6,7]). DIHS is associated with reactivations of various herpesviruses [3,4,5,6,7] and has many short- and long-term sequelae and complications [8,9,10,11,12]. In this patient, EBV reactivation was observed during the course of DIHS and again at the onset of KFD, suggesting the pathogenic role of EBV.…”

Section: Introductionmentioning

confidence: 78%

“…Indeed, several autoimmune diseases have been reported to occur as sequelae of DIHS; they include: type 1 diabetes mellitus [9,10,11,12], sclerodermoid graft-versus-host-disease-like lesions [15] and autoimmune thyroiditis [16]. Among the environmental risk factors contributing to the etiology, EBV is the most closely associated with SLE.…”

Section: Discussionmentioning

confidence: 99%

Systemic Lupus Erythematosus Presenting with Kikuchi-Fujimoto’s Disease as a Long-Term Sequela of Drug-Induced Hypersensitivity Syndrome

et al. 2008

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Drug-induced hypersensitivity syndrome (DIHS) is a severe form of drug eruptions associated with viral reactivations. Autoimmune diseases have been reported to develop several months or years after the resolution of DIHS. We describe a 36-year-old man with cervical lymphadenopathy and an erythematous eruption affecting the face and neck, which evolved into clinically evident systemic lupus erythematosus. He had had an episode of DIHS 4 years previously, in which human herpesvirus-6 and Epstein-Barr virus (EBV) were reactivated. Expression of EBV-encoded RNA was detected in the lymph node. On the basis of findings in this patient, we suggest that EBV is pathogenically important in the sequence of events leading to the onset of systemic lupus erythematosus and that patients with a history of DIHS may be at a risk of eventually developing autoimmune diseases.

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“…6,12 Recently, fulminate type 1 DM also has been reported in patients with drug-induced hypersensitivity syndrome. 6,7,13 Type 1 DM is caused by severe insulin deficiency, resulting from autoimmune destruction of pancreatic beta cells although, in some cases, there is no evidence of autoimmunity classified as idiopathic. The viral factors have been hypothesized to induce an attack on beta cell function (eg, mumps, rubella, and coxsackievirus B4).…”

Section: Discussionmentioning

confidence: 99%