Cases reported "Coxsackievirus Infections"

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1/10. Simultaneous type 1 diabetes onset in mother and son coincident with an enteroviral infection.

    enterovirus (EV) infections have been implicated in the development of type 1 diabetes. (T1D). They may cause beta-cell destruction either by cytolytic infection of the cells or indirectly by triggering the autoimmune response. Virus was isolated from a woman at diagnosis of T1D (Tuvemo 1) and in addition, virus was isolated from her son at diagnosis of T1D at the same day (Tuvemo 2). None of the isolates could initially be serotyped by conventional methods. The Tuvemo 1 virus was genotyped and after sub-cultivation it was also serotyped as Coxsackievirus B5. The mother revealed antibodies against GAD65. The boy and the father both revealed a significant increase in neutralization antibody titre against two strains of CBV-4, clearly indicating a recent or ongoing EV infection. In addition, the brother showed such a titre rise against another CBV-4 strain (E2) and against a CBV-5 strain (4429). These results show that the whole family had a proven EV infection at the time of T1D diagnosis of the mother and the 10-years-old boy, indicating that the infection might cause or accelerate the T1D.
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keywords = diabetes
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2/10. Isolation of a virus from the pancreas of a child with diabetic ketoacidosis.

    A healthy 10-year-old boy was admitted to the hospital in diabetic ketoacidosis within three days of onset of symptoms of a flu-like illness. He died seven days later and post-mortem examination showed lymphocytic infiltration of the islets of langerhans and necrosis of beta cells. Inoculation of mouse, monkey and human cell cultures with homogenates from the patient's pancreas led to isolation of a virus. Serologic studies revealed a rise in the titer of neutralizing antibody to this virus from less than 4 on the second hospital day to 32 on the day of death. Neutralization data showed that the virus was related to a diabetogenic variant derived from Coxsackievirus B4. Inoculation of mice with the human isolate produced hyperglycemia, inflammatory cells in the islets of langerhans and beta-cell necrosis. Staining of mouse pancreatic sections with fluorescein-labeled antiviral antibody revealed viral antigens in beta cells. Both the clinical picture and animal studies suggested that the patient's diabetes was virus induced.
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keywords = diabetes
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3/10. infection by multiple viruses and lymphocyte abnormalities at the diagnosis of diabetes.

    Evidence for an ongoing adenovirus infection and preceding EB and Coxsackie B virus infections was found in a 2-year-old boy at the diagnosis of insulin-dependent diabetes. An inverted T-helper/T-suppressor lymphocyte ratio and activation of T cells with a suppressor-cytotoxic phenotype were detected. A combination of multiple viral infections may be responsible for the rapid destruction of pancreatic beta cells in this case.
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ranking = 1.280737630065
keywords = insulin-dependent, diabetes
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4/10. An outbreak of coxsackievirus B infection followed by one case of diabetes mellitus.

    During the fall of 1979, 22/250 Swedish UN soldiers serving in egypt were hospitalized with fever and gastroenteritis associated with aseptic meningitis. One of the 22 developed insulin dependent diabetes mellitus (IDDM) 10 weeks following the infection. The majority of the 22 patients showed significant titer rise for coxsackievirus B by plaque reduction neutralization test. The serology results indicate that coxsackievirus B4 most likely caused the outbreak. All 22 were also tested for islet cell cytoplasmic antibodies and islet cell surface antibodies and found negative. The individual developing diabetes mellitus had the HLA-DR phenotype 3,4, which is associated with IDDM.
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ranking = 4.687861799057
keywords = diabetes mellitus, diabetes, mellitus
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5/10. Multi-system coxsackievirus B-6 infection with findings suggestive of diabetes mellitus.

    A fatal case of Coxsackievirus B-6 (CBV-6) infection in a 4 1/2-year-old girl is reported. The disease was initially characterized by a severe meningoencephalitis and, successively, by the appearance of hyperglycaemia and glycosuria, concomitantly with complement-fixing-islet cell antibodies (CF-ICA) and ICA, diarrhoea, electrolyte disorders, arrhythmia and decrease of the IgG levels, suggesting a multi-system involvement. CBV-6 was identified by isolation from stool and cerebrospinal fluid and by detection of specific IgM antibodies.
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ranking = 3.1252411993714
keywords = diabetes mellitus, diabetes, mellitus
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6/10. Pancreatic isleitis with coxsackie virus B5 infection.

    Coxsackie group B virus infection may be responsible for some cases of insulin-dependent diabetes mellitus. However, Coxsackie B5 virus is rarely implicated in this respect. The authors observed striking pancreatic islet cell damage in an infant who died of a Coxsackie B5 virus infection. The inflammatory response consisted of mononuclear cells, and the acinar tissue was completely uninvolved.
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ranking = 1.0620479299078
keywords = diabetes mellitus, insulin-dependent, diabetes, mellitus
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7/10. Various phenotypes of diabetes mellitus at ultimate outcome of acutely developed diabetic state induced by viral infection.

    For 4 to 8 years we followed up 3 diabetic patients in whom the onset of diabetes seemed to be closely related to the well-documented Epstein-Barr virus infection (Case 1) or Coxsackie B4 virus infection (Case 2, 3). Although all developed acute ketosis-prone diabetes in the convalescent stage of the viral infections, the subsequent clinical courses were quite different from each other. Case 1 has remained consistently insulin-dependent and associated with positive islet cell antibody, gastric parietal cell antibody, thyroglobulin hemoagglutinating antibody and thyroidal microsomal hemoagglutinating antibody. Case 2 restored normal glucose tolerance. Case 3 has become noninsulin-dependent diabetes mellitus after a 6 year interval. Thus, it is reasonably presumed that virus could be responsible for the occurrence of different phenotypes of diabetes.
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ranking = 5.0680267593442
keywords = diabetes mellitus, insulin-dependent, diabetes, mellitus
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8/10. The development of Type 1 (insulin-dependent) diabetes mellitus: two contrasting presentations.

    Genetic, immunological and viral factors have been implicated in pathogenesis of Type 1 diabetes mellitus. The development of Type 1 diabetes in two siblings of patients with Type 1 diabetes studied as part of a large epidemiological study, is described. One case, a 13-year-old male not sharing either HLA haplotype with his diabetic sister, had virtually normal glucose tolerance 80 days before symptomatic presentation. He showed serological evidence of infection by Coxsackie CB4 (at diagnosis) and influenza a virus (soon after diagnosis). The other case, a 15-year-old male, had impaired glucose tolerance for over 500 days (i.e., since the diagnosis of diabetes in his HLA-identical brother) before symptomatic presentation which was not associated with serological evidence of acute viral infection. The former case was negative for islet cell antibody (cytoplasmic) when first seen though positive at diagnosis, while the latter was positive throughout. These two cases suggest contrasting interactions of the main pathogenetic factors associated with Type 1 diabetes.
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ranking = 5.8295020194742
keywords = diabetes mellitus, insulin-dependent, diabetes, mellitus
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9/10. Virologic, immunologic, and genetic factors in insulin-dependent diabetes mellitus.

    A 16-month-old girl presented with an episode of fever and acute thrombocytopenic purpura caused by a Coxsackie B5 virus. On days 13 to 23, laboratory evidence of diabetes mellitus was present, followed by a 2 1/2-month remission, then by definitive insulin-dependent diabetes. The involvement of virologic, immunologic, and genetic factors in the pathophysiology was substantiated by the following data: (1) Virus-induced glucose intolerance was produced in selected mouse strains. (2) Islet-cell antibodies were found one week before onset of diabetes; however, circulating lymphocytes of the child at that time suppressed insulin release from islets in vitro. (3) Immunogenetic analysis of the child revealed the presence of high-risk genetic markers. It is suggested that the convergence of an insulotropic variant virus, genetic predisposition, and perhaps some uncontrolled adjuvant factors, e.g. steroid therapy and DPT vaccination, may have determined insular damage and anti-islet autoimmune reactions, leading to insulin-dependent diabetes mellitus.
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ranking = 6.7722875794471
keywords = diabetes mellitus, insulin-dependent, diabetes, mellitus
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10/10. Neurogenic diabetes insipidus in a child with fatal Coxsackie virus B1 encephalitis.

    A 5 year-old boy presented with fever, sore throat, diarrhea, and general soreness which evolved into encephalitis. His cerebrospinal fluid showed a cell count of 3 mononuclear cells/microliters, protein 2800 mg/l, and growth of Coxsackie virus B1. Cardiorespiratory arrest was noted after a convulsion and infusion of diazepam. Although he was immediately resuscitated, he remained unconscious with a modified Glasgow coma score of 4 or 3. He developed neurogenic diabetes insipidus 169 hours after the convulsion and died the next day. We conclude that although Coxsackie virus infection is usually benign it may become overwhelming and be complicated with neurogenic diabetes insipidus. It is important to recognize this potential sequel by regularly monitoring weight, intake and output, plasma sodium level, and urine specific gravity.
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ranking = 1.2
keywords = diabetes
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