A Case of Acute Onset, Insulin Dependent Diabetes Following an Attack of Infectious Mononucleosis

  • Namba Mitsuyoshi
    The Second Department of Internal Medicine, Osaka University Medical School
  • Kuwajima Masamichi
    The Second Department of Internal Medicine, Osaka University Medical School
  • Fukumoto Yasuaki
    The Second Department of Internal Medicine, Osaka University Medical School
  • Toyoshima Hiroyuki
    The Second Department of Internal Medicine, Osaka University Medical School
  • Matsuyama Tatsuo
    The Second Department of Internal Medicine, Osaka University Medical School
  • Nonaka Kyohei
    The Second Department of Internal Medicine, Osaka University Medical School
  • Kurimura Takashi
    The Department of Virology, Tottori University Medical School
  • Otsu Keiji
    Osaka Prefectural Institute of Public Health
  • Arita Koji
    The Department of Pathology, Research Institute for Microbial Diseases, Osaka, University
  • Tarui Seiichiro
    The Second Department of Internal Medicine, Osaka University Medical School

Bibliographic Information

Other Title
  • 伝染性単球増加症罹患中に発症した小児若年型糖尿病の1例
  • デンセンセイ タンキュウ ゾウカショウ リカンチュウ ニ ハッショウシタ ショ
  • Sequential Changes in Serum Level of Antibody Titers Against Epstein-Barr Virus and its Implication in the Clinical Course
  • Epstein-Barrウイルス抗体価の変動と急性糖尿病の経過について

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Description

To our Knowledge, only 2 cases of acute diabetes following an attack of infectious mononucleosis (IM) have previously been reported. The case described here thus represents the third such occurrence of acute diabetes, during the clinical course of Epstein-Barr (EB) virus infection.<BR>A 7-yr-old boy was admitted due to severe diabetic symptoms. Fifty days prior to admission, he had experienced vomiting and diarrhea followed by a fever of up to 39°C for 3 weeks. One week after these symptoms had subsided, he experienced severe polydipsia, polyuria, polyphagia and lost 3 kg of body weight. On admission he displayed systemic lymphnode enlargement and hepatomegaly. His laboratory data revealed leukocytosis (9700/mm3) with 3 % atypical lymphocytes, hyperglycemia (plasma glucose 600 mg/dl) and ketonemia (β-hydroxybutyrate 4296 μM). Serological analysis showed the Paul-Bunnell heterophile antibody test to be positive (1: 224) on admission and negative one month later. The immunofluorescence test for antibody to EB viral capsid antigen was at a titer of 1: 160 on admission, rose to as high as 1: 640 after 3 weeks and persisted at the same level for a further 3 months. The titer of IgM antibody for EB virus was 1: 640 on hospitalization, decreased to 1: 40 one month later and remained at the same level for the next 3 months. The patient's histocompatibility antigen was a phenotype of HLA-AW 26, BW 40/AW 24, B 7. The antibody against a microsomal component of thyroid cells appeared at the 7th month of diabetes. After successful treatment of the acute diabetes with insulin for one month, an oral glucose (O.75 g/kg body weight) tolerance test was performed. This demonstrated an almost total absence of immunoreactive insulin response. Subsequently, the patient has remained insulin dependent for more than 1 yr. He had no family history of diabetes and had not been obese. A urinary glucose test performed 1 yr before his admission was found to be negative by inquiring about his physical record at primary school.<BR>It is thus not likely that latent diabetes became overt due to the current infection. The time lag between the acute phase of IM and the onset of diabetes also opposes such occasional aggravation. In conclusion, therefore, the acute diabetes in the present case is considered to be newly induced by an irreversible injury of pancreatic B cells infected with EB virus.

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