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Mumps with laboratory signs of subclinical pancreatitis may cause a disturbed beta-cell function
J Ludvigsson1, P Forsberg, A Frydèn
1Department of Pediatrics, Faculty of Health Sciences, Linköping University, Sweden.
Abstract:
Mumps epidemics are followed by sporadic cases of insulin dependent diabetes mellitus (IDDM). We have studied beta-cell function in 11 subjects who had had a mumps infection. They had no clinical pancreatitis but were selected as they had abnormal pancreas iso-amylase values and/or glucosuria during the mumps virus infection. At the follow-up some years later the subjects were healthy. A few HbA1-values were noted in the upper part of the normal range. Total serum insulin values were normal, but the C-peptide values were low at first follow-up 1-3 years after infection in all but two patients. These values increased in 4/7 patients during the follow-up period but were subnormal in five subjects still 3-6 years after the infection. All five patients had HLA-DR 3 and/or 4. In 7 out of 11 patients islet cell surface antibodies could be demonstrated. Our results indicate that subclinical mumps pancreatitis may initiate a reaction towards the beta-cells recognized as subnormal C-peptide levels several years later in certain patients. This might contribute to manifest IDDM many years after infection.
Insights
Mumps infection can lead to subclinical pancreatitis, affecting beta-cell function and potentially causing low C-peptide levels years later. This may contribute to the development of insulin-dependent diabetes mellitus (IDDM) in susceptible individuals.
Area of Science:
- Endocrinology
- Virology
- Immunology
Background:
- Mumps virus outbreaks are linked to increased cases of insulin-dependent diabetes mellitus (IDDM).
- Previous studies suggest a potential role for mumps infection in the pathogenesis of IDDM.
Purpose of the Study:
- To investigate beta-cell function in individuals with a history of mumps infection.
- To assess long-term effects of subclinical mumps pancreatitis on pancreatic islet cells.
Main Methods:
- Studied 11 subjects with prior mumps infection, abnormal pancreas iso-amylase, and/or glucosuria.
- Assessed beta-cell function via serum insulin, C-peptide levels, and HbA1 values during follow-up.
- Screened for islet cell surface antibodies and HLA-DR types.
Main Results:
- Subnormal C-peptide levels were observed in most subjects 1-3 years post-infection, persisting in some up to 3-6 years.
- Five patients with persistently low C-peptide levels possessed HLA-DR 3 and/or 4.
- Islet cell surface antibodies were detected in 7 of 11 subjects.
Conclusions:
- Subclinical mumps pancreatitis may trigger an autoimmune response targeting beta-cells.
- Reduced C-peptide levels years after mumps infection indicate persistent beta-cell dysfunction.
- Mumps infection could be a contributing factor to the development of IDDM in genetically predisposed individuals.