M. Hiltunen et al., SEROLOGICAL EVALUATION OF THE ROLE OF CYTOMEGALOVIRUS IN THE PATHOGENESIS OF IDDM - A PROSPECTIVE-STUDY, Diabetologia, 38(6), 1995, pp. 705-710
Citations number
20
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
To study the possible temporal association between primary cytomegalov
irus infection and the appearance of islet cell autoantibodies or the
development of insulin-dependent diabetes mellitus (IDDM) cytomegalovi
rus antibodies were analysed from follow-up sera of 46 initially non-d
iabetic siblings of diabetic children who either manifested clinical I
DDM (22 siblings) or turned islet cell antibody positive (24 siblings)
during the prospective observation (mean follow-up time 2.9 years). S
econdly, cytomegalovirus antibodies were analysed during pregnancy in
96 mothers whose child presented with IDDM before the age of 7 years a
nd in 96 control mothers who gave birth to a non-diabetic child. Third
ly, a case-control series including 90 newly-diagnosed young children
with IDDM and their 90 control subjects was analysed. No seroconversio
ns were found in cytomegalovirus antibodies during the follow-up of th
e 46 siblings indicating no temporal association with islet cell antib
ody seroconversion or manifestation of clinical diabetes. During the f
ollowup 17 (37%) siblings were constantly seronegative and 29 (63%) se
ropositive for cytomegalovirus IgG and there was no difference between
islet cell antibody positive and negative siblings. Cytomegalovirus I
gG and IgM were not different in pregnant mothers who gave birth to a
subsequently diabetic child compared to control mothers, or in newly-d
iagnosed diabetic children compared to control children. Cytomegalovir
us IgA was higher in newly-diagnosed diabetic children than in control
children (p < 0.005). This difference disappeared when only cytomegal
ovirus IgG positive individuals were analysed. No correlation was foun
d between islet cell antibodies and cytomegalovirus antibodies in newl
y-diagnosed diabetic patients. The results do not support the hypothes
is that primary cytomegalovirus infections could initiate the cascade
leading to autoimmune destruction of the beta cells.