At. Soliman et al., HIGH PREVALENCE OF ISLET-CELL ANTIBODY AND DEFECTIVE INSULIN RELEASE IN CHILDREN WITH SCHISTOSOMIASIS, Journal of tropical pediatrics, 42(1), 1996, pp. 46-49
The importance of islet cell antibodies (ICA) as a predictor of insuli
n dependent diabetes mellitus (IDDM) has been emphasized by several in
vestigators since 1974. The ICA was also detected in patients with var
ious immune-mediated diseases such as auto-immune thyroiditis. Schisto
somiasis is a wide-spread helminthic disease which affects more than 2
00 million patients all over the world. Immunological abnormalities an
d pancreatic affection are features of the disease. We studied the pre
valence of ICA in 40 children with schistosomiasis (20 males and 20 fe
males), 14 children with IDDM, and 30 of the nondiabetic siblings of p
atients with IDDM, and evaluated the oral glucose tolerance and early
release of insulin after an i.v. load of glucose in children with schi
stosomiasis, diabetics' siblings, and 10 normal age-matched controls.
The age of onset of IDDM and duration of the disease were 6.5 +/- 2.3
and 4.1 +/- 1.2, respectively, and the age of onset and duration of sc
histosomiasis were 8.3 +/- 2.7 and 2.5 +/- 1.5 years, respectively. Se
x, consanguinity, history of previous virus diseases (mumps, measles a
nd rubella), and sex maturity rating did not differ among the three st
udy groups; however, children with schistosomiasis were significantly
older. The prevalence of ICA was 50 per cent in children with IDDM, 13
per cent in the diabetics' siblings, and 25 per cent of children with
schistosomiasis. Glucose tolerance was normal in children with schist
osomiasis and diabetics' siblings. Early release of insulin after i.v.
glucose load was significantly lower in children with schistosomiasis
compared to the other two groups. In conclusion, the high prevalence
of ICA and the decreased early release of insulin in response to an i.
v. glucose load in children with schistosomiasis suggest that auto-imm
une aggression against the islet cells contributes in the pathogenesis
of pancreatic disease in these patients, and might increase the risk
for developing glucose intolerance and diabetes.