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Prepublished online as a Blood First Edition Paper on July 5, 2002; DOI 10.1182/blood-2002-06-1627.
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Blood, 15 November 2002, Vol. 100, No. 10, pp. 3757-3760
NEOPLASIA
Increased frequency of mannose-binding lectin insufficiency
among children with acute lymphoblastic leukemia
Kjeld Schmiegelow,
Peter Garred,
Birgitte Lausen,
Bente Andreassen,
Bodil Laub Petersen, and
Hans Ole Madsen
From the Pediatric Clinic II, Juliane Marie Centre,
Department of Clinical Immunology, and Department of Pathology,
Laboratory Centre, The University Hospital, Rigshospitalet, Copenhagen,
Denmark.
Epidemiological data indicate that acute lymphoblastic
leukemia (ALL) could be induced by interactions between the immune system and early childhood infections. Mannose-binding lectin (MBL)
plays a critical role in the immune response in early childhood before
specific immune protection develops. We investigated whether there may
be an association between childhood ALL and low-producing MBL
genotypes. Serum MBL levels depend on normal (A)
or defective (O) alleles, and on normal
(Y) or reduced (X) promoter activities. For
this study, 137 noninfants with ALL and 250 controls were classified
into 3 MBL genotype groups according to their influence on
the serum level of functional MBL: group I, YA/YA and
YA/XA (higher levels); group II, XA/XA and
YA/O (intermediate levels); and group III, MBL
insufficiency with XA/O or O/O
(MBL-deficient) genotypes. Compared with controls, cases
more often had low-level genotypes (I/II/III: 63 [46%]/44
[32%]/30 [22%] vs 145 [58%]/65 [26%]/40 [16%];
P = .02) and MBL deficiency (8.8% vs 2.8%;
P = .009). Thus, the ALL odds ratio for
MBL-deficient versus nondeficient individuals was 3.3 (95% CI, 1.3-8.7), whereas the ALL odds ratio for group I versus group
II/III genotypes was 0.62 (95% CI, 0.41-0.94). MBL group III patients
were significantly younger at diagnosis than patients in group I/II
(median, 3.9 vs 5.2 years; P = .04). The study shows
that the presence of low-level MBL genotypes is associated
with an increased risk of childhood ALL, particularly with early age at onset.
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