A population-based study of morbidity and mortality in mannose-binding lectin deficiency
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A population-based study of morbidity and mortality in mannose-binding lectin deficiency. / Dahl, Morten; Tybjaerg-Hansen, Anne; Schnohr, Peter; Nordestgaard, Børge G.
I: Journal of Experimental Medicine, Bind 199, Nr. 10, 17.05.2004, s. 1391-9.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - A population-based study of morbidity and mortality in mannose-binding lectin deficiency
AU - Dahl, Morten
AU - Tybjaerg-Hansen, Anne
AU - Schnohr, Peter
AU - Nordestgaard, Børge G
PY - 2004/5/17
Y1 - 2004/5/17
N2 - Reduced levels of wild-type mannose-binding lectin (MBL) may increase susceptibility for infection, other common diseases, and death. We investigated associations between MBL deficiency and risk of infection, other common diseases, and death during 24, 24, and 8 yr of follow-up, respectively. We genotyped 9,245 individuals from the adult Danish population for three MBL deficiency alleles, B, C, and D, as opposed to the normal noncarrier A allele. Hospitalization incidence per 10,000 person. yr was 644 in noncarriers compared with 631 in heterozygotes (log-rank: P = 0.39) and 658 in deficiency homozygotes (P = 0.53). Death incidence per 10,000 person. yr was 235 in noncarriers compared with 244 in heterozygotes (P = 0.44) and 274 in deficiency homozygotes (P = 0.12). After stratification by specific cause of hospitalization or death, only hospitalization from cardiovascular disorders was increased in deficiency homozygotes versus noncarriers (P = 0.02). When retested in two case control studies, this association could not be confirmed. Incidence of hospitalization or death from infections or other serious common disorders did not differ between deficiency homozygotes and noncarriers. In conclusion, in this large study in an ethnically homogeneous Caucasian population, there was no evidence for significant differences in infectious disease or mortality in MBL-deficient individuals versus controls. Our results suggest that MBL deficiency is not a major risk factor for morbidity or death in the adult Caucasian population.
AB - Reduced levels of wild-type mannose-binding lectin (MBL) may increase susceptibility for infection, other common diseases, and death. We investigated associations between MBL deficiency and risk of infection, other common diseases, and death during 24, 24, and 8 yr of follow-up, respectively. We genotyped 9,245 individuals from the adult Danish population for three MBL deficiency alleles, B, C, and D, as opposed to the normal noncarrier A allele. Hospitalization incidence per 10,000 person. yr was 644 in noncarriers compared with 631 in heterozygotes (log-rank: P = 0.39) and 658 in deficiency homozygotes (P = 0.53). Death incidence per 10,000 person. yr was 235 in noncarriers compared with 244 in heterozygotes (P = 0.44) and 274 in deficiency homozygotes (P = 0.12). After stratification by specific cause of hospitalization or death, only hospitalization from cardiovascular disorders was increased in deficiency homozygotes versus noncarriers (P = 0.02). When retested in two case control studies, this association could not be confirmed. Incidence of hospitalization or death from infections or other serious common disorders did not differ between deficiency homozygotes and noncarriers. In conclusion, in this large study in an ethnically homogeneous Caucasian population, there was no evidence for significant differences in infectious disease or mortality in MBL-deficient individuals versus controls. Our results suggest that MBL deficiency is not a major risk factor for morbidity or death in the adult Caucasian population.
KW - Adult
KW - Base Sequence
KW - Case-Control Studies
KW - DNA Primers
KW - Denmark
KW - Disease Susceptibility
KW - Genotype
KW - Heterozygote Detection
KW - Humans
KW - Incidence
KW - Infection
KW - Mannose-Binding Lectin
KW - Morbidity
KW - Mortality
KW - Neoplasms
U2 - 10.1084/jem.20040111
DO - 10.1084/jem.20040111
M3 - Journal article
C2 - 15148337
VL - 199
SP - 1391
EP - 1399
JO - The Journal of Experimental Medicine
JF - The Journal of Experimental Medicine
SN - 0022-1007
IS - 10
ER -
ID: 45524116