НВ-ВМХ, част 86 - за здравословното хранене и връзката между хрането и здравето

Autoimmune diseases (AD) have a higher prevalence in women, particularly during their
childbearing age. A growing interest is being paid to the possible consequences of maternal
disease and associated treatment on the fetus and newborn infant. If maternal disease
is characterized by the presence of IgG isotype autoantibodies, these can cross the
placenta with possible antibody-mediated damage to the fetus. In addition, immunosuppressive
and other drugs administered to the mothers during pregnancy might affect the
fetal and neonatal immune system development. Finally, mothers disease and/or treatment
could be related to neuropsychological alteration reported in some of their children.
Neonatal lupus erythematosus
Neonatal lupus erythematosus (NLE) is a
model of passively acquired autoimmune
disease (AD) in which mother’s autoantibodies
with anti-Ro/SS-A and anti-La/SSB
specificities cross the placenta and may
damage the fetus. The most common and
serious cardiac manifestation is the autoimmune-
associated congenital heart block
(CHB), which typically begins in utero during
the second or third trimester. In some
cases, CHB begins as first- or seconddegree
block and then progresses to thirddegree
block. Complete CHB, once established,
appears to be irreversible and carries
a significant morbidity and mortality.1,2 The
frequency of third-degree block in an offspring
of a mother who has anti-SSA/Ro
antibodies is estimated at 1–2%.3 Earlyonset
cardiomyopathy can occur together
with complete CHB in fetus or at birth,
however, delayed dilated cardiomyopathy
has been also reported.4-6
Other cardiac features include congenital
malformations, less advanced degrees of
block and conduction abnormalities.7-9
While the precise pathogenic mechanism
of antibody-mediated injury remains
unknown, it is clear that the antibodies
alone are insufficient to cause disease and
fetal factors are likely contributory. In vivo
and in vitro evidence supports a pathologic
cascade involving apoptosis of cardiocytes,
surface translocation of Ro and La
antigens, binding of maternal autoantibodies,
secretion of profibrosing factors (e.g.,
TGFb) from the scavenging macrophages
and modulation of cardiac fibroblasts to a
myofibroflast scarring phenotype.10
Cutaneous transient manifestations of
neonatal lupus erythematosus usually
appear as erythematous and often annular
lesions with a predilection for the eyes, face
and scalp, frequently photosensitive. The
risk of cutaneous lesions is unknown. In
most cases, the rash follows ultraviolet light
exposure, the mean age of detection is six
weeks, and the duration up to 22 weeks. All
infants had facial involvement (mainly periorbital
region), followed by the scalp, trunk,
extremities, neck and intertriginous areas. It
is not clear whether topic treatment may
improve the outcome of skin lesions.11
Less frequently documented features
include hepatobiliary disease and Hematologic
abnormalities, both associated with
maternal anti-SSA/Ro-SSB/La antibodies
and generally self-limited; hepatic and
hematologic involvement are grouped
under the heading of neonatal lupus syndromes.
12,13 It is uncommon for children
with neonatal
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