Thank you for your question. Responding to all of your questions
directly would require extensive research of medical journals.
However, I found some strong journal articles on Pre-eclampsia and its
relation to hypertension and placental abruption among other things.
The information I have provide is a broad survey of the current
medical literature on Pre-eclampsia and should provide you with
important information. I start with a broad journal article, then
present specific excerpts from articles relating to your specific
concernsm and finally I provided a list of sources for further
research.
Please let me know if I can clarify this response in any way.
*Backround Information
(this article seems to address a lot of your questions:
Lancet 2000; 356 (9237): 1260-1265
October 7, 2000
TITLE: Pre-eclampsia
SOURCE: Department of Obstetrics and Gynaecology, St James's
University Hospital, Leeds LS9 7TF, UK (Prof J J Walker FRCOG)
(e-mail: j.j.walker@leeds.ac.uk)
AUTHOR: James J Walker
ABSTRACT: Pre-eclampsia is associated with significant morbidity and
mortality for mother and baby, but it resolves completely post partum.
Despite a steady reduction in maternal mortality from the disorder in
more developed countries, it remains one of the most common reasons
for a woman to die during pregnancy. The disorder starts with a
placental trigger followed by a maternal systemic response. Because
both this systemic response and the woman's reaction to it are
inconsistent, the clinical presentation varies in time and substance,
with many different organ systems affected. With the increasing
understanding of the disease process, there have been advances in
management, such as antihypertensive therapy, magnesium sulphate, and
fluid restriction.
TEXT:
In the UK, the number of maternal deaths from hypertension in
pregnancy has fallen steadily over the past few decades (figure 1) n1
as has the complication rate. n2 However, in other parts of the world,
the rates of mortality and morbidity remain high n3 and will continue
to be so until there are general improvements in maternity services.
Trials on prevention have been disappointing, n4 so the mainstays of
management of hypertension in pregnancy are integrated antenatal care,
access to monitoring services, stabilisation of the maternal
condition, and delivery of the baby on the best day in the best way to
benefit both mother and child. Antenatal care must provide easy access
to monitoring services. n5
Epidemiology
The epidemiology of pre-eclampsia is complicated by differences in
definitions and inaccuracy of diagnosis. A single blood-pressure
reading of 140/90 mm Hg or above is not uncommon in pregnancy and was
reported in nearly 40% of pregnant women in one study. n6 Such a
finding carries little risk to the mother or fetus. Persistent
hypertension is diagnosed if a high reading is found on two occasions
at least 4 h apart. Persistent hypertension occurs in around 12-22% of
pregnancies, n7-n9 depending on the populations and definitions used.
The type of hypertension can be further defined on the basis of other
clinical signs, particularly proteinuria and abnormalities of
coagulation. n10
Hypertension in pregnancy can be classified into two main groups
(panel 1): women who are hypertensive when they become pregnant n11
and those who become hypertensive for the first time in the second
half of pregnancy. n9 Blood pressure generally falls in the first and
second trimesters; therefore women with high blood pressure before the
20th week of gestation are assumed to have pre-existing hypertension.
Although these definitions are important for research and
epidemiological purposes, they are less important clinically. All
women with raised blood pressure must be carefully monitored for the
associated features of pre-eclampsia. Although well-controlled
essential hypertension is benign, the frequency of superimposed
pre-eclampsia is between 15% and 25%, increasing the maternal and
fetal risk. n12, n13
Pre-eclampsia is twice as common in primigravid women as in women
having second or later pregnancies. n14 However, with a change of
partner, the risk in a multiparous woman increases; this effect
suggests that primipaternity is important. Particular men seem to have
an increased risk of fathering a pre-eclamptic pregnancy. n15 Women
who become pregnant with donor eggs have a higher frequency of
pre-eclampsia than women pregnant with their own eggs; n16 this
finding suggests that any new fetal factors are important, not
necessarily those of paternal origin.
Pathophysiology
Pre-eclampsia is the result of an initial placental trigger, which has
no adverse effect on the mother, and a maternal systemic reaction that
produces the clinical signs and symptoms of the disorder. n17
Placental trigger
Pre-eclampsia occurs only in the presence of a placenta. Although it
is associated with a failure of the normal invasion of trophoblast
cells, leading to maladaptation of maternal spiral arterioles, n18 it
can also be associated with hyperplacentation disorders such as
diabetes, hydatidiform mole, and multiple pregnancy. The maternal
arterioles are the source of blood supply to the fetus (figure 2), and
maladaptation of these vessels can interfere with normal villous
development. In some cases, compensation can occur, but, in others,
poor villous development results in placental insufficiency. n19
Secondary damage, such as fibrin deposition and thrombosis, can then
occur within the placenta. These features are found in cases of
placental insufficiency, whether pre-eclampsia is present or not. n20
Not all women with the potential placental trigger develop
pre-eclampsia, therefore the maternal response must be the decisive
factor in development of systemic disease.
Maternal response
Although pre-eclampsia is said to be a vascular endothelial disorder,
n21 it is a multisystem disorder with various forms. This variation
could be due to different vascular beds being affected to varying
degrees, but later research has shown that there is a strong maternal
inflammatory response. n17 Although this response has been described
in the placental bed, n22 there is far broader immunological systemic
activity. n17 These changes may explain many of the clinical signs,
including the endothelial-cell dysfunction.
Because pre-eclampsia is diagnosed by the presence of hypertension and
proteinuria, the rest of the systemic features can vary from mild
cases with little systemic involvement, to multiorgan failure. How
extensively the disease develops depends on various modifying factors,
which could be genetic or environmental in origin.
Figure 1: Maternal mortality associated with pre-eclampsia and eclampsia
[SEE FIGURE IN ORIGINAL]
Hereditary factors
Pre-eclampsia can be familial, n23 but various groups have studied the
genetic basis of this disorder and no persistent results have been
obtained with obvious population differences. A single pre-eclampsia
gene is unlikely; there are probably several modifier genes along with
environmental factors. n24 There have been conflicting results for the
genes that encode angiotensinogen, superoxide dismutase, tumour
necrosis factor [alpha], methylene-tetrahydrofolate reductase, factor
V Leiden, and endothelial nitric oxide synthase. These studies
concentrated on maternal genetics and ignored the potential paternal
and fetal influences. n15 The results of large multicentre studies
with the use of modern chip technology for genome scanning with
multiple microsatellite markers are awaited to clarify the role of
genetics in the pathophysiology of pre-eclampsia. n24
Panel 1: Classification of hypertension in pregnancy
Pre-existing hypertension (3-5% of pregnancies) n11
Hypertension before pregnancy or found earlier than 20 weeks of
gestation or persisting after the pregnancy ends. Most such patients
have essential hypertension but some have renal disease and other
medical disorders.
Pregnancy-associated hypertension (12% of pregnancies) n9
Hypertension occurring de novo after the 20th week of pregnancy and
settling within 6 weeks of delivery. This category is divided into two
groups.
Gestational hypertension (6-7%)--Hypertension alone with no associated features.
Pre-eclampsia (5-6%)--Hypertension with proteinuria of at least 0.3 g
in 24 h (24 h urine collection or protein/creatinine ratio).
Superimposed pre-eclampsia (25% of women with pre-existing hypertension) n12, n13
Signs and symptoms of pre-eclampsia in woman with pre-existing hypertension.
Eclampsia
Convulsions in any woman who has, or then presents with, hypertension
in pregnancy of any cause.
Diagnosis and assessment
Hypertension is the most common diagnostic sign, although some women
present with convulsions, abdominal pain, or general malaise. Because
there are no specific diagnostic investigations, the initial diagnosis
of pre-eclampsia remains clinical. The classification of severity is
mainly based on the blood-pressure value and the presence of
proteinuria; further characterisation is based on the other
accompanying signs. n25
Measurement of blood pressure
There has been much controversy about the method of measuring blood
pressure in pregnancy. In the UK, Korotkoff phase IV is generally
used, but in other parts of the world, clinicians use Korotkoff phase
V. A study by Brown and colleagues suggested that Korotkoff phase V is
preferable. n26 What is important is that the method used is
consistent and documented. For measurement of blood pressure, the
woman should be rested and reclining at an angle of 45 [degrees]. The
blood-pressure cuff should be of appropriate size and placed at the
level of the heart. Because of the normal blood-pressure variation,
several readings should be used to confirm the diagnosis.
In normal pregnancy, there are substantial cardiovascular changes with
a 50% increase in cardiac output and blood volume, which is
accompanied by a fall in blood pressure due to peripheral
vasodilation. The changes in pre-eclampsia tend to be the reverse.
Severe disease is generally associated with a low cardiac output and a
high peripheral resistance. However, Bosio and colleagues n27 found
both high-output and low-output states and peripheral resistance
within a range from normal to high among women with hypertensive
disorders of pregnancy. More importantly, serial studies have shown a
cross-over effect from high output plus low resistance to low output
plus high resistance as the disease progresses. n27
In pre-eclampsia, the urine protein excretion rises above a threshold
of 0.3 g per 24 h. This finding is generally associated with the
classic pathological finding of glomeruloendotheliosis, n28 which is
not permanent but recovers after delivery. The presence of proteinuria
confirms the diagnosis of pre-eclampsia and the concomitant increase
in risk for both mother and fetus. n29 The risk is related simply to
the presence of proteinuria; it is not affected by the absolute value
of or the increase in urinary protein excretion. n30
Figure 2: Diagram of maternal/placental interface showing
spiral-artery blood flow and villous structure
[SEE FIGURE IN ORIGINAL]
Blood pressure and proteinuria can be readily assessed in the
antenatal-care setting. If abnormalities are found, the woman should
be admitted to hospital or referred to an antenatal day unit for
further investigations. n5
The loss of serum protein and the increase in capillary endothelial
permeability lead to a decrease in intravascular volume and increased
tissue oedema. n31 All organs can be affected, including the liver
(producing abdominal pain), brain (producing headache and convulsion),
and the lungs (producing breathlessness). Peripheral oedema also
occurs, but it is variable and is not a useful diagnostic sign. The
decrease in blood volume can lead to an increase in maternal
haemoglobin concentration and is associated with an increased risk of
intrauterine growth restriction. n29
In normal pregnancy, the platelet count can fall below 200 x 10<9>/L
because of the normal maternal blood-volume expansion. In
pre-eclampsia, the platelet count falls further and is associated with
progressive disease. n29 This fall is probably a result of both
increased consumption and intravascular destruction. Associated
coagulation abnormalities are unlikely if the count is above 100 x
10<9>/L. n32 A low platelet count is one component of the HELLP
syndrome (haemolysis, elevated liver enzymes, and low platelets),
which carries a particular risk to the mother. n33
Serum concentrations of uric acid fall in normal pregnancy because
renal excretion increases. In pre-eclampsia, there can be a rise in
uric acid concentrations that correlates with poorer outcome for both
mother and baby. n33 This rise is due mostly to a decrease in renal
excretion, but there is probably also increased production secondary
to tissue ischaemia and oxidative stress. This variable is a
particularly sensitive marker of disease progression and risk.
Liver involvement in pre-eclampsia is very varied but is the cause of
the upper epigastric pain commonly seen in the disorder. The liver
swells as a result of local oedema secondary to inflammatory
infiltrates and obstructed blood flow in the sinusoids. Haemorrhage
can occur beneath the liver capsule and may be so extensive as to
cause rupture of the capsule into the peritoneal cavity. If a
haematoma or haemorrhage is suspected, the liver should be examined by
ultrasonography. n34 Liver involvement can be assessed by measurement
of alanine aminotransferase and aspartate aminotransferase activities
in serum; they increase in pre-eclampsia as a result of leakage across
cell membranes. Rises in these enzymes are part of the HELLP syndrome.
n33 With substantial liver involvement there are coagulation
abnormalities that result from hepatic dysfunction and not
disseminated intravascular coagulation, which is a rare complication
of pre-eclampsia in the absence of placental abruption. n35
Renal function is generally maintained in pre-eclampsia until the late
stage. In normal pregnancy, there is an increase in creatinine
clearance with a concomitant decrease in serum creatinine and urea
concentrations. If creatinine concentrations are high early in the
disease process, underlying renal disease should be suspected. In
severe disease, rises in serum creatinine can be seen and are
associated with worsening outcome. n25 Acute renal failure is now rare
in pre-eclampsia in more developed countries; n1, n36 most cases are
associated with haemorrhage or sepsis. Most cases of renal failure are
due to acute tubular necrosis, and most patients recover with no
long-term renal impairment. n36 Acute cortical necrosis, a permanent
cause of renal failure, occurs in less than 4% of all cases of renal
failure in pre-eclampsia. n37
Numbers of neurological sequelae, such as eclampsia and stroke, are
decreasing, n2 perhaps because of earlier intervention and delivery or
environmental factors. The fall in incidence antedates the use of
antihypertensive drugs and magnesium sulphate. n2 Cerebral oedema is
associated with convulsions and can be seen on computed tomography and
magnetic resonance imaging. This disorder has been described as
posterior leucoencephalopathy syndrome (PLES). n38 It is not a new
diagnosis but a radiological description. The cerebral oedema may
antedate eclampsia, because occipital-lobe blindness n39 can occur in
the absence of eclampsia and is completely reversible.
*Hypertension and Pre-ecampsia
Heart Disease Weekly
December 7, 2003
HEADLINE: OBSTETRICS: Brachial artery flow-mediated dilation
assessments predict pre-eclampsia
BODY:
Brachial artery flow-mediated dilation assessments predict pre-eclampsia.
"Endothelial injury and increased vascular reactivity are involved in
the pathogenesis of pre-eclampsia (pregnancy-induced hypertension). To
investigate whether flow-mediated dilation (endothelium-dependent
dilation) and the reactive hyperemic response can predict
pre-eclampsia, we prospectively measured flow-mediated dilation and
the Doppler flow velocity pattern (V, cm/s) in the brachial artery
using high-resolution ultrasound in 43 pregnant women (32plusmn5 years
old) in the second half of their pregnancy, and compared the findings
with traditional risk factors," scientists in Japan stated.
"Regarding the Doppler flow velocity pattern, the pulsatility index
(PI)=(systolic V-diastolic V)/mean V and resistance index
(RI)=(systolic V-diastolic V)/systolic V were calculated," they said.
"For the flow-mediated dilation, the per cent diameter changes were
determined based on those from baseline to hyperemic conditions. Nine
women suffered from pre-eclampsia and 34 women remained normotensive.
Only flow-mediated dilation was found to be significantly lower in the
subsequently developed pre-eclampsia patients (1.6plusmn1.0% in
subsequently developed pre-eclampsia patients vs. 11.0plusmn4.5% in
normotensive patients, p<0.05)," reported B. Takase and colleagues,
National Defense Medical College, Research Center.
"Neither the other traditional factors nor the Doppler flow velocity
pattern were significantly different between the subsequently
developed pre-eclampsia and normotensive patients. If a normal cutoff
value of 3.0% obtained from age-matched 14 nonpregnant women
(32plusmn7 years old) in our laboratory was used, the positive
predictive value of flow-mediated dilation (<3.0%) for subsequent
pre-eclampsia is 90% and the negative predictive value is 100%," they
noted.
"In conclusion, flow-mediated dilation in brachial artery can be a
simple and noninvasive modality to predict pre-eclampsia."
Takase and colleagues published their study in Journal of Human
Hypertension (Flow-mediated dilation in brachial artery in the second
half of pregnancy and prediction of pre-eclampsia. J Hum Hypertension,
2003;17(10):697-704).
For additional information, contact B. Takase, National Def Med
College, Research Center, 3-2 Namiki, Tokorozawa, Saitama 3598513,
Japan.
The publisher's contact information for the Journal of Human
Hypertension is: Nature Publishing Group, Macmillan Building, 4 Crinan
St., London N1 9XW, UK.
The information in this article comes under the major subject areas of
Angiology, Cardiology, Hypertension Risk Factor and Obstetrics.
This article was prepared by Heart Disease Weekly editors from staff
and other reports.
Lancet 2000; 355 (9198): 81-82
January 8, 2000
TITLE: Maternal blood pressure and birthweight
Hypertension in pregnancy is a leading cause of maternal and neonatal
mortality and morbidity, so a large proportion of antenatal care goes
to the detection and management of this disorder. Antihypertensive
drug therapy is an important part of management strategy. The effect
of such therapy on the baby's birthweight has been examined by P von
Dadelszen and colleagues in their meta- analyses, reported in today's
Lancet, of up to 45 randomised controlled trials.
The investigators noted the effect of change in mean arterial blood
pressure (MAP) in a novel way. MAPs were calculated for blood pressure
at entry to the trial and before delivery. Changes in MAPs (DeltaDMAP)
between these two times were compared between drug and placebo groups.
A DeltaDMAP of 10 mm Hg meant that the MAP had fallen by 10 mm Hg more
in the treatment than in the placebo group. Drug/drug and drug/placebo
comparisons were made. For drug/drug comparisons beta-blockers were
arbitrarily assigned to be the experimental intervention and
methyldopa to be the control. 38 trials related to therapy for
hypertension of late onset in pregnancy; the remainder were trials of
therapy for chronic hypertension. The agents used were
alpha-methyldopa, various beta- blockers, thiazides, ketanserin,
hydralazine, calcium-channel blockers, and clonidine. Despite this
striking heterogeneity, fall in blood pressure was significantly
related to the proportion of small-for-gestational-age (SGA) infants
and inversely to the mean birthweight.
A fall in blood pressure of 10 mm Hg was associated with a 145 g
decrease in birthweight. This was the maximum effect between trials.
Only one trial showed a mean fall in blood pressure greater than 10 mm
Hg and, paradoxically, in that trial the approximately 16 mm Hg fall
in blood pressure was associated with no change in birthweight.
Nevertheless, the relation held statistically, although only 16% of
the variation in birthweight could be accounted for by the change in
blood pressure.
The investigators excluded two trials. One was by Butters et al,n 1*
which showed a remarkably large fall in birthweight for a relatively
small fall in blood pressure. This trial has been considered an
outlier in other meta-analyses,n 2* and it has also been subject to
methodological controversy.n 2* The other trial, which compared
nicardipine with labetalol, was also an obvious outlier from
inspection of the data of von Dadelszen's meta-analysis.
No other predictor variables, such as type of hypertension, severity
of hypertension, nature of the hypotensive agent, or the length of
therapy was thought to be related to birthweight or rate of SGA
births.
Oncology Business Week
March 28, 2004
HEADLINE: PRE-ECLAMPSIA: Hypertension condition during pregnancy
linked to increased cancer risk
BODY:
Women with a history of pre-eclampsia are at increased risk of cancer,
particularly cancers of the stomach, breast, ovary, lung, and larynx,
according to new research.
Previous studies have shown either no association or have suggested a
protective association between pre-eclampsia and cancer, but the
evidence is inconsistent.
Ora Paltiel, Hadassah-Hebrew University, Israel; and colleagues at the
Albert Einstein College of Medicine of Yeshiva University and the
Mailman School of Public Health, Columbia University, both in New
York, published their findings on the British Medical Journal website
on March 5, 2004 (www.bmj.com, Online First section).
The researchers compared the incidence of cancer among 37,033 women
who delivered babies in three large hospitals in West Jerusalem during
1964-76.
After pre-eclampsia there was an overall excess of cancer when all
sites were combined. The risk of breast cancer was significantly
increased for pre-eclamptic women after taking into account
differences in age and number of births prior to entry into the study,
Paltiel and associates reported.
The risk of cancers of the stomach, ovary, lung, or larynx were also
significantly increased after adjusting for age.
The authors suggest that certain environmental and genetic factors may
contribute to the development of both pre-eclampsia and cancer in
Middle Eastern populations.
Drug Week
January 9, 2004
HEADLINE: HYPERTENSION: Pre-eclampsia correlates with reduced plasma
coenzyme Q10 levels
BODY:
Pre-eclampsia correlates with reduced plasma coenzyme Q10 levels.
According to published research from Ecuador, "pre-eclampsia is a
common (approximately 7% of all pregnancies) disorder of human
pregnancy in which the normal hemodynamic response to pregnancy is
compromised. Despite many years of intensive research, the
pathogenesis of pre-eclampsia is still not fully understood. The
objective of the present study was to investigate the concentration of
coenzyme Q10 in normal pregnancy and pre-eclampsia."
"Pregnant women (n = 18), women with pre-eclampsia. (n = 12), and
nonpregnant normotensive women (n = 22) were included. Plasma levels
of coenzyme Q10 were measured by high-performance liquid
chromatography. Plasma coenzyme Q10 levels were significantly higher
in normal pregnant women (mean = 1.08, SEM = 0.08 micromol/l; p<0.005)
in comparison to nonpregnant women (mean = 0.86, SEM = 0.16
micromol/1) and women with pre-eclampsia (mean = 0.7, SEM = 0.03
micromol/l; p<0.0001)," said E. Teran and colleagues, Central
University of Ecuador, Biomedical Center.
"These results demonstrated that during pre-eclampsia there is a
significant decrease in plasma levels of coenzyme Q10 compared to
normal pregnant women, and compared to those who are not pregnant,"
researchers concluded.
*Pre-eclampsia and its Relation to Placental Abruption:
TITLE: Effect of antioxidants on the occurrence of pre-eclampsia in
women at increased risk: a randomised trial
Lancet 1999; 354 (9181): 810-816
September 4, 1999
The primary outcome measure was the ratio PAI-1/PAI-2 and the
secondary outcome measure the frequency of pre-eclampsia, which was
defined prospectively according to the guidelines of the International
Society for the Study of Hypertension in Pregnancy.n 29* Gestational
hypertension was defined as two recordings of diastolic blood pressure
of 90 mm Hg or higher at least 4 h apart, and severe gestational
hypertension as two recordings of diastolic blood pressure of 110 mm
Hg or higher at least 4 h apart or one recording of diastolic blood
pressure of at least 120 mm Hg. Proteinuria was defined as excretion
of 300 mg or more in 24 h or two readings of 2+ or higher on dipstick
analysis of midstream or catheter urine specimens if no 24 h
collection was available. Women were classified as previously
normotensive or with chronic hypertension before 20 weeks' gestation.
For previously normotensive women, pre-eclampsia was defined as
gestational hypertension with proteinuria and severe pre-eclampsia as
severe gestational hypertension with proteinuria. For women with
chronic hypertension, superimposed pre-eclampsia was defined by the
new development of proteinuria. For this study, all women were
allocated to an outcome category on the basis of their blood pressure
before delivery.
Other adverse perinatal outcomes were: placental abruption (the
presence of retroplacental clot at delivery and abdominal pain,
bleeding, or both immediately before delivery); spontaneous preterm
delivery (before 37 weeks' gestation); intrauterine death; and small-
for-gestational-age infants (on or below the 10th centile for
gestation and sex, corrected for maternal height, weight, parity, and
ethnic origin by customised centile chartsn 30*).
Pediatrics 2004; 113: 35-41
January, 2004
Outcomes and Confounding Variables
The primary study outcome was presence or absence of risk-adjusted,
predischarge mortality or major morbidity, including BPD, severe ICH,
severe ROP, or severe NEC. These morbidities were chosen because of
demonstrated relationships to long-term neurodevelopmental outcomes of
VLBW infants. [n22-n24] Morbidities were counted among survivors and
when possible also among infants who died. The composite outcome of
death or major morbidity was chosen as the primary outcome to account
for possible trade-offs between death and major morbidity. Secondary
outcomes included death alone and death in combination with each major
morbidity.
Information on factors previously shown to affect the selected study
outcomes were included as independent variables in multivariable
regression analyses. Possible confounders included both infant and
maternal variables unrelated to the care provided by clinicians and
practice variables related to clinician decision making. The infant
and maternal variables were birth weight, gestational age, race (white
or nonwhite), gender, multiple gestation pregnancy, SGA status,
5-minute Apgar score <5, and maternal hypertension or preeclampsia.
Practice variables included CRIB score, use of antenatal
glucocorticoids, and use of intrapartum antibiotic. We chose to
evaluate separately practice variables to emphasize possible
opportunities to modify care to improve outcome.
Pediatrics 2003; 112: 570-577
September, 2003
During week 1, trypsinogen-1 showed a positive correlation with
gestational age (r = 0.36, P < .001). The concentration of
trypsinogen-1 did not correlate with proteinuric preeclampsia,
antenatal glucocorticoid treatment, BW, severity of acute respiratory
distress, or duration of mechanical ventilation (data not shown).
A weak negative correlation was observed between trypsinogen-2
concentration during week 1 and BW (r = -0.26, P = .005), whereas
there was no correlation with gestational age during week 1 or 2 (data
not shown). No association existed between trypsinogen-2 and antenatal
glucocorticoid treatment. Trypsinogen-2 was significantly higher
during weeks 1 and 2 in infants who were born to mothers with
proteinuric preeclampsia than in those who were born to mothers with
chorioamnionitis or premature rupture of the membranes or in those who
were born to mothers without these complications (Fig 2). The infants
who were born to mothers with proteinuric preeclampsia (n = 11) were
of a higher GA (mean [+/-SD]: 28.6 +/- 1.8 weeks vs 26.6 +/- 1.8
weeks, respectively; P = .003) but had more severe acute respiratory
distress as indicated by a lower initial arterial to alveolar oxygen
tension ratio (aAPO[2]; mean [+/-SD] 0.15 +/- 0.07 vs 0.33 +/- 0.22; P
= .02). A negative correlation existed between trypsinogen-2 during
weeks 1 and 2 and surfactant maturity, as measured as L/S ratio in TAF
(week 1: r = -0.36, P = .001; week 2: r = -0.66, P < .0001).
Furthermore, the presence of phosphatidyl glycerol in TAF was
associated with lower trypsinogen-2 levels during weeks 1 and 2 (Table
2). Trypsinogen-2 was higher in infants with an initial aAPO[2]
</=0.22 and in those who needed treatment with surfactant (Table 2).
The concentration of trypsinogen-2 during week 1 showed a positive
correlation with duration of mechanical ventilation (r = 0.30, P =
.001).
Pediatrics 2003; 112: 583-587
September, 2003
We evaluated predictors that might be associated with failure of the
second indomethacin course: gestational age, birth weight, sex,
exposure to antenatal betamethasone, maternal diagnoses of
chorioamnionitis and preeclampsia, presence of respiratory distress
syndrome, ventilator support score, maximum serum creatinine after the
initial course of indomethacin, fluid administration (normalized to
body weight) during the first 96 hours of life (data not shown),
indomethacin treatment approach (symptomatic versus prophylactic),
year of birth (December 1, 1991, to December 21, 1996, vs January 1,
1997, to June 15, 2001), number of indomethacin doses and the
cumulative dose administered in the initial course, the postnatal age
when infants were treated initially and when they were retreated for
symptomatic reopening, the number of days between indomethacin
treatment courses, the results of the Doppler examination after the
initial course of indomethacin, and temporally related sepsis at
indomethacin retreatment. These univariate analyses revealed that the
only significant predictor of PDA ligation after the second course of
indomethacin was the demonstration (by Doppler) of persistent ductus
flow after the first course of indomethacin (Tables 1 and 2). Among
the 32 newborns who received a second course of indomethacin, 9 had
persistent ductus flow on Doppler examination after the initial
indomethacin course. All of these newborns ultimately met our criteria
for surgical ligation of a hemodynamically significant PDA after the
second course of indomethacin. In contrast, only 9 of (39%) 23
newborns with absent Doppler flow after the initial indomethacin
course developed a hemodynamically significant PDA and underwent
surgical ligation after the second course (P = .002, [chi]<2>
analysis).
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assessments predict pre-eclampsia
Search Strategy
Lexis-Nexis Search:
"Pre-eclampsia" or "preeclampsia"
also used various narrowing search terms to limit the field
Thanks again for your question.
Regards,
Anthony (adilorenga) |
