Gynecologists. Obstet Gynecol. 2011;118: 751–753.)
Other oral hypoglycemics, such as the sulfonylureas, have inferior data and
increase risk of adverse effects.
J.B. is a good candidate for insulin therapy because she is greater than 30 weeks’
gestation and has a fasting blood sugar level less than 110 mg/dL. Doses should be
increased or decreased to achieve glycemic control.
RISK OF DEVELOPING DIABETES MELLITUS
CASE 49-4, QUESTION 4: Why is J.B. at risk for developing diabetes mellitus after delivery?
Glucose tolerance normalizes after delivery for most women. Women with GDM,
however, have a 15% to 50% chance of developing nongestational diabetes within 5
72 The highest risk is in women who are obese or were diagnosed before
24 weeks’ gestation or who had marked hyperglycemia during or soon after
pregnancy. The risk of developing GDM in a future pregnancy is estimated to be 50%
J.B. should try to minimize the potential for development of insulin resistance by
exercising and maintaining a normal weight. She should also have her glucose
checked with a 2-hour OGTT at her postpartum appointment 6 weeks after delivery
and then at least every 1 to 3 years with screening of either fasting blood sugar or
HgbA1c. In addition, J.B. should be instructed about the importance of using an
effective birth control method to prevent unplanned pregnancies. She also needs to
schedule regular appointments with her primary-care clinician.
QUESTION 1: T.D., a 37-year-old G1, P0, obese black woman was diagnosed with stage 1 hypertension
Hypertensive disease occurs in 5% to 8% of all pregnancies and is a major cause
of maternal and perinatal morbidity and mortality.
80 From 15% to 24% of maternal
deaths in developed countries are attributed to hypertensive disorders in
81,82 Hypertension in pregnancy is defined as a systolic BP of at least 140
mm Hg or a diastolic BP of at least 90 mm Hg on two separate occasions at least 6
Women with pregnancy-associated hypertension can be grouped into the following
categories: chronic hypertension, preeclampsia–eclampsia, preeclampsia
superimposed on chronic hypertension, and gestational hypertension.
delivery, gestational hypertension is ultimately delineated as either (a) transient
hypertension of pregnancy if preeclampsia is absent during delivery and BP
normalizes by 12 weeks postpartum or (b) chronic hypertension if BP remains
Chronic hypertension is defined as hypertension diagnosed before conception or
before the 20th week of gestation, or hypertension persisting beyond 12 weeks
80 Hypertension noted after the 20th week of gestation might be difficult to
classify, particularly if a woman has had inadequate prenatal care without
Women with chronic hypertension, similar to T.D., commonly have a normal BP
during the first half of pregnancy because of the physiologic decline of BP during the
83 BP usually returns to the prepregnancy level by the third trimester.
T.D.’s diastolic pressure decreased from the prepregnancy levels of 90 to 95 mm Hg
to 86 to 90 mm Hg during the second trimester. It is normal for T.D.’s BP to increase
during the third trimester. These changes in BP make it difficult to differentiate
chronic hypertension from preeclampsia during the second half of pregnancy in
women with late prenatal care or inadequate BP monitoring. It is also difficult to
diagnose preeclampsia superimposed on existing hypertension using BP
measurements alone. A sharp increase in T.D.’s pressure of more than 30 mm Hg
systolic or more than 15 mm Hg diastolic could be consistent with preeclampsia.
Without coexisting proteinuria (≥0.3 g/24 hours or ≥1+ in a random urine sample) or
evidence of renal dysfunction, a diagnosis of preeclampsia would be a reach.
has no proteinuria, and a normal SCr and serum UA. T.D has chronic hypertension,
but it is unlikely that T.D. has preeclampsia at this time.
CASE 49-5, QUESTION 2: What risk factors does T.D. have for developing preeclampsia?
Preeclampsia is a pregnancy-specific condition usually occurring after 20 weeks’
gestation and consisting of hypertension with proteinuria.
multiple organ systems (e.g., kidney, liver, hematologic, CNS). The signs and
symptoms are often unpredictable and can be mistaken for other disorders. Because
edema is so common in normal pregnancy and is not specific, it is no longer used as a
criterion for the diagnosis of preeclampsia. Preeclampsia is a consequence of
progressive placental and maternal endothelial cell dysfunction, increased platelet
aggregation, and loss of arterial vasoregulation. A variant of preeclampsia is
Hemolysis, elevate Liver enzymes, Low Platelet count (HELLP) syndrome, which
consists of hemolysis (H), elevated liver (EL) enzymes, and low platelet (LP) count.
HELLP can also be life–threatening and may not always present with proteinuria and
When women with preeclampsia exhibit seizures, the term eclampsia is used.
Women with preeclampsia may unpredictably progress rapidly from mild-to-severe
preeclampsia and to eclampsia within days or even hours. Eclampsia is a potentially
preventable complication of preeclampsia. About 20% of women who experience
eclampsia have a diastolic BP less than 90 mm Hg or no proteinuria.
The term gestational hypertension is used when BP is increased during pregnancy
or is increased in the first 24 hours postpartum in a woman without signs or
symptoms of preeclampsia and without preexisting hypertension.
gestational hypertension are at high risk of recurrence during subsequent pregnancies.
Preeclampsia occurs most commonly during the first pregnancy (two-thirds of
cases). Obesity and increasing maternal age are risk factors.
increase the risk for preeclampsia include diabetes mellitus or insulin resistance and
renal disease. Pregnancy-associated risk factors include multifetal gestations, urinary
tract infection, certain fetal chromosomal anomalies, and hydatidiform moles. A
family history of a sister or mother with preeclampsia significantly increases the risk
of developing preeclampsia. Women with previous preeclampsia are at high risk for
recurrence in subsequent pregnancies, particularly if it developed before 30 weeks’
In addition to her age and obesity, chronic hypertension is the most
significant aspect of T.D.’s medical history, which confers a 25% risk of developing
CASE 49-5, QUESTION 3: What subjective and objective data should be monitored in T.D. for the
T.D. should have her BP monitored frequently. If protein is detected in a random
urinalysis, then a 24-hour urine collection for protein and creatinine can be repeated
to determine accurately the degree of proteinuria and severity of disease.
ultrasounds should be obtained to assess fetal growth because IUGR is common in
pregnant women with chronic hypertension. T.D. should be taught to recognize and
immediately report all signs and symptoms of preeclampsia, such as nondependent
edema (i.e., swelling of face or hands), headaches, and visual disturbances. The
latter two are signs of severe preeclampsia and may indicate impending eclampsia.
Upper abdominal pain also can be a sign of severe preeclampsia, indicating hepatic
86 Because T.D. has chronic hypertension, worsening of
hypertension alone may not be a reliable sign of superimposed
preeclampsia. Proteinuria is the best indicator of superimposed preeclampsia in a
pregnant woman with chronic hypertension and no renal disease.
CASE 49-5, QUESTION 4: Should T.D.’s chronic hypertension be treated with antihypertensive drugs to
The goal of antihypertensive therapy for women with chronic hypertension during
pregnancy is to minimize the risks to the mother of an elevated BP without
compromising placental perfusion.
84 The value of treating pregnant women with
chronic antihypertension drugs remains an area of ongoing debate. A sustained
diastolic BP of more than 100 mm Hg may cause maternal vascular damage,
especially if the diastolic pressure is more than 105 to 110 mm Hg.
unlikely with a diastolic BP of less than 100 mm Hg. Therefore, many clinicians
recommend treatment with antihypertensive drugs to lower diastolic pressures of
80 Treatment of a diastolic BP of less than 100 mm Hg
should be reserved for women with chronic hypertension and target organ damage
(e.g., left-ventricular hypertrophy) or underlying renal disease because
antihypertensive drugs can decrease placental blood flow, which might increase fetal
88,89 Treatment of mild-to-moderate hypertension is associated with
a decrease in the risk of developing severe hypertension by approximately 50%, but
the overall risk of developing preeclampsia is unchanged.
evidence of a reduction in the risk of stillbirth, fetal growth restriction, or preterm
birth if women with chronic hypertension with systolic BP of 140 to 169 mm Hg or
diastolic BP of 90 to 109 mm Hg are given antihypertensive therapy.
women treated with antihypertensive therapy were more likely to experience adverse
drug effects compared with those who received placebo or were untreated.
Antihypertensive therapy, however, is required to reduce the risk of cardiovascular
morbidity such as heart or renal failure and acute risk of stroke in pregnant women
with severe hypertension (diastolic >110 mm Hg).
T.D. has normal renal function and her BP is less than 100 mm Hg; she does not
need antihypertensive drug treatment at this time. If T.D. had been on drug therapy
before conception, some experts would have her continue during the pregnancy.
In such cases, however, the doses of the antihypertensive agents often need to be
lowered or discontinued altogether to prevent hypotension because the maternal BP
naturally decreases during the second trimester. Perinatal outcomes in women with
untreated chronic hypertension who do not progress to preeclampsia are similar to
those of the general obstetric population.
85 Although chronic hypertension is a major
risk factor for preeclampsia, treating T.D.’s uncomplicated mild chronic
hypertension is unlikely to prevent the development of preeclampsia.
CASE 49-5, QUESTION 5: When T.D. returns to the clinic 2 weeks later at 30 weeks’ gestation, her BP
Methyldopa, a centrally acting α-agonist that decreases sympathetic outflow to
decrease BP, is the most commonly used antihypertensive agent for chronic treatment
of hypertension in pregnancy in the United States. The usual starting dose of 750 to
1,000 mg/day, to be administered in three to four daily divided doses, can be
increased to 2 or 3 g/day if needed. Higher doses may be needed to control BP in
Methyldopa, classified as category B for fetal risk, has the longest and best safety
record of all antihypertensive agents during pregnancy. Despite its common use, few
adverse effects have been reported in neonates exposed to methyldopa in utero. In
addition, no congenital anomalies are associated with methyldopa.
Dizziness and sedation, accompanied by a loss of energy, are among the most
common adverse effects reported by pregnant women.
effects occur early in therapy and tend to subside, but may recur with an increased
dosage. Problems with postural hypotension usually do not occur in pregnant
91 Patients should be monitored for methyldopa-induced liver damage.
drugs used to treat hypertension in pregnancy include labetalol and calcium-channel
blockers. A review of drug therapies for the treatment of chronic hypertension in
pregnancy is listed in Table 49-4.
T.D. should be started on methyldopa 500 mg PO 3 times daily. If T.D. cannot
tolerate the side effects, she can be switched to labetalol 200 mg PO twice daily. The
only antihypertensive drugs absolutely contraindicated during pregnancy are ACEI
and angiotensin II receptor blockers because of the association with fetal and
newborn morbidity and mortality.
demonstrates fetal growth restriction. Laboratory results are as follows:
Aspartate aminotransferase (AST), 25 units/L
Alanine aminotransferase (ALT), 16 units/L
The causes of preeclampsia currently remain unknown. Although the pathogenesis
begins early in pregnancy, the disease is not clinically evident until the latter half of
the pregnancy and persists until the fetus is delivered.
placental vascular bed changes and endothelial cell dysfunction are integral to the
Early in a normal pregnancy, the trophoblastic migration and invasion of the uterine
spiral arteries result in physiologic changes within the placental vascular bed that
facilitate maximal intervillous blood flow. The physiologic changes within these
spiral arteries are responsible for creating a fixed low-resistance arteriolar circuit,
which increases blood supply to the growing fetus. In preeclampsia, these
physiologic changes do not occur completely, resulting in decreased perfusion and,
consequently, placental ischemia.
An intact vascular endothelium assists in preserving the integrity of vasculature,
mediating immune and inflammatory responses, preventing intravascular coagulation,
and modulating the contractility of the underlying smooth muscle cells.
In normal pregnancy, prostacyclin is increased 8 to 10 times, creating an increased
ratio of prostacyclin to thromboxane A2
98 The biologic dominance of prostacyclin
along with nitric oxide plays an important role in maintaining vasodilation throughout
pregnancy. Prostacyclin may be responsible for vascular refractoriness to angiotensin
II in normal pregnancy. In preeclampsia, the ratio of prostacyclin to thromboxane A2
is biologically dominant during preeclampsia, leading
to increased vascular sensitivity to angiotensin II and norepinephrine.
increased release of thromboxane A2
is believed to be caused by endothelial cell
dysfunction. The end result is vasospasm, which further increases endothelial cell
98 Reduced activity of nitric oxide synthase and
decreased nitric oxide-dependent or nitric oxide-independent endothelium-derived
relaxing factor are believed to increase the vasoconstrictive potential of pressures
Drugs for Treatment of Chronic Hypertension in Pregnancy and Lactation
Methyldopa 750–1,000 mg/day start
Longest safety record in pregnancy. Considered a first-line
88 Dizziness, sedation, and lack of energy are common
symptoms, which tend to resolve. Can cause liver toxicity.
Low breast milk concentrations, so considered safe in breastfeeding
Labetalol 200–400 mg/day start,
Combined α- and β-receptor antagonist properties.
methyldopa owing to fewer side effects. Neonatal effects
could include bradycardia and hypotension. Low
concentration in breast milk and generally considered safe in
Other β-blockers Various Atenolol in particular associated with decreased placental
IUGR thought to be related to βblocker-induced increased vascular resistance in mother and
fetus. Atenolol, acebutolol, metoprolol, nadolol, and sotalol
can have high milk-to-plasma ratios and accumulate in breast
milk, creating potential risk for neonatal blockade.
Propanolol found in only small amounts in breast milk and
generally considered safe, but infants should be monitored for
hypotension, bradycardia, and blood glucose changes
amlodipine. Concentrations of nifedipine in breast milk are
low and considered compatible with breast-feeding
Diuretics Various Not first-line agents, although probably safe.
regarding potential interference with normal blood volume
expansion in pregnancy. Avoid if preeclampsia or IUGR
already present. Concentration low in breast milk, but may
ACEI or ARB Contraindicated Contraindicated in pregnancy in all trimesters. Fetal renal
failure when used after first trimester, resulting in
oligohydramnios, limb contractures, pulmonary hypoplasia,
skull hypoplasia, and irreversible neonatal renal failure.
Increased risk major birth defects with first-trimester ACEI
75 Minimal amounts of captopril and enalapril in
breast milk and both considered compatible with breastfeeding.
229 Minimal amounts of benazepril in breast milk
Endothelial cell dysfunction in pregnancy is thought to be caused by oxidative
stress. Intermittent hypoxic and reperfusion injury that occurs as a consequence of
decreased placental perfusion may increase oxidative stress.
eventually leads to disruption of the vascular lining, which causes leaking capillary
membranes, allowing fluid to leak into the interstitium.
results in hypovolemia, hemoconcentration, and consequently an increase in
hematocrit. The loss of plasma volume, vasospasm, and microthrombi decrease
perfusion of the kidney, CNS, liver, and other organs. The loss of intravascular
proteins in the urine secondary to renal damage, and through damaged epithelia,
decreases plasma oncotic pressure and leads to a rapid onset of nondependent
edema. The imbalance of endogenous procoagulants and anticoagulants produces
platelet consumption and results in thrombocytopenia and coagulation defects.
T.D.’s diastolic BP is now higher than it was before her pregnancy and has
increased by 12 mm Hg in the last 3 weeks. Although an increase in BP by itself is
not diagnostic of preeclampsia, the new finding of proteinuria confirms the diagnosis.
Other evidence for preeclampsia includes the elevated serum UA concentration,
which is a sensitive marker for preeclampsia, and elevated SCr.
headaches, visual disturbances, and abdominal pain, which are symptoms of severe
preeclampsia. The transaminases and platelet count are normal; therefore, she does
not have HELLP syndrome at this time. T.D.’s clinical presentation is consistent with
mild preeclampsia; however, a 24-hour urine collection should be obtained to
measure protein excretion, quantify the urine output, and further rule out severe
The delivery of the fetus is the only cure for preeclampsia and would be the best
treatment option for T.D. if she were at more than 37 weeks’ gestation. T.D. has mild
disease, however, and is not close to term. Her delivery should be postponed
because premature delivery increases neonatal morbidity and mortality. T.D.’s
fetus is somewhat growth restricted, which is common in women with chronic
hypertension, with or without superimposed preeclampsia. If T.D.’s fetus is severely
growth restricted or if subsequent fetal biophysical testing is abnormal, premature
80 Because neither of these is evident in the present
circumstances, T.D. should continue her pregnancy under very close medical
supervision. It has been suggested that continued hospitalization is appropriate for
women with preterm onset of mild preeclampsia, such as T.D.
for rapid intervention in case of rapid progression of disease or associated
complications. Probably, a role exists for outpatient monitoring of some select
women with very frequent maternal and fetal monitoring, and rehospitalization for
T.D. is also a candidate for administration of glucocorticoids for fetal lung
maturation (see Case 49-7, Question 7). Bed rest in the lateral decubitus position is
usually suggested and may help reduce BP and promote diuresis by decreasing
vasoconstriction and improving renal and uteroplacental perfusion.
T.D. should have her BP measured regularly each day. Liver transaminases,
platelets, and creatinine should be measured periodically and whenever her clinical
status changes. She also should be assessed for symptoms of severe preeclampsia
(e.g., headaches, visual disturbances, epigastric or right upper-quadrant pain). Fetal
80 One approach is to perform a modified biophysical
profile, a test performed to ensure fetal well-being using ultrasonography measuring
fetal breathing, tone, movement, and amniotic fluid volume with an assessment in
fetal heart rate, twice a week and whenever maternal clinical status changes, and an
ultrasound for fetal growth every 3 to 4 weeks.
CASE 49-5, QUESTION 8: T.D.’s BP for about 2 weeks ranged from 140 to 150 mm Hg systolic and 90 to
Estimated fetal weight by ultrasound is 1,700 g, which is between the 10th and 25th percentile for a
this diagnosis in T.D., and what complications may occur?
T.D. has developed severe preeclampsia.
84 Her systolic and diastolic BP are
greater than 160 and 112 mm Hg, respectively. She has greater than 3+ protein in a
random urine sample, and her SCr is elevated. She complains of headaches and
visual disturbances. T.D. is also thrombocytopenic as her platelet count is
95,000/μL. Although her liver transaminases are currently normal, she may be
developing HELLP syndrome, a variant of severe preeclampsia associated with a
high incidence of maternal and perinatal morbidity and mortality. Therefore, her
laboratory values should continue to be monitored even as delivery is being planned.
T.D. is at risk for cerebral hemorrhage, cerebral edema, encephalopathy,
coagulopathies, pulmonary edema, liver failure, renal failure, and eclamptic
85,86 Severe preeclampsia is dangerous not only to T.D. but also to her fetus
because uteroplacental perfusion is compromised. T.D. requires drug treatments to
both lower her BP and prevent eclampsia, as well as delivery.
ACUTE TREATMENT OF SEVERE HYPERTENSION
CASE 49-5, QUESTION 9: How should T.D.’s severe hypertension be treated?
The goal of antihypertensive therapy in T.D. is to prevent cerebral complications
(e.g., encephalopathy, hemorrhage).
85 Although it is important to reduce the maternal
BP, it must be accomplished gradually while the fetus is in utero because a sudden
large drop in maternal BP could result in the reduction of uteroplacental perfusion.
Because of the potential for fetal bradycardia during or after acute treatment of
maternal hypertension, continuous fetal heart rate monitoring should be considered.
Hydralazine, a direct arterial smooth muscle dilator, has in the past been the drug of
choice for the acute treatment of severe hypertension in pregnancy.
induces a baroreceptor-mediated tachycardia and increases cardiac output, which
increases uterine blood flow because the BP is lowered.
The onset of antihypertensive effect for hydralazine ranges from 10 to 20 minutes,
and duration of action ranges from 3 to 6 hours after an IV dose.
of hydralazine should not be repeated more frequently than every 20 to 30 minutes to
91 Nausea, vomiting, tachycardia, flushing, headache, and
tremors could occur. Some of these hydralazine-induced adverse effects mimic
symptoms associated with severe preeclampsia and imminent eclampsia, making it
difficult for a clinician to differentiate between drug-associated and disease-related
91 Fetal hydralazine serum concentrations are reportedly the same as or
higher than maternal serum concentrations, but drug-associated fetal abnormalities
Labetalol is also a commonly used drug to treat severe hypertension during
pregnancy. It should be administered IV in increasing doses of 20, 40, and 80 mg
every 10 minutes to a cumulative dose of 300 mg or until the diastolic pressure is
101 The onset of action is within 5 minutes, and its effect peaks
in 10 to 20 minutes with a duration of action ranging from 45 minutes to 6 hours.
IV labetalol is as effective as IV hydralazine in lowering BP in patients with
hypertension during pregnancy, but has fewer reported adverse effects.
meta-analysis of β-blocker trials for the treatment of hypertension in pregnancy,
labetalol was associated with less maternal hypotension, fewer cesarean deliveries,
and no increase in perinatal mortality.
also does not appear to decrease uteroplacental blood flow even with a decrease
91 Labetalol reduces cerebral perfusion pressure, which occurs in up
to 43% of women with severe preeclampsia, without negatively affecting cerebral
103 Decreased cerebral perfusion pressure may prevent progression to
eclampsia. However, it should be avoided in women with asthma and
104,105 Labetalol has also been associated with higher
rates of neonatal bradycardia and hypotension than hydralazine, but not higher rates
of neonatal intensive care admission.
Nifedipine has been used in doses of 10 mg for acute treatment of severe
hypertension during pregnancy because it can be given orally.
effective in decreasing BP without reducing uteroplacental blood flow or decreasing
fetal heart rate. Short-acting nifedipine capsules are no longer recommended for the
treatment of acute hypertensive urgency, however, because of the risk of stroke or
myocardial infarction, and it was never FDA-approved for this indication.
Immediate-release nifedipine continues to be used to treat hypertension in pregnancy,
however, because this unique patient population may not be at high risk for ischemic
events secondary to atherosclerotic disease.
88 Calcium gluconate or calcium chloride
should be available for IV administration in the event of sudden hypotension. Caution
should be used when giving nifedipine to women concomitantly treated with
magnesium sulfate because these drugs have synergistic effects, causing hypotension
Several studies comparing immediate-release oral nifedipine with IV labetalol in
hypertensive emergencies of pregnancy have found them to be equally effective in
107,108 Nifedipine lowers BP to less than 160 mm Hg systolic and less
than 100 mm Hg diastolic earlier than labetalol,
107 but it increases cardiac index
(see Chapter 21, Hypertensive Crises). The use of sustained-release nifedipine
capsules as an alternative is associated with a delay in BP control to 45 to 90
minutes, which is probably not acceptable.
Hydralazine 5 mg IV for 1 to 2 minutes should be administered to T.D. and
repeated in doses of 5 to 10 mg every 20 to 30 minutes to a cumulative dose of 20
85 T.D. should have repeated measurements of her BP at 15-minute intervals.
Because intervillous blood flow depends on maternal perfusion pressure, the goal is
to decrease the diastolic pressure to not less than 90 mm Hg.
maternal BP excessively may decrease uteroplacental perfusion and compromise the
fetus. A hypotensive overshoot can be observed with hydralazine, particularly in the
setting of volume depletion, which is typical of preeclampsia.
of hydralazine are not effective in lowering T.D.’s diastolic to less than 100 mm Hg,
labetalol 20 mg IV every 10 to 15 minutes can be given.
CASE 49-5, QUESTION 10: T.D. will undergo an induction of labor for her severe preeclampsia. Which
medication should be given to T.D. to prevent seizures?
The precise mechanism of anticonvulsant action of magnesium for the prevention
and treatment of eclamptic seizures is unknown. The anticonvulsant activity may be
partly mediated through blockade of an excitatory amino acid receptor, N-methyl-Daspartate.
106 Seizures are thought to be caused by decreased cerebral blood flow
because of vasospasm. Magnesium sulfate is a potent cerebral vasodilator and
increases the synthesis of prostacyclin, an endothelial vasodilator. It also causes a
dose-dependent decrease in systemic vascular resistance, which may explain its
transient hypotensive effect. Magnesium may also protect against oxidative injury to
Although termination of the pregnancy is the definitive treatment for severe
preeclampsia, the intrapartum and immediate postpartum periods are also the periods
of greatest risk for eclampsia.
84 Although the incidence of eclampsia is extremely
low, maternal morbidity and mortality are high.
In the United States, it has been
usual practice to treat all preeclamptic women with magnesium sulfate during labor
and for 12 to 24 hours postpartum.
In the United Kingdom, however, it is common
to reserve magnesium sulfate therapy for severe preeclampsia.
magnesium sulfate prevention of the progression of disease in mildly preeclamptic
women had been largely anecdotal in the past. In a large international study of more
than 10,000 women, published in 2002, magnesium sulfate clearly decreased the risk
of eclampsia in preeclamptic women by 58% compared with placebo.
observational study of nearly 2,500 women with mild preeclampsia (BP of 140/90
mm Hg and 1+ protein) found an incidence of eclampsia of about 1% without the use
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