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Chinese Medical Journal 2012;125(11):2067-2069 2067

Case report

Chronic hypertension superimposed on preeclampsia at 13

gestational weeks: a case report with reviewZHU Yu-chun, SUN Yu and YANG Hui-xia

Keywords: preeclampsia; second pregnancy trimester; induced abortion

Preeclampsia is represented by hypertension and proteinuria in pregnancy. It usually occurs after 20 gestational weeks.

There are few reports on preeclampsia before 20 gestational weeks. In this case, we report a patient with chronic

hypertension superimposed with preeclampsia at 13 gestational weeks.

Chin Med J 2012;125(11):2067-2069

reeclampsia, according to its definition, is represented

by hypertension and proteinuria in a pregnancy atover 20 weeks of gestation.1

Although its pathogenesis isstill unclear, the onset of preeclampsia is believed torelate to poor second placentation and remodeling of thespiral arteries. Therefore, it usually occurs after 20gestational weeks. There are few reports on preeclampsiabefore 20 gestational weeks

2,3and it is especially rare

before 15 weeks. Most of these cases are associated withtrophoblastic disease, triploidy, or antiphospholipidsyndrome. In this case, we report a patient with chronichypertension superimposed with preeclampsia at 13gestational weeks.

CASE REPORT

A 25-year-old woman (gravida 2 para 1) was admitted at14 gestational weeks on October 25, 2007, withhypertension that had persisted for 1 week. Her menstrualperiods had been regular before pregnancy. One weekpreviously, her blood pressure (BP) was found to be170/120 mmHg at a local clinic, with 3+ proteinuria ondipstick urinalysis. She did not complain and was nottreated. Three days later, her BP rose to 190/130 mmHgand she was recommended to take labetalol. However,she did not follow the doctors advice. Later, she was

admitted to our hospitals emergency center with a BP of180/120 mmHg and 2+ proteinuria; nonetheless, she stilldid not complain. The patient had no history ofhypertension. During her annual physical examination, 6months before her pregnancy, her BP was 120/70 mmHgand she had a normal urinalysis. She had had an artificialabortion in a previous pregnancy. There was a familyhistory of pregnancy-induced hypertension and diabeteson her mothers side and hypertension on her fathersside. At admission, the patients BP was 160/130 mmHg.No remarkable abnormalities were found during thephysical examination.

After admission, she was given oral nifedipine anddiazepam. She complained of headaches andlight-headedness. Furthermore, because her BP remained

at 180/100 mmHg, intravenous phentolamine was added

to her medication. On the second day of her admission,she complained of light-headedness, nausea andvomiting. With a BP of 170/120 mmHg, mannitol wasadministered to control her intracranial pressure and thenifedipine dosage was increased to 30 mg twice daily. Anexamination for optic fundi displayed normal results.Ultrasound revealed normal fetal anatomy and gestationconsistent with 14 weeks. Urinalysis showed 1+ to 2+proteinuria. Blood cell count, liver and renal functions,myocardial enzyme levels and coagulation function werenormal. Blood potassium was 2.87 mmol/L and becamenormal after intravenous supplementation. Abdominal,renal, adrenal and cardiac ultrasound investigationsrevealed normal results. As the patients BP was poorlycontrolled and the onset of preeclampsia was abnormallyearly, the decision to terminate the pregnancy was made.At that time, intra-amniotic ethacridine was administered.Two days later, the patient delivered a fetus of 12 cm inlength with no gross abnormalities. The placenta also didnot display gross abnormalities. After delivery, her BPwas well controlled and an oral antihypertensive wasadministered instead of intravenous nitroprusside. Her 24hour urinary protein excretion (24hUPE) totaled 0.56 g.Her thyroid function was normal, as were measures ofurine catecholamines, corticosteroids and 24-hour urinary

vanillylmandelic acid (VMA) excretion. Creatinineexcretion rate was 113 ml/min. The patient wasdischarged on the fifth postnatal day with traceproteinuria on dipstick urinalysis.

The patient did not take the prescribed antihypertensivedrugs on a regular basis. Consequently, her BP rose to170/120 mmHg on one occasion. Nine weeks after thetermination of pregnancy, she consulted an internal

P

DOI: 10.3760/cma.j.issn.0366-6999.2012.11.041Department of Obstetrics and Gynecology, Peking University FirstHospital, Beijing 100034, China (Zhu YC, Sun Y and Yang HX)

Correspondence to: Dr. YANG Hui-xia, Department of Obstetricsand Gynecology, Peking University First Hospital, Beijing 100034,China (Tel and Fax: 86-10-83573226. Email: yanghuixia@bjmu.edu.cn)

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Chin Med J 2012;125(11):2067-20692068

physician. Her blood liver and renal functions,corticosteroid rhythm, postural stimulation test of rennin,aldosterone test and 24-hour VMA excretion were allfound to be normal. Oral antihypertensive medication wasrecommended and she began to take isosorbidemononitrate and hyzaar regularly. Three months after the

intervention, her BP returned to normal, with negativeproteinuria.

After almost one year, the patient became pregnant againand this time took labetalol to maintain a normal BP. Hercondition remained stable during the first trimester andthe 24hUPE was 0.18 g during the second trimester, withBP fluctuating between 130150/80100 mmHg. OnApril 7, 2009, at 30 gestational weeks, she complained ofheadache and light-headedness. Her BP rose to 160/110mmHg with 4+ proteinuria. She was admitted to ouremergency center. Despite the oral hypertensive drug

treatment, her BP remained unstable at 200/120 mmHgon the second day of her admission. As a result, thepatient underwent a Cesarean section and gave birth to a1100 g baby. The 24h UPE turned out to be 15.19 g,which verified severe preeclampsia. Postnatally, her BPbecame well-controlled. The patient was discharged onthe seventh postnatal day. Her baby stayed in the NICUfor 5 weeks and was discharged in good health with nosevere complications.

DISCUSSION

In this case, the patients prenatal BP and urinalysis were

both normal during the first pregnancy. Hypertension andproteinuria occurred at the 13th gestational week.Although this onset time was not consistent with thedefinition of preeclampsia, the clinical manifestationswere. Hypertension and proteinuria improved postpartum,which also infers that pregnancy induced the disease. As aresult, the patient was diagnosed with severepreeclampsia during the first pregnancy. At first, beforethe patient reached her 20th gestational week, webelieved she suffered from pure preeclampsia.However, because the patient remained hypertensive for 6weeks after the first pregnancy (a condition which she

maintained unless she took antihypertensive drugs), weconcluded that chronic hypertension was a more accuratediagnosis. The second pregnancy verified this diagnosis.The patient was then superimposed with severepreeclampsia during the third trimester. Therefore, a veryearly onset of hypertension/preeclampsia, even if theprenatal file is negative, should alert the clinician toconsider a diagnosis of chronic hypertension. Close andregular follow-up on these patients is an absoluterequirement. These patients future pregnancies are ofhigh risk and prenatal care should be enhancedaccordingly.

In this case, the patient displayed evident hypertension

with mild proteinuria, headache and hypokalemia.

Therefore, we should consider secondary hypertension as

a differential diagnosis. From the normal results of renal

function tests and ultrasound investigations of the kidney

and adrenal glands, we could rule out hypertension

caused by renal parenchyma disease or renal artery

dysfunction. According to the normal levels of urinary

catecholamine, corticosteroid and 24-hour VMA

excretion, pheochromocytoma and hypercortisolismcould be ruled out. Primary hyperaldosteronism could

also be excluded based on the postural stimulation test of

rennin.

According to the literature, preeclampsia before 20 weeks

of gestation is usually related to triploidy, trophoblastic

disease or antiphospholipid syndrome. There are currently

eight case reports about preeclampsia before 20 weeks, 4

of which are about trophoblastic disease and triploidy,2-5

one of which is about antiphospholipid syndrome6

and the

other three focus on pure preeclampsia.7-9

Approximately 10% of patients with trophoblastic diseasewill present with symptoms of hypertension, proteinuria

and edema, generally before 20 weeks of pregnancy.

Thus, for these cases, trophoblastic disease and triploidy

should be considered first. In this case, we could exclude

these possibilities. According to the literature, most cases

involved a partial hydatidiform mole with triploidy.

Antiphospholipid syndrome is also reported to be

associated with early onset preeclampsia, which usually

occurs at 2530 weeks gestation. The three cases of one

report6

all presented with HELLP syndrome, two of

which coincided with hepatic infarction. However, one

case control study showed that a positiveantiphospholipid antibody status does not always lead to

of preeclampsia.10

In our case, the patient had no history

of miscarriages or thrombosis. We did not evaluate her

antiphospholipid antibodies so we cannot exclude

antiphospholipid syndrome as a cause. In 2003, Hazra

first reported a case of pure preeclampsia at 17 weeks

gestation, as opposed to reporting triploidy, trophoblastic

disease and antiphospholipid syndrome.7

The patient

recovered completely after the termination of her

pregnancy. As a result, Hazra questioned the opinion of

the absence of preeclampsia before 20 weeks of gestation.

In 2006, Imasawa from Japan reported a case of purepreeclampsia at 14 weeks gestation; the main

manifestation was heavy proteinuria of the nephritic

syndrome.8

The renal biopsy pathology was compatible

with glomerular changes in preeclampsia. All the

symptoms disappeared within 3 months postnatally. In

2008, Ivan et al9

reported a case of hypertension and

proteinuria in a 17-year-old woman at 19 weeks of

gestation. This teenager presented with refractory

hypertension and heavy proteinuria, so induction of labor

was performed. Renal biopsy was also performed, and

this verified glomerular capillary endotheliosis consistent

with preeclampsia. The latter cases confirm that

preeclampsia can indeed occur before 20 weeks of

gestation and the relevant glomerular capillary

endotheliosis can occur as early as 14 weeks gestation.

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Chinese Medical Journal 2012;125(11):2067-2069 2069

Thyroid dysfunction can also cause preeclampsia.Alfadda et al

11reported a preeclampsia-like syndrome

associated with severe hypothyroidism in a20-week-pregnant woman. Hypothyroidism can lead tovascular smooth muscle contraction in systemic and renalvessels. In our case, we could exclude this consideration

because the patient displayed normal thyroid function.

At present, the pathogenesis of preeclampsia is unclear,but is believed to be a two-stage process. First, shallowand ineffective placentation takes place, with decreasedtrophoblastic invasion leading to placental dysfunctionand hypoxia. The second stage begins when solublecytokines are released, including soluble fms-liketyrosine 1 (sFlt1) and soluble endoglin, which causessystemic endothelial dysfunction.

12According to

Baumann et al,13

the increase in circulating sFlt1 levelscan be detected as early as the first trimester, predicting

the onset of preeclampsia. The normal second stage ofplacentation, involving trophoblastic invasion that dilatesthe spiral arteries and decreases resistance, usually occursat 1820 weeks of gestation. Thus the traditional opinionis that preeclampsia occurs later than 20 weeks ofgestation. However, the disease can be diagnosed oncethere is uteroplacental hypoinfusion and placentalischemia. Ischemia occurs typically in cases ofhypertension, diabetes, antiphospholipid syndrome,systemic lupus erythematosus. In a report

7on a twin

pregnancy, a 12-cm uterine myoma affected the bloodsupply and contributed to the pathogenesis. Based on thisconsideration, when there is placental ischemia,

preeclampsia can indeed occur before 20 weeks ofgestation. In our case, the pathogenesis seems to havebeen chronic hypertension.

In conclusion, we report a case of preeclampsia at 13gestational weeks that ultimately turned out to bepreeclampsia superimposed on a state of chronichypertension. Nonetheless, pure preeclampsia seems tobe possible before 20 weeks. There should be furtherdiscussion on the definition of preeclampsia and furtherresearch on its pathogenesis. Finally, it is essential tooffer such patients further follow-ups and appropriate

prenatal care.

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(Received December 20, 2011)Edited by CHEN Li-min