Atypical severe preeclampsia (PE) at \20 weeks of gestation is an extremely rare yet serious cause of perinatal morbidity [1]. Severe PE that occurs at \20 weeks of gestation has been reported with molar change in the placenta; however, data describing this condition in cases without molar change are limited. To our knowledge, there is only one reported case of severe PE without molar change at 15 weeks of gestation [2]. We describe the clinical course of a pregnancy without molar change that was complicated by atypical severe PE superimposed on chronic hypertension at 19 weeks of gestation.A 40-year-old gravid 2, para 1 woman was referred at 12 weeks of gestation with multiple risk factors affecting her pregnancy, including hypertension, a family history of cardiovascular disease (father suffered from hypertension and ischemic cardiovascular disease at 48 years), severe PE at 28 weeks in a previous pregnancy, obesity (body mass index 27.2), advanced maternal age, and conception by intracytoplasmic sperm injection (ICSI) and transfer of a single embryo. At referral, mild hypertension (148/94 mmHg) without proteinuria was observed and at 18 weeks of gestation, her blood pressure was 137/94 mmHg without proteinuria. At 19 3/7 weeks, the following findings suggested atypical severe PE superimposed on chronic hypertension: blood pressure 165/98 mmHg, urinary protein excretion 400 mg/day, extreme edema in the hands and lower extremities, and headache. A first and a second trimester ultrasound screening test did not reveal any abnormalities except for bilateral early diastolic notches in the uterine artery (uterine artery pulsatility index, 1.92; [95th percentile). At 19 5/7 weeks, the patient's body weight increased by 3 kg in 2 days, and this weight gain was associated with exacerbation of edema and oliguria. Her blood pressure and 24-h urinary protein excretion increased to 175/102 mmHg and 6.2 g, respectively. She did not show any clinical symptoms of systemic lupus erythematosus and did not present any autoantibody such as anti-dsDNA, anti-Sm, antiphospholipid, and antinuclear antibody. In addition, platelet count and liver function tests were normal. Although magnesium sulfate and nicardipine hydrochloride were administered, her blood pressure remained high at 185/113 mmHg. The pregnancy was terminated and a 250 g stillborn male was delivered at 20 4/7 weeks. Pathological examination of the placenta revealed an absence of physiologic transformation in the decidual segment of the spiral artery and ischemic changes, such as increase in cytotrophblastic cellular proliferation, syncytial knot formation, and hyalinized villous spots; however, there was no evidence of molar change. Protein excretion decreased to 200 mg/day on postpartum day 2 and disappeared by day 7. She was prescribed nifedipine (30 mg/day) to control her blood pressure, which was 130-140/80-90 mmHg on postpartum day 8, and she was subsequently discharged in good health.Very little is known about severe PE at \20 weeks of gestation [1-3]. Sibai et al...