Hemolysis, Elevated Liver Enzymes, And Low Platelets Research Articles

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Liver Transplantation for Acute Liver Failure at 11-Week Gestation with Successful Maternal and Fetal Outcome

Acute liver failure (ALF) during pregnancy is very uncommon. Pregnancy-specific liver conditions like hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome and acute fatty liver of pregnancy can cause ALF at term or postpartum, but, typically occur during the third trimester. Most of these patients recover spontaneously after delivery, but, on occasion, they require liver transplantation in the postpartum period. However, ALF during the first and second trimester of pregnancy requiring antepartum liver transplantation is rare. Only fifteen cases of liver transplantation during pregnancy have been reported, and very few occurred during the first trimester. We report a Woman who developed acute liver failure during the first trimester of pregnancy and underwent successful liver transplantation at 11-week gestation, followed by successful delivery of the fetus at 30 weeks. To our knowledge, this is the earliest case of successful liver transplantation during pregnancy followed by successful fetal outcome. We discuss management of the patient and fetus before, during, and after liver transplantation and review the literature on antepartum liver transplant in pregnancy.

A Case of HELLP Syndrome with Multiple Complications

Hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome is a rare complication of pregnancy. The mortality rate associated with HELLP syndrome increases when life-threatening complications occur. A 37-year-old woman at 37 weeks of gestation developed severe cerebral hemorrhage at the beginning of labor induction and was transferred to our hospital, where HELLP syndrome was diagnosed. She developed disseminated intravascular coagulation (DIC), hepatic hematoma, and cerebral infarction after surgery. On day 68, she was transferred to her local hospital. Careful observation and rapid management can save patients with severe complications of HELLP syndrome.

HELLP Needs Aggressive Help

HELLP (Hemolysis Elevated Liver Enzymes and Low Platelets) syndrome is a multi-system pregnancy associated disorder, commonly seen in patients with pre-eclampsia but can occur alone. It is significantly associated with maternal-fetal morbidity and mortality. A triad of hemolysis elevated liver enzymes and thrombocytopenia after 24 weeks of gestation is diagnostic of this syndrome. HELLP syndrome is classified depending on simple parameters but it dictates severity of the disease. Frequently encountered complications with HELLP syndrome are hemorrhagic stroke, disseminated intravascular coagulation, pulmonary edema, acute renal failure and hepatic rapture. The aggressive supportive care of failing organs with high dose of steroids will decrease the duration of HELLP syndrome, decreases intensive care and hospital stay of these patients as well as reduction in fetal complications. HELLP syndrome is associated with significant increase in morbidity and mortality of pregnant patients; hence it is of vital importance that not only obstetrician, but acute care physicians and intensivist should be aware of this clinical entity. We report a case of Classl, normotensive postpartum HELLP syndrome complicated by pulmonary edema and acute renal failure, successfully managed in our intensive care unit.

Pregnancy-Induced Shifts in Von Willebrand Factor (VWF) Parameters Support a Prolongation in VWF Survival

Abstract 33Levels of the hemostatic protein von Willebrand Factor (VWF) are known to increase markedly during pregnancy. The mechanism by which VWF levels are increased has long been thought to be due to estrogen stimulation of vascular endothelial cells to synthesize and release more VWF. We hypothesized an alternate scenario in which prolongation of VWF survival contributes to the overall increase in VWF levels during pregnancy.To test this hypothesis, we measured VWF parameters in a repository of plasma samples acquired longitudinally over healthy pregnancies. Third trimester and postpartum (≥ 6 weeks) samples were available for 45 pregnancies, while prepregnancy, first, and second trimester samples were also available on a subset of pregnancies. VWF propeptide (VWFpp) and VWF antigen (VWF:Ag) levels were determined by ELISA (GTI Diagnostics), Factor VIII:C (FVIII:C) was performed by a one-stage assay, and ADAMTS13 activity was measured via cleavage of an enzyme-linked peptide substrate. ABO blood group, a known modifier of VWF:Ag levels and VWF survival, was determined by ABO allele-specific PCR (GTI Diagnostics).We found VWFpp, VWF:Ag, and FVIII:C levels were all significantly increased in the third trimester, as expected, while ADAMTS13 activity remained unchanged (see Table 1). Furthermore, the VWFpp:Ag ratio dropped by nearly half, consistent with a prolongation in VWF survival, while the VWFpp also rose, supporting a coexistent increase in VWF production. Unexpectedly, the decrease in the VWFpp:Ag ratio could be detected early during pregnancy, before the second trimester. Also surprisingly, we observed the VWF:Ag/FVIII:C ratio increase significantly during pregnancy. In a subset analysis of the data categorized by ABO blood group (group O, A, or B), the observed differences in VWF parameters between the third trimester and baseline remained statistically significant for all blood types.Table 1VWF parameters (+/− 1SD) in 45 healthy pregnancies.3rd TrimesterPostpartump-valueVWF:Ag (U/dL)192 +/− 7282 +/− 308.3 × 10−15VWFpp (U/dL)160 +/− 42132 +/− 310.00015FVIII:C (% Activity)200% +/− 63%114% +/− 38%6.9 × 10−11ADAMTS13 (% Activity)119 +/− 30122 +/− 330.599VWFpp/Ag Ratio0.91 +/− 0.271.75 +/− 0.631.4 × 10−13VWF/FVIII Ratio1.03 +/− 0.450.77 +/− 0.270.00054p-values determined using Student's two-tailed, paired t-testCollectively, these data point to previously unsuspected and biologically relevant qualitative changes in VWF during pregnancy. In a model accounting for the volume expansion of pregnancy and evidence of increased VWF production (and assuming one compartment, single-order kinetics, and a stable VWFpp half-life), we calculated that an increase in the half-life of VWF (1.9 fold) would account for the observed excess in VWF:Ag in the third trimester. Furthermore, the change in the VWF/FVIII ratio suggests a pregnancy-induced alteration in the VWF:FVIII stoichiometry such that pregnancy-associated VWF carries less FVIII. This new model of pregnancy-induced VWF change has direct relevance to the prothrombotic state of pregnancy, and could relate to the increased risk of venous thromboembolism (VTE), the major cause of maternal mortality in the developed world. This fresh perspective on the shifts in VWF and FVIII levels which occur in healthy pregnancy may also lend new insight into the mechanisms underlying the derangements of VWF which accompany other life-threatening pregnancy-associated complications, such as preeclampsia and HELLP (hemolysis, elevated liver enzymes, and low platelet syndrome). Disclosures:No relevant conflicts of interest to declare.

Induction of labour versus expectant monitoring for gestational hypertension or mild pre-eclampsia between 34 and 37 weeks' gestation (HYPITAT-II): a multicentre, open-label randomised controlled trial.

BackgroundGestational hypertension (GH) and pre-eclampsia (PE) can result in severe complications such as eclampsia, placental abruption, syndrome of Hemolysis, Elevated Liver enzymes and Low Platelets (HELLP) and ultimately even neonatal or maternal death. We recently showed that in women with GH or mild PE at term induction of labour reduces both high risk situations for mothers as well as the caesarean section rate. In view of this knowledge, one can raise the question whether women with severe hypertension, pre-eclampsia or deterioration chronic hypertension between 34 and 37 weeks of gestation should be delivered or monitored expectantly. Induction of labour might prevent maternal complications. However, induction of labour in late pre-term pregnancy might increase neonatal morbidity and mortality compared with delivery at term.Methods/DesignPregnant women with severe gestational hypertension, mild pre-eclampsia or deteriorating chronic hypertension at a gestational age between 34+0 and 36+6 weeks will be asked to participate in a multi-centre randomised controlled trial. Women will be randomised to either induction of labour or expectant monitoring. In the expectant monitoring arm, women will be induced only when the maternal or fetal condition detoriates or at 37+0 weeks of gestation. The primary outcome measure is a composite endpoint of maternal mortality, severe maternal complications (eclampsia, HELLP syndrome, pulmonary oedema and thromboembolic disease) and progression to severe pre-eclampsia. Secondary outcomes measures are respiratory distress syndrome (RDS), neonatal morbidity and mortality, caesarean section and vaginal instrumental delivery rates, maternal quality of life and costs. Analysis will be intention to treat. The power calculation is based on an expectant reduction of the maternal composite endpoint from 5% to 1% for an expected increase in neonatal RDS from 1% at 37 weeks to 10% at 34 weeks. This implies that 680 women have to be randomised.DiscussionThis trial will provide insight as to whether in women with hypertensive disorders late pre-term, induction of labour is an effective treatment to prevent severe maternal complications without compromising the neonatal morbidity.Trial RegistrationNTR1792 Clinical trial registration: http://www.trialregister.nl

Rhino-orbital zygomycosis in a patient with pregnancy related liver disease and multi-organ failure

Zygomycosis is an infection due to the fungi Zygomycetes, which, despite being ubiquitous, rarely cause disease in humans. Predisposing conditions include diabetic ketoacidosis, hematologic malignancies, iron overload, multiorgan failure, chronic liver disease, renal failure, metabolic acidosis and immunosuppressed state [1–3]. Zygomycosis can rarely occur in pregnancy as a complication of diabetic ketoacidosis [1]. We report zygomycosis occurring in a non-diabetic woman with pregnancy—related liver disease and multi-organ failure. A 20-year-old woman presented to our center at 38 weeks of gestation (primigravida) with history of swelling of feet and fatigue for 10 days, breathlessness, and jaundice (3 days), and abdominal pain (1 day). She had no prior major illness. She had not taken any drug known to cause liver dysfunction. On presentation, she was conscious and oriented, her blood pressure was 140/90 mmHg, pulse rate was 124/min and respiratory rate was 36/min. She was icteric and pale. Abdominal examination showed a gravid uterus; there was no ascites or palpable mass. Urinalysis revealed proteinuria and pelvic ultrasound showed intrauterine death of the fetus. Her laboratory results were: hemoglobin 13 gm%, white cell count 12,800/cmm, platelet count 56,000/cmm, serum bilirubin 16.6 mg/dL, alanine transaminase 130 IU/L, creatinine 3.4 mg/dL, random blood sugar 160 mg/dL, lactate dehydrogenase 892 IU/L, and INR 4.2. Arterial blood gas analysis showed pH 7.2, lactate 7.3 mmol/L, anion gap 12.6 and, base excess −17.5. Etiological work up for liver dysfunction like peripheral smear for malaria and serology for hepatitis viruses (hepatitis A, B, C and E) was non-contributory. Her blood culture was sterile. A diagnosis of pregnancy—related liver dysfunction [Diagnostic criteria for acute fatty liver of pregnancy (AFLP) and pre-eclamptic liver dysfunction and hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome were met] with intra-uterine death was made. She was started on piperacillin with tazobactam and metronidazole intravenously. After a failed attempt to induce vaginal delivery, she underwent emergency cesarean section under blood product coverage 22 h after admission to our hospital. The baby delivered was a macerated stillbirth. There was 750 mL of ascites drained and 500 mL of blood loss during the surgery. She was maintained on the same antibiotics in intensive care unit and was on mechanical ventilation with other supportive measures. Hemodialysis was instituted, with which acidosis resolved partially (pH 7.35), but she had persistent lactic acidemia (lactate >4 mmol/L) with worsening liver functions and recurrent hypoglycemia. A. Goel (*) :U. Zachariah : C. E. Eapen Department of GI Sciences, Christian Medical College, Vellore 632 004, India e-mail: drashish_goel@yahoo.com

Standardized Mississippi Protocol Treatment of 190 Patients with HELLP Syndrome: Slowing Disease Progression and Preventing New Major Maternal Morbidity

Objective. To evaluate the effectiveness of the Mississippi Protocol (MP) to treat HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Methods. Uniform early initiation of MP (corticosteroids, magnesium sulfate, systolic blood pressure control) was studied prospectively in patients admitted with severe preeclampsia/class 1 or class 2 HELLP syndrome. Results. One hundred and ninety patients between 2000 and 2007 received MP without suffering maternal death, stroke, or liver rupture. Only 39 of 163 patients (24%) not class 1 when MP began progressed to class 1 disease; only 18.2% of class 1 and 2.4% of class 2 subsequently developed major maternal morbidity. Conclusion. Early initiation of MP inhibits HELLP syndrome disease progression and severity.

428: Apoptosis pathway is involved in hemolysis, elevated liver enzyme, and low platelet (HELLP) syndrome and intrauterine growth restriction (IUGR)

The neurotrophin family comprises molecules involved in growth, differentiation, survival, regeneration, normal functions of the neuronal system, and in angiogenesis. We investigate the expression pattern of neurotrophic signaling molecules in pregnancies complicated by HELLP (Hemolysis, Elevated Liver enzymes and Low Platelet count) syndrome and IUGR.

Recurrence risks of hypertensive diseases in pregnancy after HELLP syndrome

To determine the recurrence risk for hypertensive diseases in pregnancy after HELLP (Hemolysis Elevated Liver enzymes and Low Platelets) syndrome in a first pregnancy. The study was designed as a cohort study investigating 148 Caucasian primiparae with a diagnosis of HELLP syndrome in a first pregnancy and at least one subsequent pregnancy conducted beyond the 24th gestational week. Diagnoses were verified by reviewing medical records and classified according to ISSHP (International Society for the Study of Hypertension in Pregnancy) criteria. The recurrence risk of HELLP syndrome or other hypertensive disorders in the subsequent pregnancy was calculated with regard to disease severity in the index pregnancy. Among 148 pregnancies subsequent to HELLP syndrome, 56.1% of the women were normotensive. The recurrence rate was 12.8% for HELLP syndrome, 16.2% for pre-eclampsia, and 14.2% for gestational hypertension only. Women with HELLP syndrome ≤32 gestational weeks tended to show a greater risk of complicated subsequent pregnancies compared to women presenting with HELLP after 32 gestational weeks. Women with a diagnosis of HELLP syndrome are at a strongly increased risk of recurrent HELLP syndrome, pre-eclampsia or gestational hypertension, however, currently no clinical or laboratory parameters allow the prediction of recurrence risk in any individual case.

Clinical review: Special populations - critical illness and pregnancy

Critical illness is an uncommon but potentially devastating complication of pregnancy. The majority of pregnancy-related critical care admissions occur postpartum. Antenatally, the pregnant patient is more likely to be admitted with diseases non-specific to pregnancy, such as pneumonia. Pregnancy-specific diseases resulting in ICU admission include obstetric hemorrhage, pre-eclampsia/eclampsia, HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome, amniotic fluid embolus syndrome, acute fatty liver of pregnancy, and peripartum cardiomyopathy. Alternatively, critical illness may result from pregnancy-induced worsening of pre-existing diseases (for example, valvular heart disease, myasthenia gravis, and kidney disease). Pregnancy can also predispose women to diseases seen in the non-pregnant population, such as acute respiratory distress syndrome (for example, pneumonia and aspiration), sepsis (for example, chorioamnionitis and pyelonephritis) or pulmonary embolism. The pregnant patient may also develop conditions co-incidental to pregnancy such as trauma or appendicitis. Hemorrhage, particularly postpartum, and hypertensive disorders of pregnancy remain the most frequent indications for ICU admission. This review focuses on pregnancy-specific causes of critical illness. Management of the critically ill mother poses special challenges. The physiologic changes in pregnancy and the presence of a second, dependent, patient may necessitate adjustments to therapeutic and supportive strategies. The fetus is generally robust despite maternal illness, and therapeutically what is good for the mother is generally good for the fetus. For pregnancy-induced critical illnesses, delivery of the fetus helps resolve the disease process. Prognosis following pregnancy-related critical illness is generally better than for age-matched non-pregnant critically ill patients.

Platelet monitoring follow-up in a pregnant patient with HELLP syndrome

Monitoring the course of platelet function in HELLP (haemolysis, elevated liver-enzymes and low platelets) syndrome is important for clinical decision-making. We present a primigravid woman developing HELLP syndrome at 29 weeks and 6 days. Platelet function was monitored by multiple electrode aggregometry (MEA), platelet function analyzer (PFA-100®), platelet count and mean platelet volume (MPV) over an 11-day period. MPV and PFA-100® seem better predictors for platelet function than platelet levels.

Effects of Hypoxia-Inducible Factor-1α Overexpression in Pregnant Mice: Possible Implications for Preeclampsia and Intrauterine Growth Restriction

Preeclampsia and intrauterine growth restriction (IUGR) are pregnancy-specific disorders that share a common pathophysiology. Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that plays an important role in placental development. HIF-1α is elevated in preeclamptic placentas and induces soluble vascular endothelial growth factor receptor-1 (sFLT-1), a central factor in preeclampsia and IUGR pathogenesis. Our objective was to investigate the effects of HIF-1α overexpression on pregnancy in mice. C57BL/6J pregnant mice were systemically administered either adenovirus expressing stabilized HIF-1α (cytomegalovirus [CMV]-HIF), luciferase control (CMV-Luc), or saline on gestational day 8. Pregnant mice overexpressing HIF-1α had significantly elevated blood pressure and proteinuria compared with pregnant controls. HIF-1α mice showed fetal IUGR, decreased placental weights, and histopathological placental abnormalities compared with control mice. Glomerular endotheliosis, the hallmark lesion of preeclampsia, was demonstrated in the kidneys of these mice relative to the normal histology in control mice. Moreover, liver enzyme levels were significantly elevated, whereas complete blood counts revealed significant anemia and thrombocytopenia in CMV-HIF mice compared with controls. Blood smears confirmed microangiopathic hemolytic anemia in CMV-HIF mice, consistent with HELLP (hemolysis, elevated liver enzymes, and low platelets)-like syndrome. CMV-HIF mice showed elevation in serum sFLT-1 and soluble endoglin, providing a mechanistic explanation for the observations. Collectively, our results suggest a possible role for HIF-1α in the pathogenesis of both preeclampsia and IUGR.

Left ventricular function many years after recovery from pre-eclampsia

Epidemiological observations have shown that women with pre-eclampsia are at increased risk for subsequent development of cardiovascular disease. We evaluated maternal haemodynamics in asymptomatic women many years after pre-eclampsia and HELLP (haemolysis, elevated liver enzymes and low platelets) syndrome. Case-control study. University-based department of obstetrics. Forty-eight women, 13-18 years after the affected pregnancy: 17 women with a history of HELLP syndrome, 14 women with a history of pre-eclampsia and 17 women following normal pregnancy (control group). Echocardiographic examination was performed in all groups, recording the isovolumetric contraction time and isovolumetric relaxation time (ICT + IVRT), ejection time (ET), myocardial performance index (MPI), transmitral early to atrial filling velocity ratio (MV-E/MV-A), stroke volume (SV) and cardiac output (CO). Cardiac function. Women with previous HELLP syndrome showed a significantly increased MPI (0.34 versus 0.26; P = 0.008) and ICT + IVRT (442.16 versus 415.03; P = 0.01); MV-E/A, SV, ET and CO were not significantly different. Women with a history of pre-eclampsia showed a significantly increased MPI (0.36 versus 0.26; P = 0.006) and decreased ET (317.3 versus 328.93; P = 0.04); ICT + IVRT, MV-E/A, SV and CO were not significantly different. This study confirms epidemiological observations that women with pre-eclampsia are at increased risk for subsequent development of cardiovascular disease. Many years after HELLP syndrome or pre-eclampsia, asymptomatic women have an increased risk for impaired cardiac function as shown by an increased MPI.

Placental Protein-13 and Pregnancy-Associated Plasma Protein-A as First Trimester Screening Markers for Hypertensive Disorders and Small for Gestational Age Outcomes

Objective. To investigate the role of placenta protein 13 (PP13) and pregnancy-associated plasma protein-A (PAPP-A) in hypertensive disorders and small for gestational age (SGA) during first trimester of pregnancy. Methods. In this case–control study, first trimester serum samples (11+0 to 13+6 weeks) were retrieved from frozen storage of which 452 were from normal pregnancies and 47 samples were identified to have pregnancies with at least one of the following adverse outcomes: SGA, preeclampsia (PE), hemolysis, elevated liver enzymes, and low platelets (HELLP), or gestational hypertension (GH). PP13 concentrations were measured by a new AutoDELFIA method. Levels of PAPP-A were measured for a first trimester screening program using Kryptor analyzer. Results. First trimester levels of PAPP-A are significantly lower in cases of SGA, PE, and most subgroups including HELLP. Levels of PP13 were not found to differ between control and affected pregnancies. Conclusion. PP13 needs to be studied further as our results contrast the majority of previous studies.

Thrombotic Microangiopathy and Occult Neoplasia

Thrombotic thrombocytopenic purpura (TTP), which is typically characterized by fever and central nervous system manifestations and hemolytic uremic syndrome (HUS), in which renal failure is a prominent feature are the most common thrombotic microangiopathies (TMAs). TTP is usually associated with a severe deficiency of ADAMTS13 [a metalloproteinase involved in the degradation of von Willebrand factor (vWF) multimers], causing excessive accumulation of ultra-large vWF multimers and platelet aggregation with organ failure. By contrast, patients with HUS or other TMAs usually display a normal or at least detectable ADAMTS13 activity. A TMA may be occasionally developed in association with HELLP (haemolysis, elevated liver enzymes, and low platelet count) syndrome, infections, cancer and bone marrow transplantation. In cancer patients, TMA may be related to chemotherapeutic regimens or the malignant disease itself. Occasionally, TMA is the first manifestation of an occult cancer, and in large series approximately 3% of patients who were originally diagnosed with TTP, were in fact harboring an occult malignancy. The pathogenesis of cancer-associated TMAs is not completely elucidated, but probably the most important factor is endothelial damage. However, cancer-associated TMAs show some distinct features that should promptly lead to complementary investigations for an underlying malignancy. Weakness, cough and dyspnoea, fever, weight loss, bone and abdominal pain are the most common presenting symptoms. Generally, biochemistry reveals markedly increased LDH levels, increased alkaline phosphatase and the blood smear shows erythromyelemia. Bone marrow biopsy is a valuable tool in order to establishing malignant seeding. Treatment of the underlying neoplasia is the mainstay of therapy and there is no role for plasmapheresis or plasma infusions.

First‐trimester placental growth factor as a marker for hypertensive disorders and SGA

The objective of this study was to examine first-trimester maternal serum placental growth factor (PlGF) levels in pregnancies which later develop hypertensive and growth complications. In this case-control study, PlGF levels were measured by AutoDELFIA immunoassay platform. There were 47 cases of at least one of the following adverse outcomes: pre-eclampsia (PE), small for gestational age (SGA), haemolysis elevated liver enzymes and low platelets (HELLP) and gestational hypertension (GH) and 452 matched controls. PlGF levels were significantly lower in cases of all PE, early PE, HELLP, all SGA, early SGA and SGA without PE, but not in GH, late PE, late SGA, PE with SGA or PE without SGA or HELLP. Low levels of first-trimester PlGF provide a good indicator of SGA complications and some hypertensive disorders, in particular severe cases of PE such as early onset and HELLP syndrome.

The use of angiogenic biomarkers to differentiate non-HELLP related thrombocytopenia from HELLP syndrome

Objective. Preeclampsia (PE) is diagnosed using clinical criteria and in atypical cases the diagnosis may be inaccurate as there are no specific tests to confirm or exclude PE. This study sought to evaluate the utility of angiogenic biomarkers, sFlt1, sEng and PlGF to distinguish patients with gestational thrombocytopenia and immune thrombocytopenic purpura (ITP) from patients with thrombocytopenia resulting from the HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome, a complication of severe PE.Methods. Serum was collected and the angiogenic biomarkers of patients with ITP and gestational thrombocytopenia (N = 9) were compared to patients with HELLP (N = 11) and PE (N = 11). Circulating levels of these angiogenic biomarkers were also compared by gestational age to 1564 randomly selected normotensive women from the Calcium for Preeclampsia Prevention study.Results. Patients with non-HELLP thrombocytopenia had lower sFlt1 (7.3 ± 3.8 ng/ml vs. 15.5 ± 5 ng/ml, P < 0.001), lower sEng (8.7 ± 3.6 vs. 34 ± 17, P < 0.001) and higher PlGF (484 ± 412 vs. 66.3 ± 44, P = 0.003) than patients with HELLP syndrome. Angiogenic factor abnormalities in patients with PE were similar to patients with HELLP syndrome, suggesting a common pathogenesis. Patients with non-HELLP thrombocytopenia had angiogenic profiles similar to normotensive controls, whereas patients with HELLP syndrome had levels higher than the 90th percentile for sFlt1 and sEng and lower than the 10th percentile for PlGF.Conclusions. Angiogenic biomarkers may be useful in excluding conditions that mimic PE.

Rheumatic mitral valve disease in pregnancy

A 32-year-old Nepalese woman with known rheumatic mitral valve disease presented 17 weeks into her first pregnancy with exertional breathlessness and wheezing, leading to expectoration of foamy pink liquid. Her history included percutaneous balloon mitral valvotomy at the age of 25 years, after which she had remained asymptomatic and fully active. She had three episodes of acute pulmonary oedema and was transferred to a tertiary centre for further management. An echocardiogram suggested severe mitral stenosis (mitral valve area 1.0 cm2) and pulmonary hypertension (mean pulmonary artery pressure 87 mmHg). She had further episodes of pulmonary oedema despite maximal medical therapy with diuretics, cardioselective beta blockers (dose limited because of systolic hypotension), digoxin, nitrates and anticoagulation. At 21 weeks' gestation, an emergency St Jude metallic valve was implanted. Unfortunately, intrauterine death occurred 2 days postoperatively, likely caused by pre-eclampsia or haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome. The patient recovered well and continues on warfarin and a small dose of beta blocker.

Family history of hypertension as an important risk factor for the development of severe preeclampsia

To determine the risk of preeclampsia in a population with respect to maternal and sister histories of chronic hypertension, preeclampsia and eclampsia. A case-control study of severe preeclampsia. Maternity hospital in Natal, Brazil. A total of 412 subjects were enrolled, 148 cases and 264 controls. Personal and familial histories of hypertensive disorders. Odds ratio estimates of preeclampsia with respect to family history of hypertensive diseases. Women with a history of hypertensive disorders were more frequent in the case group (p = 0.001). Women whose mothers had a history of hypertension (p = 0.003), preeclampsia (p = 0.007) or eclampsia (p = 0.038) were at increased risk of severe preeclampsia. The risk of preeclampsia was greater when the woman had a sister with a history of hypertension (OR 2.60, 95% CI 1.60-4.21, p < 0.001), preeclampsia (OR 2.33, 95% CI 1.58-3.45, p < 0.001), or eclampsia (OR 2.57, 95% CI 1.28-5.16, p = 0.008). The risk of preeclampsia was also higher for women who had both a mother and sister with a history of hypertension (OR 3.65, 95% CI 1.65-8.09, p = 0.001). A family history of hypertensive disorders increased the risk of eclampsia and hemolysis elevated liver enzymes and low platelet (HELLP) syndrome in a Brazilian population.