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      Differentiating Hemolysis, Elevated Liver Enzymes, and Low Platelet Count Syndrome and Atypical Hemolytic Uremic Syndrome in the Postpartum Period

      1 , 2 , 3 , 4
      Hypertension
      Ovid Technologies (Wolters Kluwer Health)

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          Abstract

          Pregnancy-associated atypical hemolytic uremic syndrome (aHUS) is a life-threatening thrombotic microangiopathy which may be mistaken for hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. We sought to identify laboratory parameters that differentiate aHUS and HELLP syndrome in the postpartum period. PubMed was searched from inception to March 2018 to identify cases of aHUS in the postpartum period, while cases of HELLP syndrome were identified from a cohort of deliveries at our institution from January 2015 to December 2018. Postpartum laboratory data were abstracted as either peak values (AST [aspartate transaminase]; creatinine; LDH [lactate dehydrogenase]) or nadir values (hemoglobin; platelet count). Differences were compared using the t test, Wilcoxon Rank Sum, or χ 2 test, and receiver operating characteristic (ROC) curve analyses were performed. We identified 46 cases of aHUS and 45 cases of HELLP syndrome in the postpartum period. Women with HELLP syndrome were older, but rates of nulliparity and cesarean delivery, and gestational age at delivery, were similar between groups. Peak serum creatinine and LDH values after delivery were the most useful to diagnose aHUS with area under the curve 0.996 (95% CI, 0.99–1.0) and 0.91 (95% CI, 0.83–0.98) respectively. Serum creatinine ≥1.9 mg/dL, LDH ≥1832 U/L, or serum creatinine ≥1.9 mg/dL in combination with LDH ≥600 U/L were the optimal thresholds for diagnosing pregnancy-associated aHUS. We conclude that standard laboratory data, most specifically peak serum creatinine and LDH, may be used to differentiate aHUS and HELLP syndrome in the postpartum period.

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          Most cited references60

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          Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin, Number 222.

          (2020)
          Hypertensive disorders of pregnancy constitute one of the leading causes of maternal and perinatal mortality worldwide. It has been estimated that preeclampsia complicates 2-8% of pregnancies globally (). In Latin America and the Caribbean, hypertensive disorders are responsible for almost 26% of maternal deaths, whereas in Africa and Asia they contribute to 9% of deaths. Although maternal mortality is much lower in high-income countries than in developing countries, 16% of maternal deaths can be attributed to hypertensive disorders (). In the United States, the rate of preeclampsia increased by 25% between 1987 and 2004 (). Moreover, in comparison with women giving birth in 1980, those giving birth in 2003 were at 6.7-fold increased risk of severe preeclampsia (). This complication is costly: one study reported that in 2012 in the United States, the estimated cost of preeclampsia within the first 12 months of delivery was $2.18 billion ($1.03 billion for women and $1.15 billion for infants), which was disproportionately borne by premature births (). This Practice Bulletin will provide guidelines for the diagnosis and management of gestational hypertension and preeclampsia.
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            Syndromes of thrombotic microangiopathy.

            This review article covers the diverse pathophysiological pathways that can lead to microangiopathic hemolytic anemia and a procoagulant state with or without damage to the kidneys and other organs.
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              Terminal complement inhibitor eculizumab in atypical hemolytic-uremic syndrome.

              Atypical hemolytic-uremic syndrome is a genetic, life-threatening, chronic disease of complement-mediated thrombotic microangiopathy. Plasma exchange or infusion may transiently maintain normal levels of hematologic measures but does not treat the underlying systemic disease. We conducted two prospective phase 2 trials in which patients with atypical hemolytic-uremic syndrome who were 12 years of age or older received eculizumab for 26 weeks and during long-term extension phases. Patients with low platelet counts and renal damage (in trial 1) and those with renal damage but no decrease in the platelet count of more than 25% for at least 8 weeks during plasma exchange or infusion (in trial 2) were recruited. The primary end points included a change in the platelet count (in trial 1) and thrombotic microangiopathy event-free status (no decrease in the platelet count of >25%, no plasma exchange or infusion, and no initiation of dialysis) (in trial 2). A total of 37 patients (17 in trial 1 and 20 in trial 2) received eculizumab for a median of 64 and 62 weeks, respectively. Eculizumab resulted in increases in the platelet count; in trial 1, the mean increase in the count from baseline to week 26 was 73×10(9) per liter (P<0.001). In trial 2, 80% of the patients had thrombotic microangiopathy event-free status. Eculizumab was associated with significant improvement in all secondary end points, with continuous, time-dependent increases in the estimated glomerular filtration rate (GFR). In trial 1, dialysis was discontinued in 4 of 5 patients. Earlier intervention with eculizumab was associated with significantly greater improvement in the estimated GFR. Eculizumab was also associated with improvement in health-related quality of life. No cumulative toxicity of therapy or serious infection-related adverse events, including meningococcal infections, were observed through the extension period. Eculizumab inhibited complement-mediated thrombotic microangiopathy and was associated with significant time-dependent improvement in renal function in patients with atypical hemolytic-uremic syndrome. (Funded by Alexion Pharmaceuticals; C08-002 ClinicalTrials.gov numbers, NCT00844545 [adults] and NCT00844844 [adolescents]; C08-003 ClinicalTrials.gov numbers, NCT00838513 [adults] and NCT00844428 [adolescents]).
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                Author and article information

                Contributors
                (View ORCID Profile)
                (View ORCID Profile)
                Journal
                Hypertension
                Hypertension
                Ovid Technologies (Wolters Kluwer Health)
                0194-911X
                1524-4563
                September 2021
                September 2021
                : 78
                : 3
                : 760-768
                Affiliations
                [1 ]From the Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, CA (R.M.B.)
                [2 ]Department of Obstetrics and Gynecology, University of Utah Health (K.M.)
                [3 ]Division of Nephrology, Department of Medicine, Washington University School of Medicine in St. Louis (A.J.)
                [4 ]Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, Yale University, New Haven, CT (M.G.).
                Article
                10.1161/HYPERTENSIONAHA.121.17311
                34275337
                905b6f3e-4312-4ff2-b619-8de0cc906db4
                © 2021
                History

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