Postpartum corticosteroids: Accelerated recovery from the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP)

Magann, Everett F.; Perry, Kenneth G.; Meydrech, Edward F.; Harris, Robert L.; Chauhan, Suneet P.; Martin, James N.

doi:10.1016/0002-9378(94)90055-8

Cited by 150 publications

(57 citation statements)

References 9 publications

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“…Autoimmune mechanisms have been postulated, including autoantibodies directed against certain types of phospholipids or trophoblastic constituents (34). As a result, corticosteroid therapy has been applied in severe preeclampsia, with encouraging preliminary results (35).…”

Section: Figurementioning

confidence: 99%

Patients with preeclampsia develop agonistic autoantibodies against the angiotensin AT1 receptor

Wallukat¹,

Homuth²,

Fischer³

et al. 1999

J. Clin. Invest.

748

627

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Preeclampsia usually occurs after week 20 of gestation and features hypertension and an increased peripheral vascular resistance. The mechanisms are unknown (1). Several lines of evidence implicate angiotensin II (Ang II) and its binding site, the AT 1 receptor. Preeclamptic patients manifest exaggerated pressor responses to Ang II. Gant et al. (2) infused Ang II into pregnant patients from week 10 of pregnancy onward and observed that those who later developed sustained hypertension required diminishing amounts of Ang II to obtain a similar pressor response. One possible explanation for this phenomenon might be increased expression of the AT 1 receptor. Baker et al. (3) also performed Ang II infusion experiments in pregnant patients and identified five patients who subsequently developed hypertension after week 20. These women were compared with seven who did not develop hypertension. The platelets of the preeclamptic women exhibited increased calcium signaling and increased binding sites for Ang II. The authors suggested increased stimulus-effect coupling in terms of Ang II responses in preeclamptic patients. We also observed increased cytosolic calcium responses in the platelets of preeclamptic patients in response to Ang II (4). However, circulating levels of Ang II are not increased in preeclampsia (5-7). In an earlier study of patients with essential hypertension, we observed a remarkably high incidence of circulating antibodies that cross-reacted with the α1-adrenoceptor and stimulated its signaling mechanism (8). In the present study, we tested the hypothesis that circulating antibodies to a vascular receptor might be responsible for the hypertension observed in preeclampsia. We employed a bioassay of beating neonatal rat cardiomyocytes, as well as Western blotting and confocal microscopy. We found that immunoglobulin from preeclamptic women contains a factor that binds to, and stimulates, the AT 1 receptor. MethodsCell culture. Isolation and cultivation of neonatal heart cells were performed as described previously (9). Briefly, single cells were dissociated from the minced ventricles of Wistar rats (1-2 days old) with a 0.25% solution of crude trypsin and were cultured as monolayers with a density of 800 cells/mm 2 in Halle SM 20-I medium equilibrated with humidified air. The medium contained 10% heat-inactivated FCS and 2 µmol/l fluorodeoxyuridine (Serva, Heidelberg, Germany) the latter to prevent proliferation of nonmuscle cells. On the third or fourth days, the cells were incubated for 2 h in 2 ml fresh serum-containing medium. Seven to 10 selected cells or synchronously contracting cell clusters per flask were counted for 15 s. This procedure was Immune mechanisms and the renin-angiotensin system are implicated in preeclampsia. We investigated 25 preeclamptic patients and compared them with 12 normotensive pregnant women and 10 pregnant patients with essential hypertension. Antibodies were detected by the chronotropic responses to AT 1 receptor-mediated stimulation of cultured neonatal rat cardio...

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Section: Figurementioning

confidence: 99%

Patients with preeclampsia develop agonistic autoantibodies against the angiotensin AT1 receptor

Wallukat¹,

Homuth²,

Fischer³

et al. 1999

J. Clin. Invest.

748

627

View full text Add to dashboard Cite

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“…20 As antenatal steroids were given to an equal number of subjects in each study arm it is unlikely this treatment would have affected the trial outcome. Furthermore, patients with HELLP were specifically excluded from study participation.…”

Section: Discussionmentioning

confidence: 99%

The hemodynamic effects of intravenous digoxin-binding fab immunoglobulin in severe preeclampsia: a double-blind, randomized, clinical trial

et al. 2009

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Objective: An endogenous digitalis-like factor (EDLF) has been implicated in the pathophysiology of preeclampsia (PE). This hypothesis is supported by two cases of preeclampsia in which administration of digoxin immune Fab (DIF) reduced mean arterial pressure (MAP). Study Design: To study this observation further, we performed a double-blind, placebo-controlled, randomized clinical trial to examine the effects on MAP of intravenous DIF given after delivery in 26 subjects with severe preeclampsia. Treating obstetricians were blinded to subject assignment and were allowed to use standard antihypertensive drugs during the trial. Results: The primary outcome, a significant difference in blood pressure between the two groups over the 24-h period of observation after the intervention, was not supported. However, mean MAP was significantly lower in the DIF-treated subjects for the first 4 h after therapy as compared with controls (P ¼ 0.05). Six subjects (46.2%) in the placebo arm were given conventional antihypertensive medications by their obstetrician for blood pressure >160 mm Hg systolic or >110 mm Hg diastolic, compared with zero subjects in the treatment arm (P ¼ 0.01). A trend towards increased creatinine clearance was observed in DIF-treated subjects (137.6 ± 42.6 versus 104.1 ± 43.4, P ¼ 0.07). Conclusion: These results support the hypothesis that EDLF contributes to the elevated blood pressure in preeclampsia and suggests a possible role for DIF as a treatment for this condition.

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“…В первые два дня отклонения в лабораторных показателях дости-гают пика, а затем нормализуются в течение 3-11 дней, хотя некоторые авторы указывают на более продолжи-тельные сроки [3,16,17]. В послеродовом периоде на-значают кортикостероиды, которые способствуют бо-лее быстрой нормализации лабораторных показателей и артериального давления [20].…”

Section: классификация болезней печени у беременных [3 4]unclassified

Изменение Функциональных Печеночных Тестов При беременности

Zaytsev¹

2022

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Заболевания печени, связанные с беременностью, встречаются приблизительно у 3 % беременных и являются важной причиной как материнской, так и фетальной смертности. В последние годы были получены значимые данные относительно патогенеза, диагностики и лечения этих болезней. В публикуемом обзоре акцент сделан на изменении показателей функциональных печеночных тестов у беременных как при физиологически протекающей беременности, так и при заболеваниях печени, являющихся следствием беременности, а также на механизмах этих изменений. Приводятся сведения о сроках нормализации функциональных печеночных тестов после родоразрешения или при естественном течении заболевания.

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Postpartum corticosteroids: Accelerated recovery from the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP)

Cited by 150 publications

References 9 publications

Patients with preeclampsia develop agonistic autoantibodies against the angiotensin AT1 receptor

Patients with preeclampsia develop agonistic autoantibodies against the angiotensin AT1 receptor

The hemodynamic effects of intravenous digoxin-binding fab immunoglobulin in severe preeclampsia: a double-blind, randomized, clinical trial

Изменение Функциональных Печеночных Тестов При беременности

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