Complement C3a expression and tryptase degranulation as promising histopathological tests for diagnosing fatal amniotic fluid embolism

Fineschi, Vittorio; Riezzo, Irene; Cantatore, Santina; Pomara, Cristoforo; Turillazzi, Emanuela; Neri, Margherita

doi:10.1007/s00428-009-0730-1

Cited by 42 publications

(40 citation statements)

References 37 publications

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“…An anaphylactic or complement activation reaction to some fetal components may explain the mechanism of disease [19] . Benson et al [20] showed that complement activation was found along with high levels of STN, that the levels of complement C3 and C4 were two-to threefold lower than normal, and did not implicate mast cell degranulation (anaphylaxis) as the cause of AFE.…”

Section: Discussionmentioning

confidence: 99%

Fatal Factors of Clinical Manifestations and Laboratory Testing in Patients with Amniotic Fluid Embolism

Naruse

Noguchi

et al. 2010

Gynecol Obstet Invest

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Aims: To identify factors leading to fatality of patients with amniotic fluid embolism (AFE). Methods: Patients who had fatal or nonfatal AFE were registered at the Hamamatsu University School of Medicine in the Department of Obstetrics and Gynecology from 1992 to 2006. Data collected included information about demographics and clinical characteristics. The fatal factors among these data were identified using χ² analysis and the Mann-Whitney test. Results: One hundred and thirty-five patients met the criteria, which included fatal (n = 65) and nonfatal AFE (n = 70). Maternal full-term gestational weeks, multiparous and noncesarean sections were the risk factors for death found in this study (p < 0.01). Sialyl Tn levels (mean ± SD) in the serum of patients with fatal AFE (69.7± 126.4 U/ml) were higher compared to those with nonfatal AFE (48.3± 161.8 U/ml; p = 0.003). Each of three items (cardiac arrest, dyspnea or loss of consciousness) was more common in fatal AFE (p < 0.01). Maternal pregnancy and labor complications were not associated with the distinction between fatal and nonfatal AFE. Conclusion: Factors associated with patients with fatal AFE were identified. These included multiparity, noncesarean section at full-term and the three symptoms mentioned above. Sialyl Tn levels could be a possible prognostic fatality factor.

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Section: Discussionmentioning

confidence: 99%

Fatal Factors of Clinical Manifestations and Laboratory Testing in Patients with Amniotic Fluid Embolism

Naruse

Noguchi

et al. 2010

Gynecol Obstet Invest

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“…High serum levels of mast cell-derived tryptase and complements have supported the contribution of anaphylaxis and complement activation to the pathogenesis of AFE, though the results have been somewhat inconsistent [3]. Meanwhile, immunohistochemistry demonstrated mast cell degranulation with tryptase-positive materials outside the cells in AFE lungs [4]. However, there is no report on uterine anaphylaxis related to AFE.…”

Section: Introductionmentioning

confidence: 99%

Amniotic Fluid Embolism Induces Uterine Anaphylaxis and Atony following Cervical Laceration

Tamura

Nagai

Maeda

et al. 2014

Gynecol Obstet Invest

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Amniotic fluid embolism (AFE) is a rare, high-risk obstetric complication primarily found in the lungs and potentially related to anaphylaxis. Tryptase release from the mast cell reflects anaphylaxis. Case report and findings: A female, aged over 40 years, presented with uterine atony and lethal hemorrhage after induced vaginal labor. Cervical laceration was accompanied by severe hemorrhage. Stromal edema and myometrial swelling were consistent with uterine atony. Alcian blue staining and zinc coproporphyrin immunostaining disclosed AFE, which was more prominent in the uterus than in the lungs. Tryptase immunostaining was diffuse and prominent around the activated mast cells (halos) in the uterus, including the cervix. Similar distribution of findings on the AFE markers, tryptase halos, complement receptor C5aR, and atony in the uterus suggested the causality of AFE to anaphylaxis, complement activation and atony. It is probable that disseminated intravascular coagulation (DIC), induced by AFE, uterine atony and cervical laceration, caused the lethal hemorrhage. It is likely that AFE, in association with cervical laceration, induces uterine anaphylaxis, complement activation, atony, DIC and lethal hemorrhage.

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“…In this report, the patient did not have multiple risk factors beyond the African descent and premature rupture of ovular membranes. Large population cohort studies indicate that these two risk factors have adjusted odds ratios (with confi dence interval of 95%) of 2.4 (1.5 -3.6) and 1.4 (0.6 -2.0)/0.7 (0.4 -1.5), respectively, for amniotic fl uid embolism (Conde-Agudelo and Romero 2009).The complement activation in this case may have been secondary to the immunological disease of the patient (Fineschi et al 2009). …”

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confidence: 84%

“…The complement activation in this case may have been secondary to the immunological disease of the patient (Fineschi et al 2009). …”

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confidence: 93%

Placental and infant metastasis of maternal melanoma: A new case

Carolis

Garofalo

Degennaro

et al. 2014

Journal of Obstetrics and Gynaecology

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Obstetric Case Reports 417 diagnostic resources, support and a multidisciplinary team trained for clinical emergencies in pregnancy are essential for the successful treatment of such severe cases.Risk factors for amniotic embolism include maternal age below 20 and above 35 years, elderly primigravidity, grand multiparity, black race, previous caesarean section, induction of labour, caesarean delivery, forceps delivery, vacuum delivery, multiple pregnancy, placenta previa, abruptio placenta, pre-eclampsia, eclampsia, diabetes, premature rupture of membranes, chorioamnionitis, dystocia, polyhydramnios, foetal macrosomia, cervical laceration and uterine rupture (Conde-Agudelo and Romero 2009). In this report, the patient did not have multiple risk factors beyond the African descent and premature rupture of ovular membranes. Large population cohort studies indicate that these two risk factors have adjusted odds ratios (with confi dence interval of 95%) of 2.4 (1.5 -3.6) and 1.4 (0.6 -2.0)/0.7 (0.4 -1.5), respectively, for amniotic fl uid embolism (Conde-Agudelo and Romero 2009).The complement activation in this case may have been secondary to the immunological disease of the patient (Fineschi et al. 2009).Probably there is a complex and still unknown immune component in the pathogenesis of amniotic fl uid embolism. Pregnant women with autoimmune diseases should be observed with careful attention to serious adverse events such as this. Th ere are still no methods for fast diagnosis; however, confi rmation of this event can be directed to the investigation of the complement system (Harboe et al. 2006;Staff ord and Sheffi eld 2007).

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Complement C3a expression and tryptase degranulation as promising histopathological tests for diagnosing fatal amniotic fluid embolism

Cited by 42 publications

References 37 publications

Fatal Factors of Clinical Manifestations and Laboratory Testing in Patients with Amniotic Fluid Embolism

Fatal Factors of Clinical Manifestations and Laboratory Testing in Patients with Amniotic Fluid Embolism

Amniotic Fluid Embolism Induces Uterine Anaphylaxis and Atony following Cervical Laceration

Placental and infant metastasis of maternal melanoma: A new case

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