Recurrent Massive Perivillous Fibrin Deposition and Chronic Intervillositis Treated With Heparin and Intravenous Immunoglobulin: A Case Report

Abdulghani, Sahar H.; Moretti, Felipe; Gruslin, Andrée; Grynspan, David

doi:10.1016/j.jogc.2017.03.089

Cited by 27 publications

(20 citation statements)

References 24 publications

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“…Since then, this lesion has been described by a variety of terms that include "massive chronic intervillositis", "chronic histiocytic intervillositis", "chronic intervillositis of unknown etiology", "intervillitis", "chronic intervillositis", "chronic histiocytic intervillositis of unknown etiology", "massive perivillous histiocytosis", and "massive histiocytic chronic intervillositis [64,65]. CHIV can be accompanied by increased fibrin deposition [66], which in some cases is so extreme as to be classified as massive perivillous fibrin deposition [67,68]. The most important microscopic differential diagnosis for CHIV is the chronic stage of placental malaria, in which accumulations of histiocytes in the intervillous space also occur [69].…”

Section: Discussionmentioning

confidence: 99%

Placental Pathology of COVID-19 with and without Fetal and Neonatal Infection: Trophoblast Necrosis and Chronic Histiocytic Intervillositis as Risk Factors for Transplacental Transmission of SARS-CoV-2

Schwartz

Morotti

2020

Viruses

126

112

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The mechanism(s) by which neonates testing positive for coronavirus disease 2019 (COVID-19) acquire their infection has been largely unknown. Transmission of the etiological agent, SARS-CoV-2, from mother to infant has been suspected but has been difficult to confirm. This communication summarizes the spectrum of pathology findings from pregnant women with COVID-19 based upon the infection status of their infants and addresses the potential interpretation of these results in terms of the effects of SARS-CoV-2 on the placenta and the pathophysiology of maternal-fetal infection. Placentas from pregnant women with COVID-19 and uninfected neonates show significant variability in the spectrum of pathology findings. In contrast, placentas from infected maternal-neonatal dyads are characterized by the finding of mononuclear cell inflammation of the intervillous space, termed chronic histiocytic intervillositis, together with syncytiotrophoblast necrosis. These placentas show prominent positivity of syncytiotrophoblast by SARS-CoV-2, fulfilling the published criteria for transplacental viral transmission as confirmed in fetal cells through identification of viral antigens by immunohistochemistry or viral nucleic acid using RNA in situ hybridization. The co-occurrence of chronic histiocytic intervillositis and trophoblast necrosis appears to be a risk factor for placental infection with SARS-CoV-2 as well as for maternal-fetal viral transmission, and suggests a potential mechanism by which the coronavirus can breach the maternal-fetal interface.

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Section: Discussionmentioning

confidence: 99%

Placental Pathology of COVID-19 with and without Fetal and Neonatal Infection: Trophoblast Necrosis and Chronic Histiocytic Intervillositis as Risk Factors for Transplacental Transmission of SARS-CoV-2

Schwartz

Morotti

2020

Viruses

126

112

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“…Many have suggested that there is an immunological basis for the pathology similar to the other pathologies described herein. The host vs placental/fetal semi‐allograft hypothesis for this lesion is based on the following facts: there is a significant recurrence risk, there is an increased incidence of the lesion in women with antiphospholipid antibody syndrome (APAS) and other autoimmune pathologies ; discordances have been reported in both monochorionic and dichorionic placentas; and that immunotherapy treatment seems to have a protective affect . Another theory is that maternal thrombophilia is a significant factor associated with the pathology .…”

Section: Massive Perivillous Fibrin Deposition/maternal Floor Infarctmentioning

confidence: 99%

“…Additional serum markers may be helpful and include an elevated msAFP , sENG, and sVEGFR‐1 . Treatment modalities have been reported with some success including primarily thrombolytic therapies (aspirin, heparin) with or without combining immunologically directed treatments (e.g., IVIG) . One report notes a live birth with normal post‐natal follow‐up at 2 years in a woman with a history of four consecutive losses presumably all due to MFI/MPFD (one case confirmed) who was treated with a combination of thrombolytic therapy (aspirin and heparin), IVIG, and an ‘innovative therapy’ of a statin (pravastatin) to ‘correct’ her angiogenic/antiangiogenic imbalance thought to be causational of her recurrent MFI/MPFD .…”

Section: Massive Perivillous Fibrin Deposition/maternal Floor Infarctmentioning

confidence: 99%

Placental pathologic lesions with a significant recurrence risk – what not to miss!

Chen

Roberts

2017

APMIS

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Here, we review three important placental pathologies with significant clinical implications and recurrence risks. They are, in order of most to least frequently seen, villitis of unknown etiology, chronic histiocytic intervillositis, and massive perivillous fibrin deposition (also known as maternal floor infarction). These entities occur in both preterm and term gestations and are observed more frequently with maternal and obstetric disorders including prior pregnancy loss, hypertension/preeclampsia, and autoimmune disease. They are associated with, and probably the cause of, significant perinatal morbidity and mortality including intrauterine growth restriction, fetal and neonatal demise, and fetal/neonatal neurocompromise (seizures and cerebral palsy). All three entities have high recurrence risks, with recurrence rates ranging from 34 to 100%. The histologic features of villitis of unknown etiology, chronic histiocytic intervillositis, and massive perivillous fibrin deposition are described herein. We discuss the clinical associations and suggest the subsequent clinical and pathological evaluation. Hypotheses as to the biology of these lesions are reviewed.

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“…Multiple treatment strategies have been employed in CHI, including various combinations of aspirin, lowmolecular-weight heparin, corticosteroids, hydroxychloroquine, and IVIG. 11,[13][14][15] These have had mixed results. A recent case report 14 of a mother with recurrent severe IUGR who had a dramatic response to IVIG, heparin, and ASA prompted a similar treatment strategy for our patient.…”

Section: Discussionmentioning

confidence: 99%

“…11,[13][14][15] These have had mixed results. A recent case report 14 of a mother with recurrent severe IUGR who had a dramatic response to IVIG, heparin, and ASA prompted a similar treatment strategy for our patient. Unfortunately, our patient did not experience the same response.…”

Section: Discussionmentioning

confidence: 99%

Diffuse Subamniotic Calcification: A Novel Pattern of Placental Calcification

Nohr

Wright

2020

Pediatr Dev Pathol

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Two primary patterns of placental calcification have been described, each with distinctive pathophysiology and clinical relevance. We report a novel pattern of diffuse subamniotic calcification. It occurred in a 25-week placenta involved by recurrent chronic histiocytic intervillositis (CHI) associated with severe intrauterine growth restriction (IUGR) and intrauterine fetal demise (IUFD). This was the mother’s third stillbirth related to CHI, despite treatment with intravenous immunoglobulin (IVIG), prednisone, low-molecular-weight heparin, and acetylsalicylic acid (ASA). On placental examination, the majority of the fetal surface was calcified. This variably formed a continuous band or dispersed calcium microparticles. Electron microscopy demonstrated associated electron dense deposits highly suggestive of immune complex deposition. CHI explains recurrent IUGR and stillbirth, but has not been associated with calcification or immune complex deposition. We hypothesize IVIG therapy may have caused immune complex deposition and subsequent dystrophic calcification, supported by its rare association with immune complex deposition disorders in the kidney. Identification of additional cases with this pattern of calcification, with additional studies on fresh tissue including immunofluorescence, electron microscopy and mass spectrometry, may aid in elucidating the underlying pathophysiology and clinical significance of this unusual lesion.

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Recurrent Massive Perivillous Fibrin Deposition and Chronic Intervillositis Treated With Heparin and Intravenous Immunoglobulin: A Case Report

Cited by 27 publications

References 24 publications

Placental Pathology of COVID-19 with and without Fetal and Neonatal Infection: Trophoblast Necrosis and Chronic Histiocytic Intervillositis as Risk Factors for Transplacental Transmission of SARS-CoV-2

Placental Pathology of COVID-19 with and without Fetal and Neonatal Infection: Trophoblast Necrosis and Chronic Histiocytic Intervillositis as Risk Factors for Transplacental Transmission of SARS-CoV-2

Placental pathologic lesions with a significant recurrence risk – what not to miss!

Diffuse Subamniotic Calcification: A Novel Pattern of Placental Calcification

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