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Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome
Hepatic infarction is uncommon due to the dual blood supply from the hepatic artery and portal vein. The majority of the cases are caused following liver transplant or hepatobiliary surgery, hepatic artery occlusion, or shock. Hepatic infarction is a rare complication of hemolysis, elevated liver en...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cureus
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9056947/ https://www.ncbi.nlm.nih.gov/pubmed/35506117 http://dx.doi.org/10.7759/cureus.23724 |
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author | Paudel, Anish C Altomare, John F Shogbesan, Oluwaseun Lee, Andrew Desai, Parth Noain, Jesus S Khanal, Suravi |
author_facet | Paudel, Anish C Altomare, John F Shogbesan, Oluwaseun Lee, Andrew Desai, Parth Noain, Jesus S Khanal, Suravi |
author_sort | Paudel, Anish C |
collection | PubMed |
description | Hepatic infarction is uncommon due to the dual blood supply from the hepatic artery and portal vein. The majority of the cases are caused following liver transplant or hepatobiliary surgery, hepatic artery occlusion, or shock. Hepatic infarction is a rare complication of hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. HELLP is an obstetrical emergency requiring prompt delivery. The presence of elevated liver enzymes, mainly alanine aminotransferase and aspartate aminotransferase in pre-eclampsia, should warrant diagnosis and treatment in the line of HELLP syndrome. Our patient with underlying sickle cell trait presented with features of HELLP syndrome in her third trimester of pregnancy. She underwent cesarean delivery on the same day of the presentation. The liver enzymes continued to rise following delivery and peaked on postoperative day two. Contrast computed tomography scan showed multifocal hepatic infarctions. Pre-eclampsia by itself is a state of impaired oxygenation and can lead to hepatic hypoperfusion, and appeared to be a clear contributor to the hepatic infarction in this case. However, this case also raises the question of whether the underlying sickle cell trait might have potentiated the hepatic infarction. Although sickle cell disease is well known to cause hepatic infarctions, it is unknown whether the sickle cell trait affects the liver to a similar extent as sickle cell disease. In addition, there have been case reports of sickle cell trait causing splenic infarcts and renal papillary necrosis, but it remains unclear if it can be directly associated with hepatic infarction. |
format | Online Article Text |
id | pubmed-9056947 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Cureus |
record_format | MEDLINE/PubMed |
spelling | pubmed-90569472022-05-02 Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome Paudel, Anish C Altomare, John F Shogbesan, Oluwaseun Lee, Andrew Desai, Parth Noain, Jesus S Khanal, Suravi Cureus Internal Medicine Hepatic infarction is uncommon due to the dual blood supply from the hepatic artery and portal vein. The majority of the cases are caused following liver transplant or hepatobiliary surgery, hepatic artery occlusion, or shock. Hepatic infarction is a rare complication of hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. HELLP is an obstetrical emergency requiring prompt delivery. The presence of elevated liver enzymes, mainly alanine aminotransferase and aspartate aminotransferase in pre-eclampsia, should warrant diagnosis and treatment in the line of HELLP syndrome. Our patient with underlying sickle cell trait presented with features of HELLP syndrome in her third trimester of pregnancy. She underwent cesarean delivery on the same day of the presentation. The liver enzymes continued to rise following delivery and peaked on postoperative day two. Contrast computed tomography scan showed multifocal hepatic infarctions. Pre-eclampsia by itself is a state of impaired oxygenation and can lead to hepatic hypoperfusion, and appeared to be a clear contributor to the hepatic infarction in this case. However, this case also raises the question of whether the underlying sickle cell trait might have potentiated the hepatic infarction. Although sickle cell disease is well known to cause hepatic infarctions, it is unknown whether the sickle cell trait affects the liver to a similar extent as sickle cell disease. In addition, there have been case reports of sickle cell trait causing splenic infarcts and renal papillary necrosis, but it remains unclear if it can be directly associated with hepatic infarction. Cureus 2022-04-01 /pmc/articles/PMC9056947/ /pubmed/35506117 http://dx.doi.org/10.7759/cureus.23724 Text en Copyright © 2022, Paudel et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Internal Medicine Paudel, Anish C Altomare, John F Shogbesan, Oluwaseun Lee, Andrew Desai, Parth Noain, Jesus S Khanal, Suravi Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome |
title | Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome |
title_full | Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome |
title_fullStr | Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome |
title_full_unstemmed | Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome |
title_short | Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome |
title_sort | hepatic infarction in a patient with sickle cell trait presenting with hellp syndrome |
topic | Internal Medicine |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9056947/ https://www.ncbi.nlm.nih.gov/pubmed/35506117 http://dx.doi.org/10.7759/cureus.23724 |
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