scholarly journals High rates of de novo malignancy compromise post‐heart transplantation survival

2021 ◽  
Vol 36 (4) ◽  
pp. 1401-1410
Author(s):  
Katherine Giuliano ◽  
Joseph K. Canner ◽  
Eric Etchill ◽  
Alejandro Suarez‐Pierre ◽  
Chun W. Choi ◽  
...  
2018 ◽  
Vol 71 (1) ◽  
pp. 40-49 ◽  
Author(s):  
Jong-Chan Youn ◽  
Josef Stehlik ◽  
Amber R. Wilk ◽  
Wida Cherikh ◽  
In-Cheol Kim ◽  
...  

2020 ◽  
Author(s):  
Katherine Giuliano ◽  
Joseph Canner ◽  
Eric Etchill ◽  
Alejandro Suarez Pierre ◽  
Chun Choi ◽  
...  

2020 ◽  
Vol 39 (4) ◽  
pp. S126-S127
Author(s):  
K. Giuliano ◽  
J.K. Canner ◽  
E.W. Etchill ◽  
A. Suarez-Pierre ◽  
A.K. Velez ◽  
...  

2020 ◽  
Author(s):  
Chie Bujo ◽  
Eisuke Amiya ◽  
Masaru Hatano ◽  
Masaki Tsuji ◽  
Hisataka Maki ◽  
...  

2019 ◽  
Vol 38 (4) ◽  
pp. S274
Author(s):  
R. Asleh ◽  
X. Li ◽  
H. Alnsasra ◽  
A. Briasoulis ◽  
B. Smith ◽  
...  

2016 ◽  
Vol 35 (4) ◽  
pp. S64-S65
Author(s):  
J. Youn ◽  
L.B. Edwards ◽  
L.H. Lund ◽  
J. Stehlik ◽  
S. Kang ◽  
...  

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Naruki Higashidate ◽  
Suguru Fukahori ◽  
Shinji Ishii ◽  
Nobuyuki Saikusa ◽  
Naoki Hashizume ◽  
...  

Abstract Background Apart from Kasai’s procedure, liver transplantation (LTx) has dramatically improved the outcome of children with biliary atresia (BA). However, de novo malignancy has been reported to be one of the major causes of late mortality after LTx among adults. We report a rare case of de novo gastric cancer developing after LTx for BA received during childhood. Case presentation A 21-year-old male patient who had undergone LTx for BA at age 2 years occasionally visited our outpatient clinic due to symptoms of epigastric pain and dysphagia. Endoscopic examination and computed tomography revealed advanced gastric cancer at the gastroesophageal junction with multiple liver metastases. Despite systemic chemotherapy, the disease progressed, resulting in patient’s death 2 years after the diagnosis. Conclusions De novo malignancy in the absence of post-transplant lymphoproliferative disease is rare in pediatric patients who received LTx. To the best of our knowledge, no report has been available on the development of gastric cancer after LTx for BA during childhood. Primary physicians should therefore establish a follow-up plan for patients receiving LTx for BA considering the potential for the development of de novo malignancy, including gastric cancer, despite its rarity.


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Nicholas S Wilcox ◽  
Stuart Prenner ◽  
Marisa Cevasco ◽  
Courtney Condit ◽  
Amy Goldstein ◽  
...  

Case Presentation: A 29-year-old male with LVH diagnosed in childhood was admitted with acute HF. TTE showed LVEF 5-10% and LV thrombi for which he was anticoagulated. He received inappropriate ICD shocks due to T wave oversensing, leading to cardiogenic shock requiring VA-ECMO support. Serum lactate peaked at 17 mmol/L due to cardiac and metabolic decompensation. He underwent heart transplantation (HT) on hospital day (HD) 8 and tolerated standard immunosuppression. First endomyocardial biopsy showed acute cellular rejection requiring pulse steroids. He was discharged on HD 33. Trio whole exome and mitochondrial genome sequencing revealed biallelic variants in complement component 1Q subcomponent-binding protein ( C1QBP ), due to a maternally inherited likely pathogenic variant c.612C>G (p.F204L in exon 5) and an apparently de novo deletion of 17p13.2, spanning exons 4-6 of C1QBP and exon 6 of the RPAIN gene. Mitochondrial genome sequencing of the explanted heart revealed multiple large-scale mitochondrial DNA deletions at 33% heteroplasmy. Discussion: C1QBP variants are associated with mitochondrial and multi-organ dysfunction. Only 12 patients exhibiting biallelic C1QBP variants are reported. Four died in the peripartum period due to fetal hydrops or HF; 5 exhibited early-onset cardiomyopathy (CM); 3 others had late-onset ophthalmoplegia without CM. The p.F204L variant has been reported in 1 patient with compound C1QBP p.F204L/p.C186S heterozygosity who died from hydrops fetalis and a second with p.F204L homozygosity with late-onset ophthalmoplegia and skeletal myopathy without CM. Differences in the size, heteroplasmy, and tissue distribution of mitochondrial genome secondary deletions may explain variability in disease onset and progression. We present the first patient with biallelic pathogenic C1QBP gene variants with mitochondrial CM to undergo HT and highlight the diagnosis and management of an exceptionally uncommon genetic disorder.


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