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• W2918910433 abstract "Potential conflict of interest: Nothing to report. To the Editor: LoPiccolo et al.1 describe the very effective clinical management of severe portal hypertension associated with nodular regenerative hyperplasia (NRH), developing acutely during melanoma treatment with pembrolizumab. Pembrolizumab is a novel immunoglobulin G4 antibody targeting the antiprogrammed death‐1 receptor on lymphocytes, and therefore physiologically serving as an immune check‐point blocker. NRH is a rare diffuse architectural disturbance of the liver that is thought to be caused by uneven microperfusion, secondary to endothelial damage of the small portal vein radicles.2 It is likely that NRH is overall underdiagnosed due to its slow‐evolving nature, but in an unknown proportion of individuals it progresses to histological nodularity (<3 mm) with no fibrosis, clinically significant portal hypertension, and end‐stage liver disease.2 Due to the frequent association with immune‐mediated and hemato‐oncological conditions and/or use of medications interfering with the lymphocyte functions (e.g., azathioprine, 6‐thioguanine, busulfan, cyclophosphamide, oxaliplatin),2 it has been tempting to contemplate a putative immune background to NRH. A particularly strong association has been observed with common variable immune deficiency (CVI), noted in between 5%‐12% of all CVI patients.3 Most of the patients with NRH and CVI have autoimmune‐like manifestations, such as idiopathic thrombocytopenic purpura, scleroderma, psoriasis, vasculopathies, autoimmune hemolytic anemia, or arthritis.3 CVI has not been defined molecularly, but the principal immunological features involve B cell and T cell abnormalities with defective interleukin‐4 signaling, resulting in poor antibody production and frequent hypogammaglobulinemia.3 A possible explanation for the link was suggested when one‐third of NRH patients were found to have cytotoxic CD8+ T cells in hepatic sinusoids adjacent to atrophic areas. These CD8+ T cells specifically target apoptotic sinusoidal endothelial cells, according to clonality studies, and thus rule out the “passenger lymphocyte” effect.4 The similar CD8+ T cell infiltrate findings were reproduced with associated hepatic tissue increase in interferon‐γ production in NRH with CVI.3 Finally, one report described NRH in adult sibling pairs from three unrelated families with no triggering factors in history and severe clinical phenotypes.5 Although LoPiccolo et al.1 suggest the idiosyncratic nature of this rare complication in background of immune check blockade, we wonder whether patients with NRH should be subjected to formal immunological studies and the emerging large‐scale genetic sequencing studies involving subtler immunological aberrations. Although NRH is likely a heterogeneous condition, it is conceivable that a proportion could have a verifiable underlying immune dysregulation." @default.
• W2918910433 created "2019-03-11" @default.
• W2918910433 creator A5067392447 @default.
• W2918910433 date "2019-05-29" @default.
• W2918910433 modified "2023-09-26" @default.
• W2918910433 title "Letter to the Editor: Is Nodular Regenerative Hyperplasia an Immune‐Mediated Phenomenon?" @default.
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• W2918910433 doi "https://doi.org/10.1002/hep.30596" @default.
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