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Other venous disorders
Published in Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland, Manual of Venous and Lymphatic Diseases, 2017
Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland
Non-cirrhotic portal fibrosis (idiopathic portal hypertension) is characterized by portal hypertension and splenomegaly, but with preserved liver function and patent hepatic and portal veins.5 The condition probably results from a genetically-based auto-immune injury.
Clinico-pathological features in fatal COVID-19 infection: a preliminary experience of a tertiary care center in North India using postmortem minimally invasive tissue sampling
Published in Expert Review of Respiratory Medicine, 2021
Animesh Ray, Deepali Jain, Ayush Goel, Shubham Agarwal, Shekhar Swaroop, Prasenjit Das, Sudheer Kumar Arava, Asit Ranjan Mridha, Aruna Nambirajan, Geetika Singh, S. Arulselvi, Purva Mathur, Sanchit Kumar, Shubham Sahni, Jagbir Nehra, Mouna Bm, Neha Rastogi, Sandeep Mahato, Chaavi Gupta, S Bharadhan, Gaurav Dhital, Pawan Goel, Praful Pandey, Santosh Kn, Shitij Chaudhary, Vishakh C Keri, Vishal Singh Chauhan, Niranjan Mahishi, Anand Shahi, Ragu R, Baidnath K Gupta, Richa Aggarwal, Kapil Dev Soni, Neeraj Nischal, Manish Soneja, Sanjeev Lalwani, Chitra Sarkar, Randeep Guleria, Naveet Wig, Anjan Trikha
Liver biopsy cores were obtained from 29 of these 37 patients. In eight patients (27.58%) acute submassive hepatic necrosis was identified, while four (13.79%) biopsies showed features of acute-on-chronic liver failure (ACLF) with evidence of hepatic necrosis (Figures 5–7). Four of the biopsies showing acute hepatic necrosis (Figure 5e) also showed prominent microvesicular steatosis (Figure 6b, 6d & 7d). In one of the liver biopsies showing features of ACLF, histological features were suggestive of acute exacerbation of autoimmune inflammation (Figures 6e & 7b). However, the most common histological finding across the biopsies was Kupffer cell hypertrophy [21 (72.41%)] (Figures 5f & 6d). In three biopsies (10.3%) there were features of non-cirrhotic portal fibrosis (NCPF), in the form of obliterative portal venopathy in two biopsies with focal sinusoidal fibrotic occlusions (Figures 5c & 6f). Portal inflammation, interface hepatitis, or lobular necroinflammatory activities were not identified in these three cases. While significant portal mononuclear cell infiltrates were identified in 13 (44.82%) biopsies, in only three biopsies the portal inflammation was dense and in four portal inflammation was moderate (Figures 6e & 7b). Lobular inflammation was identified only in five (17.24%) cases (Figure 6e). In four biopsies (13.79%), there was centrizonal hemorrhagic necrosis, histologically suggestive of heart failure. Macrovesicular steatosis in zone 3 and zone 2 were identified in four biopsies (13.79%) [Figures 5e, 6a & 6c], while diffuse macrovesicular steatosis was noted in one biopsy (Figure 7). Out of the liver biopsies showing macrovesicular steatosis, two had a history of chronic hypothyroidism, while all of these patients received steroids as a part of their COVID-19 related management regimen. In two of the biopsies from patients with hypothyroidism, we also identified prominent nuclear glycogenization. Four of this index cohort of liver biopsies had features within normal histological limits. Hepatic necrosis was noted in heterogeneous pattern, while zone 3 predominant necrosis was seen in eight biopsies (Figure 5e), diffuse transacinar necrosis was noted in two, and focal irregular lobular necrosis pattern was identified in three biopsies. Other features of hepatocyte damage, viz. ballooning, acidophil bodies, and Kupffer cell hypertrophy were also prominent in most of the liver biopsies, except the histologically normal biopsies (Figure 7a). Intracanalicular and intracytoplasmic cholestasis in hepatocytes were identified in seven biopsies (24.13%), while ductular cholestasis was identified in one biopsy with other features of associated sepsis-related changes (Figure 6c).