Hepatocellular Adenoma Risk Factors of Hemorrhage

Abstract Background Hepatocellular adenoma (HCA) subtypes are considered as risk factors for malignant transformation; thus, an accurate diagnosis is important. We report a case of resected HCA previously diagnosed as unclassified HCA using immunohistochemistry, subsequently discovered to harbor a mutation in exon 3 of the beta (β)-catenin gene using deoxyribonucleic acid (DNA) sequencing. Case presentation The patient was a 26-year-old woman who was referred to our hospital because of a 150-mm tumor in the right lobe of the liver. Considering the possibility of malignancy, we performed right lobe hepatectomy. Based on the histopathological and immunohistochemical findings, the tumor was diagnosed as an unclassified HCA. Next, we performed sequencing of DNA isolated from the tumor and identified a mutation in exon 3 of β-catenin, suggesting that the tumor contained an activating mutation of the β-catenin gene. Conclusion β-Catenin mutations in HCA cannot be detected by immunohistochemistry alone, and molecular analysis is required to accurately diagnose and evaluate its prognosis.

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A Multicenter, 10-Year Experience With Hepatocellular Adenoma: Risk Factors and Disease Course

The American Surgeon ◽

10.1177/00031348211011084 ◽

2021 ◽

pp. 000313482110110

Author(s):

Trevor S. Silva ◽

Michael Sung ◽

Daniel W. Nelson ◽

Andrew L. DiFronzo ◽

Victoria V. O’Connor

Keyword(s):

Risk Factors ◽

Contraceptive Use ◽

Hepatocellular Adenoma ◽

Modifiable Risk Factors ◽

Disease Course ◽

Predominant Symptom ◽

Acute Rupture ◽

Long Term Follow Up ◽

The Impact

Background Management of hepatocellular adenoma (HA) is marked by a paucity of recent studies. Long-term follow-up data from an equal access health care system may facilitate our understanding of the natural disease course of HA and identify modifiable risk factors. Methods A multi-institutional, retrospective review of patients with HA from 2008-2017 was performed. Patient demographics, disease characteristics, and clinical outcomes were analyzed. Results Of 124 patients identified, 94% were women with a mean age at diagnosis of 39.5 years (range 20-82). Median follow-up was 22.5 months (range 0-114) with thirty-four (27.4%) patients eventually undergoing hepatectomy. Mean BMI of the study population was 30.5 kg/m2 (range 16-72). Stratified by size, average BMI for adenomas ≥5 cm was 34 kg/m2 compared to 28 kg/m2 for those <5 cm ( P < .05). The predominant symptom at presentation was abdominal pain (41.1%), while just 4% presented with acute rupture. Overall incidence of the malignancy was 2.5%. Among all patients, oral contraceptive use was documented in 74 (59.7%) patients, of whom 36 (29.0%) discontinued OC for at least six months. Regression after OC cessation occurred in seven patients (19.4%) while the majority (77.8%) remained stable. Discussion This decade-long review analyzing the impact of modifiable risk factors identifies a direct correlation between BMI and hepatocellular adenoma size. Rupture and malignant transformation are rare entities. Cessation of OC appears to be an effective strategy in the management of hepatic adenoma. Further investigations are warranted to determine if addressing modifiable risk factors such as BMI might induce further HA regression.

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Steatohepatitis-Like Changes in Hepatocellular Adenoma

American Journal of Clinical Pathology ◽

10.1093/ajcp/aqaa075 ◽

2020 ◽

Vol 154 (4) ◽

pp. 525-532

Author(s):

Yongjun Liu ◽

Yoh Zen ◽

Matthew M Yeh

Keyword(s):

Risk Factors ◽

Type 2 Diabetes ◽

Risk Factor ◽

Liver Disease ◽

Fatty Liver Disease ◽

Hepatocellular Adenoma ◽

Clinical Parameters ◽

Nonalcoholic Fatty Liver ◽

Clinical Records

Abstract Objectives Our aim was to investigate the frequency of steatohepatitic morphology in hepatocellular adenoma (HCA) and correlate with its clinical parameters and risk factors underlying nonalcoholic fatty liver disease (NAFLD) or nonalcoholic steatohepatitis (NASH). Methods We examined a series of 41 liver resection specimens diagnosed with HCA for steatohepatitic changes. Background nonneoplastic liver was also evaluated. Clinical records were reviewed for risk factors of NAFLD/NASH. Results Six steatohepatitic HCAs (SH-HCAs) were identified, with an overall prevalence of six (14.6%) of 41, of which three were HNF1α inactivated and three were inflammatory, but none were β-catenin mutated. Five of the six patients with SH-HCA had at least one known risk factor for NAFLD/NASH, including obesity (n = 4; 66.7%), diabetes (n = 5; 83.3%), hypertension (n = 3; 50%), and dyslipidemia (n = 1; 16.7%). Compared with the patients without SH-HCA, the patients with SH-HCA had a higher frequency of type 2 diabetes, obesity, and hypertension. Of the six SH-HCAs, background nonneoplastic liver showed significant steatosis in three (50%) cases and steatohepatitic changes in one (16.7%) case. Conclusions Approximately 15% of HCAs in our series demonstrated steatohepatitic changes. Lack of such morphology in β-catenin–mutated subtype suggests reassurance in this morphologic variant of HCA.

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Abstract B85: Genetic variation in the base excision repair pathway, environmental risk factors and colorectal adenoma risk

Cancer Prevention Research ◽

10.1158/1940-6207.prev-12-b85 ◽

2012 ◽

Vol 5 (11 Supplement) ◽

pp. B85-B85

Author(s):

Roman Corral ◽

Juan Pablo Lewinger ◽

Amit D. Joshi ◽

A. Joan Levine ◽

David Van Den Berg ◽

...

Keyword(s):

Risk Factors ◽

Genetic Variation ◽

Colorectal Adenoma ◽

Base Excision Repair ◽

Environmental Risk ◽

Excision Repair ◽

Repair Pathway ◽

Base Excision Repair Pathway ◽

Base Excision ◽

Adenoma Risk

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Risk factors for malignant transformation of hepatocellular adenoma to hepatocellular carcinoma: protocol for systematic review and meta-analysis

BMJ Open ◽

10.1136/bmjopen-2020-045733 ◽

2021 ◽

Vol 11 (8) ◽

pp. e045733

Author(s):

Tharusan Thevathasan ◽

Teresa Colbatzky ◽

Moritz Schmelzle ◽

Johann Pratschke ◽

Felix Krenzien

Keyword(s):

Risk Factors ◽

Hepatocellular Carcinoma ◽

Systematic Review ◽

Malignant Transformation ◽

Meta Analysis ◽

Hepatocellular Adenoma ◽

Assessment Tools ◽

Controlled Trials ◽

Cochrane Central Register ◽

Modifiable Factors

IntroductionHepatocellular adenomas (HCAs) are solid liver tumours that are usually found incidentally during routine medical check-ups. Multiple modifiable and non-modifiable factors constitute a risk for the malignant transformation of HCAs to hepatocellular carcinoma (HCC), which has emerged to be one of the fastest growing causes of cancer-related mortality globally. This study protocol for a planned systematic review and meta-analysis documents the methodological approach to identify risk factors and their risk estimates for the transformation from HCA to HCC.Methods and analysisTwo independent reviewers will systematically search and extract data from studies in patients of all ages published between January 1970 and June 2021 on PubMed, MEDLINE, EMBASE, Cumulative Index to Nursing and Allied Health Literature, Scopus Web of Science, Ovid, The Cochrane Hepatobiliary Group Controlled Trials Register and The Cochrane Central Register of Controlled Trials by using an a priori defined search strategy. Study quality will be rated with the National Institute of Health quality assessment tools. Disagreements will be resolved by consensus with a third independent reviewer. The primary outcome will be the odds ratio (OR) of developing HCC in patients with prediagnosed HCA depending on the exposure to risk factors. HCC diagnosis must be inferred based on imaging techniques or pathology. We will use R V.4.0.2 to conduct meta-analyses and generate pooled ORs based on random effects models. Results will be presented as forest plots. Cochran’s Q and I2 test will be performed to assess heterogeneity between included studies. Funnel plots and Egger’s weighted regression will be used to evaluate publication bias.Ethics and disseminationNo ethical approval is required as we will use and analyse data from previously published studies in which informed consent was obtained. The results will be disseminated in a peer-reviewed journal on completion.PROSPERO registration numberCRD42020206578.

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Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

Clinical Science ◽

10.1042/cs20190999 ◽

2019 ◽

Vol 133 (22) ◽

pp. 2283-2299

Author(s):

Apabrita Ayan Das ◽

Devasmita Chakravarty ◽

Debmalya Bhunia ◽

Surajit Ghosh ◽

Prakash C. Mandal ◽

...

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Chronic Inflammation ◽

Ex Vivo ◽

Human Subjects ◽

Critical Role ◽

Atherosclerotic Cardiovascular Disease ◽

Tnf Α ◽

Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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