Several cases will be presented to put into practice the principles of the algorithmic approach to core biopsy interpretation of the liver. There will be examples of (i) diffuse liver pathology, ...including comorbidity, (ii) liver allograft transplant pathology, and (iii) focal liver pathology. The focus will be on pattern recognition and cell profiling, differential diagnosis, diagnostic utility of ancillary tests such as special stains and immunohistochemistry, and the importance of close clinicopathological correlation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Focal liver lesions with glandular features encompass inflammatory, hyperplastic, hamartomatous to neoplastic lesions. They can be solid/cystic, solitary/multiple, occurring in a normal/diseased ...liver. Hepatobiliary entities should be segregated before considering nonhepatobiliary conditions.
In small tissue samples such as fine needle aspiration (FNA) or core biopsy, the diagnostic issues are to distinguish/recognize cystic from solid lesions, primary from metastatic adenocarcinoma, poorly differentiated adenocarcinoma from poorly differentiated hepatocellular carcinoma (HCC), rare glandular entities, mimics and pitfalls.
FNA of neoplastic cysts, such as mucinous cystic neoplasm and biliary intraductal papillary neoplasm (IPN) with biliary intraepithelial neoplasia (BilIN) or malignant transformation, may not yield totally diagnostic material.
Adenocarcinomas with dirty necrosis favor colorectal metastases. Intrahepatic cholangiocarcinoma (ICC) has many faces.
It is virtually impossible to distinguish ICC from metastatic pancreaticobiliary adenocarcinomas unless intrahepatic BilIN or carcinoma-in-situ is identified.
Pseudoacini may mimic true acini.
Papillary pattern is more likely to indicate metastases or ICC rather than biliary IPN.
An ambivalent glandular/epithelioid pattern may represent mixed hepatobiliary carcinoma.
Extrahepatic α-fetoprotein-producing adenocarcinomas may metastasize to the liver.
Benign mimics include brisk ductular reaction and reactive biliary atypia.
Malignant mimics include neuroendocrine tumors, HCC with pseudoacinar pattern, and epithelioid hemangioendothelioma. Beware of gastrointestinal contamination in endoscopic ultrasound-guided FNA.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Pathological lesions occur in the liver in primary hepatic disorders and in extrahepatic/ systemic diseases with hepatic involvement. Diseases may have acute or chronic manifestations. Comorbidities ...may exist.
Pattern recognition is the mainstay of liver biopsy interpretation. A kaleidoscope of morphological patterns exists. One pattern can be caused by more than one etiology. One etiology can produce more than one pattern. Histopathological findings evolve with disease progression or resolution. Therapy may modify the picture.
A 3-step algorithmic approach to liver biopsy reporting is presented. To avoid bias, biopsies are analysed blind initially to arrive at a morphological diagnosis based solely on descriptive histological findings. Differential clinical diagnoses are then prioritized according to ones area of practice. The final diagnosis is rendered after close clinicopathological correlation.
The basic morphological patterns are: portal hepatitis; periportal (interface) hepatitis; lobular hepatitis; cholestasis/cholestatic hepatitis; steatosis/steatohepatitis; granulomas/ granulomatous hepatitis; necrosis; fibrosis/cirrhosis; and minimal change. Helpful features include abnormalities in hepatocytes, bile ducts, Kupffer cells, hepatic stellate cells, sinusoids and blood vessels; various pigments; viral inclusions and organisms; and aberrant cells. An exclusionary diagnosis may be just as useful as a definitive one to aid decision-making and further patient management. Best practice depends on dedicated hepatology teamwork.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
There have been increasing reports of food-borne zoonotic transmission of hepatitis E virus (HEV) genotype 3, which causes chronic infections in immunosuppressed patients. We performed phylogenetic ...analyses of the HEV sequence (partial and full-length) from 1 patient from the Middle East who underwent liver transplantation, and compared it with other orthohepevirus A sequences. We found the patient to be infected by camelid HEV. This patient regularly consumed camel meat and milk, therefore camelid HEV, which is genotype 7, might infect human beings. Our finding links consumption of camel-derived food products to post-transplantation hepatitis E, which, if detected at early stages, can be cured with antiviral therapy and reduced administration of immunosuppressive agents.
Hepatocellular carcinoma (HCC) is known for its histomorphologic heterogeneity. Immunohistochemistry (IHC) can help in the comparative morphologic evaluation of HCC, its variants and their mimics. ...Some of these diagnostic challenges can be attributed to (i) the variety of neoplasms that can arise from the hepatic stem cell lineage; (ii) the spectrum of well-differentiated hepatocellular nodular lesions; (iii) the liver being a target for metastases with some of these histologic entities mimicking variants of HCC or actually arising in the liver; and (iv) the limitations of serum alpha-fetoprotein (AFP). The role of IHC is in the distinction of benign hepatocellular nodules from reactive hepatocytes; WD-HCC from benign hepatocellular nodules; poorly differentiated HCC from cholangiocarcinoma and metastases; and determination of histogenesis of malignant tumor; and of primary site of origin of malignant tumor. A panel of antibodies has more discriminant value. AFP expression usually indicates malignancy in a hepatocellular nodule and hepatocytic histogenesis of a malignancy. Polyclonal carcinoembryonic antigen (pCEA) and CD10 stain bile canaliculi in better-differentiated HCC. HepPar1 is generally accepted as a hepatocytic marker. However, not all HCC stain uniformly and not all HepPar1-positive tumors are of hepatocytic origin or arise in the liver. Mature hepatocytes and hepatocellular nodules stain with CAM 5.2, CK 8, and 18 but not with CK 7, 19, 20, or AE1/AE3. Biliary epithelium expresses CK 7 and 19. CD 34 highlights sinusoidal capillarization. AFP, pCEA/CD10, and CD34 are useful for ascertainment of malignancy in hepatocellular nodules; HepPar1 and cytokeratins to be included if histogenesis is the issue. IHC results should be interpreted in the larger context of the case.
Primary liver carcinomas with both hepatocytic and cholangiocytic differentiation have been referred to as “combined (or mixed) hepatocellular‐cholangiocarcinoma.” These tumors, although described ...over 100 years ago, have attracted greater attention recently because of interest in possible stem cell origin and perhaps because of greater frequency and clinical recognition. Currently, because of a lack of common terminology in the literature, effective treatment and predictable outcome data have been challenging to accrue. This article represents a consensus document from an international community of pathologists, radiologists, and clinicians who have studied and reported on these tumors and recommends a working terminology for diagnostic and research approaches for further study and evaluation. Conclusion: It is recommended that diagnosis is based on routine histopathology with hematoxylin and eosin (H&E); immunostains are supportive, but not essential for diagnosis. (Hepatology 2018;68:113‐126).
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Progression of liver fibrosis still occurs in some patients with chronic hepatitis B virus (HBV) infection despite antiviral therapy. We aimed to identify risk factors for fibrosis progression in ...patients who received antiviral therapy.
We conducted a longitudinal study of patients with chronic HBV infection and liver biopsies collected before and after 78 weeks of anti-HBV therapy. Fibrosis progression was defined as Ishak stage increase ≥ 1 or as predominantly progressive classified by P-I-R system (Beijing Classification). Levels of HBV DNA and HBV RNA in blood samples were measured by real-time quantitative PCR. HBV RNA in liver tissue was detected by in situ hybridization.
A total of 239 patients with chronic HBV infection with paired liver biopsies were included. Among the 163 patients with significant fibrosis at baseline (Ishak ≥ stage 3), fibrosis progressed in 22 patients (13%), was indeterminate in 24 patients (15%), and regressed in 117 patients (72%). Univariate and multivariate analyses revealed that independent risk factors for fibrosis progression were higher rate of detected HBV DNA at week 78 (odds ratio, 4.84; 95% CI, 1.30–17.98; P = .019) and alcohol intake (odds ratio, 23.84; 95% CI, 2.68–212.50; P = .004). HBV DNA was detected in blood samples from a significantly higher proportion of patients with fibrosis progression (50%) at week 78 than patients with fibrosis regression (19%) or indeterminate fibrosis (26%) (P = .015), despite low viremia (20–200 IU/mL) in all groups. The decrease of serum HBV RNA from baseline in the fibrosis regression group was larger than that in the fibrosis progression group.
In a longitudinal study of patients with chronic HBV infection, we associated liver fibrosis progression at week 78 of treatment with higher rates of detected HBV DNA. We propose that a low level of residual HBV may still promote fibrosis progression, and that patients’ levels of HBV DNA should be carefully monitored.
Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are benign hepatocellular tumors. The risk of bleeding and malignant transformation of HCA are strong arguments to differentiate HCA ...from FNH. Despite great progress that has been made in the differential radiological diagnosis of the 2 types of nodules, liver biopsy is sometimes necessary to separate the 2 entities. Identification of HCA subtypes using immunohistochemical techniques, namely, HNF1A-inactivated HCA (35–40%), inflammatory HCA (IHCA), and beta-catenin-mutated inflammatory HCA (b-IHCA) (50–55%), beta-catenin-activated HCA (5–10%), and unclassified HCA (10%) has greatly improved the diagnostic accuracy of benign hepatocellular nodules. If HCA malignant transformation occurs in all HCA subgroups, the risk is by far the highest in the β-catenin-mutated subgroups (b-HCA, b-IHCA). In the coming decade the management of HCA will be more dependent on the identification of HCA subtypes, particularly for smaller nodules (<5 cm) in terms of imaging, follow-up, and resection.
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FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UL, UM, UPUK
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