Liver and Biliary Pathology — MCQs
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A 62-year-old man presents with disorientation, jaundice, splenomegaly, and ascites. Laboratory tests show elevated ALT, AST, alkaline phosphatase, and bilirubin. A liver biopsy reveals alcoholic hepatitis with Mallory bodies. These cytoplasmic structures are composed of interwoven bundles of which of the following proteins?
Nutmeg liver is a characteristic finding in which condition?
Anti-LKM-2 autoantibody is seen in drug-induced liver injury. It is directed against which of the following structures?
Amyloid deposits in the liver are initially seen in which location?
What is the commonest benign tumor of the liver?
All of the following are true about fibrolamellar hepatocellular carcinoma except:
Given below is the histopathology of a liver biopsy of a patient with hemochromatosis. Which of the following special stains has been used?
Fatty liver is due to accumulation of which substance?
"Crumbled egg appearance" in liver is seen in which of the following conditions?
What is the most important risk factor for hepatocellular carcinoma?
Liver and Biliary Pathology Indian Medical PG Practice Questions and MCQs
Question 291: A 62-year-old man presents with disorientation, jaundice, splenomegaly, and ascites. Laboratory tests show elevated ALT, AST, alkaline phosphatase, and bilirubin. A liver biopsy reveals alcoholic hepatitis with Mallory bodies. These cytoplasmic structures are composed of interwoven bundles of which of the following proteins?
- A. a1-Antitrypsin
- B. b-Amyloid (Ab)
- C. Intermediate filaments (Correct Answer)
- D. Prion protein (PrP)
Explanation: **Explanation:** The correct answer is **Intermediate filaments**. **Mechanism and Pathophysiology:** Mallory bodies (also known as Mallory-Denk bodies) are eosinophilic, rope-like cytoplasmic inclusions found in hepatocytes [1]. They are primarily composed of tangled masses of **cytokeratin intermediate filaments** (specifically CK8 and CK18) that have been ubiquitinated and cross-linked. This occurs due to cellular stress, often from chronic alcohol consumption, which leads to protein misfolding and the failure of the proteasomal degradation system. **Analysis of Incorrect Options:** * **A. ̑1-Antitrypsin:** Deficiency of this protein leads to the accumulation of misfolded ̑1-antitrypsin in the endoplasmic reticulum of hepatocytes, appearing as **PAS-positive, diastase-resistant globules**, not Mallory bodies [1]. * **B. ̢-Amyloid (A̢):** This protein is associated with Alzheimer’s disease (extracellular plaques) and systemic amyloidosis, but it is not a component of the intracellular inclusions seen in alcoholic hepatitis. * **D. Prion protein (PrP):** Abnormal folding of PrP is characteristic of transmissible spongiform encephalopathies (e.g., Creutzfeldt-Jakob disease), affecting the central nervous system rather than the liver. **NEET-PG High-Yield Pearls:** * **Mallory Bodies are NOT pathognomonic for Alcoholic Liver Disease.** They are also seen in Non-alcoholic Steatohepatitis (NASH), Wilson disease, Primary Biliary Cholangitis (PBC), and Alpha-1 antitrypsin deficiency. * **Staining:** They are highlighted by **Ubiquitin** stains. * **Histological Triad of Alcoholic Hepatitis:** Hepatocyte swelling (ballooning), Mallory bodies [1], and neutrophilic infiltration. * **Key Protein:** Remember **Cytokeratin 8/18** as the specific intermediate filament involved. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 388-390.
Question 292: Nutmeg liver is a characteristic finding in which condition?
- A. Chronic venous congestion (Correct Answer)
- B. Hyperaemia of the liver
- C. Hepatic thrombosis
- D. Acute hepatic congestion
Explanation: **Explanation:** **Nutmeg liver** is the classic macroscopic description for **Chronic Venous Congestion (CVC)** of the liver, most commonly resulting from congestive heart failure [1], [2]. **1. Why Chronic Venous Congestion is correct:** In CVC, there is persistent back-pressure from the right heart into the hepatic veins. This leads to blood pooling in the **centrilobular areas (Zone 3)**, causing congestion and pressure atrophy of hepatocytes [1]. Grossly, these congested areas appear dark reddish-brown [2]. In contrast, the **periportal areas (Zone 1)** receive better oxygenation and may undergo fatty change, appearing pale/yellow. The alternating pattern of dark (congested) and light (fatty) areas resembles the cut surface of a nutmeg seed [1], [3]. **2. Why other options are incorrect:** * **Hyperaemia:** This is an *active* process due to increased arterial inflow (e.g., inflammation). It results in a bright red, warm organ, not the mottled pattern of CVC. * **Hepatic Thrombosis (Budd-Chiari Syndrome):** While this causes venous outflow obstruction, it typically presents with acute, severe congestion and hepatomegaly [3]. The classic "nutmeg" pattern requires *chronic* duration to allow for the distinct contrast between centrilobular necrosis and periportal fatty change. * **Acute Hepatic Congestion:** The liver is enlarged and cyanotic, but there hasn't been enough time for the characteristic fatty changes or architectural remodeling to create the nutmeg appearance [2]. **High-Yield Facts for NEET-PG:** * **Microscopic hallmark:** Centrilobular (Zone 3) necrosis and hemorrhage [2]. * **Cardiac Cirrhosis:** Long-standing CVC can lead to fibrosis, termed "cardiac cirrhosis" [3]. * **Zone 3 Vulnerability:** Zone 3 is most susceptible to congestion and hypoxia because it is furthest from the hepatic artery [3]. * **Common Cause:** Right-sided heart failure is the most frequent etiology [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 401-402. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 126. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 870-872.
Question 293: Anti-LKM-2 autoantibody is seen in drug-induced liver injury. It is directed against which of the following structures?
- A. Cytochrome P450 (Correct Answer)
- B. Cytoplasm
- C. Biliary tract
- D. Focal tract
Explanation: ### Explanation **Correct Option: A. Cytochrome P450** Anti-Liver Kidney Microsome (LKM) antibodies are a group of autoantibodies directed against specific metabolic enzymes located within the endoplasmic reticulum (microsomes) of hepatocytes and renal tubular cells. * **Anti-LKM-2** is specifically associated with **Drug-Induced Liver Injury (DILI)**, most notably caused by the drug **Ticrynafen** (a diuretic). * The target antigen for Anti-LKM-2 is **Cytochrome P450 2C9 (CYP2C9)**. The drug acts as a hapten, modifying the P450 enzyme and triggering an immune response against it. **Analysis of Incorrect Options:** * **B. Cytoplasm:** While these antibodies react with antigens located in the cytoplasm (specifically the endoplasmic reticulum), "Cytochrome P450" is the specific molecular target [1]. In NEET-PG, the most specific biochemical target is always the preferred answer. * **C. Biliary tract:** Antibodies against the biliary tract (specifically the interlobular bile ducts) are characteristic of **Primary Biliary Cholangitis (PBC)**, where the hallmark antibody is Anti-Mitochondrial Antibody (AMA) [1]. * **D. Focal tract:** This is a distractor term with no specific clinical relevance to LKM antibodies or autoimmune liver disease. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-LKM-1:** Target is **CYP2D6**. It is the hallmark of **Autoimmune Hepatitis (AIH) Type 2** (typically seen in children/young females) [1]. * **Anti-LKM-2:** Target is **CYP2C9**. Associated with **Drug-induced hepatitis** (Ticrynafen). * **Anti-LKM-3:** Target is **UDP-glucuronosyltransferase**. Associated with **Hepatitis D (Delta)** infection and AIH Type 2. * **Anti-SLA/LP:** Most specific antibody for Autoimmune Hepatitis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 845-846.
Question 294: Amyloid deposits in the liver are initially seen in which location?
- A. Space of Disse (Correct Answer)
- B. Hepatic parenchyma
- C. Intrahepatic ducts
- D. Portal tract
Explanation: **Explanation:** **1. Why the Space of Disse is Correct:** Amyloidosis of the liver involves the extracellular deposition of misfolded protein fibrils [2]. In the liver, the **Space of Disse** (the perisinusoidal space between the sinusoidal endothelium and the hepatocytes) is the initial and primary site of deposition [1]. As amyloid accumulates here, it compresses the adjacent hepatocytes and narrows the sinusoidal lumen [1]. This leads to pressure atrophy of hepatocytes, eventually resulting in the characteristic appearance of "amyloid replacement" of the hepatic parenchyma. **2. Why the Other Options are Incorrect:** * **Hepatic parenchyma:** While the parenchyma is eventually destroyed and replaced by amyloid, the deposition is *extracellular* [2]. It does not start inside the hepatocytes themselves but rather exerts external pressure on them from the Space of Disse. * **Intrahepatic ducts:** Amyloid deposition rarely involves the biliary tree directly; clinical jaundice is uncommon in hepatic amyloidosis unless the disease is very advanced. * **Portal tract:** While amyloid can be found in the walls of the hepatic arteries within the portal tracts (especially in AL amyloidosis), the classic initial site for parenchymal involvement and the primary diagnostic feature in liver biopsies is the Space of Disse. **3. NEET-PG High-Yield Pearls:** * **Gross Appearance:** The liver becomes enlarged, firm, and has a pale, "waxy" or "lardaceous" appearance. * **Staining:** Amyloid shows **Apple-green birefringence** under polarized light when stained with **Congo Red** [1]. * **Clinical Presentation:** Hepatomegaly is common, but liver function is often preserved until late stages [3]. Significant jaundice is a poor prognostic sign. * **Classification:** Hepatic involvement is common in both Primary (AL) and Secondary (AA) amyloidosis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-266. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 135-136.
Question 295: What is the commonest benign tumor of the liver?
- A. Hematoma
- B. Hemangioma (Correct Answer)
- C. Adenoma
- D. Cholangioma
Explanation: **Explanation:** **1. Why Hemangioma is Correct:** Cavernous hemangioma is the **most common benign primary tumor of the liver**. These are mesenchymal tumors composed of large, endothelial-lined vascular channels [1]. They are typically small, asymptomatic, and discovered incidentally during imaging or autopsy. While they can occur at any age, they are more frequently identified in adults. **2. Why the other options are incorrect:** * **Hematoma (Option A):** A hematoma is a localized collection of blood outside blood vessels, usually resulting from trauma or surgery. It is a reactive process, not a neoplastic tumor. * **Adenoma (Option B):** Hepatic Adenomas are benign epithelial tumors [1]. While clinically significant due to their association with **oral contraceptive pills (OCPs)** and the risk of rupture or malignant transformation, they are much rarer than hemangiomas [1]. * **Cholangioma (Option D):** Also known as bile duct adenoma, these are rare, small, benign tumors of the biliary epithelium. They are significantly less common than hemangiomas. **3. NEET-PG High-Yield Pearls:** * **Imaging:** On CT/MRI, hemangiomas show a characteristic **"centripetal filling"** pattern (peripheral globular enhancement with gradual central filling). * **Clinical Caution:** Biopsy is generally **contraindicated** if a hemangioma is suspected due to the high risk of intraperitoneal hemorrhage. * **Size:** Hemangiomas >10 cm are termed "Giant Hemangiomas." * **Most common primary malignant tumor:** Hepatocellular Carcinoma (HCC). * **Most common liver tumor overall:** Metastatic deposits (most commonly from the colon). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 874.
Question 296: All of the following are true about fibrolamellar hepatocellular carcinoma except:
- A. Alpha-fetoprotein (AFP) is typically not elevated.
- B. Recurrence of the tumor is common.
- C. Neurotensin levels may be elevated.
- D. The tumor is well demarcated and encapsulated. (Correct Answer)
Explanation: ### Explanation **Fibrolamellar Hepatocellular Carcinoma (FL-HCC)** is a distinct variant of hepatocellular carcinoma that typically occurs in young adults (20–40 years) without underlying cirrhosis or hepatitis B/C infection. **1. Why Option D is the Correct Answer (The "Except"):** While FL-HCC often appears as a large, firm, solitary mass with a characteristic **central stellate scar** (mimicking Focal Nodular Hyperplasia), it is **not encapsulated**. Although it may appear well-demarcated from the surrounding non-cirrhotic liver, it lacks a true fibrous capsule, which is a common misconception in imaging and gross pathology. **2. Analysis of Other Options:** * **Option A (AFP levels):** Unlike conventional HCC, serum **Alpha-fetoprotein (AFP) is characteristically normal** in FL-HCC [1]. This is a high-yield diagnostic differentiator. * **Option B (Recurrence):** Although FL-HCC has a better prognosis than conventional HCC (due to the absence of cirrhosis), it is still a malignant tumor. **Recurrence is common** after surgical resection, often occurring in the liver or as metastatic spread to regional lymph nodes. * **Option C (Neurotensin):** FL-HCC is associated with unique biochemical markers. Serum **neurotensin** and vitamin B12-binding capacity (transcobalamin) are frequently elevated. **3. NEET-PG High-Yield Clinical Pearls:** * **Microscopy:** Characterized by large, polygonal cells with abundant eosinophilic cytoplasm (due to mitochondria) and prominent nucleoli, separated by **parallel (lamellar) bundles of collagen**. * **Genetic Marker:** A highly specific recurrent **DNAJB1-PRKACA fusion gene** is found in almost all cases of FL-HCC. * **Gender:** Occurs equally in males and females (unlike conventional HCC, which favors males). * **Prognosis:** Better than conventional HCC because the background liver is healthy, allowing for more aggressive surgical resection [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 399-400.
Question 297: Given below is the histopathology of a liver biopsy of a patient with hemochromatosis. Which of the following special stains has been used?
- A. Von Kossa stain
- B. Alcian blue stain
- C. Perls' Prussian blue stain (Correct Answer)
- D. Crystal violet stain
Explanation: ***Perls' Prussian blue stain*** - **Perls' Prussian blue stain** is the gold standard for detecting **iron deposits** in tissues, which appears as blue granules in hepatocytes in hemochromatosis. - This stain specifically detects **ferric iron (Fe³⁺)** by forming a blue precipitate when potassium ferrocyanide reacts with iron in acidic conditions. *Von Kossa stain* - **Von Kossa stain** is used to detect **calcium deposits** in tissues, not iron deposits. - It would show **black deposits** where calcium is present, which is not relevant for diagnosing hemochromatosis. *Alcian blue stain* - **Alcian blue stain** is used to detect **mucins** and **acidic mucopolysaccharides** in tissues. - It has no utility in detecting **iron deposits** and would not assist in confirming hemochromatosis diagnosis. *Crystal violet stain* - **Crystal violet stain** is primarily used to detect **amyloid deposits** in tissues (Congo red is more commonly used). - It does not detect **iron** and would not be helpful in evaluating hemochromatosis liver pathology.
Question 298: Fatty liver is due to accumulation of which substance?
- A. Triglycerides (Correct Answer)
- B. LDL
- C. Lipoprotein a
- D. VLDL
Explanation: **Explanation:** **Steatosis (Fatty Change)** refers to the abnormal accumulation of lipids within parenchymal cells, most commonly occurring in the liver [1]. **1. Why Triglycerides (Option A) is correct:** The liver is the central organ for lipid metabolism. Fatty liver occurs when there is an imbalance between the delivery/synthesis of lipids and their utilization/export [1]. The specific form of lipid that accumulates in the cytoplasm of hepatocytes is **Triglycerides**. This happens due to various mechanisms: increased entry of free fatty acids (FFA), increased synthesis of fatty acids, decreased oxidation of fatty acids, or impaired exit of lipoproteins. **2. Why the other options are incorrect:** * **LDL (Option B):** Low-Density Lipoprotein is a transport vehicle for cholesterol in the blood. While high levels are associated with atherosclerosis, it is not the primary storage form of fat within hepatocytes. * **Lipoprotein a (Option C):** This is a specific type of LDL particle linked to cardiovascular risk; it does not play a role in the pathology of steatosis. * **VLDL (Option D):** Very Low-Density Lipoprotein is the form in which triglycerides are **exported** from the liver. A deficiency in the synthesis of the protein component (apolipoproteins) prevents VLDL formation, leading to the entrapment of triglycerides *inside* the liver, thus causing fatty liver. **High-Yield Clinical Pearls for NEET-PG:** * **Most common causes:** Alcohol abuse and Non-Alcoholic Fatty Liver Disease (NAFLD) associated with obesity/diabetes [2]. * **Gross Appearance:** The liver becomes enlarged, heavy (up to 4-6 kg), yellow, and greasy [2]. * **Microscopy:** Clear vacuoles within hepatocytes that displace the nucleus to the periphery (Macrovesicular steatosis) [2]. * **Special Stains:** Since fat is dissolved during routine processing (alcohol/xylene), it must be visualized in **frozen sections** using **Sudan IV** or **Oil Red O** (stains orange-red). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 73. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 848-854.
Question 299: "Crumbled egg appearance" in liver is seen in which of the following conditions?
- A. Hepatic adenoma
- B. Chronic amoebic liver abscess
- C. Hydatid liver disease (Correct Answer)
- D. Haemangioma
Explanation: **Explanation:** **Hydatid Liver Disease (Option C)** is caused by the larval stage of the cestode *Echinococcus granulosus*. [1] The "crumbled egg appearance" (also known as the **Water-lily sign**) is a classic radiological and pathological feature. It occurs when the endocyst (the inner germinal layer) ruptures and collapses into the cyst fluid, appearing as irregular, wavy membranes floating within the cavity. This appearance is characteristic of a Stage CE3a cyst (WHO classification), indicating a transitional phase where the parasite is no longer viable. **Why other options are incorrect:** * **Hepatic Adenoma (Option A):** These are benign epithelial tumors associated with oral contraceptive use. [2] They typically present as a well-circumscribed mass with a "cold" appearance on sulfur colloid scans, not a crumbled membrane appearance. * **Chronic Amoebic Liver Abscess (Option B):** Caused by *Entamoeba histolytica*, this is classically associated with **"Anchovy sauce pus"** (a reddish-brown, odorless necrotic material). It does not contain internal membranes. * **Haemangioma (Option C):** The most common benign liver tumor. [2] On imaging, it shows peripheral globular enhancement with "centripetal fill-in" on contrast CT, rather than a cystic crumbled appearance. **High-Yield Clinical Pearls for NEET-PG:** * **Casoni’s Test:** An immediate hypersensitivity skin test used for diagnosis (now largely replaced by ELISA). * **Layers of Hydatid Cyst:** Pericyst (host-derived), Ectocyst (outer laminated), and Endocyst (inner germinal). * **Treatment:** PAIR (Puncture, Aspiration, Injection, Re-aspiration) is a minimally invasive treatment option. * **Complication:** Rupture of the cyst can lead to life-threatening **Anaphylactic shock**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 403-404. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 874.
Question 300: What is the most important risk factor for hepatocellular carcinoma?
- A. Alcoholic hepatitis
- B. Schistosomiasis
- C. Cirrhosis (Correct Answer)
- D. Fasciolopsis buski infestation
Explanation: **Explanation:** **Hepatocellular Carcinoma (HCC)** is the most common primary malignancy of the liver [1]. The correct answer is **Cirrhosis**, as it is the single most important precursor and risk factor for HCC, regardless of the underlying etiology [1][2]. 1. **Why Cirrhosis is correct:** Approximately **80-90% of HCC cases** develop in a cirrhotic liver [1]. The pathophysiology involves a cycle of chronic inflammation, continuous hepatocyte death, and compensatory regeneration. This increased cellular turnover leads to the accumulation of genetic mutations and the formation of dysplastic nodules, which eventually progress to carcinoma. In the NEET-PG context, remember: "Cirrhosis is the common denominator for HCC." 2. **Why other options are incorrect:** * **Alcoholic hepatitis:** While chronic alcohol consumption leads to cirrhosis (which then causes HCC), the acute inflammatory state of alcoholic hepatitis itself is not the primary risk factor compared to the established architectural change of cirrhosis [3]. * **Schistosomiasis:** This leads to "pipestem" fibrosis and portal hypertension, but it is **not** typically associated with an increased risk of HCC. * **Fasciolopsis buski:** This is an intestinal fluke. It is **Clonorchis sinensis** and **Opisthorchis viverrini** (liver flukes) that are associated with **Cholangiocarcinoma**, not HCC. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause worldwide:** Chronic Hepatitis B infection (HBV can cause HCC even *without* cirrhosis due to DNA integration) [2]. * **Most common cause in the West/India:** Hepatitis C and Alcoholic Cirrhosis [3]. * **Tumor Marker:** Alpha-fetoprotein (AFP) is used for screening and monitoring [1]. * **Aflatoxin B1:** Produced by *Aspergillus flavus*, it causes a specific mutation in the **p53 gene (codon 249)**, significantly increasing HCC risk [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 399-400. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 876-877. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 388-389.
Practice by Chapter
Jaundice and Cholestasis
Practice Questions
Viral Hepatitis
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Alcoholic and Non-alcoholic Fatty Liver Disease
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Drug and Toxin Induced Liver Injury
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Cirrhosis and Its Complications
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Metabolic Liver Diseases
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Liver Tumors
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Gallbladder and Biliary Tract Diseases
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Congenital Liver Diseases
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Liver Transplantation Pathology
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