Author's Accepted Manuscript
Primary hepatic diffuse large B cell lymphoma: Unusual presentation and imaging features Ekta Dhamija MD, Kumble S. Madhusudhan MD, FRCR, S. Shalimar MD, DM, Prasenjit Das MD, Deep N. Srivastava MD, Arun K Gupta MD
www.elsevier.com/locate/enganabound
PII: DOI: Reference:
S0363-0188(14)00140-6 http://dx.doi.org/10.1067/j.cpradiol.2014.12.002 YMDR330
To appear in:
Curr Probl Diagn Radiol
Cite this article as: Ekta Dhamija MD, Kumble S. Madhusudhan MD, FRCR, S. Shalimar MD, DM, Prasenjit Das MD, Deep N. Srivastava MD, Arun K Gupta MD, Primary hepatic diffuse large B cell lymphoma: Unusual presentation and imaging features, Curr Probl Diagn Radiol, http://dx.doi.org/10.1067/j.cpradiol.2014.12.002 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
TITLE PAGE Title: Primary Hepatic Diffuse Large B cell Lymphoma: Unusual presentation and Imaging features Running title: Primary hepatic lymphoma
Authors: 1. Ekta Dhamija, MD1 2. Kumble S Madhusudhan, MD, FRCR1 3. Shalimar, MD, DM2 4. Prasenjit Das, MD3 5. Deep N Srivastava, MD1 6. Arun K Gupta, MD1
Authors belong to and work performed at: Department of Radiodiagnosis1, Gastroenterology2 and Pathology3 All India Institute of Medical Sciences New Delhi, India-110029
Corresponding author: Dr K S Madhusudhan, MD, FRCR Assistant Professor Department of Radiodiagnosis All India Institute of Medical Sciences New Delhi, India 110029 Contact no. +91 9868398826 Email: [email protected]
Source of grants, funding: Nil Conflict of interest: None
Primary Hepatic Diffuse Large B cell Lymphoma: Unusual presentation and Imaging features
Abstract Primary hepatic lymphoma is an uncommon malignancy affecting the liver with limited reports and series in the literature. Imaging appearance is not well described with no definite features suggesting a diagnosis and may mimic other focal hepatic lesions. However, biopsy is needed in most of the cases for confirmation. We report a case of 22-year-old pregnant female who on ultrasonography showed a large heteroechoic solitary liver mass mimicking focal nodular hyperplasia. Further evaluation after parturition with contrast enhanced MRI showed a large mass with central scar and peripheral diffusion restriction and contrast enhancement which was atypical. Biopsy confirmed it as lymphoma. The case illustrates unusual presentation and MRI features, including diffusion weighted imaging, of primary hepatic lymphoma in a young female.
Primary Hepatic Diffuse Large B cell Lymphoma: Unusual presentation and Imaging features Introduction Lymphomatous infiltration of liver occurs in almost half the cases of secondary lymphoma, in contrast to primary hepatic lymphoma (PHL) which is extremely rare constituting approximately 0.4% of extranodal disease and only 0.016% of all non-Hodgkin’s Lymphoma (NHL) [1]. PHL
refers to involvement of only liver with no splenic, lymph nodal or any other lymphoid organ involvement [1]. It affects predominantly males (Male: female ratio of 3.1:1) in the fifth decade of life [2]. Literature provides limited information on its mode of presentation and diagnosis with ultrasonography (USG), computed tomography (CT) and Magnetic Resonance Imaging (MRI) in the form of few case reports and series. We present a case of primary hepatic lymphoma in a young pregnant female presenting with sonographically detected liver mass mimicking focal nodular hyperplasia but whose MRI performed later showed atypical findings. Case history A 22-year-old pregnant female in 6th month of gestation presenting with complaints of sudden onset pain and swelling in the region of right hypochondrium showed a heteroechoic lesion of approximate size of 11 x 10 cm in the right lobe of liver, showing target appearance. She had with no history of fever or jaundice. The laboratory tests including liver enzymes, hemogram and serum alpha-fetoprotein were unremarkable. The patient was managed conservatively and followed up with repeated USG till parturition. Initial contrast enhanced Computed Tomography (CECT) in venous phase depicted a lobulated hypodense mass with central non-enhancing irregular scar in segments 4B and 5 of liver (Figure 1). The patient was referred to our institute with a provisional diagnosis of focal nodular hyperplasia. For further characterization of the lesion, contrast enhanced MRI with gadobenate dimeglumine (Multihance, Bracco) was performed which showed the lobulated mass located in central and periportal location of hepatic parenchyma. The mass was hypointense on T1-weighted and heterogeneously hyperintense on T2-weighted images with differential hyperintense signal of central irregular part (scar). The lesion showed diffusion restriction in the periphery and free diffusion in the central scar (Figure 2). The peripheral part of the mass showed progressively increasing contrast enhancement in
arterial, venous and delayed phases. The central scar showed vascularity and contrast enhancement in the delayed phases (10 min and one hour). The background liver showed normal signal intensity and morphology without any evidence of chronic liver disease or cirrhosis (Figure 3). The presence of diffusion restriction, central scar and progressive contrast enhancement were atypical for focal nodular hyperplasia (FNH) and a differential diagnosis of lymphoma and intrahepatic cholangiocarcinoma (ICC) was suggested. Subsequently, USG guided core biopsy of the lesion was performed and histopathological examination revealed diffuse infiltration of the lesion by intermediate to large sized atypical lymphoid cells with high mitotic activity and many scattered tingible body macrophages (Figure 4A). Only occasional residual hepatocytes were seen. These atypical cells were immunopositive for CD20, bcl2 and bcl6 (Figure 4B & C). These cells were negative for CD3 and MUM1. Thus, a diagnosis of Non Hodgkins lymphoma, diffuse large B cell type was established. CT scan of chest and abdomen done subsequently showed no other abnormality and no superficial lymph nodes could be palpated on physical examination. A final diagnosis of primary hepatic lymphoma was made. Patient was counseled and referred to medical oncology for initiation of chemotherapy. However, patient did not give consent for the treatment and was lost to follow up. Discussion Primary hepatic lymphomatous involvement is rare, occurring in less than one percent of lymphoma cases [1,2]. Due to the rarity of the disease there is inadequate data in English literature on its presentation and characteristic imaging features. Patients of PHL often present with fever, weight loss, night sweats and right upper quadrant pain and rarely with jaundice, or
features of hepatic failure [3]. The exact etiology is not known but it has been associated with viral hepatitis (Hepatitis B and C), HIV, Ebstein Barr viral infections and immunodeficiency state [4-6]. Elevated level of liver enzymes has also been reported [7,8]. Clinical examination may be normal or may show hepatomegaly. In our patient laboratory tests for viral markers were negative. PHL may present as single/ multiple nodules or diffuse infiltration. Imaging features of PHL are often non-specific and may mimic other benign or malignant hepatic tumors. Lymphomatous deposit may be seen as hypoechoic nodules or lesions with target appearance on USG [8]. ON CT scan, the lesions are mostly hypodense and may show peripheral enhancement [7,9]. Calcification may be occasionally seen. On MRI, the lesion appears hypointense on T1-weighted and mildly hyperintense on T2-weighted images. Mild contrast enhancement is seen although it has been suggested that contrast enhancement is higher in lesions with higher T2 signal [10]. Peripheral enhancement is occasionally seen [2,11]. The role of diffusion weighted MRI in PHL has not been described in literature. Similar to lymphoma at any other site, PHL also shows diffusion restriction owing to its cellularity. This helped us in suggesting a diagnosis of a malignant lesion, possibly lymphoma. The presence of central hyperintense scar on T2-weighted images in our patient with enhancement during hepatobiliary phase of contrast enhanced MRI can be confused with other lesions like ICC, FNH and rarely fibrolamellar carcinoma (FLC) or hepatocellular carcinoma (HCC). The normal levels of AFP, normal morphology of underlying liver and absence of arterial hyperenhancement and venous washout on MRI excludes HCC and FLC. Typically, FNH is nearly isointense to liver on T1 & T2 weighted images, with arterial phase contrast enhancement which becomes isointense to liver parenchyma in porto-venous phase. Absence of capsular retraction or biliary dilatation makes possibility of ICC less likely.
Other differentials of metastases or hepatic abscess can be excluded based on clinical and biochemical parameters. Histopathological examination is needed in all the cases for a final diagnosis [9]. Majority of the PHL are B-cell (63%) and T-cell lymphoma (25%). Diffuse large B-cell is the most commonly encountered subtype [8]. Other histologic subtypes of PHL include high-grade tumours (lymphoblastic and Burkett lymphoma, 17%), follicular lymphoma (4%), diffuse histiocytic lymphoma (5%), lymphoma of the mucosa-associated lymphoid tissue type, anaplastic large-cell lymphoma, mantle cell
lymphoma,
and T
cell-rich B-cell
lymphoma
[12]. with
immunophenotype supporting the diagnosis. Reed Sternberg like cells or polymorphous cell background was not noted. No other primary malignancies of hepatocyte origin were noted histologically. In conclusion, PHL is a rare malignancy which should be considered as a differential for solitary lesions of liver with central scar. The demonstration of central scar has not been described in PHL, but presence of diffusion restriction on MRI should raise a suspicion. Biopsy is however needed for confirmation.
References: 1. Ma YJ, Chen EQ, Chen XB, Wang J, Tang H. Primary hepatic diffuse large B cell lymphoma: A case report. Hepat Mon. 2011;11:203–5 2. Coenegrachts K, Vanbeckevoort D, Deraedt K, Van Steenbergen W. MRI findings in primary non-Hodgkin's lymphoma of the liver. JBR-BTR 2005;88:17-9. 3. Haider FS, Smith R, Khan S. Primary hepatic lymphoma presenting as fulminant hepatic failure with hyperferritinemia: a case report. J Med Case Rep 2008:279. doi: 10.1186/1752-1947-2-279. 4. Mizorogi F, Hiramoto J, Nozato A, Takekuma Y, Nagayama K, Tanaka T, et al. Hepatitis C virus infection in patients with B-cell non-Hodgkin's lymphoma. Intern Med 2000;39(2):112-7. 5. Bronowicki JP, Bineau C, Feugier P, Hermine O, Brousse N, Oberti F et al. Primary lymphoma of the liver: clinical-pathological features and relationship with HCV infection in French patients. Hepatology 2003;37:781-7. 6. Villafae MF, Trione N, Corti M, Mendez N, Gancedo E, Zamora N, et al. Case Report: Primary Liver AIDS Related Lymphoma. Inst. Med. trop. S. Paulo Journal 2006; 48: 22931. 7. Steller EJ, van Leeuwen MS, van Hillegersberg R, Schipper ME, Rinkes IH, Molenaar IQ. Primary lymphoma of the liver - A complex diagnosis. World J Radiol 2012;4:53-7. doi: 10.4329/wjr.v4.i2.53.
8. Elsayes KM, Menias CO, Willatt JM, Pandya A, Wiggins M, Platt J. Primary hepatic lymphoma: imaging findings. J Med Imaging Radiat Oncol 2009;53:373-9.
doi:
10.1111/j.1754-9485.2009.02081.x. 9. Gazelle GS, Lee MJ, Hahn PF, Goldberg MA, Rafaat N, Mueller PR. US, CT, and MRI of primary and secondary liver lymphoma. J Comput Assist Tomogr. 1994;18:412–5 10. Kelekis N.L., Semelka R.C., Siegelman E.S., Ascher S.M., Outwater E.K., Woosley J.T., Reinhold C., Mitchell D.G.: Focal hepatic lymphoma: magnetic resonance demonstration using current techniques including gadolinium enhancement. MRI, 1997, 15: 625-636.
11. Bilaj F, Berdica L, Dhima A, Vreto G. Magnetic resonance imaging findings in primary lymphoma of the liver: a case report. J Med Case Rep. 2012; 6: 282 12. Masood A, Kairouz S, Hudhud KH, Hegazi AZ, Banu A, Gupta NC. Primary nonHodgkin lymphoma of liver. Curr Oncol. 2009;16:74-7.
LEGENDS OF FIGURES: Figure 1: CECT demonstrating hypodense non enhancing mass: Venous phase CT scan shows presence of well defined hypodense mass in the hepatic parenchyma involving both lobes of liver (arrows in a & b). Central area is relatively more hypodense than rest of the mass, representing central scar. Background liver has no evidence of cirrhosis. Note made of thrombosed portal vein with cavernoma formation at hepatic hilum (arrowheads in a) Figure 2: Precontrast MRI of Primary Hepatic Lymphoma: Axial and coronal MR images demonstrate a large solitary mass in the central hepatic parenchyma which is hypointense on T1 WI (a) and iso to hyperintense on T2 WI (b & c), relative to the background liver and spleen. Central scar has hyperintense signal as compared to the rest of mass (arrowheads in b). On DWI and ADC (c), marked restriction is seen in its periphery. Figure 3: Axial T1 W post contrast images: The mass exhibits peripheral rim enhancement in the arterial phase (arrows in a) with gradual centripetal filling in during porto-venous (b) and venous (c) phases. Few vessels are seen coursing through the central scar (black arrowheads in b). Hepatobiliary phase at 1-hour reveals pooling of contrast in the central scar (black arrowheads in d) Figure 4: Photomicrograph shows diffuse infiltration by a large atypical lymphoid cell population with frequent apoptic bodies (arrows in a, H&E x40). These atypical cells were immunopositive for CD20 and bc16 {b (CD20); C (bc16) x100}
Fig 1
Fig 2
Fig 3
Fig 4
Primary hepatic diffuse large B cell lymphoma: Unusual presentation and imaging features Ekta Dhamija MD, Kumble S. Madhusudhan MD, FRCR, S. Shalimar MD, DM, Prasenjit Das MD, Deep N. Srivastava MD, Arun K Gupta MD
www.elsevier.com/locate/enganabound
PII: DOI: Reference:
S0363-0188(14)00140-6 http://dx.doi.org/10.1067/j.cpradiol.2014.12.002 YMDR330
To appear in:
Curr Probl Diagn Radiol
Cite this article as: Ekta Dhamija MD, Kumble S. Madhusudhan MD, FRCR, S. Shalimar MD, DM, Prasenjit Das MD, Deep N. Srivastava MD, Arun K Gupta MD, Primary hepatic diffuse large B cell lymphoma: Unusual presentation and imaging features, Curr Probl Diagn Radiol, http://dx.doi.org/10.1067/j.cpradiol.2014.12.002 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
TITLE PAGE Title: Primary Hepatic Diffuse Large B cell Lymphoma: Unusual presentation and Imaging features Running title: Primary hepatic lymphoma
Authors: 1. Ekta Dhamija, MD1 2. Kumble S Madhusudhan, MD, FRCR1 3. Shalimar, MD, DM2 4. Prasenjit Das, MD3 5. Deep N Srivastava, MD1 6. Arun K Gupta, MD1
Authors belong to and work performed at: Department of Radiodiagnosis1, Gastroenterology2 and Pathology3 All India Institute of Medical Sciences New Delhi, India-110029
Corresponding author: Dr K S Madhusudhan, MD, FRCR Assistant Professor Department of Radiodiagnosis All India Institute of Medical Sciences New Delhi, India 110029 Contact no. +91 9868398826 Email: [email protected]
Source of grants, funding: Nil Conflict of interest: None
Primary Hepatic Diffuse Large B cell Lymphoma: Unusual presentation and Imaging features
Abstract Primary hepatic lymphoma is an uncommon malignancy affecting the liver with limited reports and series in the literature. Imaging appearance is not well described with no definite features suggesting a diagnosis and may mimic other focal hepatic lesions. However, biopsy is needed in most of the cases for confirmation. We report a case of 22-year-old pregnant female who on ultrasonography showed a large heteroechoic solitary liver mass mimicking focal nodular hyperplasia. Further evaluation after parturition with contrast enhanced MRI showed a large mass with central scar and peripheral diffusion restriction and contrast enhancement which was atypical. Biopsy confirmed it as lymphoma. The case illustrates unusual presentation and MRI features, including diffusion weighted imaging, of primary hepatic lymphoma in a young female.
Primary Hepatic Diffuse Large B cell Lymphoma: Unusual presentation and Imaging features Introduction Lymphomatous infiltration of liver occurs in almost half the cases of secondary lymphoma, in contrast to primary hepatic lymphoma (PHL) which is extremely rare constituting approximately 0.4% of extranodal disease and only 0.016% of all non-Hodgkin’s Lymphoma (NHL) [1]. PHL
refers to involvement of only liver with no splenic, lymph nodal or any other lymphoid organ involvement [1]. It affects predominantly males (Male: female ratio of 3.1:1) in the fifth decade of life [2]. Literature provides limited information on its mode of presentation and diagnosis with ultrasonography (USG), computed tomography (CT) and Magnetic Resonance Imaging (MRI) in the form of few case reports and series. We present a case of primary hepatic lymphoma in a young pregnant female presenting with sonographically detected liver mass mimicking focal nodular hyperplasia but whose MRI performed later showed atypical findings. Case history A 22-year-old pregnant female in 6th month of gestation presenting with complaints of sudden onset pain and swelling in the region of right hypochondrium showed a heteroechoic lesion of approximate size of 11 x 10 cm in the right lobe of liver, showing target appearance. She had with no history of fever or jaundice. The laboratory tests including liver enzymes, hemogram and serum alpha-fetoprotein were unremarkable. The patient was managed conservatively and followed up with repeated USG till parturition. Initial contrast enhanced Computed Tomography (CECT) in venous phase depicted a lobulated hypodense mass with central non-enhancing irregular scar in segments 4B and 5 of liver (Figure 1). The patient was referred to our institute with a provisional diagnosis of focal nodular hyperplasia. For further characterization of the lesion, contrast enhanced MRI with gadobenate dimeglumine (Multihance, Bracco) was performed which showed the lobulated mass located in central and periportal location of hepatic parenchyma. The mass was hypointense on T1-weighted and heterogeneously hyperintense on T2-weighted images with differential hyperintense signal of central irregular part (scar). The lesion showed diffusion restriction in the periphery and free diffusion in the central scar (Figure 2). The peripheral part of the mass showed progressively increasing contrast enhancement in
arterial, venous and delayed phases. The central scar showed vascularity and contrast enhancement in the delayed phases (10 min and one hour). The background liver showed normal signal intensity and morphology without any evidence of chronic liver disease or cirrhosis (Figure 3). The presence of diffusion restriction, central scar and progressive contrast enhancement were atypical for focal nodular hyperplasia (FNH) and a differential diagnosis of lymphoma and intrahepatic cholangiocarcinoma (ICC) was suggested. Subsequently, USG guided core biopsy of the lesion was performed and histopathological examination revealed diffuse infiltration of the lesion by intermediate to large sized atypical lymphoid cells with high mitotic activity and many scattered tingible body macrophages (Figure 4A). Only occasional residual hepatocytes were seen. These atypical cells were immunopositive for CD20, bcl2 and bcl6 (Figure 4B & C). These cells were negative for CD3 and MUM1. Thus, a diagnosis of Non Hodgkins lymphoma, diffuse large B cell type was established. CT scan of chest and abdomen done subsequently showed no other abnormality and no superficial lymph nodes could be palpated on physical examination. A final diagnosis of primary hepatic lymphoma was made. Patient was counseled and referred to medical oncology for initiation of chemotherapy. However, patient did not give consent for the treatment and was lost to follow up. Discussion Primary hepatic lymphomatous involvement is rare, occurring in less than one percent of lymphoma cases [1,2]. Due to the rarity of the disease there is inadequate data in English literature on its presentation and characteristic imaging features. Patients of PHL often present with fever, weight loss, night sweats and right upper quadrant pain and rarely with jaundice, or
features of hepatic failure [3]. The exact etiology is not known but it has been associated with viral hepatitis (Hepatitis B and C), HIV, Ebstein Barr viral infections and immunodeficiency state [4-6]. Elevated level of liver enzymes has also been reported [7,8]. Clinical examination may be normal or may show hepatomegaly. In our patient laboratory tests for viral markers were negative. PHL may present as single/ multiple nodules or diffuse infiltration. Imaging features of PHL are often non-specific and may mimic other benign or malignant hepatic tumors. Lymphomatous deposit may be seen as hypoechoic nodules or lesions with target appearance on USG [8]. ON CT scan, the lesions are mostly hypodense and may show peripheral enhancement [7,9]. Calcification may be occasionally seen. On MRI, the lesion appears hypointense on T1-weighted and mildly hyperintense on T2-weighted images. Mild contrast enhancement is seen although it has been suggested that contrast enhancement is higher in lesions with higher T2 signal [10]. Peripheral enhancement is occasionally seen [2,11]. The role of diffusion weighted MRI in PHL has not been described in literature. Similar to lymphoma at any other site, PHL also shows diffusion restriction owing to its cellularity. This helped us in suggesting a diagnosis of a malignant lesion, possibly lymphoma. The presence of central hyperintense scar on T2-weighted images in our patient with enhancement during hepatobiliary phase of contrast enhanced MRI can be confused with other lesions like ICC, FNH and rarely fibrolamellar carcinoma (FLC) or hepatocellular carcinoma (HCC). The normal levels of AFP, normal morphology of underlying liver and absence of arterial hyperenhancement and venous washout on MRI excludes HCC and FLC. Typically, FNH is nearly isointense to liver on T1 & T2 weighted images, with arterial phase contrast enhancement which becomes isointense to liver parenchyma in porto-venous phase. Absence of capsular retraction or biliary dilatation makes possibility of ICC less likely.
Other differentials of metastases or hepatic abscess can be excluded based on clinical and biochemical parameters. Histopathological examination is needed in all the cases for a final diagnosis [9]. Majority of the PHL are B-cell (63%) and T-cell lymphoma (25%). Diffuse large B-cell is the most commonly encountered subtype [8]. Other histologic subtypes of PHL include high-grade tumours (lymphoblastic and Burkett lymphoma, 17%), follicular lymphoma (4%), diffuse histiocytic lymphoma (5%), lymphoma of the mucosa-associated lymphoid tissue type, anaplastic large-cell lymphoma, mantle cell
lymphoma,
and T
cell-rich B-cell
lymphoma
[12]. with
immunophenotype supporting the diagnosis. Reed Sternberg like cells or polymorphous cell background was not noted. No other primary malignancies of hepatocyte origin were noted histologically. In conclusion, PHL is a rare malignancy which should be considered as a differential for solitary lesions of liver with central scar. The demonstration of central scar has not been described in PHL, but presence of diffusion restriction on MRI should raise a suspicion. Biopsy is however needed for confirmation.
References: 1. Ma YJ, Chen EQ, Chen XB, Wang J, Tang H. Primary hepatic diffuse large B cell lymphoma: A case report. Hepat Mon. 2011;11:203–5 2. Coenegrachts K, Vanbeckevoort D, Deraedt K, Van Steenbergen W. MRI findings in primary non-Hodgkin's lymphoma of the liver. JBR-BTR 2005;88:17-9. 3. Haider FS, Smith R, Khan S. Primary hepatic lymphoma presenting as fulminant hepatic failure with hyperferritinemia: a case report. J Med Case Rep 2008:279. doi: 10.1186/1752-1947-2-279. 4. Mizorogi F, Hiramoto J, Nozato A, Takekuma Y, Nagayama K, Tanaka T, et al. Hepatitis C virus infection in patients with B-cell non-Hodgkin's lymphoma. Intern Med 2000;39(2):112-7. 5. Bronowicki JP, Bineau C, Feugier P, Hermine O, Brousse N, Oberti F et al. Primary lymphoma of the liver: clinical-pathological features and relationship with HCV infection in French patients. Hepatology 2003;37:781-7. 6. Villafae MF, Trione N, Corti M, Mendez N, Gancedo E, Zamora N, et al. Case Report: Primary Liver AIDS Related Lymphoma. Inst. Med. trop. S. Paulo Journal 2006; 48: 22931. 7. Steller EJ, van Leeuwen MS, van Hillegersberg R, Schipper ME, Rinkes IH, Molenaar IQ. Primary lymphoma of the liver - A complex diagnosis. World J Radiol 2012;4:53-7. doi: 10.4329/wjr.v4.i2.53.
8. Elsayes KM, Menias CO, Willatt JM, Pandya A, Wiggins M, Platt J. Primary hepatic lymphoma: imaging findings. J Med Imaging Radiat Oncol 2009;53:373-9.
doi:
10.1111/j.1754-9485.2009.02081.x. 9. Gazelle GS, Lee MJ, Hahn PF, Goldberg MA, Rafaat N, Mueller PR. US, CT, and MRI of primary and secondary liver lymphoma. J Comput Assist Tomogr. 1994;18:412–5 10. Kelekis N.L., Semelka R.C., Siegelman E.S., Ascher S.M., Outwater E.K., Woosley J.T., Reinhold C., Mitchell D.G.: Focal hepatic lymphoma: magnetic resonance demonstration using current techniques including gadolinium enhancement. MRI, 1997, 15: 625-636.
11. Bilaj F, Berdica L, Dhima A, Vreto G. Magnetic resonance imaging findings in primary lymphoma of the liver: a case report. J Med Case Rep. 2012; 6: 282 12. Masood A, Kairouz S, Hudhud KH, Hegazi AZ, Banu A, Gupta NC. Primary nonHodgkin lymphoma of liver. Curr Oncol. 2009;16:74-7.
LEGENDS OF FIGURES: Figure 1: CECT demonstrating hypodense non enhancing mass: Venous phase CT scan shows presence of well defined hypodense mass in the hepatic parenchyma involving both lobes of liver (arrows in a & b). Central area is relatively more hypodense than rest of the mass, representing central scar. Background liver has no evidence of cirrhosis. Note made of thrombosed portal vein with cavernoma formation at hepatic hilum (arrowheads in a) Figure 2: Precontrast MRI of Primary Hepatic Lymphoma: Axial and coronal MR images demonstrate a large solitary mass in the central hepatic parenchyma which is hypointense on T1 WI (a) and iso to hyperintense on T2 WI (b & c), relative to the background liver and spleen. Central scar has hyperintense signal as compared to the rest of mass (arrowheads in b). On DWI and ADC (c), marked restriction is seen in its periphery. Figure 3: Axial T1 W post contrast images: The mass exhibits peripheral rim enhancement in the arterial phase (arrows in a) with gradual centripetal filling in during porto-venous (b) and venous (c) phases. Few vessels are seen coursing through the central scar (black arrowheads in b). Hepatobiliary phase at 1-hour reveals pooling of contrast in the central scar (black arrowheads in d) Figure 4: Photomicrograph shows diffuse infiltration by a large atypical lymphoid cell population with frequent apoptic bodies (arrows in a, H&E x40). These atypical cells were immunopositive for CD20 and bc16 {b (CD20); C (bc16) x100}
Fig 1
Fig 2
Fig 3
Fig 4
