1.Histopathology of a benign bile duct lesion in the liver: Morphologic mimicker or precursor of intrahepatic cholangiocarcinoma.
Clinical and Molecular Hepatology 2016;22(3):400-405
A bile duct lesion originating from intrahepatic bile ducts is generally regarded as an incidental pathologic finding in liver specimens. However, a recent study on the molecular classification of intrahepatic cholangiocarcinoma has focused on the heterogeneity of this carcinoma and has suggested that the cells of different origins present in the biliary tree may have a major role in the mechanism of oncogenesis. In this review, benign intrahepatic bile duct lesions—regarded in the past as reactive changes or remnant developmental anomalies and now noted to have potential for developing precursor lesions of intrahepatic cholangiocarcinoma—are discussed by focusing on the histopathologic features and its implications in clinical practice.
Bile Duct Neoplasms/*pathology
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Bile Ducts/pathology
;
Bile Ducts, Intrahepatic
;
Cholangiocarcinoma/*pathology
;
Diagnosis, Differential
;
Humans
;
Liver/pathology
2.Undifferentiated embryonal sarcoma of the liver in an adult patient.
Kyu Ho LEE ; Mussin Nadiar MARATOVICH ; Kyoung Bun LEE
Clinical and Molecular Hepatology 2016;22(2):292-295
Undifferentiated embryonal sarcoma of the liver (UESL) is rare primary hepatic sarcoma and is known to occur in pediatric patients. This case is the UESL occurred in a 51-year old male patient. Multilocular cystic lesion was composed of primitive spindle cells without specific differentiation. This rare case would help to review differential diagnosis of primary sarcoma in liver and cystic neoplasm of the liver.
Abdomen/diagnostic imaging
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Biomarkers, Tumor/blood
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Desmin/metabolism
;
Diagnosis, Differential
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Humans
;
Immunohistochemistry
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Liver Neoplasms/blood/*pathology/surgery
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Magnetic Resonance Imaging
;
Male
;
Middle Aged
;
Vimentin/metabolism
3.Sarcomatoid hepatocellular carcinoma with mixed osteoclast-like giant cells and chondroid differentiation.
Clinical and Molecular Hepatology 2014;20(3):313-316
No abstract available.
Carcinoma, Hepatocellular/*pathology/therapy
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Cell Differentiation
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Chondrocytes/pathology
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Embolization, Therapeutic
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Ethanol/administration & dosage
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Giant Cells/pathology
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Humans
;
Immunohistochemistry
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Liver Neoplasms/*pathology/therapy
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Magnetic Resonance Imaging
;
Male
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Middle Aged
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Osteoclasts/pathology
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Vimentin/metabolism
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alpha-Fetoproteins/analysis
4.What Is Antibody-Mediated Rejection in Histologic Diagnosis in Liver Recipients?.
The Journal of the Korean Society for Transplantation 2017;31(1):1-5
Antibody-mediated rejection (AMR) is a rare event in liver transplantation compared to other solid organs such as the kidney and heart because of the different immunologic reactions in the liver and it ability to compensate for damage. Although it is not easy to define the histological features that help diagnosis because of its rarity, a few histologic features such as portal eosinophilia with eosinophilic endothelialitis have been reported as useful for diagnosis of acute AMR in presensitized patients. C4d staining is not a good indicator of AMR in liver grafts because of its low sensitivity and specificity. AMR is an emerging cause of chronic graft failure, especially in high risk patients having preformed or de novo donor specific alloantibodies (DSA). Some histologic parameters including interface hepatitis, lobular inflammation, portal collagenation, portal venopathy, and sinusoidal fibrosis, have been suggested as chronic AMR to predict graft fibrosis and survival in DSA positive patients. In conclusion, recent studies have resulted in the histological diagnostic criteria of AMR becoming more specific; however, confirmation of AMR still requires strong clinical evidence for alloantibodies.
Collagen
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Diagnosis*
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Eosinophilia
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Eosinophils
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Fibrosis
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Graft Rejection
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Heart
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Hepatitis
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Humans
;
Inflammation
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Isoantibodies
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Kidney
;
Liver Transplantation
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Liver*
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Sensitivity and Specificity
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Tissue Donors
;
Transplants
5.Histologic and Molecular Pathogenesis of Gallbladder Cancer
Korean Journal of Pancreas and Biliary Tract 2018;23(1):1-6
Adenocarcinoma is the major histology of gallbladder cancer. There are three subtypes of adenocarcinoma of the gallbladder: biliary, intestinal, and gastric foveolar subtypes. Also, there are three premalignant lesions of gallbladder adenocarcinoma: adenoma, biliary intraepithelial neoplasia (BilIN), and intracystic papillary neoplasm (ICPN). Premalignant lesion is hyperplasia of dysplastic epithelial cells with no evidence of stromal invasion. BilIN is invisible in gross inspection but can be microscopically identified around invasive tumor or chronic cholecystitis. ICPN is grossly identified as exophytic polypoid mass or diffuse friable thickening of mucosa and composed of mucinous epithelial cells with papillary and tubular arrangement. Dysplasia of BilIN and ICPN is classified by using a three-tiered system and high grade dysplasia is the same group with carcinoma in situ. Adenoma and ICPN have some ambiguities in definition and re-establishment of diagnostic criteria is needed for reproducibility of diagnosis. KRAS, TP53, and CDKN2A are the representative altered molecules in gallbladder cancer. Molecular alteration during dysplasia-carcinoma sequence is too heterogenous depending to the risk factors and type of premalignant lesion to explain the whole process by single process. Over-expression of COX2, mutation of TP53, impairment of mitochondrial DNA were reported in early hyperplastic or metaplastic epithelium. Loss of heterozygosity (LOH) of 3p, 8p chromosomes and amplification of HER2 were reported in low grade dysplasia and LOH of 9p, 18q, 22q, 17p chromosomes and mutation of CDK2A were reported in high grade dysplasia/carcinoma in situ.
Adenocarcinoma
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Adenoma
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Bile Pigments
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Carcinogenesis
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Carcinoma in Situ
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Cholecystitis
;
Diagnosis
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DNA, Mitochondrial
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Epithelial Cells
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Epithelium
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Gallbladder Neoplasms
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Gallbladder
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Hyperplasia
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Loss of Heterozygosity
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Mucins
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Mucous Membrane
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Precancerous Conditions
;
Risk Factors
6.Detection of Residual Leukemia with Reverse Transcription-polymerase Chain Reaction from Patients with AML1/ETO Positive Acute Myeloid Leukemia in Remission.
Kyoung Bun PARK ; Jae Jin LEE ; Hwi Joong YOON ; Si Young KIM ; Young Il KIM ; Kyoung Sam CHO
Korean Journal of Hematology 2003;38(1):15-22
BACKGROUND: One of the most frequent cytogenetic abnormality in acute myeloid leukemia (AML) is t(8;21) (q22;q22), with rearrangement of the AML1 gene on chromosome 21q22 and the ETO gene on chromosome 8q22. In adult AML1/ETO-associated leukemia patients, chemotherapy alone results in cure rates that are comparable to or better than those achieved with allogenic bone marrow transplantation. Despite the relatively good prognosis of AML1/ETO fusion transcript, relapse of leukemia remains the most common cause of treatment failure. Monitoring minimal residual disease (MRD) in leukemia has two main aims : to assess the effectiveness of treatment and to detect early signs of relapse. Reverse transcription-polymerase chain reaction (RT-PCR)- based methods is the rapid and sensitive method in the identification of this molecular abnormality. The purpose of this study is to ensure the usefulness of the RT-PCR technique for detecting MRD in AML1/ETO-associated leukemia patients in remission and to establish the correlation of the serial detection of AML1/ETO fusion transcripts after complete remission and long-term outcome. METHODS: From the bone marrow aspirates of 25 AML1/ETO positive AML patients, serial detection of AML1/ETO fusion trascripts was performed using RT-PCR. RESULTS: AML1/ETO fusion transcripts were positive in 14 cases who did not show t(8;21). In serial assay, AML1/ETO fusion transcripts was positive in 9 cases and negative in 13 cases at 10 weeks after complete remission. AML1/ETO fusion transcripts (+) group has 107.4+/-18.2 months suvival and AML1/ETO fusion transcripts (-) group has 47.3+/-18.0 months survival. However, there is no significance (P=0.11). CONCLUSION: This study suggests that the early negative conversion of AML1/ETO fusion transcript may be the good prognostic predictor. The RT-PCR technique is useful for detecting minimal residual disease in leukemia patients in remission and it may improve the therapeutic strategy for leukemia.
Adult
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Male
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Female
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Humans
;
Bone Marrow Transplantation
7.Differential Expression of Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases in Thioacetamide-Induced Chronic Liver Injury.
Soo Young PARK ; Hye Won SHIN ; Kyoung Bun LEE ; Min Jae LEE ; Ja June JANG
Journal of Korean Medical Science 2010;25(4):570-576
Hepatic fibrogenesis, a complex process that involves a marked accumulation of extracellular matrix components, activation of cells capable of producing matrix materials, cytokine release, and tissue remodeling, is regulated by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). The MMP-TIMP balance can regulate liver fibrogenesis. The aim of this study was to evaluate the expression patterns of MMPs and TIMPs during thioacetamide (TAA)-induced liver fibrogenesis. Chronic liver injury was induced with TAA (200 mg/kg i.p.) for 4 or 7 weeks in male Sprague-Dawley rats. Hepatic injury and fibrosis were assessed by hematoxylin-eosin (H&E) staining, and collagen deposition was confirmed by Sirius Red staining. The level of hepatic injury was quantified by serological analysis. The transcriptional and translational levels of alpha-smooth muscle actin (alpha-SMA), MMPs, and TIMPs in the liver were measured by Western blotting, RT-PCR, and immunohistochemistry. MMP, TIMP, and alpha-SMA were observed along fibrotic septa and portal spaces around the lobules. TAA treatment increased transcription of both MMPs and TIMPs, but only TIMPs showed increased translation. The dominant expression of TIMPs may regulate the function of MMPs to maintain liver fibrosis induced by TAA.
Animals
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Collagen/metabolism
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Extracellular Matrix/chemistry/metabolism
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*Liver Cirrhosis/chemically induced/metabolism/pathology
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Male
;
Matrix Metalloproteinases/genetics/*metabolism
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Rats
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Rats, Sprague-Dawley
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Thioacetamide/*toxicity
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Tissue Inhibitor of Metalloproteinases/genetics/*metabolism
8.Prognosis of Hepatocellular Carcinoma after Liver Transplantation: Comparative Analysis with Partial Hepatectomy.
Kyuho LEE ; Kyoung Bun LEE ; Nam Joon YI ; Kyung Suk SUH ; Ja June JANG
Journal of Pathology and Translational Medicine 2017;51(1):79-86
BACKGROUND: Liver transplantation (LT) is the treatment of choice for hepatocellular carcinoma (HCC). The aim of this study was to investigate the recurrence rate of HCC after LT and prognostic factors for recurrence by comparing LT with non-transplanted resection. METHODS: The participants were 338 patients who underwent LT between 1996 and 2012 at Seoul National University Hospital (LT group) and 520 HCC patients who underwent partial hepatectomy between 1995 and 2006 (control group, non-LT group). RESULTS: In the LT group, 68 of 338 patients (19.8%) showed relapse, and the recurrence rate was lower than that in the non-LT group (64.9%, 357/520, p < .001). Stratification analysis by American Joint Committee on Cancer (AJCC) stage showed that the stage I-II LT group had a lower recurrence rate than the non-LT group. Univariate comparative analysis demonstrated that multiplicity of tumor, tumor size, gross type, Edmondson- Steiner (ES) nuclear grade, extent of tumor, angioinvasion, AJCC stage, Milan criteria, University of California at San Francisco criteria on explant pathology (all p < .001), positive expression of cytokeratin 19 (p = .002), and preoperative α-fetoprotein (AFP) (p < .001) were predictors of tumor recurrence. In multivariate analysis, LT, preoperative AFP, multiplicity of tumor, extent of tumor, size of tumor, and ES nuclear grade were independent prognostic factors. CONCLUSIONS: LT might have a protective effect against the late recurrence of stage I-II HCC compared to non-LT, and the prognostic factors for recurrence were similar to previously well-known prognostic factors for HCC.
California
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Carcinoma, Hepatocellular*
;
Hepatectomy*
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Humans
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Joints
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Keratin-19
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Liver Transplantation*
;
Liver*
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Multivariate Analysis
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Pathology
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Prognosis*
;
Recurrence
;
Seoul
9.Diagnostic Accuracy of Endoscopic Ultrasound-Guided Fine Needle Aspiration Cytology of Pancreatic Lesions.
Hae Woon BAEK ; Min Jee PARK ; Ye Young RHEE ; Kyoung Bun LEE ; Min A KIM ; In Ae PARK
Journal of Pathology and Translational Medicine 2015;49(1):52-60
BACKGROUND: Endoscopic ultrasound-guided fine needle aspiration cytology (EUS-FNAC) is currently the most commonly used procedure for obtaining cytologic specimens of the pancreas. It is accurate, minimally invasive, safe and cost-effective. However, there is discrepancy between cytological and surgical diagnoses. This study was aimed at evaluating the diagnostic accuracy of EUS-FNAC of the pancreas. METHODS: We performed a retrospective review of 191 cases of pancreatic lesions initially diagnosed by EUS-FNAC with subsequent histological diagnosis between 2010 and 2012 in the Department of Pathology, Seoul National University Hospital. Cytologic and surgical diagnoses were categorized into five groups: negative, benign, atypical, malignant, and insufficient for diagnosis. Subsequently, 167 cases with satisfactory yield in both surgical and cytology specimens were statistically analyzed to determine correlations with diagnosis. RESULTS: In comparison to surgical diagnoses, cytologic diagnoses were true-positive in 103 cases (61.7%), true-negative in 28 cases (16.8%), false-positive in 9 cases (5.4%), and false-negative in 27 cases (16.1%). The diagnostic accuracy was 78.4%, sensitivity was 79.2%, and specificity was 75.7%. The positive predictive value was 92.0%, and negative predictive value was 50.9%. CONCLUSIONS: EUS-FNAC has high accuracy, sensitivity, specificity and positive predictive value. Overcoming the limitations of EUS-FNAC will make it a useful and reliable diagnostic tool for accurate evaluation of pancreatic lesions.
Diagnosis
;
Endoscopic Ultrasound-Guided Fine Needle Aspiration*
;
Pancreas
;
Pathology
;
Retrospective Studies
;
Sensitivity and Specificity
;
Seoul
10.A Case of Minimal Change Nephrotie Syndrome Associated with Diclofenac.
Kyoung Bun PARK ; Yo Seb HAN ; Tae Won LEE ; Myung Jae KIM ; Moon Ho YANG ; Chun Gyoo IHM
Korean Journal of Nephrology 2000;19(3):547-551
NSAIDs are now the most widely prescribed of all drugs for the therapy of a large variety of disorders including rheumatologic disorders, and so the population of patients who are at risk for adverse effects of these drugs is rapidly expanding. A number of renal and electrolyte problems have been associated with the use of NSAIDs, including alterations in glome-rular filtration rate, hyperkalemia, acute interstitial nephritis and papillary necrosis. While the use of NSAIDs has also been associated with minimal change nephrotic syndrome, this complication has almost invariably occured in association with an acute interstitial nephritis. Recently, we experienced a case of minimal change nephrotic syndrome without significant interstitial inflammation associated with the use of NSAIDs. This patient is a 64-year-old female who developed the generalized edema and about 10kg of weight gain since three days ago. She had taken the anti-inflammatory drugs for five years intermittently and started taking diclofenac sodium, 25mg orally three times a day, 10 days before admission for increasing pain in her knees. Laboratory findings disclosed the following values WBC 5,200/mm3 with only 0.6% eosinophils, total serum protein 4.0g/dL, albumin 1.2 g/dL, BUN 17mg/dL, creatinine 0.8mg/dL, sodium 140 mmol/L, potassium 4.0mmol/L, chloride 113mmol/L, total cholesterol 338mg/dL, triglyceride 203mg/dL; 24-hour protein excretion 3.6g, creatinine clearance 52.8 mL/min ; serologic tests were unremarkable. A renal biopsy revealed no abnormality except for focal mild interstitial infiltration of chronic inflammatory cells with a few atrophic tubules on light microscopy. Immunofluorescence studies showed diffuse trace mesangial deposits of IgM, and electromicroscopy revealed diffuse obliteration of the epithelial foot process and villous transformation of the epitherial cell cytoplasms without electrondense deposits. These findings were consistent with minimal-change disease. Diclofenac was discontinued on admission because of the likelihood the renal disease was drugrelated and she treated with low-dose(40-80mg/d) of furosemide. Fourteen days after stopping diclofenac, her massive edema and weight gain resolved and laboratory studies showed a 24-hour urine protein excretion of 80mg and serum albumin of 2.7g/dL. There has been no relapse for five months since then.
Anti-Inflammatory Agents, Non-Steroidal
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Biopsy
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Cholesterol
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Creatinine
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Cytoplasm
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Diclofenac*
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Edema
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Eosinophils
;
Female
;
Filtration
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Fluorescent Antibody Technique
;
Foot
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Furosemide
;
Humans
;
Hyperkalemia
;
Immunoglobulin M
;
Inflammation
;
Knee
;
Microscopy
;
Middle Aged
;
Necrosis
;
Nephritis, Interstitial
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Nephrosis, Lipoid
;
Potassium
;
Recurrence
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Serologic Tests
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Serum Albumin
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Sodium
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Triglycerides
;
Weight Gain