Serum-ascites Albumin Gradient Research Articles

Possible use of 2D shear wave liver elastography in new-onset ascites evaluation

BackgroundNo data on the use of 2D shear wave elastography exists regarding the evaluation of the new-onset ascites causality.AimsTo determine whether 2D shear wave elastography can help in the non-invasive assessment of the new-onset ascites cause. To assess the applicability of liver stiffness measured by 2D shear wave elastography using Esaote MyLab Nine apparatus in patients with ascites.MethodsIn 52 consecutive patients with new-onset ascites (January 2020 to October 2021), liver stiffness using 2D shear wave elastography was prospectively measured. The reliable measurements were used for further analysis. Relevant clinical and laboratory data was collected.ResultsThe calculated liver stiffness measurement cut-off value of 14.4 kPa held 94% accuracy, 100% sensitivity, and 83% specificity when determining ascites with serum ascites albumin gradient ≥11 g/L. Reliable 2D shear wave elastography success rate was 84%.Conclusions2D shear wave elastography may potentially be used to differentiate transudative from exudative ascites, especially in patients with portal hypertension and peritoneal carcinomatosis.

Aetiology and diagnostic utility of serum ascites albumin gradient in children with ascites

BackgroundAscites in children is multifactorial and serum ascites albumin gradient (SAAG) ≥1.1 helps differentiate portal hypertension (PHTN) related from non-PHTN ascites. AimsWe evaluated the aetiology and diagnostic accuracy of SAAG in children with ascites. MethodsChildren with ascites were retrospectively evaluated. Etiological diagnosis was based on clinical presentation and investigations. All cases with ascitic fluid analysis and a definite diagnosis were included for calculating the utility of SAAG. ResultsWe enrolled 878 children (568[64.7%] boys). Majority were PHTN related (638[72.7%]) and secondary to acute viral hepatitis (98,15.4%), acute liver failure (185,29%), chronic liver disease (276,43.3%) and Budd-Chiari syndrome (79,12.4%). Other causes included tubercular (46,5.2%), pancreatic (32,3.6%), chylous (20,2.3%), biliary (12,1.4%), pseudoascites (16,1.8%), infections (46,5.2%), nephrotic (26,2.9%), malignancy (23,2.6%), cardiac (9,1.0%) and others (10,1%). SAAG (n = 305) correctly differentiated PHTN and non-PHTN ascites in 272 (89.2%) cases, with a high sensitivity (97%), specificity (93%) and diagnostic accuracy (95.8%). Reasons for inaccurate SAAG included mixed ascites (n = 9), different day serum and ascitic fluid albumin estimation (n = 5), serum albumin ≤1.1 g/dL (n = 2), chylous ascites (n = 3), hypergammaglobulinemia (n = 1), albumin infusions (n = 1) and unexplained (n = 12). ConclusionsNearly 27% children had non-PHTN related ascites. SAAG differentiates PHTN from non-PHTN ascites with a diagnostic accuracy of 95%.

Severe Mitral Stenosis Presenting as Chronic Liver Disease: A Rare Case Report

High Serum Ascites Albumin Gradient (SAAG) ascites in severe rheumatic mitral stenosis is very uncommon. Hereby, the authors present a similar case with this rare combination. The present case report describes a 42-year-old male with no history of hypertension or diabetes, but occasional alcohol consumption, who presented to department with complaints of recurrent anasarca over the past five years. The electrocardiogram showed an irregular R-R interval with no P waves, indicating atrial fibrillation. Ascitic fluid analysis revealed a high serum ascites albumin gradient with low ascitic protein levels. The patient responded well to treatment and was discharged with appropriate medications. He was referred to a higher centre with cardiothoracic surgical facilities for mitral valve replacement and tricuspid annuloplasty. The present case report highlights the uniqueness of the combination of severe rheumatic mitral stenosis and ascites.

Differential diagnosis of ascites: etiologies, ascitic fluid analysis, diagnostic algorithm.

Ascites is the pathological accumulation of fluid within the peritoneal cavity. It often occurs as results of liver cirrhosis, malignant neoplasia, tuberculous infection, cardiac insufficiency, renal diseases, etc. Determining the etiology is an essential step in the management of patients with new-onset ascites. Abdominal paracentesis with appropriate ascitic fluid analysis is probably the most cost-effective method of determining the cause of ascites. We performed a literature search of PubMed and identified articles published in the field of ascites, to evaluate diagnostic values of various parameters in defining the etiologies of ascites and then provides diagnostic algorithm for patients with new-onset ascites. In patients with ascites, the constituent ratio of underlying etiology varies between developed and developing countries. It is a challenge to define the etiologies of ascites in developing countries. Routine ascitic fluid analysis should include the serum ascites albumin gradient (SAAG), total protein concentration, cell count and differential. Optional ascitic fluid analysis includes cholesterol, fluid culture, cytology, tumor markers, lactate dehydrogenase, adenosine deaminase (ADA), triglyceride, amylase, glucose, brain natriuretic peptide (BNP), etc. Our review evaluated diagnostic values of the above parameters in defining the etiologies of ascites. Diagnostic algorithm established in this review would provide a practical and convenient diagnostic strategy for clinicians in diagnosing patients with new-onset ascites.

Case Report On Diagnosis of Malignancy with Serum-Ascites Cholesterol Gradient

Ascites are the accumulation of fluid in the Abdomen. It happens due to clinical complications from various diseasesthat cause signs and symptoms. Cirrhosis, malignant ascites, and abdominal tuberculosis are the most common causes of ascites.The multiple etiologies of ascites make determining the cause difficult. Several techniques can aid in the differential diagnosis ofascites. However, the techniques are more expensive, invasive, and require more time. As a result, a less expensive and fastermethod of diagnosis, at least as a screening test, would greatly benefit clinicians. Albumin and Cholesterol in serum and ascitic fluidare parameters that would help screen and diagnose cancer. The serum-ascites albumin gradient or gap (SAAG) is a medicalcalculation that helps determine the cause of ascites. In addition, the serum ascites cholesterol gradient (SACG) aids in thedifferential diagnosis.The case study aims to evaluate the significance of serum-ascites cholesterol gradient (SACG) in diagnosingovarian carcinoma. This case report includes a 53-year-old woman who presented to the surgical department with anorexia,indigestion, heartburn, pain or discomfort in the abdominal and pelvic regions, nausea, early satiety, bloating, and weight loss for1 month. She was diagnosed with ovarian carcinoma. The gradients of serum-ascites albumin and serum-ascites Cholesterol werecalculated. Later, the results were compared to Ca-125, an ovarian cancer marker. SAAG showed low sensitivity but high specificityand poor diagnostic performance. Her diagnosis of ovarian carcinoma was confirmed and she was advised to follow up with theoncologist. The current case report will help understand the contribution of the ascitic fluid and serum parameters in a case ofovarian cancer with ascites of unknown etiology.

Specificity and Sensitivity of Ascitic Fluid Total Protein (AFTP) and Serum Ascitic Albumin Gradient (SAAG) in Diagnosis Etiology of Ascites

Specificity and Sensitivity of Ascitic Fluid Total Protein (AFTP) and Serum Ascitic Albumin Gradient (SAAG) in Diagnosis Etiology of Ascites

CLINICAL PROFILE OF ASCTES BASED ON PRESENTATION AND LABORATORY FINDINGS:AN INSTITUTIONAL EXPERIENCE FROM MAHARASHTRA,INDIA

Introduction: Ascites is the fluid collection in the potential space of the peritoneal cavity. Alcoholic liver disease and intra-abdominal malignancy are two major etiologies behind it. Also, diagnosis of tuberculous ascites should be thought of due to endemicity. Cirrhotic patients at any time during the course of disease, invariably present with ascites which is one of the marker of decompensation. In our context, etiology behind ascites and its correlation with symptoms and clinical findings not yet studied, so present study is conceptualised. Aim: To study clinical profile of ascites based on presentation and laboratory findings Methods: This is a cross-sectional retrospective descriptive hospital based record review of patients presented with ascites in a tertiary center of Maharashtra . One hundred fourteen patients with ascites under regular follow up of SMBT Hospital were reviewed. Data regarding presenting complaints, examination findings, relevant investigations during first visit and final diagnosis were retrieved from our own record keeping and recorded information were then evaluated. Results: Patients having ascites have myriad of symptoms and signs, commonest clinical feature being icterus (74, 64.9%). Most of them were anemic at presentation. Forty-two (36.8%) had high blood urea and 36 (31.5%) with high creatinine suggesting approximately 30-40% cases presented with deranged renal function test. Ninety-three (81.5%) had raised total serum bilirubin. Similarly, PT/INR derangements were in 74 (64.9%) and 57 (50%) suggesting deranged liver function. Serum albumin was less than 3.5 gram/decilitre in 83(72.8%) cases. Among the patients studied, 80 (70.1%) had high Serum-Ascites Albumin Gradient (SAAG) suggesting transudative type of ascites and rest 34 had low SAAG suggesting exudative type of ascites. Overall assessment revealed, majority of patients (71.05%) had Chronic liver disease (CLD) as the cause of ascites. Conclusions: Ascites due to chronic liver disease was the main finding with etiology supported by laboratory findings. Significant numbers of the patients had deranged renal function on top of liver function derangement, so these parameters need to be properly taken care of.

Ascites and Chronic Liver Disease in Children.

Development of ascites in children with chronic liver disease is the most common form of decompensation. It is associated with a poor prognosis and increased risk of mortality. A diagnostic paracentesis should be performed in liver disease patients with- new-onset ascites, at the beginning of each hospital admission and when ascitic fluid infection (AFI) is suspected. The routine analysis includes cell count with differential, bacterial culture, ascitic fluid total protein and albumin. A serum albumin-ascitic fluid albumin gradient of ≥1.1g/dL confirms the diagnosis of portal hypertension. Ascites has been reported in children with non-cirrhotic liver disease like acute viral hepatitis, acute liver failure and extrahepatic portal venous obstruction. The main steps in management of cirrhotic ascites include dietary sodium restriction, diuretics and large-volume paracentesis. Sodium should be restricted to maximum of 2mEq/kg/d (max 90mEq/d) of sodium/day. Oral diuretic therapy comprises of aldosterone antagonists (e.g., spironolactone) with or without loop-diuretics (e.g., furosemide). Once the ascites is mobilized, the diuretics should be gradually tapered to the minimum effective dosage. Tense ascites should be managed with a large-volume paracentesis (LVP) preferably with albumin infusion. Therapeutic options for refractory ascites include recurrent LVP, transjugular intrahepatic porto-systemic shunt and liver transplantation. AFI (fluid neutrophil count ≥250/mm3) is an important complication, and requires prompt antibiotic therapy. Hyponatremia, acute kidney injury, hepatic hydrothorax and hernias are the other complications.

Role of Serum Ascites Albumin Gradient In The Etiologic Diagnosis of Ascites

Background: Classification based on ascitic fluid protein has been challenged on several occasions in diverse clinical situations, including cirrhotic patients on extended diuretic treatment, cardiac ascites, 1/3 individuals with malignant ascites, spontaneous bacterial peritonitis, and even normal ascitic fluid. Objective: The study’s objective was to observe the role of serum ascites albumin gradient (SAAG) in diagnosing Ascites. Methods: This cross-sectional observational study was conducted at the Department of Medicine, Sylhet M.A.G. Osmani Medical College Hospital, Bangladesh. with a total of 100 participants with ascites following the inclusion and exclusion criteria of the study. Result: The most prevalent cause of ascites was cirrhosis, observed in 56% of the participants. Among the 56 cirrhosis patients, mean ± S.D. values of AFTP, AFAlb, SAlb, and SAAG were 2.1±1.2, 0.8±0.6, 3.1±0.7, and 2.2±0.7 respective units accordingly. According to ascitic fluid albumin values, a statistically significant relation was observed between cirrhosis and tuberculosis (P<0.01) and cirrhosis vs malignancy (P<0.01) cases. According to serum ascitic albumin gradient values, a similar significant association was also found between cirrhosis vs tuberculosis (P<0.01) and cirrhosis vs malignancy (P<0.01) cases. Conclusion: SAAG is an essential laboratory tool for the correct aetiological diagnosis of ascites. J Dhaka Med Coll. 2022; 31(1) : 120-124

PREDICTION OF ESOPHAGEAL VARICES BASED ON SERUM-ASCITES ALBUMIN GRADIENT (SAAG) IN CIRRHOTIC PATIENTS

1.Introduction Cirrhosis is the end stage of chronic liver disease. Ascites and esophageal varices (EVs) are the most common complications of portal hypertension (PHT), with an incidence of approximately 50% [1]. Since effective preventive modalities have been established for variceal haemorrhage, early detection of EVs is critical for primary prevention of bleeding. Upper gastrointestinal endoscopy (UGE) remains the gold standard for screening [2,3]. However, many studies have been conducted to predict PHT and EV with a diverse rate of accuracy. All patients with cirrhosis should undergo UGE screening to identify those at high risk of bleeding and who may benet from primary prophylaxis, since EVs are an independent predictive factor and an early complication of cirrhosis. The test should also be repeated during the follow-up of patients with cirrhosis without EVs, who are at risk of bleeding, with or without decompensation [1]. Though UGiscopy is the gold standard to screen patients for variceal development; but has has many drawbacks such as being relatively expensive, invasive, and restrictive [4]. Such a screening test should be simple, rapid, reproducible, and inexpensive [5–7]. The serum ascites albumin gradient (SAAG) is a minimally invasive method that is precise and has been described in the classication of ascitic uid(AF) based on the presence or absence of PHT [8]. Many Studies have been performed to identify non-invasive parameters for the prediction of EVs in patients newly diagnosed with cirrhosis [5]. SAAG can be considered an indirect parameter for the detection of EVs and is useful in regions where there are limitations to perform UGE. The aim of our study was to evaluate the role of SAAG in the prediction of EVs in cirrhotic patients with ascites.

Outcomes after hospitalisation with spontaneous bacterial peritonitis over a 13-year period: a retrospective cohort study.

Assess outcomes in patients with an index presentation of spontaneous bacterial peritonitis (SBP) over a 13-year period. SBP, a bacterial infection of ascites, has a poor prognosis. Retrospective cohort study assessing mortality (standardised to 32 months) and prognostic factors in patients with SBP during two periods: period 1 (June 2006-November 2012) and period 2 (December 2012-May 2019). The study included 178 patients who were followed up for 11.6 (29.2) months. Mortality was high, with 12-, 24- and 32-month survival being 32%, 26% and 24%, respectively. Inpatient mortality was 36% with mortality in those surviving hospitalisation being 62%. Serum creatinine at the time of SBP diagnosis was an independent predictor of mortality at 32 months [hazard ratio (HR) 1.002, P = 0.023] and inpatient mortality (HR 1.003, P = 0.035). Positive ascitic fluid culture and ascitic fluid neutrophil count were independent predictors of 32-month (HR 1.679, P = 0.008) and inpatient mortality (HR 1.0001, P = 0.005), respectively. Patients in period 2 had lower ascitic fluid albumin (5.9 ± 3.3 g/L vs. 10.8 ± 5.4 g/L, P < 0.001), higher ascitic fluid neutrophil count (815.0 cells/mm3 vs. 345.0 cells/mm3, P < 0.001) and higher rates of hepatorenal syndrome-acute kidney injury (58 vs. 35%, P = 0.002). Mortality at 32 months and mortality in those surviving hospitalisation were similar at 78 vs. 73%, P = 0.392 and 66 vs. 58%, P = 0.355, for periods 1 and 2, respectively. Despite more advanced initial presentations, mortality rates have remained similar over the last 13 years. Serum creatinine at the time of SBP diagnosis is an independent predictor of mortality.

Risk factors, clinical indicators, and pathological findings of abomasal ulcers in tropical dairy buffaloes.

The current study aimed at identifying the risk factors and initial diagnostic aids for abomasal ulcers. The risk factor analysis confirmed a significant association (P < 0.05) of abomasal ulcers with concentrate-rich diets (OR, 4.795; CI, 1.212-15.974) and concurrent disorders (OR, 2.978; CI, 0.987-8.980), while the buffaloes in early lactation (OR, 2.777; CI, 0.703-10.972) showed a higher tendency (P = 0.078) for the disorder. The depressed demeanour, dark or black manure (melena), anemia, tachycardia, decreased milk production, anorexia, tachypnea, absence of rumination, abdominal guarding, kyphosis, and tachypnea were the most frequent clinical signs. Subjecting the abomasal fluid for cultural isolation, gram staining, and stormy clot fermentation test identified the presence of clostridium perfringes, while screening through uniplex PCR detected cpa toxin. The buffaloes affected with type-3 and 4 abomasal ulcers exhibited a higher peritoneal fluid to serum ratio of total protein, albumin, and glucose with a low (P < 0.01) serum-ascites albumin gradient (SAAG) concentration compared to reference values of healthy buffaloes. The first two principal components of PCA explained 54.50% of the total variances with lymphocytes, creatine kinase, and rumen chloride levels as the top contributors to dimension I, and albumin, total protein, sodium, and methylene blue reduction time (MBRT) for rumen liquor as the major contributors to dimension II. The vector plot revealed lymphocytopenia, decreased hemoglobin, hypoalbuminemia, hypokalemia, decreased rumen pH, neutrophilia, eosinophilia, leucocytosis, greater MBRT, and higher rumen chloride, serum creatine kinase, and blood urea nitrogen as the major indicators for abomasal ulcers. Histopathological studies revealed infiltration of inflammatory cells in the mucosa along with multifocal areas of necrosis, degeneration, and eroded muscle structure. The study projected a few high-scored clinical signs and extremely variable clinical indicators as initial diagnostic aids of abomasal ulcers, which can be confirmed by ultrasonography and peritoneal fluid examination.

A Rare Hemorrhagic, Orange-Colored Ascites, Challenging Traditional Ascitic Fluid Analysis.

Analysis of ascitic fluid can offer useful information in developing and supporting a differential diagnosis. As one of the most prevalent complications in patients with cirrhosis, ascitic fluid aids in differentiating a benign condition from malignancy. Both the gross appearance of the ascitic fluid, along with fluid analysis, play a major role in diagnosis. Here, we discuss a patient with liver cirrhosis, esophageal varices, hepatitis C, and alcohol abuse, who had a paracentesis performed, which revealed a turbid, viscous, orange-colored ascitic fluid that has not been documented in literature. Ascitic fluid is routinely analyzed based on gross appearance, cell count, and serum ascites albumin gradient (SAAG) score. An appearance of turbidity or cloudiness has commonly suggested an inflammatory process. In our case, fluid analysis revealed a red blood cell count of 24 250/mcL, further suggesting inflammation. However, it also revealed an insignificant number of inflammatory cells, with a total nucleated cell count of 14/mcL. This rich-orange color has posed a challenge in classification and diagnosis of the underlying cause of ascites, with one classification system suggesting inflammation, while another suggesting portal hypertension. Furthermore, we have traditionally relied on the SAAG score to aid in determining portal hypertension as an underlying cause of ascites. With a 96.7% accuracy rate, the SAAG score incorrectly diagnosed portal hypertension in this patient. In this article, we aim to explore how this rare, orange-colored ascitic fluid has challenged the traditional classification system of ascites.

Correlation between serum ascites albumin gradient and esophageal varices in patients with chronic liver disease

Correlation between serum ascites albumin gradient and esophageal varices in patients with chronic liver disease

A Case Report on Primary Collapsing Glomerulopathy in a Filipino Post-partum Female and An Updated Review of Literature

Collapsing Glomerulopathy (CG) is a rare entity presenting as nephrotic syndrome and rapidly progressive renaldeterioration. It has been first identified among African-American patients and subsequently dubbed HIV-associated nephropathy after a number of patients with HIV were found to have CG. It has re-emerged recently among patients with COVID-19. To our knowledge, this is the first case of primary collapsing glomerulopathy in the country to be published.The case is a 36-year-old Filipino female admitted due to bipedal edema which started 2 weeks post-partum. Shehas no comorbidities and social history was negative for illicit drug use. Initial work up showed hypoalbuminemia and diffuse hepatic disease on ultrasound. She was referred to a gastroenterologist where albumin infusion and paracentesis was done but with no improvement. She developed anasarca and was admitted. Paracentesis obtained minimal ascitic fluid. Serum ascites albumin gradient was low and baseline laboratories showed high creatinine, hypoalbuminemia, and albuminuria. 24-hour urine protein was 11 grams, ANA and anti-DsDNA were negative and c3 and c4 levels were normal. Hepatitis profile was negative for infection. Abdominal CT scan revealed multiple hypoenhancing lesions. Tumor markers CA-125, CA 19-9 and CA 15-3 were high. Breast ultrasound showed simple breast cyst. Gynecology consult was called where pap smear was negative for atypical cells. Surgery service recommended monitoring for the pancreatic and breast lesions. Kidney biopsy was delayed due to new onset bacterial pneumonia. COVID-19 RT-PCR test was negative. Patient was discharged improved with no edema. On follow up, the kidney biopsy result came out to be collapsing glomerulopathy. HIV test was then done and was negative. Bipedal edema and albuminuria recurred. She was started on tacrolimus. She has been on regular follow up and currently has no edema, no proteinuria and normal creatinine level. This is an interesting case as the primary glomerular disease has been masked by the earlier laboratory findingswhich led us to think of liver disease then a paraneoplastic nephrotic syndrome. Ultimately, the renal biopsy revealed the diagnosis. This serves as an index case for primary collapsing glomerulopathy in a Filipino patient on remission after being treated with tacrolimus.

Causes Of Ascites And Its Correlation With Serum-Ascites Albumin Gradient In Patients Admitted At Medical Wards In A Tertiary Hospital In Ghana.

Objective: Ascites can be classified depending on whether it results from portal hypertension (PH) or non-portal hypertension (NPH) causes. This classification is relevant because the modes of evaluation and management are different for these two groups. Serum-ascites albumin gradient (SAAG) has been proposed in many studies to categorise ascites better than ascetic fluid total protein. This has not been determined in Ghanaian patients with ascites. The aim of this study was to determine the aetiology of ascites and to assess the performance of SAAG in the classification of portal versus non-portal hypertension ascites among patients admitted to a tertiary hospital in Ghana.&#x0D; Methodology: A cross-sectional study was conducted at the Korle-Bu Teaching hospital, where 140 patients with ascites were recruited within the study period. Data on socio-demography, clinical features, and results of relevant laboratory investigations and imaging studies were collected using pretested questionnaires&#x0D; Results: The mean age of patients was 44.7±13.2 years. Chronic liver disease (CLD) was the major cause of ascites in this study representing 73.57%. SAAG had a sensitivity of 91.59%, positive predictive value of 95.15% and diagnostic accuracy of 90.0% in classifying ascites as due to a PH or NPH.&#x0D; Conclusion: CLD was the major cause of ascites in Ghanaian patients. SAAG has satisfactory diagnostic accuracy in differentiating ascites related to PH from NPH causes. This could be used as a first line investigation in the aetiological diagnosis of ascites for initiation of prompt treatment.

Diagnostic accuracy of serum ascites albumin gradient (SAAG) in a contemporary unselected medical cohort.

To describe the different aetiologies of ascites and test the validity of serum ascites albumin gradient (SAAG) and cytology in a contemporary unselected medical cohort. All adult patients admitted to Nottingham University Hospitals, UK, between 1 May 2013 and 30 April 2018 with new-onset radiologically-confirmed ascites were included. Data were analysed to determine the distribution of different aetiologies of ascites and the diagnostic accuracy of SAAG in portal hypertension and cytology in malignancy as underlying causes of ascites. Over 5 years, 286 patients presented with new-onset ascites; 122 surgical cases were excluded. Most patients were men (n = 84, 51.2%) over 50 years of age (n = 142, 86.6%). Cirrhosis accounted for 54.9% (n = 90) of the cases of ascites followed by malignancy (n = 48, 29.3%) and cardiac failure (n = 10, 6.1%). SAAG ≥11 g/L had a sensitivity of 85.5% and specificity of 60.6% for diagnosing portal hypertension as a cause of ascites (diagnostic accuracy = 78.5%, 95% confidence interval (CI): 69.8-85.5; area under the curve (AUC) = 0.756, 95% CI: 0.652-0.860). Ascitic fluid cytology was positive in 50% of malignant cases and 66% of primary peritoneal carcinomatosis cases. The underlying aetiology and the validity of available tests varied substantially compared with previous reports.

S3127 Peritoneal Tuberculosis in an Immunocompetent Patient With Findings of Chronic Liver Disease and Peritoneal Carcinomatosis

Introduction: Peritoneal tuberculosis (PT) accounts for 1-2% of all tuberculosis cases. Diagnosis of PT can be challenging due to non-specific symptoms, insidious onset, and variable imaging findings. We present a case of PT presenting with ascites and imaging studies suggestive of chronic liver disease (CLD), and peritoneal carcinomatosis. Case Description/Methods: A 48-year-old man presented to our clinic with complaints of increased abdominal girth, weight loss, and night sweats for the past 3 months. Physical exam revealed soft and distended abdomen with shifting dullness. Laboratory tests showed a mild anemia of Hb at 13.0 g/dL (13.1-17.2) and ESR at 34 mm/h (0-15). Abdominal ultrasound (US) revealed the presence of free abdominal fluid, and diffuse heterogenous granular liver parenchyma supporting the diagnosis of CLD. His liver tests were within normal ranges. Ascitic fluid analysis revealed serum ascites albumin gradient (SAAG) of 0.2 g/dL, WBCs of 1.70 × 103 cells/dL (91.8% lymphocytes). Ascitic fluid cytology was negative for malignant cells. Ascitic fluid acid-fast bacilli (AFB) test and mycobacterial culture were negative. Adenosine deaminase (ADA) level in ascitic fluid was 108.5 U/L (0-40). Interferon-gamma release assay (IGRA) test was positive. Contrast-enhanced computed tomography (CT) scan revealed normal liver parenchyma, diffuse thickening and nodularity of the peritoneum, and thickening of omentum with omental cake appearance. CT scan was suggestive of peritoneal carcinomatosis. EGD and colonoscopy were unremarkable. With consistent clinical history, SAAG < 1.1, ascitic fluid with lymphocytic predominance, high ADA levels, and positive IGRA, a diagnosis of PT was made. Anti-tuberculosis treatment was initiated, and the patient’s clinical symptoms have improved. CT scan at the end of treatment showed the resolution of ascites and peritoneal findings (Figure 1). Discussion: Ascites is the most common presenting symptom of PT. High suspicion of PT is important in the setting of ascites of unknown origin. Despite the US findings were suggestive of CLD in this patient, CT scan revealed normal liver findings. Differing PT from peritoneal carcinomatosis might be challenging due to overlapping findings on imaging. Ascitic fluid analysis of SAAG < 1.1, high ADA levels, positive IGRA test should lead towards the diagnosis of PT. AFB and mycobacterial culture of the ascitic fluid may often have low diagnostic yield in PT. Early diagnosis and treatment are important to prevent complications.Figure 1.: A1, A2, Before treatment; axial contrast-enhanced computed tomography scan showing moderate ascites, and diffuse thickening and nodularity of peritoneum. Imaging is suggestive of peritoneal carcinomatosis. B1, B2, After treatment; resolution of ascites and peritoneal findings.

S1783 Noncirrhotic Portal Hypertension and Pancreaticogastric Fistula Complicating Acute Pancreatitis With Fluid Collections

Introduction: Noncirrhotic portal hypertension constitutes an increase in pressure of the portal venous system in the absence of cirrhosis. This is a rare condition; however, it is insufficiently acknowledged given its decreased prevalence in North America and Europe compared to other nations. We present a rare case of noncirrhotic portal hypertension and pancreatico-gastric fistula complicating acute pancreatitis with an acute fluid collection and resultant portal vein narrowing. Case Description/Methods: A 55-year-old man with history of alcohol use disorder presented to the emergency department with worsening abdominal pain 2 weeks after discharge for uncomplicated acute pancreatitis. Lipase was 48 IU/L (normal 11-82 IU/L). CT abdomen showed increasing peripancreatic fluid collection with marked narrowing of the main portal vein, which appeared near threadlike, and narrowing of the bifurcation of the portal vein extending into the left portal vein. The splenic vein was also severely narrowed (Figure A). He was discharged home with outpatient follow-up, however, returned to the ED for intractable pain one month later. A CT abdomen showed florid changes of pancreatitis with pseudocyst formation with new foci of air within the collection concerning for fistulous tract formation with the gastric lumen (Figure B). The portal vein and splenic vein narrowing improved, but the narrowing of the right and left portal veins worsened. He underwent upper endoscopy which showed a small area of White "milky" base in the posterior wall of the incisura angularis which was suggestive of fistulous opening in the area (Figure C). Four columns of small distal esophageal varices were also noted. During admission, paracentesis was performed for ascites. Serum ascites albumin gradient was over 1.1 consistent with ascites due to portal hypertension – likely due to the portal vein narrowing. Patient was discharged in stable, improved condition. Discussion: Although portal hypertension normally presents in cirrhotic patients, it may rarely present in the absence of cirrhosis by conditions such as portal vein thrombosis or portosinusoidal vascular disease. Compression of the portal vein from an acute pancreatic fluid collection is an extremely rare cause of noncirrhotic portal hypertension. Clinicians should have a high index of suspicion for complications related to portal hypertension such as ascites or varices in patients with a prolonged course of acute pancreatitis without cirrhosis.Figure 1.: (A) Contrast CT abdomen showing marked narrowing of the main portal vein, which appears near threadlike. (B) One of 2 foci of air in the collection at the anterior superior aspect of the pancreatic body. Appears inseparable from the posterior wall of the gastric body, concerning for fistulous involvement. (C) Area of White “milky” base in the posterior wall of the incisura angularis. This area was rinsed, however re-accumulated despite no obvious opening seen.

S3143 Rare Case of Plasma Cell Infiltration-Induced Cirrhosis

Introduction: Multiple myeloma (MM) is a type of malignancy that arises from the unorganized replication of plasma cells within the bone marrow. The overproduction of these cells damages systems throughout the body leading to early asymptomatic symptoms that can rapidly progress to systemic signs of disease. Liver involvement with MM is less common and generally occurs through plasma cell infiltration, light chain/amyloid deposition, and biliary obstruction. Though it can occur, the probability of it presenting near the time of diagnosis of MM is very rare and associated with poorer outcomes. Case Description/Methods: A 59-year-old male presented with generalized weakness, shortness of breath and weight gain. Physical exam showed sign of ascites and hepatomegaly. PMH was significant for esophageal cancer and a recent diagnosis of MM. No history of acute or chronic liver disease or cirrhosis risk factors. CT scan showed cardiomegaly, bilateral pleural effusions, pulmonary edema, and cirrhosis with abdominal ascites. Labs was unremarkable other than normocytic anemia. An echocardiogram showed mild reduced ejection fraction (47%) with speckle tracking suggestive of cardiac amyloidosis. Abdominal ultrasound confirmed appearance of cirrhosis, ascites, and right pleural effusion. Cirrhosis work up revealed negative hepatitis panel, normal alpha-1 antitrypsin, and normal ceruloplasmin. EGD was performed and ruled out extracellular vesicles (EV) but noted type I isolated gastric varices. Liver biopsy confirmed cirrhosis and showed portal tract damage with severe extensive plasma cell infiltration. Additionally, fragments of hepatic parenchymal showed disrupted lobular architecture by septal fibrosis and nodular formation. Immunohistochemistry was positive for CD3, CD20, CD5, BCL2, CD79a, and CD138 as well as increased lambda light chain compared to free kappa light chain. Despite extensive treatment including repeated thoracentesis and paracentesis, patient eventually developed in to decompensating liver cirrhosis (Figure 1). Discussion: In previous studies, plasma cell infiltration of the liver was seen in about 40% of cases of MM, but rarely lead to cirrhosis. This case is unique in that the patient had liver failure caused by cirrhosis and that it was some of the presenting symptoms. Whether due to masked signs or aggressive onset, the outcome for this diagnosis is poor and more specific factors observing liver function could have provided a more favorable outcome.Figure 1.: Cirrhosis secondary to plasma cell infiltration. Table 1. - Total Protein 5.0 g/dL Serum Ascites Albumin Gradient (SAAG) 1.9 g/dL Left Hepatic Vein Pressure 25 Hg Left Portal Vein Pressure 29 Hg Portosystemic Pressure Gradient 5 Hg EUS Guided Shear Wave Elastography of Liver 27 kPa