P3974 - A Challenging Case of Inflammatory Ascites Successfully Treated With Immunosuppression

Tuesday, October 24, 2023

10:30 AM – 4:00 PM PT

Location: Exhibit Hall

Has Audio

Presenting Author(s)

Xing Li, MD, MBA

Massachusetts General Hospital
Boston, MA

Xing Li, MD, MBA, Karin Andersson, MD
Massachusetts General Hospital, Boston, MA

Introduction: Ascites can be due to portal hypertensive causes such as cirrhosis (accounting for 80% of the cases) or non-portal hypertensive causes ranging from malignancies, infections to autoimmune conditions. Idiopathic inflammatory ascites is a rarely described diagnosis, with only a few case reports in the literature. We describe here an interesting case of new-onset refractory ascites in a 30-year-old woman.

Case Description/Methods: The patient developed, after a non-complicated laparoscopic cholecystectomy, new large-volume ascites and severe acute kidney injury (AKI). Her initial labs are shown in table A. Her ascitic fluid had low serum ascites albumin gradients and lymphocytosis. Her imaging showed non-nodular liver, no splenomegaly or biliary abnormality. Initial concern was for advanced chronic liver disease, due to her heavy alcohol use. Her liver biopsy revealed steatohepatitis with stage 3 fibrosis (figure A), but her hepatic venous pressure gradient (HVPG) was only 6 mmHg (borderline portal hypertension). The ascites was refractory to weekly large volume paracentesis, prompting broader work-up that was unrevealing, including a repeat HVPG with liver biopsy that confirmed prior results. Ultimately, she underwent direct portal pressure measurement to definitively rule out portal hypertension with a HVPG of 4 mmHg. Her AKI was felt to be from acute tubular necrosis and managed with hemodialysis. After extensive evaluation, she was felt to have idiopathic inflammatory ascites, and started on prednisone with improvement in ascites re-accumulation. She was transitioned to anakinra, under rheumatology guidance. She had steady response, with eventual complete resolution of her ascites after six months, and renal recovery soon after.

Discussion: Despite evidence of advanced chronic liver disease in this patient likely from alcohol-related liver disease, she did not have portal hypertension. For non-portal hypertensive ascites, tuberculosis and carcinomatosis are the two most common causes. Idiopathic inflammatory ascites is a rare entity, in this case supported by her elevated CRP; ascitic fluid lymphocytosis in the absence of malignancy, infection, and rheumatologic disorders; and response to prednisone. Mycophenolate mofetil has been used to treat this condition in another case report. To our knowledge, use of anakinra, chosen here for its safety profile, for inflammatory ascites has not been reported. Complete resolution of inflammatory ascites may require months of treatment.

Figure: Liver biopsy showing macrovesicular steatosis as well as ballooning degeneration of hepatocytes consistent with steatohepatitis in Figure A, and bridge-like fibrosis between portal tracts consistent with stage 3 out of 4 fibrosis in Figure B.

Lab results
Sodium	129 mmol/L (L)
Creatinine	5.3 mg/dL (H)
Blood urea nitrogen	58 mg/dL (H)
Albumin	4 g/dL
Aspartate aminotransferase	130 U/L (H)
Alanine aminotransferase	30 U/L
Alkaline phosphatase	101 U/L
Total bilirubin	0.8 mg/dL
White blood count (WBC)	13 K/uL (H)
Hemoglobin	12 g/dL
Platelet	342 K/uL
International normalized ratio (INR)	1.3 (H)
C reactive protein	50 mg/dL (H)
Additional lab results
Rheumatologic	Antinuclear ab 1:40, smooth muscle ab negative, Immunoglobulin G 431 mg/dL (L), C3 complement 42 mg/dL (L), C4 complement 31 mg/dL, negative anti-Ro ab, anti-La ab, antinuclear ribonucleoprotein ab, antineutrophilic cytoplasmic antibody, anti-cyclic citrullinated peptide ab and rheumatoid factor
Infectious	Nonreactive hepatitis A, B, C, Epstein-Barr virus, human immunodeficiency virus ab, negative hepatitis B and C viral load, negative Brucella, Chlamydia/Gonorrhea, Coccidioides, Histoplasma serologies, negative TSPOT
Peripheral blood flow cytometry	Negative for monoclonal B-cell, T-cell or blasts
Urinalysis	Urine sodium < 20 mmol/L, 3 -5 RBCs/hpf, 10 - 20 WBC/hpf, protein/creatinine 0.16
Ascitic fluid studies	Serum ascites albumin gradient 0.9, total protein 4.6 g/dL, glucose 104 mg/dL, triglyceride 9 mg/dL, bilirubin 0.2 mg/dL, amylase 51 U/L, total nucleated cells 507 (24% neutrophils, 63% lymphocytes, 6% monocytes, 5% macrophages), cytology negative, bacterial, fungal, and mycobacterial cultures negative
Imaging studies
Ultrasound	Patent hepatic vasculature
Computed tomography abdomen/pelvis	Fatty liver, no focal lesion, no splenomegaly, large ascites, no lymphadenopathy
Magnetic resonance cholangiopancreatography	Normal liver, no biliary dilation or biloma
Kidney ultrasound	No hydronephrosis
Pelvic ultrasound	Normal
Echocardiogram	Normal
Right heart catheterization	Right atrium 3 mmHg, pulmonary capillary wedge 5 mmHg

Disclosures:

Xing Li indicated no relevant financial relationships.

Karin Andersson indicated no relevant financial relationships.

Xing Li, MD, MBA, Karin Andersson, MD. P3974 - A Challenging Case of Inflammatory Ascites Successfully Treated With Immunosuppression, ACG 2023 Annual Scientific Meeting Abstracts. Vancouver, BC, Canada: American College of Gastroenterology.