Supplementary Material for: Case Report: An unusual cause of massive ascites

Introduction: Ascites, the abnormal accumulation of fluid within the peritoneal cavity, is commonly associated with decompensated liver cirrhosis, primary or secondary malignancy, right-sided heart failure, and peritoneal tuberculosis. The underlying pathophysiology is usually related to one of portal hypertension, hypoalbuminaemia, or peritoneal inflammation. When these common causes are excluded, autoimmune aetiologies such as systemic lupus erythematosus (SLE) should be considered, albeit being rare. SLE is a chronic, multisystem autoimmune disease with diverse manifestations, and serositis is a recognised but variably expressed feature. Lupus peritonitis, a form of serosal inflammation leading to ascites, occurs infrequently and is often overshadowed by more typical pulmonary or pericardial involvement. We report an unusual case of massive painless ascites as the presenting feature of SLE in a middle-aged man, underscoring the diagnostic challenges of this rare presentation. Case Presentation: A 43-year-old man presented to the Emergency Department with a two-week history of painless, progressive abdominal distension. He denied any associated symptoms and a thorough physical examination was unremarkable except for ascites. An extensive diagnostic panel followed to identify the cause of ascites, as the hepatobiliary system appeared normal on imaging and serum ascites albumin gradient was less than 1.1, making cirrhosis and portal hypertension unlikely. Echocardiogram and thyroid function tests were normal. His autoimmune serological markers revealed the presence of anti-Smith and anti-RNP antibodies, and the patient fulfilled the 2019 EULAR/ACR classification for Systemic Lupus Erythematosus. Discussion: Ascites as the initial presentation of SLE is uncommon, especially massive ascites. Lupus peritonitis, the underlying mechanism, is thought to result from immune complex deposition and complement activation leading to peritoneal inflammation and exudative effusion. In this patient, the absence of typical features such as rash, arthritis, or haematological abnormalities initially obscured the diagnosis. This case illustrates how SLE can present insidiously and emphasizes the need for thorough autoimmune evaluation in unexplained exudative ascites once hepatic, cardiac, malignant, and infectious causes have been excluded. The rapid response to corticosteroid therapy underscores the importance of early recognition and immunosuppressive treatment to prevent complications.