Approximately 20% of cirrhotic patients with ascites develop umbilical herniation. These patients usually suffer from multisystemic complications of cirrhosis, have a significantly higher risk of infection, and require accurate surveillance– especially in the context of the coronavirus disease 2019 pandemic. The rupture of an umbilical hernia, is an uncommon, life-threatening complication of large-volume ascites and end-stage liver disease resulting in spontaneous paracentesis, also known as Flood syndrome. Flood syndrome remains a challenging condition for clinicians, as recommendations for its management are lacking, and the available evidence for the best treatment approach remains controversial. In this paper, four key questions are addressed regarding the management and prevention of Flood syndrome: (1) Which is the best treatment approach–conservative treatment or urgent surgery? (2) How can we establish the individual risk for herniation and possible hernia rupture in cirrhotic patients? (3) How can we prevent umbilical hernia ruptures? And (4) How can we manage these patients in the conditions created by the coronavirus disease 2019 pandemic?

Hepatic encephalopathy is a neuropsychiatric complication of liver cirrhosis the symptoms of which may vary from imperceptible to severe, invaliding, and even lethal. Minimal hepatic encephalopathy is also important because of its tendency to impair patients' cognitive functions and quality of life. The polyetiological pathogenesis of hepatic encephalopathy is intensively studied. A general consensus exists that not only excess of ammonia but also inflammatory, oxidative, and other processes are significant in the development of hepatic encephalopathy.

BACKGROUND Immunoglobulin G4-related disease (IgG4-RD) is a multisystemic mass forming immune-mediated disease that affects almost every organ and is a diagnostic challenge for every clinician. There is a lack of adequate epidemiological data worldwide, and evidence-based treatment recommendations are not yet established. We report the first case of IgG4-RD from Lithuania and the Baltic Sea region presented with thyroiditis, orbital myositis, orbitopathy, uveitis, scleritis, sialadenitis, autoimmune pancreatitis and prostatitis. CASE SUMMARY A 54-year-old Caucasian male was admitted to our tertiary Centre complaining of severe weight loss, diarrhoea, abdominal pain, salivary gland swelling, sicca symptoms and diplopia. On examination, bilateral palpable masses in the projection of major salivary glands, severe protrusion of the left eyeball and cachexia were noted. The patient was previously diagnosed with autoimmune thyroiditis and endocrine ophthalmopathy. The magnetic resonance imaging (MRI) of the head revealed enlarged extraocular muscles indicating orbital myositis. The biopsy from the salivary gland mass indicated sialadenitis. Abdominal MRI showed signs of autoimmune pancreatitis, and a serological test revealed the elevated serum IgG4 concentration. The patient was then diagnosed with IgG4-RD and successfully treated with prednisolone. There was a significant clinical, serological and radiological improvement after one month of treatment and no signs of relapse within twenty months. However, it took almost 18 years and the efforts of eight different medical specialists to establish the correct diagnosis. CONCLUSION A comprehensive approach to the patient is essential to improving the recognition of rare immune system conditions, such as IgG4-RD.

BACKGROUND The inflammatory myofibroblastic tumor (IMT) is a rare, idiopathic, usually benign, mass-forming disease with myofibroblastic proliferation and a varying amount of inflammatory cells. Although it can affect various organs, the biliary tract is a rare localization of primary IMT, clinically, endoscopically and radiologically imitating cholangiocarcinoma. The treatment options are based only on clinical practice experience. CASE SUMMARY A 70-year-old woman was referred to our center due to progressive fatigue, weight loss, abdominal pain, night sweats, and elevated liver enzymes. Magnetic resonance cholangiopancreatography and endoscopic retrograde cholangiopancreatography (ERCP) revealed proximal common hepatic duct and hilar biliary strictures extending bilaterally to lobular bile ducts. Although initial clinical, endoscopic and radiological signs were typical for hilar cholangiocarcinoma, histological examination showed no signs of malignancy. In total, 8 biopsies using different approaches were performed (several biopsies from dominant stricture during ERCP and direct cholangioscopy; ultrasound-guided liver biopsy; diagnostic laparoscopy with liver and lymph node biopsies). Histological examination revealed signs of IMT, and the final diagnosis of biliary IMT was stated. Although IMT is usually a benign disease, in our case, it was complicated. All pharmacological treatment measures were ineffective. The patient still needs permanent stenting, suffers from recurrent infections and mechanical jaundice. Despite that, the patient already survived 24 mo. CONCLUSION IMT presenting with hilar biliary strictures is a unique diagnostic and clinical challenge as it is indistinguishable from cholangiocarcinoma, and there are no evidence-based treatment options. Our goal is to increase the understanding of this rare disease and its possible course.

Heparin-induced thrombocytopenia (HIT) is a lifethreatening immune complication of exposure to unfractionated heparin or low molecular weight heparins (LMWH) that occurs independently of the dose in a small percentage of patients. The clinical case and diagnosis of HIT, which started as skin necrosis will be discussed here.A 75-year-old obese woman (weight 98 kg, height 164 cm, BMI 36.4 kg/m/2) was hospitalized due to unexplained chronic abdominal pain and jaundice. Although on admission there were no clinical signs of deep venous thrombosis, she was prescribed a prophylactic dose of nadroparin 2850 U s/c; as she was motionless and after a few days of investigations, she was diagnosed with metastatic neoplasia of liver and intrahepatic ducts. After 8 days, a one 20 cm area of nonpalpable purpura with surrounding erythema and hemorrhagic vesicles on the central abdominal part was noticed (Figure 1). There was no pruritus or surrounding pain. The platelet count was decreased from 217,000/microl at hospitalization to 68,000/microl when the skin necrosis developed. Protein S, protein C, prothrombin time, and thrombin time were normal. Commercial diagnostic test kit for PF4/heparin antibodies identification of all isotypes was used (ID-PaGIA Heparin/PF4 Antibody Test (DiaMed GmbH). Two different titrations were made (1:4 and 1:32) and both of them were positive.Based on the clinical picture, nadroparin-induced skin necrosis was diagnosed. We also clinically suspected a