Case report
Four months ago, a 45-year-old Chinese female patient had yellow skin and sclera. The initial examination revealed elevated levels of transaminase and total bilirubin. Based on the patient’s clinical manifestations and relevant diagnostic test results, the diagnosis is acute hyperbilirubinemia and liver failure. During this period, the patient experienced recurrent episodes of the disease, and the treatment was mainly focused on providing supportive care to alleviate symptoms. Two week ago, the patient visited the other hospital. The MRI of the upper abdomen revealed signs of the compensatory phase of cirrhosis and acute cholecystitis. The results of abdominal color ultrasound showed an uneven liver echo and a strong echo in the liver and gallbladder wall. Liver function test results showed: ALT 182 U/L, AST 369 U/L, TBiL 250 μ mol/L, DBiL 185 μ mol/L, IBiL 65 μ mol/L, TBA 473.7 μ mol/L. ANA antibody panel test showed anti-nuclear antibody was positive, anti-nuclear antibody titer was positive.
The patient visited the Department of Hepatology of our hospital on October 11, 2022. The physical examination showed that the skin, mucous membrane, and sclera of the whole body were stained yellow, the capillaries on the face were dilated, and the spider nevi and liver palms appeared on the chest and neck. The patient reported a long history of alcohol consumption in the past. The equivalent alcohol intake was about 200g/time. Liver function test results showed: ALT 181.70 U/L, AST 319.30 U/L, TBiL 242.41 μ mo1/L, DBiL 197.62 μ mol/L, IBil 44.79 μ mol/L, TBA 544.60 μ mol/L, Hypersensitivity C-reactive protein (CRP) 11.130mg/L, IL-6 8.08 pg/ml, PCT 0.25 ng/ml, Immunoglobulin IgG 24.90 g/L, complement C3 0.65 g/L, and complement C4 0.148 g/L. Urinary routine test indicated a positive result for urinary bilirubin. Five items of hepatitis B: anti-HBe>4.20PEIU/ml, anti-HBc>5.50IU/ml. ANA antibody panel test (including anti-dsDNA) showed showed positive results for anti-nuclear antibody (ANA) at a titer of 1:1000, as well as positive results for anti-double-stranded DNA (anti-dsDNA) antibodies. Additionally, anti-ribosomal P-protein antibodies were suspected to be positive. The Coombs test was positive. There was no obvious abnormality in detecting highly sensitive B DNA, blood ammonia, and autoimmune liver. Chest and abdomen CT showed suspected liver cirrhosis, the uneven density of liver parenchyma, and cholecystitis sign. Upper abdominal MRI showed abnormal signal in liver parenchyma and cholecystitis. MR enhancement scan of upper abdomen showed large abnormal enhancement focus in the liver, hepatic sinus obstruction syndrome? Signs of cholecystitis. DWI of upper abdomen: slightly high signal in the liver. MR cholangiography (MRCP) showed gallbladder effusion and cholecystitis are considered. Color Doppler ultrasound of liver and portal vein system showed intrahepatic echo changes and intrahepatic patch echo areas; there were many strong echo spots in the liver, and the portal vein blood flow was smooth. After admission, the patient was treated with symptomatic support such as liver protection, anti-jaundice, enzyme lowering, and intestinal microflora regulation. The patient’s jaundice did not show significant improvement during hospitalization. The relevant immunologic tests were completed, and the results showed abnormalities. Considering the possibility of SLE, lupus liver, and biliary system impairment, the patient was transferred to our department for a liver function test, which revealed ALT 194.70U/L, AST 487.40U/L, TBiL 228.20 μ mo1/L, DBiL 159.90 μ mol/L, IBil 68.30 μ mol/L, and TBA 372.77 μ mo/L. The patient’s immunity was inhibited by methylprednisolone sodium succinate (40mg/Qd) and mycophenolate mofetil (0.75g/d); Polyolefinylcholine (20ml/d) and glutathione (0.6 g/Qd) improve liver function and promote bile excretion; The patients were also treated with nutritional support. Following the aforementioned treatment for two weeks, a significant reduction in the patient’s yellow skin and sclera was observed. The patient underwent a liver function test, which showed ALT 141.50U/L, AST 72.00U/L, TBiL87.50 μ mol/L, DBiL 58.60 μ mo1/L, IBil 28.90 μ mol/L, TBA 86.43umol/L. The patient presented with an acute onset of the disease and significant liver function impairment, along with a significant elevation in TBA levels. The presence of positive anti-dsDNA and anti-nuclear antibodies was observed, but the absence of AMA and other AIH-related indicators led to the exclusion of AIH. The patient’s Coombs test was positive. According to the patient’s medical history, clinical manifestations, and relevant examinations, it was determined that the primary cause of the persistent unconjugated bilirubin elevation was lupus hepatitis.