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.