Discussion
SLE is a heterogeneous disease characterized by chronic autoimmune
dysfunction of both the innate and adaptive immune systems[16]. However, the commonly used classification
criteria for SLE diseases do not include liver function impairment and
biliary tract involvement. According to the epidemiological survey[6] , up to 60% of SLE patients may have abnormal
liver function but often have no apparent clinical significance.
Multiple studies have demonstrated a significant decrease in serum
bilirubin levels among SLE/LN patients, which is closely related to
disease activity [26]. Atsushi Takahashi[20] et al. investigated SLE patients with liver
function impairment and concluded that drugs, SLE, and fatty liver are
the primary causes of liver function impairment in SLE patients.
Currently, most clinicians overlook abnormal liver function as the
primary manifestation of SLE, resulting in many patients not receiving
timely treatment. According to previous reports[3], more than half of the 15 patients with
abnormal liver function as their initial symptom were diagnosed several
weeks or even years after treatment. They were more likely to be
misdiagnosed as hepatitis or delayed SLE. Liver function impairment is
often characterized by abnormal levels of liver enzymes and the changes
in bilirubin and albumin levels. Jaundice is a recognizable ”distress
signal” that is visible to the naked eye, making it one of the common
reasons that most patients seek medical attention.
For patients presenting with liver function impairment, it is important
to consider liver diseases and hemolytic conditions, as well as
autoimmune diseases. Ellen C Ebert et al. The ANA antibody panel test of
this female patient also showed that anti-rRNP was suspiciously
positive. As early as 1993, there were literature reports that[10, 11], SLE patients complicated with chronic
active hepatitis were also anti-rRNP positive. Therefore, the positive
result of anti-rRNP antibody may indicate an association with
SLE-related hepatitis and autoimmune hepatitis (AIH), in addition to its
potential predictive value for neuropsychiatric symptoms in SLE
patients. The presence of the anti-rRNP antibody suggests a possible
association with hepatitis activity in immune-related diseases. In SLE
patients who test positive for this antibody, it is important to
consider whether the antibody is continuously expressed in the body and
monitor changes in liver function levels.
Monocytes and macrophages destroy aging red blood cells in the
circulation through hemolytic destruction by heme oxygenase (HO) and
cathepsin [8,9]. Later, uridine diphosphate
glucuronic acid transferase 1A1 (UGT1A1) in the liver, combines free
bilirubin with glucuronic acid to form binding
bilirubin[7]. Various metabolic substances in the
human body are in a dynamic state of balance. The stable levels of
various metabolic substances in the human body are maintained through a
dynamic balance between their production and the consumption of excess
metabolites [1]. In this case, we reported a
middle-aged female patient with a significant elevation of combined
bilirubin. After further investigations, all abnormal indicators were
found to be related to non-specific digestive system symptoms. Recently,
N Ferdous[27] et al. also reported a patient with
severe lupus hepatitis. Unlike the patient in Ferdous’s report, our
patient only presented with apparent jaundice. Through physical
examination, we observed typical signs of cirrhosis, such as spider
nevus and liver palm, but did not detect any symptoms of discomfort such
as ascites. Biochemical indicators improve liver function impairment,
but it is not accumulated kidney. Before the first visit, the patient
did not take any medications, and the disease has a relatively short
duration, mainly characterized by elevated levels of conjugated
bilirubin; there are specific variations in the disease background and
laboratory findings for this patient compared to others.
As we reported, for the female patient with lupus hepatitis, the liver
impairment was mainly attributed to SLE. Bile is produced by hepatocytes
and is closely linked to the liver cell metastasis
function[13]. However, when hepatocyte impairment
occurs, it can cause bile production dysfunction. Bile cannot be
transferred in time, leading to cholestasis, which increases the local
oxidative stress of the liver and increases the level of heme oxygenase
and bilirubin; when the function and expression of intrahepatic
transport proteins are disturbed, toxic bile acids will accumulate in
the cells, thus aggravating the impairment of hepatocytes and creating a
vicious cycle [12]. Prolonged cholestasis can
cause enlargement of the intrahepatic and extrahepatic bile ducts.
For SLE-related liver diseases, Gonz á lez Regueiro JA[21] and others have emphasized the importance of
firstly determining whether the liver injury is associated with SLE.
First, SLE-related lupus hepatitis should be considered. Second, other
autoimmune diseases , such as AIH, PBC, PSC, AIH-PBC/PBS(table 1), and
alternative liver diseases (mainly including SLE combined with
non-immune diseases, such as viral hepatitis, non-alcoholic hepatitis,
drug-induced hepatitis, liver injury, biliary injury, vascular injury,
and hemolysis-related disorders) should also be considered.