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.