This retrospective study emphasises that abdominal manifestations are common in pSLE. The GI involvement in pSLE is variable. Sönmez et al., in a series of cases carried out in Turkey, described gastrointestinal involvement in 27.5%. Bader-Meuner et al., in 17% of children with SLE, and in this study it was found in 50.8% of children. [5, 7]
The most common symptom in the largest pediatric series is abdominal pain. The causes of abdominal pain in SLE patients are more frequent lupus-related etiologies, among which are: lupica enteritis (EL), protein-losing enteropathy (PLE), intestinal pseudo-obstruction (IPO), acute pancreatitis (AP). Its prevalence varies in variable ranges between 15.8–100% of cases. Richer et al.  reported that 87% of the causes of abdominal pain were due to acute pancreatitis, Sönmez et al.  and Tu et al.  to lupus enteritis in 5.2% and 31.6% respectively and in Hispanic children it was found in 38.1%, the most frequent cause was associated with the use of multiple medications. Gastrointestinal symptoms in Hispanic children with SLE were significantly associated with multiple medication (p = 0.033), without finding a correlation with disease activity levels, time of evolution or antinuclear antibody positivity. [6, 9]
Sönmez et al. reported autoimmune hepatitis as the most frequent disorder associated with SLE, in 42.1%.  In contrast, in our series no patient was found. Lupus hepatitis (LH) was the most frequent (12.7%), its evolution was subclinical with a course favorable to the use of steroids, none with progression to end-stage liver disease, and although the real prevalence of hepatitis autoimmune (AIH) with SLE in our patients is unknown, it was not necessary liver biopsy for diagnosis, since the evolution was satisfactory, unlike those reported by other authors in which there is overlap of both entities and therefore the need for histological study. [4, 5]
Globally, the estimated prevalence of LE ranges between 0.2% and 14% among all SLE patients  and accounts for 29–65% cases of acute abdominal pain , in our review it was found in only 3.2% of our patients. Intestinal wall edema and ascites are important for diagnosis, and imaging studies are necessary for a definitive diagnosis. The two patients with lupus enteritis were the only ones who underwent imaging studies and responded satisfactorily to treatment with steroids and alkylating agents. Patients with lupus and severe abdominal pain require a thorough investigation as elevated disease activity is related to the presence of intra-abdominal vasculitis. 
Reported prevalence of AP in pSLE ranges between 2.6% and 6% (12–16). In the cohort described by Bader-Meunier et al., AP was the most common cause of abdominal pain . In our study, it occurred in 7.9% of patients and it was confirmed that it is significantly associated with lupus activity, in our case by the MEX-SLEDAI score (p = 0.016). [7, 11]. Figure 1. Likewise, we corroborate that the association between the administration of steroids or azathioprine and the development of pancreatitis cannot be proven significantly.
Mild elevation of transaminases occurs in up to 57.9% of patients, most of the time asymptomatically, in our case it was the most frequent biochemical alteration in 31.7% of patients and a greater elevation was demonstrated in mean values of transaminases in patients with digestive disorders, however, to attribute it to SLE, it is due to hepatotoxicity due to drugs, autoimmune hepatitis, viral hepatitis and fatty liver. [4, 11]
In our study, 58.7% of patients presented some type of nutritional impairment, in contrast to other studies conducted in adults, where it is described in less than 10% of patients. Possibly this difference is due to the fact that the disease is more serious and has greater renal involvement in children, since we significantly correlated those patients with altered nutritional status and higher levels of proteinuria (p = 0.049), on the other hand, they were not significantly associated with the time of evolution or the activity of the disease. 
Although gastrointestinal manifestations are frequent, functional digestive disorders have hardly been studied in children with SLE, in our study they occurred in 12.7% of patients, constipation being the most frequent, it is likely that medications alter gastrointestinal homeostasis, such as glucocorticoids and non-steroidal anti-inflammatory drugs, and these are potential risk factors for its development.
In our study, associations were made between antibodies and complement levels with digestive disorders, only the decrease in C4 was the only immunological parameter significantly associated in patients with lupus and digestive disorders (p = 0.033).
Abdominal ultrasound shows abnormalities in up to 79% of patients with gastrointestinal manifestations, increased echogenicity of the liver parenchyma is the most common alteration in more than 50% of patients. . On the contrary, hepatic steatosis was the most frequent alteration in our patients, and ultrasound alterations in general were described less frequently than those described in other series (62.5%). Figure 2.
Abdominal tomography has been described as abnormal in 5.5% of patients, the most common finding being thickening of the intestinal wall. In our study, only 2 patients underwent abdominal tomography, due to the severity of their symptoms, reporting thickening of the wall of the large intestine. Figure 3, in one and changes in the caliber of hepatic vessels suggestive of portal hypertension in another. Abdominal tomography should be mandatory in children with lupus who have unexplained abdominal pain to rule out findings suggestive of ischemic bowel disease.
Liver biopsies performed on patients with SLE mainly report autoimmune hepatitis (42%), hepatocellular damage (10%), toxic hepatitis (5%) and cholestatic hepatitis (5%).  In our series, only 1 patient underwent liver biopsy, with a report of hepatic steatosis. Hepatic steatosis is rarely described in children with SLE, secondary to lupus per se or corticosteroid therapy. Histopathological approach is necessary in children with SLE and elevated transaminase levels unexplained by other causes, due to the high frequency of autoimmune hepatitis and associated histopathological alterations .