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"Child`s Health" 4 (64) 2015

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Liver damage in systemic lupus erythematosus in adolescents

Authors: Lyudmila F. Bogmat, Natalya S. Shevchenko, Elena V. Matvienko - SI «Institute for children and adolescents health care of the NAMS of Ukraine», Kharkov

Categories: Pediatrics/Neonatology

Sections: Clinical researches

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Keywords

systemic lupus erythematosus, adolescents, liver, fibrogenesis.

The main objective was to investigate the liver in the adolescents with systemic lupus erythematosus (SLE). In 48 patients with SLE, aged from 12 to 18, we estimated the occurrence of liver damage (22,9%); the dependence of cytolisis formation on the grade of activity and clinical manifestation of SLE; the risk of fibrosis (in 27,3%); and the presence of fibrosis during the onset of SLE (in 9,1%).

The liver damage in SLE usually occurs in 60% of cases. Its manifestations can vary from an insignificant increase in size to a serious hepatitis. Histological investigation shows plethora, blood stagnation in the vessels, fat infiltration and necroses in the portal system. The cases of liver vasculitis, leading to infarcts and ruptures of liver with the clinical symptoms of acute abdomen, are rare. 25% patients with SLE have subclinical liver damage; 8% have SLE-connected liver damage: the actual SLE hepatitis. The most typical liver reaction provoked by damage is fibrosis. The damaging factors (inflammation, drug load, cholestasis) can activate fibrogenesis, accompanied by an increased synthesis of extracellular matrix components such as interstitial collagen, basic membrane collagen, proteoglycans, glycoproteins such as laminin and fibronectin - leading to structural changes and functional failure of liver.

Nevertheless, the existing data on the liver pathology in SLE in children and adolescents are quite poor. Clinical and laboratory instrumental signs of the liver damage lack both in diagnostic criteria of SLE and in SLICC/ACR damage index. Together with that, liver is a hidden target organ, the pathological changes in which can be registered at the fibrosis formation stage. That’s why we chose to study the liver in the adolescents with SLE at the onset of disease.

Materials and methods. The group consisted in 48 patients with SLE (mostly female (90,00 %) recovered in the clinics of cardiologic department of SI “Institute of Children and Adolescents Health Care of the NAMS of Ukraine”. The mean age of the patients was 14,4 years (172,9 ± 4,72 months). The diagnosis was based on SLICC, 2012 criteria with not less than 4 of 11 signs available (Petri M. et al.., 2012). The functional state of liver was examined with a complex of clinical laboratory, biochemical and instrumental methods (objective examination, ultrasound investigation of liver and gallbladder, the levels of bilirubin and its fractions, general cholesterol, the activities of alanine transferase (ALT), aspartate transferase (AST), alkaline phosphatase (AP). De Ritis coefficient (AST/ALT) and APRI index (Aspartate-aminotransferase-to-Platelet Radio Index) have been estimated.

Results. At the onset of SLE, the pathological changes in liver were registered in 11 of 48 patients (22,9 %): an increase in size and an increase in transaminase activity. The SLE onset age in this group was 14,1 years (169,09±5,91 months), the mean SLE duration was 4,63±1,90 months,  54,5% of the patients had sub acute onset and 63,6% had an increased activity of pathological process. 81,1% had liver cytolisis manifestations accompanied by a moderate increase in ALT (115,66±5,42 IU/l), AST (60,6±3,47 IU/l) and a significant decrease in de Ritis coefficient (down to 0,79 with its normal values 1,3-1,4). 37,4% of the patients of this group had de Ritis coefficient higher than 1,0 (AST prevailing) that is more typical for “cardiac” cytolisis. 63,6% of the patients of this group had de Ritis coefficient lower than 1,0 (ALT prevailing) that is an evidence of liver changes. Alkaline phosphatase (excretory function) and pigment metabolism did not have changes. The level of cholesterol in the serum was decreased in 30,0% of the patients. USI data showed an increase in the size of liver in 81,81% of the patients, an increase in parenchyma echogenicity and fading of ultrasound signal in deep layers.

AST positively correlated with C-rp  (r= 0,67, р<0,05), sialic acids (r= 0,66, р<0,05), glycoproteins (r= 0,62, р<0,05); ALT positively correlated with the level of circulating immune complexes (r= 0,81, р<0,001) – an evidence for the role of inflammation in liver cells damage.

Tests for fibrosis showed an increased risk of its formation in 27,3% of patients at the onset of SLE, and its reliable probability in 9,1% (APRI index 1,1).

Conclusions. Liver is involved in SLE, with high occurrence of liver damage manifested as cytolisis, a decrease in synthetic activity, signs of fibrogenesis activation and the presence of the initial stage of fibrosis in some patients at adolescent age. The degree of changes depends on SLE activity and the presence of cardiac and renal syndromes. The examination of the patients should take into account the markers of functional state of liver, including inflammatory activity and fibrosis formation. A timely discovery of such changes can benefit the therapy able to decrease their progress.


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