Echocardiographic alteration in patients with systemic lupus erythematosus affected by hepatic steatosis: a cross-sectional single center study

INTRODUCTION. Systemic Lupus Erythematosus (SLE) is a chronic inflammatory disease caused by autoimmunity. Systemic inflammation disease related may increase flogosis related damage as steatosis. In this study, we looked for a correlation between disease activity, evaluated by SLEDAI and SLICC-DI score, and heart involvement comparing those who presented a hepatic steatosis to those who do not. MATERIALS AND METHODS. We evaluated 19 SLE patients (Steat-SLE: 13 women and 6 men, aged 51.89 ± 10.37 years) between 01/01/2015 and 31/12/2018 affected by hepatic steatosis. As control group, we use 51 patients (No-Steat-SLE: 42 women and 9 men, aged 46.24 ± 14.27 years) that did not evidence of steatosis. Patients came in follow-up for revaluation and therapy adjustment. RESULTS. Anti-dsDNA Ab, C3, C4, ESR and PCR were not different between the groups. Hepatic dysfunction was not detected in Steat-SLE. No difference were found in SLEDAI, while SLICC-DI results increased if steatosis was detected (Steat-SLE 3.57 ± 3.36 vs No-Steat-SLE 2.27 ± 2.15, p<0.05). Patients with Steatosis present a longer disease (Steat-SLE 232.0 ± 129.8 vs No-Steat-SLE 121.4 ± 110.6 months, p<0.05). We highlight that patients with steatosis had an increased left ventricular mass (MLV) both as absolute value (MLV: Steat-SLE 226.2 ± 57.53 vs No-Steat-SLE 194.4 ± 58.17 gr., p<0.05) and MLV indexed (MLVi) for body surface area (BSA) (MLVi: Steat-SLE 135.0 ± 48.17 vs No-Steat-SLE 112.3 ± 27.47 gr/m2, p<0.05) but no in interventricular septum thickness. At the same time no difference was found in left atrium (LA) as volume absolute value (LAV: Steat-SLE 67.33 ± 25.97 vs No-Steat-SLE 58.45± 19.06 ml, p<0.05) while it was increased as LA volume indexed (LAVi) for body surface area (BSA) (LAVi Steat-SLE 41.67 ± 19.49 vs No-Steat-SLE 34.12 ± 9.74 ml/m2, p<0.05). Moreover, a correlation was found in both Steat and No-Steat SLE between SLICC-DI, MLV and MLVi. CONCLUSION. These data show an increase of LAVi, MLV and MLVi in patients with steatosis. At the same time, these patients present an increased disease damage and duration. This could suggest heart involvement as result of systemic inflammation similarly to that related to hepatic stetosis. At the same time, the detection of hepatic steatosis should suggest a worsening in heart damage in SLE patients.

Titolo: Echocardiographic alteration in patients with systemic lupus erythematosus affected by hepatic steatosis: a cross-sectional single center study
Autori: 
CICCO, SEBASTIANO
SUSCA, NICOLA
CRUDELE, LUCILLA
GUARASCIO, MATTEO
LEONE, PATRIZIA
PRETE, MARCELLA
RACANELLI, Vito
VACCA, Angelo
mostra contributor esterni 
Data di pubblicazione: 2019
Abstract: INTRODUCTION. Systemic Lupus Erythematosus (SLE) is a chronic inflammatory disease caused by autoimmunity. Systemic inflammation disease related may increase flogosis related damage as steatosis. In this study, we looked for a correlation between disease activity, evaluated by SLEDAI and SLICC-DI score, and heart involvement comparing those who presented a hepatic steatosis to those who do not. MATERIALS AND METHODS. We evaluated 19 SLE patients (Steat-SLE: 13 women and 6 men, aged 51.89 ± 10.37 years) between 01/01/2015 and 31/12/2018 affected by hepatic steatosis. As control group, we use 51 patients (No-Steat-SLE: 42 women and 9 men, aged 46.24 ± 14.27 years) that did not evidence of steatosis. Patients came in follow-up for revaluation and therapy adjustment. RESULTS. Anti-dsDNA Ab, C3, C4, ESR and PCR were not different between the groups. Hepatic dysfunction was not detected in Steat-SLE. No difference were found in SLEDAI, while SLICC-DI results increased if steatosis was detected (Steat-SLE 3.57 ± 3.36 vs No-Steat-SLE 2.27 ± 2.15, p<0.05). Patients with Steatosis present a longer disease (Steat-SLE 232.0 ± 129.8 vs No-Steat-SLE 121.4 ± 110.6 months, p<0.05). We highlight that patients with steatosis had an increased left ventricular mass (MLV) both as absolute value (MLV: Steat-SLE 226.2 ± 57.53 vs No-Steat-SLE 194.4 ± 58.17 gr., p<0.05) and MLV indexed (MLVi) for body surface area (BSA) (MLVi: Steat-SLE 135.0 ± 48.17 vs No-Steat-SLE 112.3 ± 27.47 gr/m2, p<0.05) but no in interventricular septum thickness. At the same time no difference was found in left atrium (LA) as volume absolute value (LAV: Steat-SLE 67.33 ± 25.97 vs No-Steat-SLE 58.45± 19.06 ml, p<0.05) while it was increased as LA volume indexed (LAVi) for body surface area (BSA) (LAVi Steat-SLE 41.67 ± 19.49 vs No-Steat-SLE 34.12 ± 9.74 ml/m2, p<0.05). Moreover, a correlation was found in both Steat and No-Steat SLE between SLICC-DI, MLV and MLVi. CONCLUSION. These data show an increase of LAVi, MLV and MLVi in patients with steatosis. At the same time, these patients present an increased disease damage and duration. This could suggest heart involvement as result of systemic inflammation similarly to that related to hepatic stetosis. At the same time, the detection of hepatic steatosis should suggest a worsening in heart damage in SLE patients.
Handle: http://hdl.handle.net/11586/253847
Appare nelle tipologie:4.2 Abstract in Atti di convegno

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