case_images: PMC3420763_01
case_images: Pretreatment echocardiography showing severely depressed left ventricular systolic function.
case_images: CRIM.RHEUMATOLOGY2011-402483.001.jpg
case_images: PMC3420763_01_CRIM.RHEUMATOLOGY2011-402483.001.jpg
case_images: fig1
case_images: There were no features suggestive of pulmonary arterial hypertension, vegetations, or clots (Figure 1).
case_images: (a) Mild distortion of architecture by enlarged portal areas and bridging fibrosis/necrosis (red arrow) [Hematoxylin and Eosin Stain, 50x]. (b) Interface hepatitis (red arrow) and portal inflammation (yellow arrow) [Hematoxylin and Eosin Stain, 100x]. (c) Lobular inflammation (red arrow) [Hematoxylin and Eosin Stain, 150x]. (d) Hydropic hepatocytes with attempted rosette formation (red arrow) [Hematoxylin and Eosin Stain, 200x].
case_images: CRIM.RHEUMATOLOGY2011-402483.002.jpg
case_images: PMC3420763_01_CRIM.RHEUMATOLOGY2011-402483.002.jpg
case_images: fig2
case_images: The revelation was that of interface hepatitis, lobular and portal inflammation with plasma cells, and hydropic changes in some of the hepatocytes with attempted rosette formation; changes that were characteristic of autoimmune hepatitis (AIH) (Figures 2(a), 2(b), 2(c), and 2(d)).
case_images: Posttreatment echocardiography showing marked improvement of left ventricular systolic function.
case_images: CRIM.RHEUMATOLOGY2011-402483.003.jpg
case_images: PMC3420763_01_CRIM.RHEUMATOLOGY2011-402483.003.jpg
case_images: fig3
case_images: In comparison to the previous echocardiographic profile, there were no mitral regurgitation or pericardial effusion in the posttreatment period (Figure 3).