A 72-year-old asymptomatic woman presented to the clinic for a checkup. She had a history of cholecystectomy, hypothyroidism, and hypertension. She had been treated with thyroid hormone (Puran  T4, 75 mug), an anti-hypertensive agent (the angiotensin-converting enzyme inhibitor Enalapril , 20 mg), an antiarrhythmic drug (Diltiazem , 90 mg), and acetylsalicylic acid (200 mg). She reported use of oral contraceptives for over 30 years. She had no history of smoking, drinking, drug abuse or family history of liver disease.
On physical examination, the liver was palpable to 6.5 cm from the right costal, and 10 cm from the appendix xiphoid; it was painless, and had a rugged and hard consistency. Laboratory studies revealed the following: red blood cells, 3,690,000/mm3; hemoglobin, 11.7 g/dL; hematocrit, 35%; platelets, 278,000/mm3; cholesterol, 186 mg/dL; triglycerides, 70 mg/dL; glucose, 85 mg/dL; TSH, 2.8 U/mL; serum creatinine, 0.7 mg/dL; ALT, 47 U/L; AST, 29 U/L; GGT, 23 U/L; alkaline phosphatase, 138 U/L; TB, 0.8 mg/dL; DB, 0.4 mg/dL; PT, 12 s; INR, 1.0; PTT, 29 s; folic acid, 11 mg/mL; alpha-fetoprotein, 2.08 ng/mL; iron, 106 mug/dL; vitamin B12, 210 pg/mL; ferritin, 170 mg/L; LDH, 384 IU/L; and CEA 2.4 ng/mL.
Abdominal ultrasound revealed an enlarged and heterogeneous liver that contained an expansive and heterogeneous lesion measuring 14 x 9.4 cm with poorly defined limits, including two echogenic nodular areas, measuring 6.3 and 3.2 cm, respectively. The gallbladder was not visualized.
Computed tomography (CT) of the upper abdomen (Figure 1) showed a heterogeneous lesion - measuring 15 x 14 x 10 cm - with a partially well-defined margin and hypodense permeating areas, some with attenuation values compatible with soft parts, and others with liquefaction located in the left liver lobe. After endovenous contrast injection, the lesion showed intense and non-homogeneous impregnation in the arterial and portal phases, with hypodense permeated areas located in the left lobe, notably parts II and III; these areas determined recoil and reduced the size of vascular structures adjacent to the liver. The injury also caused bulging of the border of adjacent liver tissue, causing a compressive effect on other abdominal structures, especially the stomach and pancreas.
Magnetic resonance (MR) imaging of the upper abdomen showed different components within the lesion. T2-weighted images in the peripheral region showed a discrete heterogeneous hyperintense signal, while the central portion was hypointense. In T1-weighted images, the signal in the periphery of the mass was similar to the muscle signal and the center of the lesion showed a signal that was clearly hypointense. Although impregnation of both components began in the arterial phase, the peripheral region showed a stronger signal during the arterial and portal phases, followed by signal decay in the late phase due to relatively rapid washout, indicative of hypervascularization. The center of the mass was far more intense in the late phase, probably due to slow flow through the vascular components (Figures 2 and 3).
Surgery and pathological analysis revealed a hepatic segment measuring 17.5 x 14 x 8 cm and weighing 1200 g that contained a 15 x 9 cm brown tumor with ill-defined limits. The tumor had a gelatinous component and showed hemorrhaged, necrotic, and cystic areas. The final diagnosis was TA. The patient progressed well and she remains asymptomatic after one year of follow up.