A 65-year-old man presented to the emergency department of our hospital with worsening general condition, jaundice and increased abdominal perimeter.
The patient works as an auxiliary in the dispatch of a novice and has no toxic habits.
During the previous four years she had been followed intermittently in gastroenterology consultations for an alteration of the hepatic profile with predominance of mild stasis.
The rest of the personal and family history was of no interest.
During these years of follow-up, multiple laboratory tests were performed, in which only the known pattern of stasis and mild thrombocytopenia were observed in some controls.
Throughout this period of time the TOG figures ranged between 31-56 IU/l; 21356 IU/l for PTG, between 27-75 IU/l; those for GGT, between 150-185 IU/l;
The total bilirubin was moved between 1.2-2.56 mg/dl. An autoimmunity study was performed, which was negative.
The same result was obtained from serology of hepatotropic and HIV viruses and tumor markers (CEA, Ca 19.9 and α-fetoprotein).
The rest of analytical data, including complete blood count, biochemistry, coagulation, ferrokinetic study, proteinogram, thyroid hormones,... were always normal.
The patient was also submitted to various imaging tests.
During these four years several abdominal ultrasounds were performed, all normal except that performed four months before admission, which reported mild stenosis enlargement.
Two CT studies, one abdominal and one abdominal-pelvic, performed seven months before admission to our center, had also been reported as normal.
Upon admission to our hospital ward, clear mucocutaneous jaundice and non-stress ascites were evident, as well as a slight deterioration in the patient's level of consciousness.
Analytically stands out: Hb: 9.6 g/dl; hematocrit: 26.9%; platelets: 37000; white blood cells: 3800; total bilirubin: 27.5 mg/dl; HCV αGT:
An abdominal ultrasound is performed, which reports liver stigmata of chronic liver disease, with multiple regeneration nodules within it, and a scant nuclear magnetic resonance, with images compatible with macronodular liver cirrhosis and ascites.
A transjugular liver biopsy was performed.
However, while the histological result of such biopsy is expected, the patient suffers an abrupt worsening of his clinical condition and respiratory function, requiring mechanical ventilation, orotracheal intubation and admission to the ICU due to distress.
He died 36 hours later.
Liver biopsy, whose result was received after the death of the patient, is reported as irregular dilatation of the sinusoids (peliosis) and proliferation of endothelial cells, without these presenting mitosis.
Necropsy was performed, which showed macroscopically liver with macronodular external surface, which shows the section spongy-peliotic areas, among which are located zones with macroscopic appearance of authentic stasis.
Search strategy focused on proliferation with sinus growth pattern, configuring recessive spaces lined by dementia cells.
Hepatic involvement is diffuse and patchy, and in some areas neoplasic intravascular growth is observed, sometimes with the presence of mitosis, some of which are inherited.
Cells are strongly positive for endothelial markers CD-31 and CD-34.
All this is compatible with primary hepatic angiosarcoma.
