We present the case of a liver transplant patient who developed severe thrombocytopenia in the early postoperative period.
This is a woman of age diagnosed with liver cirrhosis due to HCV in 1988, with Child's stage C and MELD score of 19 points at the time of diagnosis.
The previous ultrasound showed signs of cirrhosis, with partial portal thrombosis, stenosis and ascites.
Platelet counts were 90,000/mm3.
As other antecedents, the patient had a history of diabetes mellitus 2, hysterectomy and double adnexectomy 22 years earlier, which required blood transfusion (possible origin of HCV diabetes).
The donor was a 69-year-old woman who died from a hemorrhagic stroke.
The only antecedent was hypertension and two cesarean sections.
During precis seizure control, transfusion of 6 fibrinogen concentrates, 2 plasma units, 2 platelet pools, and 3 g of fibrinogen was performed.
Immunosuppression with tacrolimus and corticosteroids was initiated maintaining good renal and hepatic function.
During the first 5 days after LT platelet counts remained stable.
On the 6th day they decreased to 2,000/mm3, with the nadir of 1,000 platelets at the 8th day.
Clinically, the patient presented generalized cutaneous hematomas and melenic depositions with anemization, which required transfusion of medications.
There was no clinical infection.
She suffered a transfusion reaction to platelet transfusion, requiring premedication prior to subsequent transfusions.
Platelet counts remained refractory to transfusion of multiple pooled platelets.
Suspicion of etiology was suspected on day 8. Treatment with high doses of immunoglobulins (0.4 g/kg/day) and corticosteroids was initiated and possible drugs involved (tacrolimus, furosem) were suspended.
Abdominal ultrasound showed only a well-known anomaly.
Bone marrow puncture showed a reactive medulla, with hyperplasia of the three hematopoietic series and without maturational pairs.
Indirect antiplatelet antibodies IgM and IgG were positive, and anti-HLA I-II were negative.
The study of microsatellites (STR) by DNA techniques (10 locus and 20 alleles analyzed) in peripheral blood in two samples post-HT (7th and 60th day) of the receptor and a previous donor absence
HCV viral load was 11,000,000 IU/ml and CMV PCR was undetectable.
On day 14 post-HT platelets increased to 12,000, with Ig being discontinued, corticoid dosage decreased and tacrolimus was restarted.
Thereafter platelet counts progressively increased.
