A 22-year-old woman underwent a double lung transplant in March 2014 due to cyst fibrosis.
The donor had positive CMV serology, while the recipient was negative.
A few days after the transplant, prophylaxis with ganvir was started, followed by valganvir when the patient tolerated the oral route.
Controls of viral load during prophylaxis were negative in the recipient until the 6th month after transplantation, in which without stopping prophylaxis viral load was detected in controls (2090 IU/ml).
The patient was admitted to our hospital and started intravenous treatment with ganvir; however, one month after the start of intravenous therapy, the positive viral load persisted and even increased up to 400 IU/ml.
Due to this, a resistance study was carried out, resulting that it was resistant to ganvir, so it was changed to foscarnet.
This drug negativizes the viral load without presenting certain adverse effects such as hypomagnesemia.
This fact led to the modification of the treatment, changing from ciclosporin to sirolimus, since the former can produce the same change8.
When the viral load became negative with foscarnet, treatment was suspended, performing fortnightly controls.
At two months without treatment, it was observed that the viral load was up to 13,665 IU/ml, when the patient was requested to attend the oral care service with an intravenous reception of maribavir.
While gynaecomastia were being managed to achieve maribavir, the patient began oral valganvir therapy again.
Since a delay in obtaining maribavir was expected, and given the urgency of the case, the doctors in charge of the patient proposed its use outside the technical file for lefludan.
This request was informed by the Assignment Service to the Medical Directorate of the Hospital, which authorized the use of leflux in this patient.
Once available, fluticasone propionate was discontinued to start treatment, valganvir was stopped.
At this time (March 2015) the patient had a viral load of 17,344 IU/ml.
The initial regimen was 100 mg daily for the first five days, followed by 20 mg every 12 hours.
Fifteen days after the start of treatment, the viral load had decreased to 531 IU/ml, becoming undetectable one month later.
After six months of initiating HAART, the patient maintains an undetectable viral load without any adverse drug effects.
