Mycophenolate mofetil/tacrolimus
Cytomegalovirus infection and lack of efficacy: case reportA 56-year-old man developed cytomegalovirus infection during maintenance immunosuppressive therapy with tacrolimus and mycophenolate mofetil. Additionally, he experienced lack of efficacy during treatment with tacrolimus and mycophenolate mofetil.The man had a history of end-stage heart failure due to ischaemic cardiomyopathy for which he had undergone a left ventricular assist device implantation as a bridge to cardiac transplantation in April 2018. Both the donor and the recipient were seronegative for cytomegalovirus (CMV) prior to the transplant. He had a normal allograft function without allograft rejection. He was on tacrolimus and mycophenolate mofetil [dosages and routes not stated] for maintenance immunosuppression. In December 2019, he was hospitalised for CMV infection manifesting as fever and diarrhoea.The man received ganciclovir for 6 days and then transitioned to valganciclovir. By discharge, his fever and diarrhoea had resolved. On follow-up, the CMV DNA was undetectable. Three weeks after the discharge (i.e. in January 2020), he presented to the hospital with 10 days of ascending sensory loss and proximal muscle weakness. Physical examination was notable for sensory loss in the lower extremities to just below the knees, in the hands and forearms and on the anterior tongue. He had weakness of the deltoids, biceps and intrinsic muscles of the hand, as well as weakness with hip flexion and dorsiflexion of the feet. He had a neuropathic gait. The remainder of his examination, including the cardiopulmonary examination, was unremarkable. Laboratory investigations revealed a normal basic metabolic panel and complete blood count. His liver function tests were improving as compared to his prior admission. Thyroglobulin, thyroid peroxidase and thyroid stimulating antibodies were absent. Thiamine, vitamin B12, serum protein electrophoresis, immunofixation electrophoresis and copper levels were normal. Human immunodeficiency virus test, rapid plasma reagin, CMV PCR and Epstein-Barr virus PCR were negative. Tacrolimus level was 8.9 ng/mL. An underlying hyperthyroidism was also noted. His CRP was found to be elevated 14.4 mg/mL. An antinuclear antibodies titer was positive at 1:320 in a speckled pattern. Erythrocyte sedimentation rate was 40 mm/h. Antibodies to MAG, SGPG, Purkinje Cell/Neuronal Nuclear, Asialo-GM1, GD1A and GQ1B were negative. Antibodies to the ganglioside GD1b were elevated to 74IV. An MRI of the entire spine showed possible enhancement of the cauda equine nerve roots at the L5-S1 level. Nerve conduction studies were suggestive of subacute Guillain-Barre Syndrome. He was treated with immune-globulin and valganciclovir was discontinued. The hyperthyroidism was treated with methimazole. Shortly after the initiation of immune-globulin therapy, he developed shortness of breath. A right heart catheterisation showed borderline high filling pressures but a normal cardiac index. He was empirically treated for ...