We report clinical experience of diagnosis and treatment in four cases underwent TA-GVHD after liver transplant in 550 cases carried out in our hospital. The four patients, mean 38 years and male, with liver cancer were performed liver transplant. The immunosuppressive drugs of FK506 and MMF were given. Recovery were uneventful and liver function transferred into normal after operation. One to four weeks after transplant they complained of increasing fatigue and developed high fever, then presented skin rash from head and trunk to limbs, diarrhea, abnormal liver function (ALT mean 260 IU/L, AST mean 180 IU/L), and pancytopenia. The bone marrow biopsy showed a poorly erythroid, abnormal myeloid and megakaryocyte cell lines. Serum IgG and IgM antibodies of parvovirus B19, CMV (pp65), and EBV (IgM) were negative. Vitamin B12 and folate levels in serum were normal. Skin biopsy showed that epidermis loose and a lot of lymphocytes and monocytes infiltrate into tissue between dermis and epidermis. At clinical diagnosis of TA-GVHD the patients were protected in isolation room and FK506 and MMF were transferred or adjusted. The corticosteroid medication, dexamethasone and methyprednisolone, were given for controlling TA-GVHD progress. The other regimen consist of preventing infection with antibiotics and immunoglobulin, promoting hematopoietic recovery with G-CSF, preventing bleed and improving anemia with gamma irradiation of blood components when necessary. After two to three weeks the temperature recovered normally, skin rash disappeared, diarrhea stopped eventually, and liver function again recovered in three patients following normally up one year. The other one died from respiratory failure due to complicated pneumonia in the three weeks late. TA-GVHD is a rare complication caused by immunocompetent lymphocytes in blood used in transplant period. Although the incidence rate (<0.01%) was very low in our practice, severe TA-GVHD threatening to life can result in recipients. The diagnosis of TA-GVHD depended on clinical manifestation, skin biopsy, HLA typing and DNA analysis, if possible, between donor blood and host. The diagnosis should be distinguished from liver transplant associated GVHD and virus infection. The diagnosis of TA-GVHD can be established based mainly on their clinical manifestation, skin biopsy, and effective treatment. Because transfusion of blood were different donor resources, HLA typing and DNA analysis were difficult to be tested. Since liver transplant associated GVHD does not cause abnormal liver function, whether or not abnormal liver function is important key at difference diagnosis with TA-GVHD. Also, the virus infection should be ruled out because virus test are negative. Although the prognosis of TA-GVHD is pessimism according to literature, the three out of them in our report were effectively cured. Especially, treatment of corticosteroid medication are very important regimen. Adjusting immunosuppressive drugs, anti-infection, preventing bleed and promoting hematopoietic recovery are also essential. The gamma irradiation of blood components can be used for preventing TA-GVHD.

Disclosure: No relevant conflicts of interest to declare.

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