Interferon and antivirals
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Graft versus host disease and diarrhoea: 2 case reports In a case series of 2 patients, two men aged 56 years and 64 years were described, who developed graft versus host disease (GVHD) following administration of ledipasvir/ sofosbuvir or ribavirin and unspecified interferon for hepatitis C virus infection. Additionally, the 56-year-old man also developed diarrhoea following administration of immunosuppressant drug therapy with mycophenolate mofetil [dosages, routes, times to reactions onsets not stated; not all outcomes stated]. Case 1: The 56-year-old man underwent orthotropic liver transplantation for decompensated cirrhosis secondary to hepatitis C virus (HCV). His maintenance immunosuppressant drug therapy included mycophenolate mofetil along with concurrent tacrolimus. The donor was cytomegalovirus seropositive. One month following discharge, his liver enzymes were elevated. Consequently, a biopsy was performed, which was consistent with HCV genotype 1a. He received ledipasvir/sofosbuvir for 12 weeks. Four months after the transplant, he presented to emergency department due to intermittent generalised weakness, nausea, vomiting and fever for 1 week. Also, he had a pruritic rash on his left leg and right arm, that had been present for 4 weeks, intermittent diarrhoea with up to three to four loose stools per day, which started 2 months prior to the presentation. Upon examination, he had a body temperature of 101.2°F. Diffusely scattered hyperpigmented, minimally scaly, oval to round patches and macules were seen on the neck, chest, upper back, shoulders, to proximal upper arms. The WBC count was 70 cells/mm3, platelet count was 54,000 cells/mm3, haemoglobin was 6.2 g/dL and haematocrit was 18%. Short tandem repeat (STR) analysis for cluster of differentiation (CD3) cells showed 15% of donor CD3-positive cells (Tlymphocytes). A skin biopsy revealed interface dermatitis, vacuolar degeneration of the basal layer of the epithelium, epidermal infiltration by lymphocytes and necrotic eosinophilic keratocytes, consistent with the diagnosis of GVHD. He received treatment with unspecified broad-spectrum antimicrobials. Mycophenolate mofetil was stopped followed by tacrolimus with poor response. Subsequently, therapy was changed to prednisone and tacrolimus was re-started. After 2 weeks, repeat chimerism studies returned with 0% donor CD3 cells. However, during subsequent admissions in the following year, STR analysis for CD3 cells in his peripheral blood exhibited increasing donor lymphocytes at 16%, 32%, and 84%. Worsening symptoms and poor response to prednisone were noted. Eventually, he died due to infectious complications 221 days following the diagnosis of GVHD. Case 2: The 64-year-old man underwent orthotropic liver transplantation. He received a CMV-seropositive donor into CMV-seropositive recipient transplant. Several years prior to the transplantation, his hepatitis C virus infection was successfully treated with ribavirin and unspecified interferon. One month after the transplant, he presented with pruri
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