Fulminant hepatic failure caused by adenovirus infection following bone marrow transplantation for Hodgkin’s disease

Abstract

Summary:Adenoviruses are increasingly realised to be responsible for serious morbidity and mortality following allogeneic bone marrow transplantation. We describe a case of fulminant hepatic failure due to adenovirus serotype 2 in a 39-year-old woman who received a matched sibling allogeneic bone marrow transplant for multiply relapsed Hodgkin's disease. Isolated fulminant hepatic failure caused by this serotype of adenovirus has not previously been described. Keywords: adenovirus; hepatic failure; bone marrow transplant Case reportA 35-year-old woman presented with bulky stage IIA nodular sclerosing Hodgkin's disease involving the mediastinum. She received three full cycles of ChlVPP/ PABLOE 1 and mantle radiotherapy to the residual mass. She relapsed 2 years later in the anterior mediastinum and received mini-BEAM 2 as salvage chemotherapy. She was primed with cyclophosphamide for stem cell collection and then received high-dose therapy with stem cell rescue 3 ). The procedure was uncomplicated. Within 6 months she relapsed once more, this time with disease extending from the mediastinum into the lung parenchyma. A regimen of weekly vinca alkaloid injections prevented clinical and radiological deterioration for 11 months but then her disease progressed again. Two courses of ESHAP (without methylprednisolone) 4 were given as bulk reduction treatment before a sibling allogeneic bone marrow transplant. The conditioning regimen was Campath 1-G (20 mg daily from days −9 to −5), thiotepa (5 mg/kg on days −8 and −7), cyclophosphamide (60 mg/kg on days −6 and −5) and total body irradiation (14.4 Gy in 8 fractions from days −4 to 0). The graft was T cell depleted and the recipient was CMV positive. The transplant was uncomplicated and she was discharged on day 21. A month later she was read-

Real‐Time Blood Plasma Polymerase Chain Reaction for Management of Disseminated Adenovirus Infection

“…Genetic variability is high among adenoviruses, and we could not find a DNA sequence compatible with real-time PCR conditions that is conserved in all species of adenovirus. Therefore, we choose to target adenovirus DNA from subgenera A, B, and C, because, according to the literature, 195% of adenovirus species recovered in cases of severe adenovirus infection belong to these subgenera [1,9,14,15,16,[22][23][24]. Adenovirus species from subgenus D (types 8 and 32) and subgenus E (type 4) have been reported as responsible for the remaining 5% of cases of disseminated adenovirus infection [3,16].…”

The hepatologist in the haematologists' camp

“…It usually occurs after d 30 in paediatric recipients and after d 90 in adult recipients. Hepatic manifestations of this infection are hepatomegaly, coagulopathy, severe hepatitis and, rarely fulminant hepatic failure (Somervaille et al , 1999). PCR techniques are useful to detect adenovirus DNA in blood, sputum, urine, broncoalveolar lavage samples and liver tissue, either pre‐ or post mortem (Echavarria et al , 1999).…”

GI complications in pediatric patients post-BMT

“…The majority of the published data regarding these complications comes from adult studies. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] A paucity of information exists in the published literature regarding the incidence, range and severity of gastrointestinal (GI) complications in pediatric patients in the immediate post-BMT period. 19,20 The majority of the pediatric studies examined specific complications such as veno-occlusive disease (VOD), acute pancreatitis or typhilitis in fairly homogeneous patient populations.…”