Venoocclusive Disease of the Liver Following Bone Marrow Transplantation

Jones, Richard J.; Lee, Kamthorn S. K.; Beschorner, William E.; Vogel, Victor G.; Grochow, Louise B.; Braine, Hayden G.; Vogelsang, Georgia B.; Sensenbrenner, Lyle L.; Santos, George W.; Saral, Rein

doi:10.1097/00007890-198712000-00011

Cited by 864 publications

(632 citation statements)

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“…1) [1][2][3][4][5]. In the setting of allogeneic bone marrow transplantation, other causes of liver derangement, such as venoocclusive disease (VOD), GVHD, organ rejection, or superinfection with cytomegalovirus or herpes simplex virus, should be excluded [81,82]. Because the hepatitis is preceded or accompanied by HBV virological reactivation, its diagnosis relied heavily on the serial quantification of serum HBV viral load.…”

Section: Pathogenesis and Diagnosis Of Hbv Reactivationmentioning

confidence: 99%

Hepatitis B reactivation after chemotherapy: two decades of clinical research

Lau

2008

Hepatol Int

102

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Hepatitis due to hepatitis B virus reactivation after cytotoxic or immunosuppressive therapy is a serious cause of liver-related morbidity and mortality. With the characterization of the underlying pathogenesis, much progress in the management of this important clinical problem has been made in the past 2 decades. By year 2008, it is mandatory to screen for hepatitis B surface antigen status before initiating intensive chemotherapy or immunosuppressive therapy. All those who are hepatitis B surface antigen positive should be started on preemptive nucleos(t)ide analogues. However, there remains important issues, such as the type and duration of nucleos(t)ide analogue therapy, which need to be understood. As not all hepatitis B surface antigen-positive patients will suffer from HBV reactivation, it is therefore useful to identify risk factors related to HBV reactivation so that patients will not be treated unnecessarily with nucleos(t)ide analogues. To date, a high baseline level of viral replication, as reflected by high serum HBV DNA level, positive serum hepatitis B e antigen, and a high intrahepatic covalently closed circular DNA level, is the most important predictor for HBV reactivation. Recently, there has been an increased awareness of reactivation of occult hepatitis B virus, especially in hepatitis B virus endemic area, such as the Asia-Pacific region. Careful epidemiological study will be needed to clarify the impact of occult hepatitis B infection in patients treated with cytotoxic or immunosuppressive therapy. How important is the problem?Over the past 20 years of clinical practice at Queen Mary Hospital, we have seen a lot of progress in the management of hepatitis due to HBV reactivation in hepatitis B surface antigen carriers [1][2][3][4][5]. In the past, we saw patients who died of fulminant hepatic failure after being administered a few courses of cytotoxic therapy to treat their life-threatening lymphoma [6][7][8][9] and breast cancer [10][11][12] if they were also hepatitis B surface antigen positive. At that time, the literature report of this important clinical issue was scanty. The first report in the field was published by Wand et al. [13] who studied the effects of antitumor chemotherapeutic agents on hepatitis antigen (HBAg) and antibody (HBAb) in 25 patients with myeloproliferative and in 60 patients with lymphoproliferative disorders. This elegant study was performed at the time when only antigen and antibody associated with viral hepatitis could be semiquantified [14]. In those patients who had HBAg at the time of initiation of chemotherapy, bone marrow suppression by chemotherapeutic agents was associated with a marked increase in HBAg titer, which was then followed by hepatocellular damage, as manifested by an elevation in serum transaminase enzymes [13]. Since then, this important observation was further confirmed in other studies [8,15,16], with the rate of HBV reactivation ranging from 19% to 48%. Among them, one-quarter to half would be complicated, with severe hepatitis...

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Section: Pathogenesis and Diagnosis Of Hbv Reactivationmentioning

confidence: 99%

Hepatitis B reactivation after chemotherapy: two decades of clinical research

Lau

2008

Hepatol Int

102

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“…Veno-occlusive disease was clinically defined by right upper quadrant pain, weight gain, ascites and early hyperbilirubinemia. 18 Episodes of sepsis, determined by the presence of positive cultures, were also monitored.…”

Section: Patientsmentioning

confidence: 99%

Monitoring soluble interleukin-2 receptor levels in related and unrelated donor allogeneic bone marrow transplantation

Foley

Couban

Walker

et al. 1998

Bone Marrow Transplant

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Summary:Acute graft-versus-host disease (GVHD) is effected by donor T lymphocytes which have been stimulated by host antigens. Activated donor T lymphocytes express interleukin-2 receptor (IL-2R), which is comprised of three subunits (␣, ␤, ␥). During activation, the ␣ IL-2R subunit (CD25) is shed from the receptor complex and can be measured in the circulation. Soluble IL-2R␣ (sIL-2R) levels are increased in states of immune activation including GVHD, and could theoretically be used as a guide to therapy. Since IL-2R␣ expression is an early marker of T cell activation, we investigated: (1) if an increase in sIL-2R is specific for acute GVHD; and (2) if serial sIL-2R levels can identify patients with early GVHD, prior to the onset of clinical tissue damage (effector function). Weekly sIL-2R levels were monitored in 36 patients undergoing matched related (n ‫؍‬ 23) or matched unrelated (n ‫؍‬ 13) allogeneic bone marrow transplantation (BMT). There was no significant difference in sIL-2R levels between matched related and matched unrelated recipients. Patients with acute GVHD (n ‫؍‬ 19, 53%) demonstrated higher sIL-2R levels, than those without during weeks 2 and 3 post-BMT (P ‫؍‬ 0.02 and 0.04, Mann-Whitney U test, twotailed). In patients with acute GVHD, the rise in sIL-2R preceded the clinical signs of GVHD (16/19 patients). However, patients with sepsis demonstrated a trend towards higher sIL-2R levels at week 1 and significantly greater levels by week 4 (P = 0.02). Furthermore, patients with veno-occlusive disease (VOD) (25%) also had significantly higher sIL-2R levels at week 2 (P ‫؍‬ 0.03). We conclude that although sIL-2R levels increase in patients with acute GVHD, similar increases are seen in patients with VOD and/or sepsis and therefore, as a single biochemical marker, we find that serial measurements of sIL-2R lacks sufficient specificity to guide GVHD therapy.

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“…by the conditioning regimen with radio/chemotherapy contributes to veno-occlusive disease (VOD) of the liver, 7,8 thrombotic microangiopathy (TMA) [9][10][11] and graft-versushost disease (GVHD). 12,13 TMA is a clinical diagnosis which includes hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP); both are characterized by microangiopathic hemolytic anemia, thrombocytopenia, microvascular thrombosis and multiorgan failure.…”

mentioning

confidence: 99%

Diagnostic value of hemostatic parameters in bone marrow transplant-associated thrombotic microangiopathy

Kanamori

Maruta

Sasaki

et al. 1998

Bone Marrow Transplant

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Summary:We investigated hemostatic parameters in a prospective study of 16 patients who received bone marrow transplants (BMT). We found a significant rise in the levels of fibrinogen, plasmin-␣ 2 antiplasmin inhibitor complex, tissue-plasminogen activator·plasminogen activator inhibitor complex (t-PA·PAI), von Willebrand factor antigen, and thrombomodulin on day 14 after transplant compared with values before transplant. Protein C and thrombin-antithrombin III levels did not change significantly. No significant changes in prothrombin time ratio, activated partial thromboplastin time, or protein S were detected. Patients who had grades II-IV graft-versus-host disease (GVHD) (n = 6) showed a significantly higher level of t-PA·PAI on day 14 compared with those with grades 0-I GVHD (n = 10) (P = 0.0062). Three patients with grades II-IV GVHD developed thrombotic microangiopathy (TMA) on days 19, 19 and 62. In these patients, we noted significantly lower levels of fibrinogen (P = 0.0383), and significantly higher levels of t-PA·PAI (P = 0.0008) and thrombomodulin (P = 0.0001) on day 14 compared with those patients who did not develop TMA. These results suggest that prothrombotic states and endothelial damage may be caused by the conditioning regimen and/or acute GVHD during BMT; thrombomodulin values on day 14 post BMT may be useful in surveillance for TMA because of endothelial cell injury.

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Venoocclusive Disease of the Liver Following Bone Marrow Transplantation

Cited by 864 publications

References 0 publications

Hepatitis B reactivation after chemotherapy: two decades of clinical research

Hepatitis B reactivation after chemotherapy: two decades of clinical research

Monitoring soluble interleukin-2 receptor levels in related and unrelated donor allogeneic bone marrow transplantation

Diagnostic value of hemostatic parameters in bone marrow transplant-associated thrombotic microangiopathy

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