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Post-Transplant Complications Portal Vein Thrombosis After Hematopoietic Cell Transplantation: Frequency, Treatment and Outcome

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Post-Transplant Complications Portal Vein Thrombosis After Hematopoietic Cell Transplantation: Frequency, Treatment and Outcome Bone Marrow Transplantation (2002) 29, 329–333 2002 Nature Publishing Group All rights reserved 0268–3369/02 $25.00 www.nature.com/bmt Post-transplant complications Portal vein thrombosis after hematopoietic cell transplantation: frequency, treatment and outcome K Kikuchi, R Rudolph, C Murakami, K Kowdley and GB McDonald Gastroenterology/Hepatology Section and the Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, and the University of Washington School of Medicine, Seattle, WA, USA Summary: reported as risk factors for PVT. Decreased levels of the naturally occurring anticoagulants protein C and antithrom- Patients who develop veno-occlusive disease (VOD) of bin III have been observed in patients undergoing hemato- the liver may have low plasma levels of the natural anti- poietic cell transplantation, usually after the development coagulants protein C and antithrombin III, but large of veno-occlusive disease (VOD) of the liver,5–7 although vessel thromboses are not commonly reported in these a cause–effect relationship between decreased plasma lev- patients. We reviewed the records of 1847 consecutive els of protein C and antithrombin III and hypercoaguability patients for evidence of portal vein thrombosis. Eight has not been proven in the transplant setting. Some clinical patients (0.4%) developed portal vein thrombosis (PVT) and histologic data suggest that low plasma levels of these at a median of day +28 (range 3–58). All patients had natural anticoagulant proteins promote thrombosis after clinical evidence of VOD with ascites, a median total hematopoietic cell transplantation. For example, patients serum bilirubin 11.9 mg/dl, and median weight gain with hepatic VOD often develop deposition of fibrin in the from baseline of 7.9%. Median plasma levels of walls of terminal hepatic venules.8 In hematopoietic cell antithrombin III and protein C were low (36% and transplant patients, large vein thrombosis is an unusual 21%, respectively). Four patients with PVT died of sev- complication9 and only sporadic cases of portal vein throm- ere VOD and multi-organ failure, but PVT did not con- bosis,10 sinus vein thrombosis11 and superior vena cava tribute to death. We conclude that PVT is a rare compli- thrombosis12 have been reported. Thrombosis at the site of cation of hematopoietic cell transplant and is associated venous access catheters is more common.13,14 We now with hepatic VOD. We speculate that PVT resulted report eight patients who developed PVT after transplant, from diminished portal venous flow (related to hepatic associated with VOD and decreased plasma levels of sinusoidal obstruction to blood flow) and a hypercoagul- protein C and antithrombin III. able state (related to low circulating antithrombin III and protein C levels). Prognosis depended on the sever- ity of the underlying VOD and not PVT per se, suggest- METHODS ing that treatments directed solely toward dissolution of portal vein thrombi should be used with caution in Techniques of hematopoietic cell transplantation this setting. Bone Marrow Transplantation (2002) 29, 329–333. DOI: The techniques of hematopoietic cell transplantation at the 10.1038/sj/bmt/1703368 Fred Hutchinson Cancer Research Center have been Keywords: portal vein thrombosis; veno-occlusive dis- described previously.15 Briefly, patients underwent a mye- ease; protein C; antithrombin III; hematopoietic cell trans- loablative conditioning regimen before infusion of either plantation; thrombolytic therapy marrow or peripheral blood stem cells. The date of infusion is referred to as day 0. Patients receiving allografts were given immunosuppressive drugs to prevent GVHD, usually cyclosporine and methotrexate.16 Prophylaxis against viral Portal vein thrombosis (PVT) is a known complication of infections (acyclovir) and fungal infections (fluconazole) cirrhosis, neoplasm, intra-abdominal infection, and myelo- was routine during 1994–1998. proliferative disorders.1 Recently, both acquired and inherited hypercoagulable forms of protein C deficiency,2 antithrombin III deficiency3 and factor V Leiden4 have been Patient selection Between March 1994 and January 1998, all patients who developed signs of liver dysfunction or right upper quadrant Correspondence: Dr GB McDonald, Gastroenterology/Hepatology Section (D2–190), Fred Hutchinson Cancer Research Center, 1100 Fairview pain or ascites underwent abdominal Doppler ultrasound Avenue North, PO Box 19024, Seattle, WA 98109–1024, USA examination. PVT was diagnosed if echogenic material was Received 14 June 2001; accepted 21 October 2001 observed in the portal vein and flow signals, as assessed Portal vein thrombosis after transplant K Kikuchi et al 330 by color Doppler ultrasound, were absent.17,18 The fre- evidence of VOD of the liver on the day that PVT was quency of PVT was defined by the number of patients with diagnosed, with a median total serum bilirubin of 11.9 an ultrasound diagnosis of PVT divided by the total number mg/dl (range 2.4–21.7 mg/dl) and a median weight gain of patients who underwent hematopoietic cell transplant from pre-conditioning baseline of 7.9% (range 2–24.6%). during this time interval. Clinical and laboratory data at the All patients had developed either hepatomegaly or liver time of diagnosis of PVT, treatment, outcome and cause of pain. In patients 7 and 8, abdominal pain was related to death were noted from medical records. This retrospective liver tenderness even though hepatomegaly was not review was conducted under a protocol approved by the detected on physical examination. All patients had ascites Institutional Review Board of the Fred Hutchinson Cancer proven by ultrasound on the day of diagnosis of PVT. There Research Center. was no evidence of GVHD in any organ system at the time of diagnosis of PVT. Plasma levels of antithrombin III mea- Definition of VOD sured at the time of diagnosis of PVT in five patients were all below the normal range; the median value was 36% The clinical criteria for VOD are: (1) hepatomegaly and/or (range 22–66%). Plasma levels of protein C in six patients liver tenderness, (2) weight gain of more than 2% of the were also below the normal range; the median value was baseline weight, and (3) an elevation of serum bilirubin 20.5% (range 7–29%). In no patient was there clinical or level of more than 2 mg/dl. VOD was diagnosed if two or radiological evidence of mesenteric ischemia. more these findings developed within 30 days of transplan- tation and there was no alternative explanation for these findings.19–21 Clinical course and outcome after diagnosis of PVT (Table 2) Laboratory methods Thrombolytic therapy with human recombinant tissue plas- minogen activator (dose 20 mg/day, range 20–50, for 4 Blood specimens were collected over sodium citrate and days, range 3–9) was given to six patients. This therapy centrifuged at 4°C. Assays for protein C and antithrombin was prescribed specifically for PVT in patients 3, 7 and 8, III were performed at the Hemostasis Laboratory of the each of whom lacked clinical evidence of severe VOD at Puget Sound Blood Center, Seattle, WA, using a chromo- the time of diagnosis of PVT and who would not have been genic method for antithrombin III (Iltest AT III; Instrumen- treated with thrombolysis otherwise. Patient 3, however, tation Laboratories, Lexington, MA, USA) and a functional despite the disappearance of his PVT within 2 days after assay for protein C (American Bioproducts Company, Par- the start of thrombolytic therapy, deteriorated and died of sippany, NJ, USA). The reference range for antithrombin VOD and multi-organ failure at day 47. Patients 7 and 8 III is 85–122%, and for protein C, 78–132%. resolved their PVT and recovered from VOD but died of recurrent myeloma and graft-versus-host disease, respect- Results ively. Thrombolytic therapy was given because of clinical evidence of severe VOD and not specifically for treatment Frequency of PVT of PVT in patients 1, 4 and 5. The PVT in patients 1 and 5 did not resolve and these patients died of VOD and multi- Of 1847 patients transplanted between March 1994 and organ failure. Patient 4 had resolution of both PVT and January 1998, eight (0.4%) were diagnosed with PVT. VOD and is a long-term survivor. Thrombolytic therapy was not given to patients 2 and 6. Patient 2 had recent Patient characteristics before diagnosis of PVT (Table 1) abdominal surgery as a contraindication to thrombolysis; The median age was 48 (32–65) years. Five patients had his PVT resolved spontaneously but he died of VOD and received autologous and three allogeneic transplants fol- multi-organ failure. Patient 6 had mild VOD that resolved. lowing high-dose myeloablative therapy. The clinical con- His PVT was noted to have resolved at an ultrasound exam- ditions being treated by transplantation included leukemia ination at day 52, and he is a long-term survivor. (n = 4), myeloma (n = 2), and solid tumor (n = 2). Two patients had chronic hepatitis before transplant (hepatitis C in patient 3 and hepatitis B and C in patient 5), a risk factor Discussion for severe VOD of the liver; neither patient had clinical evidence of cirrhosis. Patient 1 had undergone laparotomy In our study, of 1847 transplanted patients, eight patients for small bowel obstruction and lysis of adhesions on day (0.4%) were diagnosed with PVT, each of whom had clini- 27 post transplant, 9 days before the diagnosis of PVT. cal evidence of VOD. As VOD develops in 30–50% of Patient 3 had undergone laparoscopic cholecystectomy for patients who undergo myeloablative hematopoietic cell 19,20,22 gallstones 1 month before transplant. All patients had transplantation at our center, we estimate the fre- engrafted, at a median of day 15 (range 9–28). quency of PVT among patients with VOD at 1%. An Aus- tralian group has previously reported three patients with PVT after autologous hematopoietic cell transplantation, Patient characteristics on the day of PVT diagnosis with a denominator of 47 patients undergoing autologous (Table 1) hematopoietic cell transplantation.10 This study and our Diagnosis of PVT was made by Doppler ultrasound at a report were retrospective and may have underestimated the median of day 28 (range 3–58).
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