Partial splenic embolization as a treatment for hypersplenism in HIV/hepatitis C virus-co-infected patients

Unzurrunzaga, Ainhoaa; Martínez, Eduardoa; Miguélez, José Luisb; Cazallas, Juana; Mayo, Joséa; Echevarría, Javierb

doi: 10.1097/QAD.0b013e3280d64a0a
Author Information

aDepartments of Infectious Diseases, Spain

bRadiology, Hospital Galdakao, 48960 Bizkaia, Spain.

Received 13 September, 2006

Accepted 21 September, 2006

Article Outline

The development of thrombocytopenia in the course of untreated chronic hepatitis C may be caused by autoimmune phenomena or the infection of platelets with hepatitis C virus (HCV), but it generally denotes portal hypertension or, in other words, advanced hepatic fibrosis or cirrhosis [1], so it carries a bad prognosis. The only therapeutic option for patients with chronic hepatitis C at present is a regimen of interferon plus ribavirin, and as the dose of both interferon and ribavirin is crucial for an optimal response [2], the haematological toxicity of this regimen must be managed with the addition of haemopoietic factors rather than by reducing the drug doses [3,4]. Experience with recombinant thrombopoietin in patients with low platelet counts is scarce, and its efficacy seems to be low [3], therefore the development of thrombocytopenia with less than 50 000 platelets/μl is a frequent cause of treatment withdrawal. On the other hand, advanced liver disease is associated with a more severe thrombocytopenia, which precludes optimal treatment in the group of patients that more critically need it. Apart from splenectomy and splenic irradiation, there are no effective therapies for this kind of thrombocytopenia. Splenic irradiation has not been proved to increase platelet counts in patients with HIV-related thrombocytopenia, and has a negative impact on immunological status [5]. Splenectomy brings about a considerable morbimortality, particularly in patients with portal hypertension, and carries an increased risk of immediate and delayed infectious complications [6]. There have been good results with laparoscopic splenectomy, but it renders patients asplenic, and data on safety in HIV/HCV-co-infected patients are lacking. Partial splenic embolization (PSE) has proved to be a useful method to resolve thrombocytopenia caused by hypersplenism [7,8]. Here we report our experience on PSE in eight HIV/HCV-co-infected patients unable to tolerate an interferon/ribavirin regimen because of thrombocytopenia secondary to hypersplenism (Table 1).

All the patients, formerly intravenous drug users, had HCV-associated liver disease, and at the time of PSE all had cirrhosis; one was in Child–Pugh class B and the remainder were in class A. Hypersplenism was diagnosed by the observation of an ultrasonographically enlarged spleen (range 480–4224 ml) and reduced blood platelet counts (range 53–134 × 109/μl). All were on successful antiretroviral therapy, with undetectable plasma HIV viral loads and CD4 cell counts of 74–667 cells/μl (median 407). Pneumococcal, Haemophilus influenzae and quadrivalent meningococcal vaccines were administered, and, after written consent, a catheter was placed, via the femoral artery, in the splenic artery distal to the dorsal pancreatic branch. Embolization was performed injecting polyvinyl particles of approximately 500–700 μ; antibiotics were also injected and continuous angiographic control was performed, so the procedure could be stopped when approximately 70% of the splenic parenchyma was embolized. All patients received intravenous analgesic (meperidine) and antiemetic (metoclopramide) medication and antibiotic prophylaxis during and after the procedure. Complications were remarkably absent, except in one patient in whom the procedure was very difficult and resulted in a massive splenic infarct, sterile peritonitis presumably caused by the injected material and later secondary bacterial peritonitis. Another patient was readmitted for persistent fever, which was proved to be secondary to a subtotal splenic infarction; in addition, he was diagnosed as having an asymptomatic splenic and left portal branch vein thrombosis. Pain was always present and required narcotic analgesics in most cases; fever was also common, but it was caused by an infectious complication in only one case. A normal platelet count was achieved in every case, and all except two patients have been able to tolerate the subsequent regimen of full-dose pegylated interferon and ribavirin; in one patient thrombocytopenia relapsed (later, several accessory spleens were discovered at laparoscopy), and another developed neutropenia refractory to granulocyte colony-stimulating factor during such regimen (another patient stopped treatment against medical advice). Five out of eight patients completed a 48-week full-dose regimen; of these, three are sustained viral responders, one is an end-of-treatment responder and one, who was an end-of -treatment responder, died later from a septic shock.

PSE preserves some residual splenic function and can restore a normal platelet count without major complications. It has recently been recommended as a pretherapy in HCV-infected patients with hypersplenism [7], including liver transplant patients [8]. Foruny et al. [9] reported their experience with eight patients, of whom three were HIV/HCV co-infected, and in all cases thrombocytopenia corrected after PSE, allowing the completion of a full-dose anti-HCV regimen in 75% of patients. In that series asymptomatic portal thrombosis developed in four patients, compared with one patient from our series.

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