Background-Thrombocytopenia in cirrhotic patients may be due to deficient production of thrombopoietin. Aims-To determine the relation between thrombopoietin and thrombocytopenia in cirrhotic patients before and after orthotopic liver transplantation. Methods-Thrombopoietinconcentrations and platelet counts were measured in 43 cirrhotic patients and 21 normal controls and serially for 14 days after transplantation in 23/43 patients. Results-27 of the 43 patients had thrombocytopenia (platelet count less than 120 × 10 9 /l; group 1) whereas 16 patients had normal platelet count (group 2). Thrombopoietin concentrations were lower in group 1 than in group 2 (92. Conclusions-Inadequate thrombopoietin production may contribute to cirrhotic thrombocytopenia. Thrombopoietin production is restored after liver transplantation leading to the resolution of thrombocytopenia. (Gut 1999;44:754-758)

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A frequent complication in patients with end-stage liver disease is portal vein thrombosis (PVT). Although PVT is not considered an absolute contraindication to orthotopic liver transplantation (OLT), more complex surgery is required and patients have more postoperative complications and greater mortality rates. We describe 2 patients who experienced complete PVT either while waiting for liver transplantation or during the workup, resulting in acute deterioration of liver function. Recanalization of the portal vein was successfully performed in both patients using transjugular intrahepatic portosystemic stent shunt (TIPS), and patency was maintained by the addition of anticoagulation therapy. They subsequently underwent successful OLTs and remain well. In conclusion, we believe that TIPS placement can be performed safely in patients with recent PVT, ensuring the patency of the portal vein until OLT. (Liver Transpl 2001;7:453-460.)

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recovery of renal function with resolution of pulmonary oedema. COMMENTIn elderly diabetic patients with renal cholesterol atheroembolism, a common precipitant is manipulation of atherosclerotic vessels during vascular surgery or angiography. It can also result from thrombolytic and anticoagulant therapy, sometimes after a considerable delay1. Spontaneous cholesterol embolism is uncommon-found by Cross2 in 1.9% of serial necropsies, always in patients over 60 years of age. The clinical features are varied and make diagnosis difficult. Risk factors for renal cholesterol atheroembolism are advanced age (mean 66 years), hypertension, coronary atherosclerosis and renal impairment3. Spontaneous renal atheroembolism often leads to progressive decline in renal function, early dialysisdependence and high mortality3; however, renal function can recover4. Flash pulmonary oedema often points to underlying atheromatous renal artery occlusion, and we suspect that this was present in our patient. Regarding treatment, there is some evidence that a statin can stabilize atherosclerotic plaques, reduce the propensity for atheroembolism and thus preserve renal function5.Recurrent spontaneous cholesterol atheroembolism, characterized here by short-lived episodes of acute renal failure and pulmonary oedema, does not seem to have been described previously. This possibility should be considered in any elderly diabetic patient with established atherosclerotic disease who presents with impaired renal function and pulmonary oedema.