Nikolaos Grammatikos

Adefovir plus lamivudine are more effective than adefovir alone in lamivudine-resistant HBeAg- chronic hepatitis B patients: A 4-year study

Background and Aim:  Adefovir dipivoxil (ADV) is effective in lamivudine (LAM)‐resistant hepatitis B e antigen‐negative (HBeAg‐) chronic hepatitis B (CHB). However, it is unclear whether LAM treatment should be continued in these patients. We aimed to compare the long‐term efficacy of adding ADV to ongoing LAM treatment versus switching to ADV monotherapy in LAM‐resistant HBeAg‐ CHB.

Spur cells and spur cell anemia in hospitalized patients with advanced liver disease: Incidence and correlation with disease severity and survival.

Aim:  Spur cell anemia (SCA) is a form of acquired hemolytic anemia seen in patients with advanced cirrhosis and particularly in patients with alcoholic cirrhosis. The aim of the present study was to evaluate the incidence of spur cells and spur cell anemia in patients with advanced liver disease and to correlate the presence of spur cell anemia with survival.

Lamivudine/pegylated interferon alfa-2b sequential combination therapy compared with lamivudine monotherapy in HBeAg-negative chronic hepatitis B.

Background and Aim:  Monotherapy has been proven insufficient in achieving sustained control of chronic hepatitis B. We aimed to assess the efficacy of combined sequential administration of lamivudine and pegylated interferon alfa‐2b in patients with hepatitis Be antigen (HBeAg)‐negative chronic hepatitis B.

Effect of lamivudine treatment in patients with decompensated cirrhosis due to anti‐HBe positive/HBeAg‐negative chronic hepatitis B

Abstract:  Lamivudine has been shown to improve liver function and reduce the need for liver transplantation (LT) in patients with decompensated HBeAg‐positive cirrhosis. Nevertheless, there is only limited experience with lamivudine in patients with anti‐HBe‐positive/HBeAg‐negative cirrhosis. The primary aim of this study was to determine whether lamivudine treatment improves liver function and subsequently pre‐LT survival or delays or obviates the need for LT in patients with anti‐HBe‐positive/HBeAg‐negative cirrhosis. Between July 1998 and June 2003, 20 consecutive patients awaiting LT were enrolled in the study. All patients showed active viral replication and were treated with lamivudine 100 mg daily. Significant clinical improvement, defined as a decrease in the Child–Pugh–Turcotte score by ≥2 points, was observed in 11 (55%) patients. The median change in the Child–Pugh–Turcotte score was −2 (range −5 to +2). The median time required to achieve a 2‐point or greater reduction in Child–Pugh–Turcotte score was 6 months (range 3–12 months). In nine patients (45%), the Child–Pugh–Turcotte score decreased to ≤6 (Childs class A cirrhosis). At last follow‐up, 14 (70%) patients were alive and waiting for LT, with a median LT‐free survival of 36 months (range 12–63 months). One patient (5%) developed resistance to lamivudine with reappearance of HBV DNA after 48 months of treatment. In conclusion, our results provide further evidence to the notion that lamivudine is beneficial in patients with decompensated anti‐HBe‐positive/HBeAg‐negative cirrhosis caused by actively replicating chronic hepatitis B.

Interferon/long-term lamivudine combination therapy in anti-HBe positive chronic hepatitis B patients.

Background:  Monotherapy with a single antiviral agent is insufficient in controlling hepatitis B virus infection in the majority of patients with anti‐HBe positive chronic hepatitis B. Interferon/long‐term lamivudine combination therapy was evaluated to determine if this strategy would improve treatment efficacy and reduce the emergence of lamivudine resistance.

Sarcoidosis-induced pericarditis in a patient with portopulmonary hypertension: a case report

Portopulmonary hypertension is a rare and severe complication of patients with cirrhosis. Sarcoidosis, a disease of unknown etiology, is also a cause of pulonary hypertension and right heart dysfunction. We report the case of a 51-year-old male patient, suffering from cirrhosis due to Wilsons disease, portal hypertension and pulmonary hypertension (PH), who developed severe pericarditis. Wilsons disease was diagnosed 8 years before his last admission to our hospital and was being successfully treated with D-penicillamine. PH was recognized 2 years before admission and being treated with bosentan. The patient complained for dyspnea at rest and the 2D echocardiogram revealed a significant amount of pericardial fluid. All other causes of acute pericarditis were excluded and his laboratory, imaging and histopathological investigation showed evidence of sarcoidosis. He underwent a therapy with corticosteroids (methylprednisolone) and his follow-up examination showed remarkable decrease of the levels of mean pulmonary artery pressure and pericardial fluid.