Nikolaos Eugenidis

Long-term Follow-up of Patients With Acute Hypertriglyceridemia-Induced Pancreatitis

Background An acute and potentially life-threatening complication of hypertriglyceridemia (HTG) is acute pancreatitis (AP). Hypertriglyceridemia, usually severe, may be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy, and use of drugs. Study The efficacy of treatment to prevent relapses in 17 patients with AP attributed to HTG was investigated in the current prospective study. The mean follow-up period of patients was 42 months. Hypertriglyceridemia-induced AP comprised 6.9% of all patients with AP (n = 246) hospitalized in our clinic during the study (6 years). Results Causative conditions of HTG-induced AP were familial HTG in eight patients, HTG caused by uncontrolled diabetes mellitus in five, HTG aggravated by drugs in two (one by tamoxifen and one by fluvastatin), familial hyperchylomicronemia (HCM) in one, and lipemia of pregnancy in one. During the acute phase of pancreatitis, patients underwent standard treatment. Thereafter, HTG was efficiently controlled with high dosages of fibrates or a fibrate plus acipimox, except for the patient with HCM, who was on a specific diet (the only source of fat was a special oil consisting of medium chain triglyceride) and taking a high dosage of acipimox. One of the patients died during the acute phase of pancreatitis with acute respiratory distress syndrome. During follow-up, maintenance treatment was successful and only one patient relapsed, because he discontinued diet and drug treatment. Conclusion Appropriate diet and drug treatment, including dose titration, of severe HTG is very effective in preventing relapses of HTG-induced AP.

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.

Small-Duct Primary Sclerosing Cholangitis. A Single-Center Seven-Year Experience

Patients with cholestatic liver function tests and histological features of primary sclerosing cholangitis (PSC) but without the typical cholangiographic changes are considered to have small-duct PSC. The incidence of small-duct PSC and the natural history still is not known. We performed a retrospective search for patients diagnosed with small-duct PSC between January 1997 and December 2003. The diagnosis of small-duct PSC was based on biochemical features of chronic cholestasis, liver biopsy findings consistent with PSC, and a normal cholangiogram on endoscopic retrograde cholangiography. Six patients fulfilled the diagnostic criteria for small-duct PSC. All patients received medical therapy. After a mean follow-up time of 26.0 ± 29.8 months (range, 7–84 months), all patients are alive. Repeated liver biopsy was performed in one patient, 58 months after the initial one, and disclosed amelioration of histological findings (reduction in the Ludwig fibrosis score from 4 to 2). During follow-up symptoms disappeared in all patients who were symptomatic at diagnosis; none of those who were asymptomatic at diagnosis developed symptoms. At the time of last follow-up all patients showed significant improvement of their biochemical variables compared to baseline. Administration of aminosalicylates seemed to be of benefit irrespective of the presence of inflammatory bowel disease. No patients underwent liver transplantation or developed cholangiocarcinoma. Even though our study included a low number of patients and the follow-up time was relatively short, we can suggest that small-duct PSC rarely progresses to large-duct PSC and does not seem to be associated with development of cholangiocarcinoma. It thus seems to represent a separate entity with a favorable prognosis.

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.

Idiopathic portal hypertension in an "inactive" HBV carrier: a case report.

Idiopathic portal hypertension belongs to the group of non-cirrhotic portal hypertension, its etiology is still unknown but its prognosis is excellent. We report a case of 45 year old female with inactive hepatitis B virus (HBV) carrier status and persistently elevated alpha-fetoprotein (AFP), presented with features of portal hypertension and without evidence of cirrhosis or fibrosis on liver biopsy.