Nikolaos Evgenidis

Low-molecular-weight heparin (enoxaparin) as adjuvant therapy in the treatment of active ulcerative colitis: a randomized, controlled, comparative study.

Heparin could be beneficial to the treatment of active ulcerative colitis because of its anticoagulant, anti‐inflammatory and immunomodulatory properties.

Severe eosinophilic infiltration in colonic biopsies predicts patients with ulcerative colitis not responding to medical therapy

Eosinophils are potent proinflammatory cells that are involved in the pathogenesis of ulcerative colitis (UC). We evaluated the infiltration of eosinophils into the lamina propria in patients with active and inactive ulcerative colitis (UC) and investigated its clinical significance, among other variables, in predicting the outcome of medical treatment in active disease.

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.

Late onset ulcerative colitis complicating a patient with Budd-Chiari syndrome: a case report and review of the literature.

We report a case of a 33-year-old female patient with Budd-Chiari syndrome because of polycythemia vera. A transjugular intrahepatic portal-systemic shunt was performed because of refractory ascites 7 months after diagnosis. She had a stable hepatic function receiving anticoagulants until 3 years later when she presented with bloody diarrheas, liver function deterioration with prolonged prothrombin time and hypoalbuminemia, encephalopathy, and ascites. Colonoscopy revealed ulcerative pancolitis and the patient was treated with corticosteroids and antibiotics. Hepatic function was stabilized in parallel to controlling ulcerative colitis and the patient is in good health until now receiving maintenance therapy for ulcerative colitis and anticoagulants for Budd-Chiari syndrome.

Focal nodular hyperplasia of the liver in a patient with primary aldosteronism

cardiolipin antibody, with both anticardiolipin IgG and IgM serotypes detected. Imaging showed hepatosplenomegaly and there were multiple discrete lesions in the liver and spleen consistent with hepatic and splenic infarcts, and minimal ascites. There was no dilatation of the biliary tree. Liver biopsy showed discrete foci of hepatic infarction with venular and arteriolar fibrin. There was no evidence of vasculitis, central vein fibrosis, zone 3 congestion or erythrocytes within the space of Disse. The hepatic parenchyma adjacent to the coagulative necrosis was normal. There was some sinusoidal dilatation in response to small vein thrombosis, but no other evidence to suggest Budd–Chiari syndrome. Skin biopsy also showed small vessel fibrin thrombi with no evidence of vasculitis. The patient rapidly responded to intravenous hydrocortisone with resolution of his symptoms and improvement in liver chemistries (Table 1), and was discharged on a reducing dose of prednisolone. The patient was non-compliant with follow up, and was admitted to hospital with recurrent catastrophic APS on a further 17 occasions over the next 7 years. Recurrent episodes of catastrophic APS primarily involved the liver with symptoms of jaundice and ascites. The patient responded rapidly to steroids on each occasion. The addition of cyclophosphamide, gglobulin and quinine did not result in a more durable remission. A brief trial of low-molecular-weight heparin was complicated by antithrombin III deficiency and was ceased, and anticoagulation with warfarin was contraindicated because of patient non-compliance. Gastrointestinal system involvement is common in catastrophic APS, with a recent review finding that 22% of patients manifest with abdominal discomfort, and that hepatic, gastrointestinal and pancreatic involvement occur in 30%, 14% and 9% of cases, respectively. Approximately 50% of patients survive their initial episode of catastrophic APS. The majority of surviving patients are managed with anticoagulation, and recurrent catastrophic APS is seen in only 26% of cases. Few patients have previously been managed with corticosteroid therapy alone, and it has been concluded that steroids do not improve the chance of recovery. In the indexed case of catastrophic APS, steroid therapy was associated with rapid recovery from catastrophic APS on numerous occasions. This suggests that steroids, in contradistinction to previous evidence, may assist in the recovery from catastrophic APS, but do not prevent recurrent disease when stopped.

Polyarteritis Nodosa in a Patient with Type 1 Autoimmune Hepatitis

Polyarteritis nodosa is a systemic necrotizing vasculitis that affects small- and medium-sized arteries. Liver involvement in patients with polyarteritis nodosa has been described, and ranges from asymptomatic elevation of aminotransferases to hepatic aneurysm rupture. We describe the case of a patient with type 1 autoimmune hepatitis and compensated liver cirrhosis who developed classic polyarteritis nodosa, complicated with cytomegalovirus and repeated urinary tract infections. After a long bedridden hospitalization, the patients condition was stabilized. She is currently in good health, with well-controlled blood pressure, and stable kidney and liver function. To our knowledge, this is the first case report in the literature with concurrent appearance of both diseases.