Esophageal variceal ligation in the secondary prevention of variceal bleeding: Result of long term follow-up.

INTRODUCTION: Long-term outcome of patients after band ligation have been poorly defined. Therefore, we conducted a long-term follow-up study to delineate the outcome of ligation in patients with portal hypertension in the Hassan II university hospital, Fes, Morocco. METHODS: Over 118 months patients treated by endoscopic variceal ligation were received regular follow- up and detailed clinical assessment of at least 24 months. RESULTS: One hundred twenty five patients were followed up for a mean of 31 months (range 12-107 months). Obliteration of the varices was achieved in 89.6 % (N = 112) of patients, with 3 +/-1.99 (range 1-8) endoscopy sessions over a period of 14 + /-6.8 weeks (range 3-28). The percentage of variceal recurrence during follow-up after ligation was 20.5 % (N = 23). Recurrence were observed in a mean of 22 months +/- 7.3 (range 3-48). Bleeding rate from recurrent varices was 30.4 % (7/23). Rebleeding from esophageal ulcers occurred in 5.6 % (7/125) of patients. Portal hypertensive gastropathy before and after eradication of varices was 17.6% (N = 22) and 44.6% (N = 50) respectively; p< 0.05. Fundal gastric varices was 30.4% (N = 38) and 35.7% (N = 40) before and after eradication of varices respectively; p> 0.05. The overall mortality was 4 % (N = 5). CONCLUSION: Band ligation was an effective technical approach for variceal obliteration with low rates of variceal recurrence, rebleeding and development of gastric varices. Furthermore, it was associated with frequent development of portal hypertensive gastropathy.

Esophageal variceal ligation for hemostasis of acute variceal bleeding: efficacy and safety.

INTRODUCTION: Endoscopic variceal ligation is widely accepted as the optimum endoscopic treatment for esophageal variceal hemorrhage. In Morocco, there are no data regarding the efficacy of this technique. Our aim was to evaluate the effectiveness and safety of endoscopic variceal ligation in the management of oesophageal variceal bleeding in cirrhosis in a located population in Morocco. METHODS: Via a retrospective study over 118 months (December 2001- October 2011), cirrhotic patients with endoscopically proven esophageal variceal hemorrhage were treated by endoscopic variceal ligation. We studied the rate of haemostasis, rebleeding, complications and mortality. RESULTS: 360 cirrhotic patients were included and 378 haemostatic variceal ligations were performed. Primary haemostasis was obtained in 96.5 % (N=365) of cases. Thirty three patients (8.7%) bled during follow-up. The rate of minor complications was 15.3 % (N=58). Retrosternal pain, fever, dysphagia and Overtube's migration developed in 8.4 % (N=32); 2.6 % (N=10); 3,7 % (N=14) and 0.5 % (N=2) of the patients respectively. Severity of these complications was mild and transient. The rate of oesophageal ulcers was 5 % (N=19), while the mortality rate by haemorrhage was 5 % (N=18). CONCLUSION: Our data showed that band ligation is an effective and safe treatment modality of esophageal variceal bleeding with low rates of rebleeding and complications.

Acute esophageal necrosis: a case report and review.

Acute esophageal necrosis, commonly referred to as "black esophagus" or "acute necrotizing esophagitis", is a rare clinical disorder with an unclear etiology. The definition excludes patients with a history of recent caustic ingestion. Oesophageal necrosis can be diagnosed at endoscopy by the presence of black necroting appearing oesophagus. Contrary to the caustic oesophagitis whose treatment is often surgical, treatment of the acute necrositing oesophagitis is primarily medical. The prognosis for patients who develop acute necrotizing oesophagitis is generally poor. We report a new case of acute necrotizing oesophagitis and undertook a literature review of this rare diagnosis.

Acute inflammatory demyelinating polyneuropathy after treatment with pegylated interferon alfa-2a in a patient with chronic hepatitis C virus infection: a case report.

INTRODUCTION: The combination of polyethylene glycol (PEG)ylated interferon (pegylated interferon) and ribavirin has been shown to be an effective treatment for chronic hepatitis C virus. In general, common side effects related to this combination therapy are mild and are well tolerated. However, peripheral neuropathy including demyelinating polyneuropathy related to PEG-interferon α2a (pegylated interferon alfa-2a) is extremely rare. In the literature, only one case of acute inflammatory demyelinating polyneuropathy related to PEG-interferon α2a has been published previously. CASE PRESENTATION: To the best of our knowledge we present only the second case of acute inflammatory demyelinating polyneuropathy related to PEG-interferon α2a, occurring in a 63-year-old Caucasian man. He developed tingling, numbness, and weakness of his upper and lower extremities with acute neurological deficits after five weeks of a combination therapy with PEG-interferon α2a and ribavirin for chronic hepatitis C virus infection. His clinical course, neurological findings, and his electromyogram results were all consistent with acute inflammatory demyelinating polyneuropathy. Our patient recovered completely after interferon was stopped and symptomatic treatment and a further electromyogram showed a disappearance of neuropathy. Four weeks later, PEG-interferon α2a was reintroduced with a gradually increasing dose without any reappearance of neurological symptoms allowing hepatitis C seroconversion. CONCLUSIONS: Recognition of this rare yet possible presentation is important for early and accurate diagnosis and treatment. This case report also suggests that the reintroduction of PEGylated interferon in patients who had presented with acute inflammatory demyelinating polyneuropathy related to interferon α may be safe, but this must be confirmed by further studies.

Acute hepatitis secondary to parenteral amiodarone does not preclude subsequent oral therapy.

Amiodarone chlorhydrate is a diiodated benzofuran derivative used to treat cardiac rhythm abnormalities. Hepatotoxicity is a relatively uncommon side effect of amiodarone and symptomatic hepatic dysfunction occurs in less than 1% to 3% of patients taking amiodarone. We report here on an unusual case of amiodarone-induced hepatotoxicity. A 29 year old woman with normal liver function was given amiodarone intravenously to treat her atrial fibrillation. She developed acute toxic hepatitis after 24 h. The intravenous form of amiodarone was immediately avoided and replaced by the oral form, using conventional loading doses as soon as the deranged liver function tests had normalized, without recurrence of the hepatitis. These observations show that the occurrence of acute hepatic impairment with intravenous amiodarone does not necessarily preclude the use of this drug by mouth and the necessity of monitoring the hepatic function of patients treated with amiodarone.