Vocal Tract Discomfort and Dysphonia in Patients Undergoing Empiric Therapeutic Trial with Proton Pump Inhibitor for Suspected Laryngopharyngeal Reflux.

INTRODUCTION: the aim of this study was to evaluate the correlation among dysphonic and vocal tract discomfort symptoms in patients who underwent empiric therapeutic trial with proton pump inhibitor (PPI) for a suspected laryngopharyngeal reflux (LPR). MATERIALS AND METHODS: A total of 34 patients with suspected LPR were enrolled in this study. All of them were evaluated using the reflux finding score, the reflux symptom Index (RSI), the vocal tract discomfort scale (VTDS), and the voice symptom scale (VoiSS) before and after the PPI treatment. RESULTS: A significant difference was found between pretreatment and posttreatment reflux finding score, RSI, VTDS, and VoiSS scores. Significant correlations among RSI, VTDS, and VoiSS before the PPI treatment were found. CONCLUSION: PPI treatment determined a significant improvement of symptoms related to dysphonia and vocal tract discomfort in patients with suspected LPR, in addition, significant correlations among the RSI, VTDS, and VoiSS scores were demonstrated thus suggesting that LPR might influence the response of questionnaires not specifically developed in order to assess the complains in LPR patient.

Primary prophylaxis of variceal bleeding in cirrhotic patients: a cohort study.

BACKGROUND: Current guidelines recommend beta-blockers for primary prevention of variceal haemorrhage in cirrhotic patients, and band ligation for patients with contraindications or intolerance to beta-blockers. However, it has been suggested that these patients may respond poorly to band ligation. AIM: We evaluated the usefulness of a strategy in which band ligation was used to treat patients with contraindications or intolerance and patients not responding to beta-blockers identified by hepatic vein pressure gradient measurement. Haemodynamic responders and patients refusing hepatic vein pressure gradient measurement were given long-term beta-blockers. METHODS: One hundred and thirty-five consecutive patients with high-risk oesophageal varices and no prior bleeding were enrolled. Twenty-five patients with contraindications (group A), 26 with intolerance to beta-blockers (group B) and 25 showing a poor haemodynamic response (Group C) underwent band ligation. Twenty-two haemodynamic responders (Group D) and 37 refusing hepatic vein pressure gradient measurement (Group E) were treated with beta-blockers. RESULTS: Median follow-up was 32 months. 12/135 patients (8.9%) bled: 3/25 (12%) in group A, 1/26 (3.8%) in group B, 0/25 (0%) in group C, 0/22 (0%) in group D and 8/37 (22.2%) in group E. Mortality was 8/135 (5.9%). CONCLUSIONS: Patients with contraindications, intolerance or not responding to beta-blockers treated with band ligation achieve protection from variceal bleeding comparable to that of good responders to beta-blockers.

Acute variceal bleeding: pharmacological treatment and primary/secondary prophylaxis.

Variceal bleeding is one of the most severe complications of portal hypertension related to liver cirrhosis. Primary prophylaxis is considered mandatory in patients with cirrhosis and high-risk oesophageal varices, and once varices have bled, every effort should be made to arrest the haemorrhage and prevent further bleeding episodes. In acute variceal bleeding, vasoactive drugs that lower portal pressure should be started even before endoscopy, and should be maintained for up to 5 days. The choice of vasoactive drug should be made according to local resources. Terlipressin, somatostatin and octreotide can be used; vasopressin plus transdermal nitroglycerin may be used if no other drug is available. In variceal bleeding, antibiotic therapy is also mandatory. In primary and secondary prophylaxis, beta-blockers are the mainstay of therapy. In secondary prophylaxis (but not in primary prophylaxis) these drugs can be combined with organic nitrates.

High-D-dimer plasma levels predict poor outcome in esophageal variceal bleeding.

BACKGROUND AND AIM: Variceal bleeding carries a high-mortality rate in patients with liver cirrhosis. Since coagulation and fibrinolysis are abnormal in these patients we evaluated whether or not abnormalities of these haemostasis systems were independently related to mortality. METHODS: Global coagulation, coagulation activation and fibrinolysis measurements were performed in 43 cirrhotics bleeding from esophageal varices at baseline and during follow-up and in 43 non-bleeding cirrhotic patients at baseline only. RESULTS: Baseline measurements of coagulation activation and fibrinolysis were more impaired in bleeders. In bleeders, prothrombin time, tissue type plasminogen activator antigen and D-dimer plasma levels were persistently more abnormal in patients who died. High-D-dimer, infection, Child-Pugh C class and MELD score >or=17 were the significant predictors of death at univariate analysis. Two different multivariate analyses to assess the independent prognostic value of these variables, one including the Child-Pugh class, the other including MELD, were performed. Independent predictors of death were high-D-dimer and infection, but not Child-Pugh class, in the former; MELD and infection, but not D-dimer, in the latter. CONCLUSIONS: Beside infection, high-D-dimer is a stronger predictor of death as compared to Child-Pugh C class, but not to a MELD score >or=17.

Diagnosis and monitoring of portal hypertension.

Currently, oesophago-gastroduodenoscopy is the standard method to diagnose the presence of oesophago-gastric varices and to estimate the risk of bleeding. It is recommended that all patients undergo endoscopic screening for varices at the time when cirrhosis is diagnosed. After screening endoscopy, patients with medium or large varices should be treated to prevent bleeding, while all other patients should undergo periodic surveillance endoscopy. However, at a given point in time a variable proportion of patients will not have varices, since the prevalence of varices is variable. Thus, screening all cirrhotic patients with endoscopy to detect the presence of varices implies a number of unnecessary endoscopies. In recent years a wealth of new methods have been proposed as alternatives to conventional oesophago-gastroduodenoscopy for the non-invasive or minimally invasive diagnosis of oesophageal varices. Three of these methods (the platelet count/spleen diameter ratio, Fibrotest and Fibroscan) are truly non-invasive. Of these, the former is promising and needs a proper validation, Fibrotest appears to be insufficiently precise, while Fibroscan needs further evaluation. Multidetector CT oesophagography and capsule endoscopy are not entirely "non-invasive", since the first requires air insufflation into the oesophagus via an orally passed tube, and the latter requires swallowing the capsule. Multidetector CT oesophagography is promising, but needs further evaluation; capsule endoscopy is safe and reliable and might be proposed as an alternative to oesophago-gastroduodenoscopy in patients unable or unwilling to undergo oesophago-gastroduodenoscopy.

Nickel and cobalt recycling from lithium-ion batteries by electrochemical processes.

The presence of LiCoO(2) and LiCo(x)Ni((1-x))O(2) in the cathodic material of Li-ion and Li-polymer batteries has stimulated the recovery of Co and Ni by hydrometallurgical processes. In particular, the two metals were separated by SX method and then recovered by electrochemical (galvanostatic and potentiostatic) processes. The metallic Ni has been electrowon at 250 A/m(2), pH 3-3.2 and 50 degrees C, with 87% current efficiency and 2.96 kWh/kg specific energy consumption. Potentiostatic electrolysis produces a very poor Ni powder in about 1 h with current efficiency changing from 70% to 45% depending on Ni concentration in the electrolyte. Current efficiency of 96% and specific energy consumption of 2.8 kWh/kg were obtained for Co at 250 A/m(2), pH 4-4.2 and 50 degrees C, by using a solution containing manganese and (NH(4))(2)SO(4). The Co powder, produced in potentiostatic conditions (-0.9 V vs. SCE, pH 4, room temperature) appears particularly suitable for Co recycling as cobaltite in new batteries.

Review article: the relevance of portal pressure and other risk factors in acute gastro-oesophageal variceal bleeding.

Gastro-oesophageal variceal bleeding is the last step in a chain of events that starts with an increased portal pressure, and is followed by the formation and progressive dilatation of gastro-oesophageal varices. When the tension of the thin wall of the varices exceeds its elastic limit, the varices rupture and bleed. Wall tension is directly proportional to variceal pressure (which is a function of portal pressure) and variceal radius, and inversely related to the thickness of the variceal wall. The above facts explain why a high portal pressure (usually determined by the hepatic venous pressure gradient, or HVPG) and the presence at endoscopy of large varices with red wheals, red spots or diffuse redness on the varices (signalling a reduced wall thickness) correlate with the risk of bleeding.

Diagnosis and treatment of portal hypertension.

Prevention of the first variceal haemorrhage should start when the patients have developed medium-sized to large varices. Non-selective beta-blockers and band ligation are equally effective in preventing the first bleeding episode. Rubber band ligation is the first choice for patients with contraindications or intolerance to beta-blockers. Treatment of acute bleeding should aim at controlling bleeding and preventing early rebleeding and complications, especially infections. Combined endoscopic (band ligation or sclerotherapy) and pharmacological treatment with vasoactive drugs can control bleeding in up to 90% of patients. Antibiotic prophylaxis is an integral part of the treatment of acute variceal haemorrhage, and must be started as soon as possible. Emergency transjugular intrahepatic portosystemic stent shunt (TIPS) is the standard rescue therapy for patients failing combined endoscopic and pharmacological treatment. All patients who survive a variceal bleed should be treated with beta-blockers or band ligation to prevent rebleeding. All patients in whom bleeding cannot be controlled or who continue to rebleed can be treated with salvage TIPS or, in selected cases, with surgical shunts. Liver transplantation should be considered for patients with severe liver insufficiency in which first-line treatments fail.

Medical treatment of portal hypertension.

Prevention of the first variceal haemorrhage should start when the patients have developed medium sized to large varices. Non-selective beta-blockers are the first-line treatment; band ligation is roughly equivalent to beta-blockers and is the first choice for patients with contraindications or intolerance to beta-blockers. Treatment of acute bleeding should aim at controlling bleeding and preventing early rebleeding and complications, especially infections. Combined endoscopic and pharmacological treatment with vasoactive drugs can control bleeding in up to 90% of patients. All patients who survive a variceal bleed should be treated with beta-blockers or band ligation to prevent rebleeding. All patients in whom bleeding cannot be controlled or who continue to rebleed can be treated with salvage TIPS or, in selected cases, with surgical shunts. Liver transplantation should be considered for patients with severe liver insufficiency in which first-line treatments fail.

[Portal hypertensive gastropathy in patients with cirrhosis of the liver]. / Gastropatia da ipertensione portale nei pazienti con cirrosi epatica.

Portal hypertensive gastropathy (PHG) is characterized by changes in the endoscopic appearance of the gastric mucosa, specific for portal hypertension. The identification of the elementary lesions of PHG allowed the development of a reproducible classification, defining mild and severe pictures, and the execution of a natural history study. This study showed a 80% overall prevalence of PHG in patient with cirrhosis of the liver and a correlation between duration of the disease and development of PHG. PHG has often been shown to be a fluctuating condition, thus suggesting that its pathophysiology is not only related to portal hypertension, but also to other, yet unknown, factors. Bleeding from PHG did not occur in patients with a recent diagnosis of liver cirrhosis. Acute and chronic bleeding occurred in 2.5% and 12% of patients, respectively. The death rate from acute PHG bleeding was lower (12.5%) than the death rate of variceal bleeding (39.1%). Vasoactive drugs can be used in the treatment of acute PHG bleeding. For chronic bleeding, non selective 13-blockers and, if needed, iron, are the treatment of choice. TIPS or surgical portosystemic shunt may be considered for acute or chronic PHG bleeding, if medical treatment fails. Clinical controlled trials are needed to evaluate the efficacy of these or other treatments.