Biomedical subjects

J Rodés

Publications and source records attributed to J Rodés.

At least 163 records · Page 9Linked to original sources

PubMed1997

Anemia worsens hyperdynamic circulation of patients with cirrhosis and portal hypertension.

This retrospective cohort study was aimed at investigating the effects of anemia on the hemodynamic disturbances associated with portal hypertension. In all, 202 consecutive nontreated portal-hypertensive patients referred for evaluation to our Hepatic Hemodynamic Laboratory were included. Compared to the nonanemic patients, anemic cirrhotic patients had an increased cardiac output (7.9 +/- 1.9 vs 7.1 +/- 2 liters/min, P < 0.01), and a decreased mean arterial blood pressure (82 +/- 11 vs 94 +/- 13 mm Hg, P < 0.0001) and systemic vascular resistance (838 +/- 235 vs 1102 +/- 356 dyn/sec/cm5, P < 0.0001). Similar results were obtained when Child A or Child B-C patients were analyzed separately. Multivariate logistic regression disclosed that hemoglobin concentration, in addition to age, sex azygos blood flow, and albumin concentration, was an independent factor influencing the degree of systemic vasodilation in cirrhotic portal-hypertensive patients. This study discloses that anemia worsens the hyperdynamic circulation associated with portal hypertension. Since hemoglobin concentration may change with time, this parameter should be taken into account when evaluating hemodynamics in portal-hypertensive patients.

Aldosterone↗

PubMed1997

Antibodies to mycobacterial 65-kD heat shock protein cross-react with the main mitochondrial antigens in patients with primary biliary cirrhosis.

Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease associated with autoimmune disorders. The aetiology is unknown, although it has been suggested that the disease may be related to infectious agents. Previous studies revealed that sera from patients with PBC react against Mycobacterium gordonae. This specific reactivity, characterized by a recognition of two membrane polypeptides of 70-65 and 55 kD, cross-react with the two major mitochondrial autoantigens of PBC. As the most immunogenic components of mycobacteria are the heat shock proteins (hsp), which have been associated with autoimmunity, this study has been undertaken to characterize whether the reacting polypeptides in PBC are hsp from M. gordonae. Cultures of M. gordonae were incubated at 37 degrees C and 46 degrees C before sonication, protein extraction and separation by SDS-PAGE. Exposure of M. gordonae to heat shock treatment resulted in membrane protein overexpression, similar to the 70-65-kD polypeptide recognized by the sera from patients with PBC. Immunoprecipitation assays with a monoclonal antibody directed against the Hsp65 kD of mycobacteria and with sera from patients with PBC revealed similar reacting profiles characterized by the precipitation of the overexpressed 65-kD polypeptide from M. gordonae. Competitive immunoblotting showed that binding of the monoclonal antibody to the Hsp65 kD protein was prevented by preincubation with sera from patients with PBC, but not with sera from healthy subjects. Furthermore, monoclonal antibody to the Hsp65 kD protein recognized the main mitochondrial autoantigens of PBC (PDH-E2 and BCKDH-E2). These data indicate the existence of cross-reacting epitopes contained on M. gordonae Hsp65 kD and the main mitochondrial antigens in patients with PBC.

Antigens, Bacterial↗

PubMed1997

The portal pressure response to beta-blockade is greater in cirrhotic patients without varices than in those with varices.

BACKGROUND & AIMS: Nonselective beta-blockers are effective in reducing portal pressure in cirrhotic patients. However, this beneficial effect is highly variable and may depend on the extent of portal system collateralization. The aim of this study was to compare portal pressure response with timolol, a nonselective beta-blocker, in cirrhotic patients with and without varices. METHODS: Portal and systemic hemodynamics were measured before and after a single oral dose of 10 mg of timolol in 50 patients with cirrhosis and portal hypertension, 15 with and 35 without esophageal varices. RESULTS: Timolol significantly decreased portal pressure in all patients (mean reduction, 20% +/- 13%; P < 0.0001). The reduction in hepatic venous pressure gradient was greater in patients without varices (-24% +/- 14%) than in those with varices (-12% +/- 8%) (P < 0.01). A decrease in the hepatic venous pressure gradient of <12 mm Hg was achieved in 7 of 12 (58%) patients without varices and a baseline pressure gradient of <12 mm Hg, but only in 3 of 15 patients with varices (20%) (P < 0.01). CONCLUSIONS: Timolol is effective in reducing portal pressure in cirrhotic patients, more so in patients without varices, suggesting that nonselective beta-blockers will be more effective in the treatment of portal hypertension when administered at early stages, before the development of varices.

Aged↗

PubMed1997

Nitric oxide production by peritoneal macrophages of cirrhotic rats: a host response against bacterial peritonitis.

BACKGROUND & AIMS: Patients and rats with cirrhosis and ascites are prone to develop peritonitis. The aim of this study was to assess whether peritoneal macrophages of cirrhotic rats without peritoneal infection produce nitric oxide and express inducible NO synthase (iNOS). METHODS: NO2- accumulation produced by macrophages from control rats and cirrhotic rats with ascites was determined. iNOS messenger RNA and protein expression were analyzed by Northern and Western blot and immunocytochemical analysis. The in vivo effects of inhibiting iNOS were investigated by giving the specific iNOS inhibitor L-N-(1-iminoethyl)-lysine (L-NIL) or sterile saline to 9 and 7 cirrhotic rats with ascites, respectively. RESULTS: Cirrhotic macrophages produced NO2- that was around fourfold greater than that of control macrophages after 30 hours in culture. Northern and Western blot and immunocytochemical analysis showed the presence of iNOS messenger RNA and protein in macrophages of cirrhotic rats. Ascites cultures were positive in all rats administered L-NIL and negative in those administered saline. CONCLUSIONS: Macrophages of cirrhotic rats produce NO and express iNOS messenger RNA and protein, and these changes are not a consequence of overt bacterial infection. Because iNOS inhibition results in peritoneal infection, these results suggest that iNOS induction in macrophages of cirrhotic rats is a host defense response to prevent bacterial peritonitis.

Animals↗

PubMed1997

Paracentesis-induced circulatory dysfunction: mechanism and effect on hepatic hemodynamics in cirrhosis.

BACKGROUND & AIMS: Therapeutic paracentesis may be associated with a circulatory dysfunction, manifested by a marked increase of the plasma renin activity and plasma norepinephrine. The aim of the study was to characterize the systemic and hepatic hemodynamic changes associated with paracentesis-induced circulatory dysfunction. METHODS: Changes in plasma renin, aldosterone, and norepinephrine, and in systemic and hepatic hemodynamics were assessed 1 hour and 6 days after complete mobilization of ascites in 37 patients treated by total paracentesis plus intravenous dextran-70 infusion. RESULTS: Paracentesis-induced circulatory dysfunction occurred in 10 patients (renin and norepinephrine increased from 9.0 +/- 10.5 to 28.8 +/- 19.0 ng.mL-1.h-1 and from 752.0 +/- 364.0 to 1223.0 +/- 294.0 pg/mL, respectively) and was associated with significant reduction in systemic vascular resistance (-13.0% +/- 2.6%; P < 0.05) and increase in hepatic venous pressure gradient (from 19.5 +/- 1.5 to 22.5 +/- 2.4 mm Hg; P < 0.01). In the remaining 27 patients, mobilization of ascites also induced a significant but smaller reduction in systemic vascular resistance (-5.0% +/- 1.6%; P < 0.05) without significant changes in renin, norepinephrine, and hepatic venous pressure gradient. CONCLUSIONS: Paracentesis-induced circulatory dysfunction is predominantly caused by an accentuation of the arteriolar vasodilation already present in untreated cirrhotic patients with ascites. The homeostatic activation of endogenous vasoactive systems may account for the increased intrahepatic vascular resistance associated with this condition.

Aged↗

PubMed1997

Arginine vasopressin induces contraction and stimulates growth of cultured human hepatic stellate cells.

BACKGROUND & AIMS: Hepatic stellate cells (HSCs) are perisinusoidal cells believed to participate in the regulation of hepatic blood flow because of their contractile properties and presence of receptors for several vasoactive factors. It is unknown whether HSCs have receptors for vasopressin, one of the most potent endogenous vasoconstrictors. This study investigated the existence of receptors for and the effects of arginine vasopressin (AVP) on cultured human HSCs. METHODS: intracellular calcium concentration ([Ca2+]i) and cell contraction were measured in individual cells loaded with fura-2 using a morphometric method with an epifluorescence microscope coupled to a CCD imaging system (Photometrics, Tucson, AZ). AVP-specific binding was measured with [3H]AVP. Mitogen-activated protein kinase (MAPk) activity and DNA synthesis were measured by in vitro phosphorylation of myelin basic protein and [3H]thymidine incorporation, respectively. Parallel experiments were performed in vascular smooth muscle cells. RESULTS: AVP elicited a dose-dependent increase in [Ca2+]i and contraction of HSCs. Moreover, AVP increased MAPk activity, DNA synthesis, and cell number. These effects were similar to those observed in vascular smooth muscle cells and were blocked by a V1 receptor antagonist. The existence of V1 receptors was further confirmed by binding studies. CONCLUSIONS: Human HSCs have V1-vasopressin receptors that induce effects similar to those observed in vascular smooth muscle cells. AVP may play a role in the regulation of HSC function.

Animals↗

PubMed1997

Endoscopic assessment of variceal volume and wall tension in cirrhotic patients: effects of pharmacological therapy.

BACKGROUND & AIMS: Variceal rupture is believed to occur when variceal wall tension is excessive. The combined use of endosonography, allowing the objective measurement of variceal radius, and endoscopic measurement of transmural variceal pressure may enable assessment of this important parameter. The aim of this study was to assess the effects on variceal hemodynamics of drugs acting through different mechanisms: decreasing portocollateral blood flow (propranolol) or resistance (isosorbide-5-mononitrate [ISMN]). METHODS: Repeated measurements of variceal radius, volume (by endosonography), and transmural pressure (using endoscopic gauge) were performed in 27 cirrhotic patients at baseline and 40 minutes after double-blind administration of placebo (n = 9), propranolol (n = 9), or ISMN (n = 9). RESULTS: Placebo had no effect. Propranolol significantly reduced variceal volume (-32% +/- 26%; P = 0.01), radius (-12% +/- 9%; P < 0.005), and pressure (-26% +/- 10%; P < 0.0001). The resulting decrease in wall tension (-34% +/- 13%; P < 0.0005) exceeded that in transmural pressure (P < 0.01). ISMN reduced transmural variceal pressure (-26% +/- 21%; P < 0.005), but not radius (-3% +/-14%; NS) and volume (-9% +/- 31%; NS). CONCLUSIONS: The combination of endosonography and endoscopic measurement of transmural variceal pressure allows quantitative estimation of variceal wall tension. Propranolol and ISMN reduce similarly transmural variceal pressure. Propranolol, but not ISMN, reduces variceal volume and radius. Therefore, despite similar decreases in variceal wall tension, propranolol may offer a greater therapeutic effect than ISMN in portal hypertension.

Adrenergic beta-Antagonists↗

PubMed1997

Pathogenesis of ascites in cirrhosis.

Much progress has been made in the recognition of factors involved in the pathogenesis of the abnormal regulation of extracellular fluid volume in cirrhosis. It is now well established that cirrhosis induces modifications in the activity of several systemic vasoactive factors which then play a major role in the development of renal dysfunction and the formation of ascites and edema. It is also evident that intrarenal factors participate in the pathogenesis of these abnormalities. Nevertheless, the available information is still limited. The link between the diseased liver and the disturbances in the vasoactive systems is not completely known but much evidence suggests that it consists of a circulatory dysfunction that affects mainly the arterial circulation and is characterized by an inability to maintain an effective arterial blood volume within normal limits. Research on the mechanisms of this circulatory dysfunction may yield clues that will help in the design of more pathophysiologically oriented therapeutic approaches to the management of ascites.

Ascites↗

PubMed1997

Bacterial infections in liver disease.

Most bacterial infections in cirrhotic patients are hospital-acquired. Urinary tract infections, spontaneous bacterial peritonitis (SBP), respiratory tract infections, and bacteremia are the most frequent bacterial infectious complications seen in cirrhotic patients. SBP is the most characteristic infectious complication of cirrhotic patients, and it is defined as the infection of a previously sterile ascitic fluid, with no apparent intra-abdominal source of infection. The incidence of SBP in cirrhotic patients admitted to hospital with ascites has been estimated to range between 7 and 23%. The diagnosis is established on the basis of clinical signs and symptoms and/or a polymorphonuclear cell count in ascitic fluid higher than 250/mm3. This diagnosis is confirmed by a positive culture in approximately 70% of the cases. The remaining 30% are considered culture-negative SBP but are empirically treated with antibiotics because severe peritonitis and death may follow if these patients are not treated. Early diagnosis, the routine use of diagnostic paracentesis in patients admitted to hospital with ascites, and, especially, the use of adequate antibiotics are very important tools in the treatment of SBP. Third-generation cephalosporins are the first-choice antibiotic treatment in SBP, although selected patients with SBP, those with normal renal function and without hepatic encephalopathy, shock, or gastrointestinal bleeding, may be treated with oral quinolones. Selective intestinal decontamination with norfloxacin is safe and useful in the primary and secondary prophylaxis of SBP, although the incidence of quinolone-resistant organisms is increasing and this may be a problem in the future.

Bacteremia↗

PubMed1997

Incidence and risk factors of hepatitis C virus infection in a haemodialysis unit.

BACKGROUND: Hepatitis viruses have become one of the main infectious problems in patients on maintenance haemodialysis. The aim of this study was to prospectively investigate the incidence of de novo hepatitis C virus (HCV) infection in a haemodialysis unit and to identify factors currently involved in HCV transmission to haemodialysis patients. METHODS: One hundred and fourteen anti-HCV negative and HCV-RNA negative patients who started long-term haemodialysis were followed for a mean period of 36 months (range 18-56). Liver tests and anti-HCV were performed at 6-month intervals. Factors that might be implicated in HCV transmission, such as blood transfusions, sexual habits, surgery and other invasive procedures, were recorded. HCV markers were re-examined in transfused blood and the HCV genotype was investigated in seroconverters to anti-HCV and in patients with previous HCV infection who were treated in the vicinity of those who seroconverted. RESULTS: Eight patients (7%) seroconverted to anti-HCV and seven of them became HCV-RNA positive. HCV markers, including HCV-RNA, were negative in the blood transfused to seroconverters. No differences between seroconverters and non-seroconverters. No differences found in other risk factors not directly related to haemodialysis. The investigation of HCV genotype suggested that HCV transmission was not restricted to patients treated in the vicinity of previously HCV infected patients. Occasional failure to observe strict measures of asepsis was detected in the haemodialysis unit and this was the only factor that might be incriminating. CONCLUSIONS: HCV acquisition in patients on haemodialysis is currently not related to blood transfusion, and nosocomial transmission within the haemodialysis unit seems to be the main mechanism of HCV infection. Extremely careful observation of preventive measures seems essential to eradicate HCV transmission in haemodialysis units.

Adult↗

PubMed1997

Hepatitis G virus infection in a haemodialysis unit: prevalence and clinical implications.

BACKGROUND: Hepatitis viruses have become one of the main infectious problems in patients on long-term haemodialysis. A new RNA virus, designated hepatitis G virus (HGV) has been recently identified. The pathogenic relevance of this virus is currently under investigation. The aim of this study was to analyse the prevalence and clinical implications of hepatitis G virus infection in patients on haemodialysis. METHODS: The presence of HGV-RNA was investigated in 96 patients on maintenance haemodialysis. Hepatitis viral markers (HBsAg, anti-HCV, HGV-RNA) and liver tests were assessed in all these patients, as well as the risk factors for hepatitis viruses acquisition. As a control group, 200 blood donors were tested for the presence of HGV-RNA. RESULTS: HGV-RNA was detected in 25 of 96 patients on haemodialysis (26%) and in six of 200 blood donors (3%) (P < 0.001). Thirteen of 25 HGV infected patients (52%) were coinfected with other hepatitis viruses (HBV and/or HCV). Evidences of chronic liver disease were more frequent in patients infected by HBV and/or HCV (61%) than in patients infected by HGV alone (17%) (P = 0.01). Although 80% of HGV infected patients had received blood products, the transfusion rate was not different from non HGV-infected patients. Time on haemodialysis was significantly shorter in patients infected with HGV alone (3.1 +/- 3.5 years) compared to patients infected with HBV and/or HCV (7.6 +/- 5.8 years) (P = 0.04). CONCLUSIONS: Patients on maintenance haemodialysis are at increased risk for HGV infection. HGV infection itself does not seem to be a frequent cause of chronic liver disease in these patients. Since the prevalence of HGV infection in blood donors is high, blood transfusion could be one of the main factors implicated in HGV transmission in patients on haemodialysis.

Adolescent↗

PubMed1997

Carbohydrate-deficient transferrin as a marker of alcohol consumption in male patients with liver disease.

Carbohydrate-deficient transferrin (CDT) has been proposed as a marker of alcohol abuse. However, its value in patients with associated liver disease is still controversial. The aim of the study was to investigate the usefulness of CDT as a marker of alcohol consumption in patients with liver disease. We measured serum levels of CDT and those of commonly used hematological and biochemical markers, mean corpuscular volume (MCV), transaminases (AST and ALT), and gamma-glutamyltransferase in 179 male subjects divided into four groups: 45 active drinkers (13 with normal liver, 21 with fibrosteatosis, and 11 with liver cirrhosis), 45 abstinent chronic alcoholics (18 with and 27 without liver disease), 58 patients with nonalcoholic liver disease, and 31 healthy controls. Serum CDT in active alcoholics was 37.5 +/- 3.6 units/liter, being significantly higher than that of abstinent alcoholics (20.3 +/- 1.5 units/liter), patients with nonalcoholic liver disease (18.1 +/- 1.1 units/liter), and controls (13.1 +/- 0.8 units/liter). Contrary to the other markers, no significant differences were observed in CDT values in relation with the presence and severity of liver disease in either the active drinkers or in the abstinent alcoholics. The sensitivity and specificity of CDT as a marker of alcoholism in the series as a whole was 64% and 82%, respectively, similar to the best conventional marker, MCV (64 and 82%). In patients with liver disease, CDT maintained good sensitivity (72%) and specificity (83%). Receiver operating characteristic analysis confirmed that CDT had a similar diagnostic value to that of MCV, but better than gamma-glutamyl-transferase and transaminases for the detection of alcohol abusers. The good diagnostic efficacy of CDT remained unchanged when analyzing only patients with liver disease. We conclude that serum CDT is a good marker of alcoholism and is less influenced than the currently used biochemical markers for associated liver disease. Thus, CDT is an effective laboratory test to detect alcohol abuse regardless of the presence of alcoholic liver disease.

Adult↗

PubMed1997

Hepatitis G virus infection in fulminant hepatic failure.

BACKGROUND: RNA sequences of the recently identified hepatitis GB virus C (HGBV-C), also named hepatitis G virus (HGV), have been detected in patients with idiopathic fulminant hepatic failure (FHF) but the role of this agent in the disease remains controversial. AIMS: To investigate the presence and implications of HGV infection in a large series of Spanish patients with FHF. PATIENTS: Sixty eight patients with FHF, including 19 with idiopathic disease, were studied. In 28 cases, studies were performed before and after liver transplantation. For comparison 200 volunteer blood donors and 22 patients transplanted for chronic liver disease were also studied. METHODS: HGV RNA was measured in serum by reverse transcriptase polymerase chain reaction of the 5' non-coding region. RESULTS: Evidence of HGV infection was found in 3% (6/200) of blood donors and in 19% (13/68) of patients with FHF. HGV infection was more frequent in patients with hepatitis B (24%, 6/25) or hepatitis D (42%, 5/12), than in patients with idiopathic disease (11%, 2/19). Half of the patients with HGV infection used illicit intravenous drugs. Specific clinical features associated with HGV infection were not identified. A very high rate of infection with HGV was observed in patients who underwent liver transplantation, either for FHF (60%, 15/24) or chronic liver disease (45%, 9/20). CONCLUSIONS: In our geographical area, HGV infection is relatively frequent in FHF, but it does not seem to play a major role in idiopathic cases.

Adult↗

PubMed1997

[Effects of percutaneous intrahepatic portosystemic shunt on splanchnic and systemic hemodynamics in patients with portal hypertension].

Transjugular intrahepatic portosystemic shunt (TIPS) is a calibrated shunt directed at reducing the portal pressure gradient with a low incidence of hepatic encephalopathy and deterioration of hepatocellular function. The present study investigated the effects of TIPS on splanchnic and systemic hemodynamics on liver function and on the development of encephalopathy. A group of 30 patients treated with TIPS were included in the study: 26 patients with hepatic cirrhosis for an hemorrhagic episode by esophageal varices not controlled by medical treatment and sclerotherapy and in 4 cases with the Budd-Chiari syndrome for ascites refractory to medical treatment. Before, at 24 hours and 2 months after TIPS, the portal pressure gradient, cardiopulmonary pressure and cardiac output, blood flow of the azygos vein, and hepatic clearance of indocyanine green as indexes of liver function were determined. TIPS significantly decreased the portal pressures gradient and azygos blood flow. This was associated with a significant increase in cardiac output and a significant decrease in peripheral vascular resistance and hepatic clearance of indocyanine green. Portal flow deviated by TIPS was greater in the 9 patients (30%) who developed hepatic encephalopathy during follow up. In conclusion, TIPS effectively reduces portal hypertension. Nonetheless, it is associated with an increase in hyperdynamic circulation, a high incidence of encephalopathy and a deterioration in liver function.

Adolescent↗

PubMed1997

[Autoimmune cholangitis or primary biliary cirrhosis without antimitochondrial antibodies?].

The term cholangitis or autoimmune cholangiopathy is applied to patients with a disease similar to primary biliary cirrhosis because of its clinical and histologic characteristics but in whom there is a repeated absence of antimitochondrial antibodies and, by the contrary, the presence of antinuclear antibodies. The initial description of these cases was carried out in 1987. Good response was observed to treatment with glucocorticoids in these first cases and others described later. A series of 13 female patients with features of autoimmune cholangitis diagnosed from 1987 to 1993 in the Hospital Clinic i Provincial from Barcelona, Spain, is retrospectively reviewed. These patients were compared with 13 patients with primary biliary cirrhosis diagnosed on the basis of clinical and histologic criteria and the presence of antimitochondrial antibodies. No relevant clinical or histological differences were observed between the two groups of patients. Six patients with autoimmune cholangitis underwent treatment with glucocorticoids with unequal response, and in 5 cases ursodeoxycholic acid was administered with a slight analytical improvement being observed. According to these results and the current data of these patients, autoimmune cholangitis should be considered as a variety of primary biliary cirrhosis, the main characteristic of which would be the absence of antimitochondrial antibodies more than that of being a specific, independent disease.

Adult↗

PubMed1997

[Class I and II histocompatibility antigens and severity of the alcoholic liver lesion].

The association between the class I and class II histocompatibility antigens (HLA) and the severity of alcoholic liver disease was studied in 102 alcoholic patients (64 males and 38 females) with liver disease. According to histologic diagnosis 41 patients had a mild hepatic lesion (12 with minimum changes, 15 with steatosis and 14 with fibrosis) and 61 patients had severe hepatic lesion (13 with alcoholic hepatitis, 35 with cirrhosis and 13 with cirrhosis and alcoholic hepatitis). No differences were found between the two groups in regards to sex, quantity and length of alcohol consumption, although the patients with mild hepatic lesion were younger than those with severe hepatic lesion (41.2 +/- 8.2 and 47.8 +/- 11.6 years, respectively). The prevalence of the A30, B16, B47, Bw56, Cw1, Cw5 and Cw7 antigens was higher in the alcoholics than in the controls, although only the A30 (12.7% vs. 4.4%, p < 0.04) and the Bw56 antigens (3.9% vs 0.1%, p < 0.001) remained significant when the p value was corrected by the number of antigens studied. These differences were due to a greater prevalence of the A30 antigens (17.0% vs. 4.4%, p < 0.001), B16 (24.3% vs. 7.5%, p < 0.01) and Bw56 (7.3% vs 0.1%, p < 0.001) in patients with mild hepatic lesion versus the controls. In contrast, these antigens were present in similar numbers in patients with severe hepatic lesion and in the controls. On the other hand, no differences were observed regarding the prevalence of the class II HLA antigens between the alcoholics and the controls, or between the two alcoholic groups. These data suggest that the alcoholics with A30, B16 and Bw56 antigens are less susceptible to developing severe liver disease.

Adult↗

PubMed1997

Management of ascites in the patient with portal hypertension with emphasis on spontaneous bacterial peritonitis.

The reintroduction of paracentesis has modified the way in which patients with ascites are treated. Transjugular intrahepatic portosystemic shunt can be an alternative treatment for patients with refractory ascites and for those patients with hepatorenal syndrome, although more studies are needed to clarify its usefulness and safety. The use of more potent and less nephrotoxic antibiotics together with an earlier diagnosis have improved the outcome of patients with spontaneous bacterial peritonitis (SBP). Oral antibiotics can be used in patients with SBP and good clinical conditions with an efficacy similar to that obtained with intravenous antibiotics. Prophylactic antibiotics in SBP should be restricted to cirrhotic patients at high risk, including bleeding cirrhotic patients, those with a past history of SBP, and those with low protein content in ascitic fluid. This chapter describes the management of ascites in patients with portal hypertension.

Anti-Bacterial Agents↗

PubMed1997

Pulmonary abscess as a complication of transarterial embolization of multinodular hepatocellular carcinoma.

Hepatic transarterial embolization has been widely used in the treatment of hepatocellular carcinoma and other liver tumors. Despite being a safe treatment, some complications associated with this procedure have been described. The most frequent adverse effect of transarterial embolization is postembolization syndrome, whereas infections account for only 3.4% of complication. We report the first case of lung abscess as a complication of transarterial embolization used in the treatment of multinodular hepatocellular carcinoma.

Carcinoma, Hepatocellular↗