Mónica González

Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Barcino, Catalonia, Spain

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Publications (11)128.26 Total impact

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    ABSTRACT: Acute portal vein thrombosis (APVT) is a rare disorder that causes chronic portal hypertension if recanalization is not obtained. However, response to anticoagulation and long-term prognosis of APVT are not well-defined. Thirty-eight patients diagnosed with APVT between 1995 and 2003 from 5 Spanish referral hospitals, in whom cirrhosis and malignancy were specifically excluded, were included in this retrospective study. The response to anticoagulation therapy and development of portal hypertension-related complications during follow-up were evaluated. Mean follow-up was 43 months (range, 6-112 months). Recanalization occurred in 12 of 27 patients receiving anticoagulation versus 0 of 11 patients who did not receive anticoagulation (P = .008). Rates of recanalization were influenced by the precocity of heparin administration and the number of underlying prothrombotic conditions. Follow-up upper endoscopy performed in 29 patients disclosed gastroesophageal varices in 16 (55%). Varices appeared as early as 1 month after APVT. However, in most patients varices were detected in successive endoscopies, mainly during the first year. Two-year actuarial probability of variceal bleeding was 12% and for ascites 16%. Five-year survival was 87%. Mortality was related to the APVT episode in 2 cases and to an underlying hematologic disorder in one. Anticoagulation achieved recanalization in about 40% of patients. Most patients not achieving recanalization will develop gastroesophageal varices during follow-up. However, development of variceal bleeding and ascites is infrequent, and survival is satisfactory.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 12/2008; 6(12):1412-7. DOI:10.1016/j.cgh.2008.07.031 · 7.90 Impact Factor
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    ABSTRACT: The use of the hepatic venous pressure gradient (HVPG) to assess the efficacy of the pharmacological treatment of portal hypertension in cirrhosis is controversial. Our aim was to establish whether target HVPG reduction predicts variceal bleeding in cirrhotic patients receiving variceal bleeding prophylaxis. Data sources were MEDLINE, EMBASE, Cochrane Controlled Trials Register, citation lists, and abstracts (most recent search March 2006). Cohorts of patients on drug therapy from randomized and nonrandomized studies correlating variceal bleeding and HVPG change were used. Heterogeneity was explored by metaregression analysis. Ten studies totaling 595 patients undergoing two HVPG measurements were identified. The RR of bleeding was lower in patients achieving an overall (HVPG <or=12 mmHg or decrease >or=20%) (0.27, 95% CI 0.14-0.52), complete (HVPG <or=12 mmHg) (0.48, CI 0.28-0.81), or partial (HVPG decrease >or=20%) (0.41, CI 0.20-0.81) response, with significant heterogeneity. Regression analysis identified the interval between the HVPG measurements significantly associated with the RR of bleeding. Heterogeneity was no longer significant after exclusion of an outlier trial, which showed the longest interval to HVPG remeasurement and the lowest quality score. Even considering nonvaluable patients because of bleeding as HVPG responders, the RR of bleeding was lower in overall responders than in nonresponders (0.66, CI 0.51-0.86). Overall response was associated with lower liver-related mortality (RR 0.58, CI 0.37-0.91). Current evidence supports the validity of HVPG end points to monitor drug therapy efficacy for variceal bleeding prophylaxis. HVPG monitoring also provides valuable prognostic information.
    The American Journal of Gastroenterology 05/2007; 102(5):1116-26. DOI:10.1111/j.1572-0241.2007.01191.x · 10.76 Impact Factor
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    ABSTRACT: In cirrhosis, repeated flares of portal pressure and collateral blood flow provoked by postprandial hyperaemia may contribute to variceal dilation and rupture. To examine the effect of the extent of the collateral circulation on the postprandial increase in portal pressure observed in cirrhosis. The hepatic venous pressure gradient (HVPG), hepatic blood flow and azygos blood flow were measured in 64 patients with cirrhosis before and after a standard liquid meal. Peak increases in HVPG (median+14.9%), hepatic blood flow (median+25.4%), and azygos blood flow (median+32.2%) occurred at 30 min after the meal. Compared with patients with marked postprandial increase in HVPG (above the median, n = 32), those showing mild (<15%, n = 32) increase in HVPG had a higher baseline azygos flow (p<0.01) and underwent a greater postprandial increase in azygos flow (p<0.02). Hepatic blood flow increased similarly in both groups. Postprandial increases in HVPG were inversely correlated (p<0.001) with both baseline azygos flow (r = -0.69) and its postprandial increase (r = -0.72). Food intake increased nitric oxide products in the azygos (p<0.01), but not in the hepatic vein. Large varices (p<0.01) and previous variceal bleeding (p<0.001) were more frequent in patients with mild increase in HVPG. Postprandial hyperaemia simultaneously increases HVPG and collateral flow. The extent of the collateral circulation determines the HVPG response to food intake. Patients with extensive collateralisation show less pronounced postprandial increases in HVPG, but associated with marked flares in collateral flow. Collateral vessels preserve their ability to dilate in response to increased blood flow.
    Gut 02/2007; 56(2):259-64. DOI:10.1136/gut.2006.095240 · 14.66 Impact Factor
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    ABSTRACT: Meta-analysis designed to provide evidence-based guidance on the effect of TIPS and paracentesis on mortality and encephalopathy in cirrhotic patients with refractory ascites. Five randomized trials published between 1989 and 2005 were identified. The five trials involved 330 patients, and none included patients >76 years, with bilirubin >5-10 mg/dl or creatinine >3 mg/dl. Ascites recurrence was lower in the TIPS arm (RR 0.56; 95% CI 0.47-0.66). TIPS was associated with a greater risk of encephalopathy (RR 1.36; 95% CI 1.1-1.68) and severe encephalopathy (RR 1.72; 95% CI 1.14-2.58). TIPS did not affect mortality, as estimated by the RR (0.93; 95% CI 0.67-1.28, random effect model) and pooled hazard ratio (RR 1.09; 95% CI 0.84-1.88). Analysis of this outcome measure was limited by significant heterogeneity among trials. Liver-related mortality was homogenous and similar in both arms. Results were unaffected by excluding trials of lower quality or with a greater number of alcoholics. Meta-analysis of trials including patients with recidivant ascites revealed a lower mortality in the TIPS arm (RR 0.68; 95% CI 0.49-0.93). In patients with refractory ascites, a better control of ascites by TIPS does not translate into improved survival and worsens encephalopathy.
    Journal of Hepatology 01/2006; 43(6):990-6. DOI:10.1016/j.jhep.2005.06.005 · 11.34 Impact Factor

  • Hepatology 12/2003; 38:295-295. DOI:10.1016/S0270-9139(03)80331-2 · 11.06 Impact Factor
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    ABSTRACT: Spontaneous bacterial peritonitis (SBP) is frequently associated with renal failure. This study assessed if systemic and hepatic hemodynamics are also affected by this condition. Standard laboratory tests, tumor necrosis factor alpha (TNF-alpha) in plasma and ascitic fluid, plasma renin activity (PRA) and norepinephrine (NE), and systemic and hepatic hemodynamics were determined in 23 patients with SBP at diagnosis and after resolution of infection. Eight patients developed renal failure during treatment. At diagnosis of infection, patients developing renal failure showed significantly higher values of TNF-alpha, blood urea nitrogen (BUN), PRA and NE, peripheral vascular resistance, and hepatic venous pressure gradient (HVPG) and lower cardiac output than patients not developing renal failure. During treatment, a significant reduction in cardiac output and arterial pressure and increase in PRA and NE, HVPG, and Child-Pugh score were observed in the first group but not in the second. Peripheral vascular resistance remained unmodified in both groups. Changes in PRA and NE correlated inversely with changes in arterial pressure and directly with changes in BUN, Child-Pugh score, and HVPG. Five patients in the renal failure group developed encephalopathy, and 6 died. In the group without renal failure, none of the patients developed encephalopathy or expired. In conclusion, patients with SBP frequently develop a rapidly progressive impairment in systemic hemodynamics, leading to severe renal and hepatic failure, aggravation of portal hypertension, encephalopathy, and death. This occurs despite rapid resolution of infection and is associated with an extremely poor prognosis.
    Hepatology 12/2003; 38(5):1210-8. DOI:10.1053/jhep.2003.50447 · 11.06 Impact Factor
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    ABSTRACT: Intestinal bacterial overgrowth and translocation, both common in cirrhosis with ascites, may lead to the activation of monocytes and lymphocytes, increased levels of proinflammatory cytokines, and enhanced synthesis of nitric oxide present in cirrhosis. Bacterial endotoxin promotes the synthesis of lipopolysaccharide (LPS)-binding protein (LBP), and forms a LPS-LBP complex that binds to CD14. This study was designed to evaluate LBP levels and their correlation to the immune response and the hemodynamic status in cirrhotic patients. Plasma LBP, endotoxin, soluble CD14 (sCD14), cytokines, renin, nitrites, and systemic vascular resistance were determined before and 4 weeks after norfloxacin or placebo in 102 cirrhotic patients and 30 controls. LBP was elevated in 42% of ascitic cirrhotic patients (15.7 +/- 0.7 versus 6.06 +/- 0.5 microg/mL, P <.01). In 60% of high LBP patients, endotoxin was within normal range. Among ascitic patients, those with high LBP showed greater (P <.05) levels of sCD14, tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), nitrites + nitrates (NOx)/creatinine, and renin, and lower vascular resistance. In the cirrhotic patients with high LBP, norfloxacin normalized (P <.01) LBP (from 16.6 +/- 0.5 to 5.82 +/- 0.8 microg/mL) and sCD14; reduced the level of cytokines, NOx/creatinine, and renin; and increased vascular resistance; but lacked effect in patients with normal LBP. Portal pressure was unchanged after norfloxacin in another group of 18 cirrhotic patients with high and 19 with normal LBP. In conclusion, the subset of ascitic cirrhotic patients with marked immune and hemodynamic derangement is identified by increased LBP levels. Amelioration of these abnormalities by norfloxacin suggests the involvement of enteric bacteria or their products in the triggering of the process.
    Hepatology 01/2003; 37(1):208-17. DOI:10.1053/jhep.2003.50038 · 11.06 Impact Factor

  • Journal of Hepatology 04/2002; 36:44-44. DOI:10.1016/S0168-8278(02)80135-0 · 11.34 Impact Factor

  • Journal of Hepatology 04/2002; 36:44-44. DOI:10.1016/S0168-8278(02)80137-4 · 11.34 Impact Factor
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    ABSTRACT: Endoscopic therapy, involving either injection sclerosis or band ligation, is considered the intervention of first choice for acute variceal bleeding (AVB). Pharmacologic agents have also been shown to be highly effective in the control of the bleeding episode. The purpose of this meta-analysis was to assess whether vasoactive drugs may improve the efficacy of endoscopic therapy (injection sclerosis or band ligation) in the control of AVB and thus increase survival rates. Computer databases and scientific meeting abstracts from 1994 to 2001 were used to search for randomized trials that compared the combined use of endoscopic and drug therapy with endoscopic therapy alone in the control of AVB. Eight trials involving 939 patients fulfilled the selection criteria and the following evaluated by standard meta-analysis methods: initial hemostasis, 5-day hemostasis, 5-day mortality, and adverse events. Combined treatment improved initial control of bleeding (relative risk [RR], 1.12; 95% confidence interval (CI), 1.02-1.23), and 5-day hemostasis (RR, 1.28; 95% CI, 1.18-1.39), with numbers of patients needed to treat (NNT) of 8 and 5, respectively. The difference in favor of combined treatment remained significant when trials that used drugs other than octreotide or that included a low proportion of alcoholic patients (<40%) or high-risk cirrhotic patients (<35%) were excluded. Mortality was not significantly decreased by combined therapy (RR, 0.73; 95% CI, 0.45-1.18). Severe adverse events were similar in both groups. In conclusion, in patients with AVB, pharmacologic agents improve the efficacy of endoscopic therapy to achieve initial control of bleeding and 5-day hemostasis, yet fail to affect mortality.
    Hepatology 04/2002; 35(3):609-15. DOI:10.1053/jhep.2002.31354 · 11.06 Impact Factor
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    ABSTRACT: It has been suggested that losartan, an angiotensin II (A-II) type 1 receptor blocker, may have a pronounced portal pressure reducing effect, far greater than that of propranolol. This randomized controlled trial compared the hemodynamic and renal effects of continued 6-week administration of losartan (n = 25) vs. propranolol (n = 15) in portal hypertensive patients with cirrhosis treated endoscopically after a variceal bleeding episode. Hepatic venous pressure gradient (HVPG), systemic hemodynamics, renal function, and vasoactive factors were measured before and at 6 weeks of treatment. Losartan did not reduce HVPG (-2% +/- 12%, NS) but significantly decreased mean arterial pressure (MAP, -8% +/- 10%, P = 0.001). On the contrary, propranolol significantly reduced HVPG (-10% +/- 11%, P = 0.003) and cardiac output (-16% +/- 12%, P = 0.001) but did not modify MAP (2.5% +/- 10%, NS). Losartan increased A-II levels, reduced aldosterone, and decreased glomerular filtration rate (GFR) in Child B patients. Propranolol did not modify renal function. Adverse events related to therapy were mild and similar in both groups. Unlike propranolol, long-term losartan administration does not significantly reduce HVPG in patients with cirrhosis treated after a variceal bleeding episode, and it caused hypotension and reduced GFR in patients with moderate liver failure. Therefore, losartan is not an alternative to propranolol in preventing variceal rebleeding.
    Gastroenterology 08/2001; 121(2):382-8. DOI:10.1053/gast.2001.26288 · 16.72 Impact Factor

Publication Stats

1k Citations
128.26 Total Impact Points


  • 2008
    • Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas
      Barcino, Catalonia, Spain
  • 2003-2007
    • Hospital Universitario Ramón y Cajal
      • Departamento de Medicina Interna
      Madrid, Madrid, Spain
  • 2002
    • University of Alcalá
      Cómpluto, Madrid, Spain
    • Complutense University of Madrid
      • Department of Medicine
      Madrid, Madrid, Spain