Quiroga, J. (Jorge)

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    Risk factors for recurrence of hepatitis C after liver transplantation.
    (Wiley-Blackwell, 1998) Civeira, M.P. (María Pilar); Peña, A. (Andrés) de la; Álvarez-Cienfuegos, J. (Javier); Sola, J. (Josu); Sangro, B. (Bruno); Prieto, J. (Jesús); Herrero, J.I. (José Ignacio); Garcia, N. (Nicolás); Quiroga, J. (Jorge)
    Recurrent hepatitis C is a frequent complication after liver transplantation for hepatitis C virus– related cirrhosis, but risk factors related to its development remain ill defined. Twenty-three patients receiving a primary liver graft for hepatitis C virus–related cirrhosis and with an assessable biopsy performed at least 6 months after liver transplantation were studied retrospectively. The end point of this study was to look for risk factors associated with the development of histologic hepatitis C in the graft. Thirty-six major variables were studied, and those reaching significance by univariate analysis were included in a multivariate analysis. Eighteen patients (78%) developed posttransplant hepatitis C. On univariate analysis, six variables showed significant predictive value: increased immunosuppression for treatment of acute rejection; pretransplant hepatocellular carcinoma; cumulative doses of prednisone at 3, 6, and 12 months after transplantation; and mean blood trough levels of cyclosporine in the first 6 months posttransplantation. On multivariate analysis, two variables retained independent statistical significance as predictors of hepatitis C recurrence, namely receipt of antirejection therapy (P 5 .0087) and lower mean cyclosporine levels in the first 6 months after transplantation (P 5 .0134). Therefore, recurrence of hepatitis C after liver transplantation seems to be at least partially related to posttransplantation immunosuppressive therapy.
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    Concurrent clarithromycin and cyclosporin A treatment
    (Oxford University Press, 1998) Álvarez-Cienfuegos, J. (Javier); Lopez-de-Ocariz, A. (A.); Sadaba, B. (Belén); Quiroga, J. (Jorge); Azanza, J.R. (José Ramón)
    Although macrolides have been associated with significant pharmacokinetic interactions, clarithromycin is considered to have a low interaction capacity. In this study, six transplant recipients treated with cyclosporin A also received clarithromycin. In all patients, the dose of cyclosporin A had to be reduced by a mean of 33% per day depending on the macrolide dose. Normalization of the dosage parameters began on the fourth day after stopping clarithromycin treatment. Co-administration of cyclosporin A and clarithromycin may lead to increases in whole blood cyclosporin levels, and appropriate dose reductions should be considered.
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    Liver transplantation in cirrhotic patients with diabetes mellitus: Midterm results, survival, and adverse events
    (Wiley-Blackwell, 2001) Pardo, F. (Fernando); Álvarez-Cienfuegos, J. (Javier); Gomez-Manero, N. (Noemí); Sangro, B. (Bruno); Prieto, J. (Jesús); Herrero, J.I. (José Ignacio); Quiroga, J. (Jorge); Blanco, J.J. (Jose J.)
    Liver cirrhosis is frequently associated with diabetes mellitus (DM), and this metabolic complication is also frequent after orthotopic liver transplantation (OLT). The aim of our study is to investigate which factors are associated with DM before and after OLT and their impact on post-OLT evolution. We evaluated the prevalence of DM among 115 liver transplant candidates with cirrhosis and assessed their evolution after OLT (median follow-up, 41 months). Sixteen candidates had DM requiring pharmacological therapy (group A), 45 candidates had DM controlled with diet (group B), and 54 candidates did not have DM (group C). One-year and 3-year actuarial survival rates were 100% and 100% for group A, 91% and 85% for group B, and 77% and 74% for group C, respectively (P <.03). Post-OLT DM was more frequent in group A. The incidence of other metabolic complications, major infections, rejection, and arterial hypertension; the need for hospitalization; and renal and graft function of patients in groups A, B, and C were similar. The only risk factor for DM 1 year after OLT on multivariate analysis was pre-OLT DM requiring pharmacological treatment. The incidence of complications, need for hospitalization, and renal and graft function 1 year after OLT for patients with post-OLT DM were similar to those of patients without post-OLT DM. In conclusion, patients with cirrhosis who have DM have a greater risk for post-OLT DM, but their midterm survival is not worse than the survival of those without DM.
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    Factors related to increased resting energy expenditure in men with liver cirrhosis
    (2016) Prieto-Frías, C. (Cesár); Conchillo, M. (M.); Payeras, M. (Marina); Iñarrairaegui, M. (Mercedes); D'Avola, D. (Delia); Frühbeck, G. (Gema); Salvador, J. (Javier); Rodriguez, M. (Macarena); Richter, J.A. (José Ángel); Mugueta, C. (Carmen); Gil-Maria, J. (Jesús); Herrero, I. (Ignacio); Prieto, J. (Jesús); Sangro, B. (Bruno); Quiroga, J. (Jorge)
    Objective Hypermetabolism in cirrhosis is associated with a high risk of complications and mortality. However, studies about underlying mechanisms are usually focussed on isolated potential determinants and specific etiologies, with contradictory results. We aimed at investigating differences in nutrition, metabolic hormones, and hepatic function between hypermetabolic and nonhypermetabolic men with cirrhosis of the liver. Patients and methods We prospectively enrolled 48 male cirrhotic inpatients. We evaluated their resting energy expenditure (REE) and substrate utilization by indirect calorimetry, body composition by dual-energy X-ray absorptiometry, liver function, and levels of major hormones involved in energy metabolism by serum sample tests. Patients with ascites, specific metabolic disturbances, and hepatocellular carcinoma were excluded. Results REE and REE adjusted per fat-free mass (FFM) were significantly increased in cirrhotic patients. Overall, 58.3% of cirrhotic patients were classified as hypermetabolic. Groups did not differ significantly in age, etiology of cirrhosis, liver function, presence of ascites, use of diuretics, β-blockers, or presence of transjugular intrahepatic portosystemic shunts. Hypermetabolic cirrhotic patients had lower weight, BMI (P< 0.05), nonprotein respiratory quotient (P< 0.01), leptin (P<0.05), and leptin adjusted per fat mass (FM) (P<0.05), but higher FFM% (P< 0.05) and insulin resistance [homeostatic model assessment-insulin resistance (HOMA-IR)] (P<0.05). Only HOMA-IR, leptin/FM, and FFM% were independently related to the presence of hypermetabolism. Conclusion Hypermetabolic cirrhotic men are characterized by lower weight, higher FFM%, insulin resistance, and lower leptin/FM when compared with nonhypermetabolic men. HOMA-IR, FFM%, and leptin/FM were independently associated with hypermetabolism, and may serve as easily detectable markers of this condition in daily clinical practice
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    Renal hemodynamics and the renin-angiotensin system in cirrhosis
    (Consejo Superior de Investigaciones Científicas, 1989) Aliaga, L. (Luis); Richter, J.A. (José Ángel); Prieto, J. (Jesús); Quiroga, J. (Jorge); Zozaya, J.M. (José Manuel)
    The interrelationship between renal hemodynamics and the renin-angiotensin-aldosterone system in 28 nonazotemic cirrhotic patients has been studied. Patients were divided into three groups: A) Patients without ascites nor edema; B) Patients with ascites and a relatively high sodium excretion (41.9 ± 12.9 mmol/day); and C) Patients with ascites and very low sodium excretion (4.8 ± 0.6 mmol/day). Renin and aldosterone levels significantly increased in group C. A significant correlation was observed between plasma aldosterone concentration and urinary sodium excretion, and between plasma renin activity and aldosterone levels. There were no significant differences in urine flow, glomerular filtration rate, effective renal plasma flow, or renal blood flow between the three groups of patients, in spite of marked differences in renin and aldosterone levels. Renal perfusion was not related to plasma renin activity either in the overall sample of patients or in the individual groups. These results show that factors other than total renal perfusion are involved in renin secretion in cirrhosis.
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    Tratamiento de la cirrosis biliar primaria con ácido ursodesoxicólico. Resultados a corto y medio plazo y relación con el estudio de la enfermedad
    (The Spanish Society of Digestive Pathology, 1991) Conchillo, F. (F.); Garcia-Villarreal, L. (Luis); Prieto, J. (Jesús); Macias, E. (Elena); Garcia-Gonzalez, N. (Nicolás); Quiroga, J. (Jorge); Zozaya, J.M. (José Manuel)
    We present the results of the treatment with ursodeoxycholic acid (UDCA, 7-9 mg/kg body weight daily) of 17 patients with primary biliary cirrhosis (8 in stages I-II; 9 in stages III-IV). At two months the mean values of alkaline phosphatase, gammaglutamiltranspeptidase, alanine and aspartate aminotransferase were reduced (p less than 0.001, p less than 0.001, p less than 0.01 and p less than 0.01 respectively). This improvement persisted without increase during the first year. At two months the total bilirubin value was reduced (p less than 0.01) associated with a reduction in the conjugated fraction (p less than 0.05). Cholesterol and gammaglobulin mean values also decreased at two months (p less than 0.05). We found no changes in IgM levels and antimitochondrial antibody titers. The improvement was similar in both groups (early I-II and advanced III-IV stages) and the treatment showed no undesirable effects either in early or advanced stages. Almost all the patients with pruritus (6 out of 7) improved with the treatment and the use of cholestyramine was reduced in all
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    Infección aguda por el VHB
    (Gobierno de Navarra. Departamento de Salud, 2004) Alegre, F. (Félix); Moreno, D. (D.); Quiroga, J. (Jorge)
    The clinical spectrum of acute hepatitis B virus infection is very broad, with clinical manifestations that range from anicteric and sub-clinical hepatitis to severe acute icteric hepatitis and even, in some cases, to fulminant hepatitis. Diagnosis depends to a large extent on the degree of clinical suspicion of hepatitis, establishing the aetiological origin of the B virus through the study of serological markers and/or DNA in the blood. Although in the majority of cases there is a favourable evolution of acute hepatitis B virus infection, with spontaneous resolution of the clinical manifestations in 4-8 weeks, progression to chronic hepatitis is not unusual in certain cases, above all in infancy. No specific treatment exists for acute hepatitis B virus infection that would reduce its severity or prevent its evolution into chronic hepatitis. However, relative rest and the administration of an hypercaloric diet are recommended. In cases of severe acute hepatitis hospital admission should be recommended; in cases of fulminant hepatitis, admission to the intensive care unit for intensive monitoring and evaluation of a liver transplantation is recommended if spontaneous improvement does not occur. This paper reviews briefly the clinical manifestations, diagnosis, prognosis and treatment of acute hepatitis B virus infection.
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    Hepatic encephalopathy after liver transplantation in a patient with a normally functioning graft: Treatment with embolization of portosystemic collaterals
    (Wiley-Blackwell, 2009) Alegre, F. (Félix); Pardo, F. (Fernando); Iñarrairaegui, M. (Mercedes); Bilbao, J.I. (José I.); Herrero, J.I. (José Ignacio); Quiroga, J. (Jorge); Diaz-Dorronsoro, L. (Lourdes)
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    Zolmitriptan: a novel portal hypotensive agent which synergizes with propranolol in lowering portal pressure
    (Public Library of Science, 2013) Banales, J.M. (Jesús M.); Alegre, F. (Félix); Chang, H.C.Y. (Haisul C. Y.); Rodriguez-Ortigosa, C.M. (Carlos M.); Garcia, M. (Mónica); Sangro, B. (Bruno); Roboredo, M. (Mercedes); Prieto, J. (Jesús); Herrero, J.I. (José Ignacio); Moran, M.A. (María Asunción); Perez-Vizcaino, F. (Francisco); Barbero, R. (Roberto); Quiroga, J. (Jorge); Carreño, N. (N.)
    OBJECTIVE: Only a limited proportion of patients needing pharmacological control of portal hypertension are hemodynamic responders to propranolol. Here we analyzed the effects of zolmitriptan on portal pressure and its potential interaction with propranolol. METHODS: ZOLMITRIPTAN, PROPRANOLOL OR BOTH WERE TESTED IN TWO RAT MODELS OF PORTAL HYPERTENSION: common bile duct ligation (CBDL) and CCl4-induced cirrhosis. In these animals we measured different hemodynamic parameters including portal venous pressure, arterial renal flow, portal blood flow and cardiac output. We also studied the changes in superior mesenteric artery perfusion pressure and in arterial wall cAMP levels induced by zolmitriptan, propranolol or both. Moreover, we determined the effect of splanchnic sympathectomy on the response of PVP to zolmitriptan. RESULTS: In both models of portal hypertension zolmitriptan induced a dose-dependent transient descent of portal pressure accompanied by reduction of portal flow with only slight decrease in renal flow. In cirrhotic rats, splanchnic sympathectomy intensified and prolonged zolmitriptan-induced portal pressure descent. Also, propranolol caused more intense and durable portal pressure fall when combined with zolmitriptan. Mesenteric artery perfusion pressure peaked for about 1 min upon zolmitriptan administration but showed no change with propranolol. However propranolol enhanced and prolonged the elevation in mesenteric artery perfusion pressure induced by zolmitriptan. In vitro studies showed that propranolol prevented the inhibitory effects of β2-agonists on zolmitriptan-induced vasoconstriction and the combination of propranolol and zolmitriptan significantly reduced the elevation of cAMP caused by β2-agonists. CONCLUSION: Zolmitriptan reduces portal hypertension and non-selective beta-blockers can improve this effect. Combination therapy deserves consideration for patients with portal hypertension failing to respond to non-selective beta-blockers.
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    Increased concentrations of tumor necrosis factor and interleukin-6 contribute to the hemostatic abnormalities in advanced liver disease
    (Karger, 1995) Paramo, J.A. (José Antonio); Rifon, J. J. (Jose J.); Rocha, E. (Eduardo); Sangro, B. (Bruno); Quiroga, J. (Jorge); Prosper-Cardoso, F. (Felipe)
    Abnormal cytokine levels have been described in patients with chronic liver disease, but studies correlating cytokine homeostasis with abnormalities in coagulation and fibrinolysis are lacking. In order to establish a link between cytokines and the hemostatic changes the following parameters were determined in 44 patients with cirrhosis (alcoholic = 15, postnecrotic = 22, others = 7): TNF-alpha, IL-6, thrombin-antithrombin (TAT) complexes, prothrombin fragment 1 + 2 (F1 + 2) and t-PA by using enzyme-linked immunosorbent assays, and PAI-1, plasminogen and alpha 2-antiplasmin (alpha 2-AP) by using chromogenic substrates. All patients were at stages B and C of Child's classification when entering the study. Mean cytokine concentrations were significantly higher in cirrhotic patients as compared to age- and sex-matched controls (p < 0.009). There was a significant increase of TAT (p < 0.02) and F1 + 2 (p < 0.001) in the patients groups, suggesting a grade of intravascular coagulation. A hyperfibrinolytic state as demonstrated by an increase of t-PA and decrease of plasminogen and alpha 2-AP was also observed (p < 0.001). We could define a subgroup of patients with cytokine values higher than 20 pg/ml. Interestingly, in this group there was a significant increase of TAT (p < 0.04) and t-PA (p < 0.02) levels and a decrease of plasminogen and alpha 2-AP (p < 0.02) as compared to values observed in patients with cytokines lower than 20 pg/ml. We conclude that high levels of TNF-alpha and IL-6 may contribute to hyperfibrinolysis and intravascular coagulation in patients with liver cirrhosis, as assessed by the increase of TAT and t-PA levels and the reduction of plasminogen and alpha 2-AP.