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El modelo de Estado federal, posee múltiples diferencias sustanciales que le distinguen de otros modelos de Estado tradicionales, principalmente porque posee una estructura dual basada en la división del poder político, con la finalidad de dotar de mayor soberanía a los Estados que lo conforman, especialmente en lo que respecta al sistema electoral y su exclusividad legislativa. En este contexto, se destaca la cláusula de comercio, que, en su defecto, sí limita la autonomía de dichos Estados, en cuanto a las relaciones mercantiles, porque las somete a un control federal. Por lo cual, el objetivo del presente trabajo fue analizar la estructura dual del federalismo, especialmente con respecto de la cláusula de comercio, para poder determinar que la autonomía de los Estados, se ve supeditada a un control federal. La metodología que se empleó fue: Método deductivo, alcance descriptivo, a través de un enfoque cualitativo por ser de tipo post-positivista, por la interpretación hermenéutica de los documentos examinados. Se concluye que, la “commerce clause”, es un elemento caracterizador del federalismo, no obstante, constituye una limitación a la autonomía de los Estados Federados, puesto que somete las relaciones mercantiles a un control federal, por tal motivo, restringe el principio de soberanía.

Vasopressin receptor-mediated vasoconstriction is considered to be involved in the pathogenesis of organ failure in acute-on-chronic liver failure (ACLF). We studied the association between six single nucleotide polymorphisms (SNPs) of the vasopressin 1a receptor gene and the development of organ failure in 826 patients admitted for acute decompensation of liver cirrhosis (n=641) or ACLF (n=185). No associations were found for SNPs with the presence of circulatory or renal failure. A C>T mutation in SNP rs7308855 and a T>A mutation in SNP rs7298346 showed an association with the presence of coagulation failure in the entire population (n=61, P=0.024 and 0.060, respectively) and in the subgroup of patients with ACLF (n=44, P=0.081 and 0.056, respectively). Genetic variation in the vasopressin 1a receptor was found not to be associated with circulatory or renal failure, but with the presence of coagulation failure in patients with acute decompensation of liver cirrhosis and ACLF.

Palatal fistula after the repair of cleft palate appears in 7.7-35% of patients. We present two cases of palatal fistula, detailing a multi-layer repair with an interpositional collagen graft.Patient 1: girl with a cleft palate operated using a Furlow technique. A reintervention was performed due to a Pittsburgh type III fistula. Patient 2: male with cleft palate operated using a Furlow technique. A reintervention was performed due to a type V fistula.We used a multilayer repair with a local rotational flap and the interposition of a collagen matrix between the nasal and oral layers. The suture was reinforced with a fibrin hemostatic adhesive. No recurrence of the fistula after 2 years.The three-layer closure is simple, safe, effective and avoids refistulizations. Interpositional grafts of a resorbable collagen membrane provide a "scaffold" for tissue growth, revascularization and epithelialization of the mucosa.La fístula palatina tras la reparación del paladar fisurado aparece en un 7,7-35% de pacientes. Presentamos dos casos de fístula palatina, detallando la técnica de reparación multicapa con injerto interposicional de colágeno.Paciente 1: niña con fisura de paladar blando, operada mediante técnica de Furlow. Se programa reintervención por fístula secundaria tipo III de Pittsburgh. Paciente 2: varón con fisura de paladar blando, operado mediante técnica de Furlow. Se programa reintervención por fístula secundaria tipo V.Reparación multicapa mediante flap rotacional y matriz de colágeno entre las capas nasal y oral. Refuerzo con adhesivo hemostático de fibrina. Ausencia de recidiva tras 2 años de seguimiento.El cierre en tres capas es sencillo y efectivo a la hora de evitar refistulizaciones. Los injertos interposicionales de membrana reabsorbible de colágeno proporcionan un “andamio” para el crecimiento de los tejidos, revascularización y epitelialización de la mucosa.

Hepatorenal syndrome (HRS) is a serious complication of end-stage liver disease, occurring mainly in patients with advanced cirrhosis and ascites, who have marked circulatory dysfunction,1 as well as in patients with acute liver failure.2 In spite of its functional nature, HRS is associated with a poor prognosis,3 4 and the only effective treatment is liver transplantation. During the 56th Meeting of the American Association for the Study of Liver Diseases, the International Ascites Club held a Focused Study Group (FSG) on HRS for the purpose of reporting the results of an international workshop and to reach a consensus on a new definition, criteria for diagnosis and recommendations on HRS treatment. A similar workshop was held in Chicago in 1994 in which standardised nomenclature and diagnostic criteria for refractory ascites and HRS were established.5 The introduction of innovative treatments and improvements in our understanding of the pathogenesis of HRS during the previous decade led to an increasing need to undertake a new consensus meeting. This paper reports the scientific rationale behind the new definitions and recommendations. The international workshop included four issues debated by four panels of experts (see Acknowledgements). The issues were: (1) evidence-based HRS pathogenesis; (2) treatment of HRS using vasoconstrictors; (3) other HRS treatments using transjugular intrahepatic portosystemic stent-shunt (TIPS) and extracorporeal albumin dialysis (ECAD); and (4) new definitions and diagnostic criteria for HRS and recommendations for its treatment.

Background & Aims: Acute-on-chronic liver failure (ACLF) is a frequent syndrome (30% prevalence), characterized by acute decompensation of cirrhosis, organ failure(s) and high short-term mortality. This study develops and validates a specific prognostic score for ACLF patients. Methods: Data from 1349 patients included in the CANONIC study were used. First, a simplified organ function scoring system (CLIF Consortium Organ Failure score, CLIF-C OFs) was developed to diagnose ACLF using data from all patients. Subsequently, in 275 patients with ACLF, CLIP-C OFs and two other independent predictors of mortality (age and white blood cell count) were combined to develop a specific prognostic score for ACLF (CLIF Consortium ACLF score [CLIF-C ACLFs]). A concordance index (C-index) was used to compare the discrimination abilities of CLIF-C ACLF, MELD, MELD-sodium (MELD-Na), and Child-Pugh (CPs) scores. The CLIF-C ACLFs was validated in an external cohort and assessed for sequential use. Results: The CLIF-C ACLFs showed a significantly higher predictive accuracy than MELDs, MELD-Nas, and CPs, reducing (19-28%) the corresponding prediction error rates at all main time points after ACLF diagnosis (28, 90, 180, and 365 days) in both the CANONIC and the external validation cohort. CLIF-C ACLFs computed at 48 h, 3-7 days, and 8-15 days after ACLF diagnosis predicted the 28-day mortality significantly better than at diagnosis. Conclusions: The CLIF-C ACLFs at ACLF diagnosis is superior to the MELDs and MELD-Nas in predicting mortality. The CLIP-C ACLFs is a clinically relevant, validated scoring system that can be used sequentially to stratify the risk of mortality in ACLF patients. (C) 2014 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Introduction: Hyponatremia is a marker of poor prognosis in patients with cirrhosis. This analysis aimed to assess if hyponatremia also has prognostic value in patients with acute-on-chronic liver failure (ACLF), a syndrome characterized by acute decompensation of cirrhosis, organ failure(s) and high short-term mortality. Methods: We performed an analysis of the Chronic Liver Failure Consortium CANONIC database in 1,341 consecutive patients admitted to 29 European centers with acute decompensation of cirrhosis (including ascites, gastrointestinal bleeding, hepatic encephalopathy, or bacterial infections, or any combination of these), both with and without associated ACLF (301 and 1,040 respectively). Results: Of the 301 patients with ACLF, 24.3% had hyponatremia at inclusion compared to 12.3% of 1,040 patients without ACLF (P, SCOPUS: ar.j, info:eu-repo/semantics/published

BACKGROUND & AIMS: Patients with cirrhosis hospitalized for an acute decompensation (AD) and organ failure are at risk for imminent death and considered to have acute-on-chronic liver failure (ACLF). However, there are no established diagnostic criteria for ACLF, so little is known about its development and progression. We aimed to identify diagnostic criteria of ACLF and describe the development of this syndrome in European patients with AD.METHODS: We collected data from 1343 hospitalized patients with cirrhosis and AD from February to September 2011 at 29 liver units in 8 European countries. We used the organ failure and mortality data to define ACLF grades, assess mortality, and identify differences between ACLF and AD. We established diagnostic criteria for ACLF based on analyses of patients with organ failure (defined by the chronic liver failure-sequential organ failure assessment [CLIF-SOFA] score) and high 28-day mortality rate (>15%).RESULTS: Of the patients assessed, 303 had ACLF when the study began, 112 developed ACLF, and 928 did not have ACLF. The 28-day mortality rate among patients who had ACLF when the study began was 33.9%, among those who developed ACLF was 29.7%, and among those who did not have ACLF was 1.9%. Patients with ACLF were younger and more frequently alcoholic, had more associated bacterial infections, and had higher numbers of leukocytes and higher plasma levels of C-reactive protein than patients without ACLF (P < .001). Higher CLIF-SOFA scores and leukocyte counts were independent predictors of mortality in patients with ACLF. In patients without a prior history of AD, ACLF was unexpectedly characterized by higher numbers of organ failures, leukocyte count, and mortality compared with ACLF in patients with a prior history of AD.CONCLUSIONS: We analyzed data from patients with cirrhosis and AD to establish diagnostic criteria for ACLF and showed that it is distinct from AD, based not only on the presence of organ failure(s) and high mortality rate but also on age, precipitating events, and systemic inflammation. ACLF mortality is associated with loss of organ function and high leukocyte counts. ACLF is especially severe in patients with no prior history of AD.

Hyponatraemia is common in patients with advanced cirrhosis and is associated with remarkable changes in brain cells, particularly a reduction in myoinositol and other intracellular organic osmolytes related to the hypo-osmolality of the extracellular fluid. It has been recently suggested that hyponatraemia may be an important factor associated with the development of overt hepatic encephalopathy (HE). To test this hypothesis, we retrospectively analysed the incidence and predictive factors of overt HE using a database of 70 patients with cirrhosis included in a prospective study comparing transjugular intrahepatic portosystemic shunts (TIPS) vs large-volume paracentesis in the management of refractory of ascites. Variables used in the analysis included age, sex, previous history of HE, treatment assignment (TIPS vs large volume paracentesis plus albumin), treatment with diuretics, serum bilirubin, serum creatinine and serum sodium concentration. Laboratory parameters were measured at entry, at 1 month and every 3 months during follow-up and at the time of development of HE in patients who developed this complication. During a mean follow-up of 10 months, 50 patients (71%) developed 117 episodes of HE. In the whole population of patients, the occurrence of HE was independently associated with serum hyponatraemia, serum bilirubin and serum creatinine. In conclusion, in patients with refractory ascites, the occurrence of HE is related to the impairment of liver and renal function and presence of hyponatraemia.

To investigate whether albumin can be substituted by less expensive plasma expanders in cirrhotic patients with tense ascites treated with total paracentesis, 88 patients (16 with renal failure) submitted to this therapeutic procedure were randomly assigned to receive IV albumin (43 patients) or dextran-70. Both substances were given at a dose of 8 g/L of ascitic fluid removed. Patients were discharged from the hospital with diuretics, and cases developing tense ascites during follow-up were treated according to their initial schedule. Total paracentesis was effective in eliminating the ascites in all but two cases in each group. Neither paracentesis plus IV albumin infusion nor paracentesis plus IV dextran-70 infusion was associated with significant changes in renal and hepatic function or serum electrolytes. The incidence of renal impairment (one case in each group), hyponatremia (three and four cases, respectively), and other complications (hepatic encephalopathy, gastrointestinal hemorrhage, bacterial infections) after paracentesis, and the clinical course of the disease as estimated by the probability of readmission to hospital during follow-up, causes of readmission, probability of survival, and causes of death were similar in the two groups of patients. The effect of paracentesis on effective intravascular volume was indirectly assessed by measuring plasma renin activity and aldosterone concentration before and 2 and 6 days after treatment, the patients being without diuretics. In patients treated with albumin, no significant changes in renin and aldosterone were observed during the entire period of observation. In contrast, both parameters increased significantly on the 6th day of treatment in patients receiving dextran-70. A significant increase in plasma renin activity and aldosterone concentration (30% over baseline values) was observed in 51% of patients treated with dextran-70 and in only 15% of those treated with albumin (x2 = 10.4; P = 0.0012). These results indicate that although dextran-70 is less efficacious than albumin in protecting cirrhotic patients treated with total paracentesis from the decrease in effective intravascular volume, it appears to be capable of preventing the renal and electrolyte complications induced by this therapeutic procedure.

In the current study digoxin-like immunoreactivity (DLIA), Na-K-ATPase inhibition and natriuretic activity of urinary extracts from 10 healthy volunteers following a low and a high-sodium intake, respectively, were measured. Detectable urinary DLIA (46.1 +/- 5.6 ng eq digoxin/day), Na-K-ATPase inhibition (182.9 +/- 22.7 nmol eq oub/day) and natriuretic activity (UNaV: 0.38 +/- 0.11 microEq/min) were observed during the low-sodium diet period in all subjects. High-sodium diet was associated with a significant increase in DLIA (87.9 +/- 9.2 ng eq digoxin/day, p less than 0.001) which parallelled changes in Na-K-ATPase inhibition (359.8 +/- 51.9 nmol eq oub/day, p less than 0.005) and natriuretic activity (UNaV: 1.33 +/- 0.3 microEq/min, p less than 0.025). These results support the contention that DLIA is related to NH.

To investigate whether paracentesis could be an alternative therapy for ascites, 117 cirrhotics with tense ascites were randomly allocated into two groups. Fifty-eight patients (group 1) were treated with paracentesis (4-6 L/day until disappearance of ascites) and intravenous albumin infusion (40 g after each tap). Fifty-nine patients (group 2) were treated with spironolactone (200-400 mg/day) plus furosemide (40-240 mg/day). Patients from group 2 not responding to diuretics were treated with a LeVeen shunt. After disappearance of ascites, patients from both groups were discharged from hospital and were instructed to take diuretics. Patients developing tense ascites during follow-up were readmitted to hospital and treated according to their initial schedule. Paracentesis was effective in eliminating the ascites in 56 patients from group 1 (96.5%) and did not induce significant changes in renal and hepatic function, plasma volume, cardiac index, peripheral resistance, plasma renin activity, plasma norepinephrine and antidiuretic hormone concentration, and urinary excretion of prostaglandin E2 and 6-keto-prostaglandin F1 alpha. Diuretics were effective in eliminating the ascites in 43 patients from group 2 (72.8%) (p less than 0.05). Ten patients in group 1 and 36 in group 2 developed complications during their first hospital stay (p less than 0.001). This difference was due to the significantly higher incidence of hepatic encephalopathy, renal impairment, and electrolyte disturbances occurring in patients treated with diuretics. The duration of hospital stay was 11.7 +/- 1.5 days for patients from group 1 and 31 +/- 2.8 days for patients from group 2 (p less than 0.001). The two groups did not differ significantly with respect to the probability of requiring readmission to hospital during follow-up, reasons for readmission, survival probability after entry into the study, and causes of death. These results indicate that paracentesis associated with intravenous albumin infusion is a fast, effective, and safe therapy for ascites in patients with cirrhosis.

The medical treatment of ascites in cirrhosis is based on sodium restriction and the administration of diuretics. Because the natriuretic potency of spironolactone is greater than that of loop diuretics (i.e., furosemide) in patients with marked sodium retention, spironolactone is the basic drug for the treatment of ascites. The simultaneous administration of spironolactone and furosemide increases the natriuretic effect of each drug and diminishes their effects on potassium metabolism. Recent studies indicate that large-volume paracentesis associated with intravenous albumin infusion is more effective than diuretic therapy in eliminating the ascitic fluid; is associated with a lower incidence of complications (hepatic encephalopathy, renal impairment, and hyponatremia); and considerably reduces the duration of hospital stay. Therapeutic paracentesis associated with intravenous albumin infusion is therefore the treatment of choice for cirrhotic patients with tense ascites. The mobilization of the ascitic fluid by paracentesis without plasma volume expansion is constantly associated with a deterioration of effective circulating blood volume and may induce renal impairment and severe hyponatremia. Dextran 70 and polygeline appear as effective as albumin in preventing these abnormalities. Cirrhotic patients treated with paracentesis require the administration of diuretics to avoid reaccumulation of ascites. Peritoneovenous shunt, a prosthesis capable to correct most abnormalities involved in the accumulation of fluid in the abdominal cavity, is an effective treatment of ascites in cirrhosis. It is especially indicated in patients who do not respond to diuretics and develop repeated episodes of ascites despite adequate treatment. The use of peritoneovenous shunting is limited by the high incidence of complications induced by the procedure, however. In addition, approximately 40% of patients develop an obstruction of the prosthesis within the first postoperative year.

The accumulation of ascites in cirrhosis has been classically attributed to the transudation of fluid from the splanchnic vascular bed to the peritoneal cavity due to the presence of portal hypertension. This transudation of fluid would induce hypovolemia responsible for the renal abnormalities frequently observed in these patients. Recent studies, however, indicate that the pathophysiology of ascites in cirrhosis is far more complex. Cirrhotic patients with ascites usually have profound disturbances in systemic hemodynamics and renal function and an activation of the endogenous vasoactive systems that contribute to the formation of ascites. In the present article the pathogenesis of these disturbances and their possible contribution to the formation of ascites are discussed.

During the XXII Congress of the Spanish Association for the Study of the Liver a questionnaire was distributed with the aim of describing the current therapeutic attitude of those attending the meeting, concerning two of the most frequent complications of cirrhosis: ascites and spontaneous bacterial peritonitis (SBP). One hundred twelve of the 135 physicians who answered the questionnaire (83%) use to treat tense ascites by therapeutic paracentesis, while 86 physicians (63.7%) managed moderate ascites with diuretics, with spironolactone being the drug most commonly used (n = 117; 87.3%). The most used diuretic schedule for the treatment of ascites was the isolated administration of spironolactone. Frusemide was associated with spironolactone only when moderate or high doses of the latter were found to be insufficient for increasing urinary sodium excretion and eliminating ascites. Following therapeutic paracentesis however, 79 of those surveyed (58.3%) administered a combination of both diuretics on initiation to avoid reaccumulation of ascitic fluid. Sixty-eight of the physicians (50.3%) used transhepatic intrajugular portosystemic shunt in the treatment of refractory ascites. Cefotaxime was the antibiotic most widely used in the treatment of SBP (n = 119; 88%). Most of the physicians surveyed performed prophylaxis of this infection (generally by the oral administration of norfloxacin) in patients with a previous history of SBP (n = 125; 92.6%) or an episode of gastrointestinal hemorrhage (n = 108; 80%) but not in those patients with no previous history of SBP and with low protein concentrations in the ascitic fluid (n = 40; 29.6%). On the appearance of SBP in patients undergoing prophylactic treatment, cefotaxime remained the antibiotic of choice (n = 104; 79%).

The IV infusion of pharmacological doses (0.05 microgram.kg-1.min-1) of atrial natriuretic peptide to 16 patients with cirrhosis and ascites induced a significant increase in sodium excretion (65 +/- 23 to 517 +/- 231 mu Eq/min), urine volume (10.7 +/- 2.3 to 15.7 +/- 3.7 mL/min), and glomerular filtration rate (89 +/- 4 to 110 +/- 4 mL/min) in only 5 patients (responders). No significant changes in these parameters (15 +/- 6 to 11 +/- 4 mu Eq/min, 5.5 +/- 1.0 to 4.2 +/- 1.1 mL/min, and 81 +/- 5 to 79 +/- 6 mL/min, respectively) were observed in the remaining patients (nonresponders). Compared with responders, nonresponders had significantly lower baseline sodium excretion (P less than 0.02), urine flow (P less than 0.05), free water clearance (2.5 +/- 0.9 vs. 6.9 +/- 2.1 mL/min; P less than 0.05), and mean arterial pressure (82 +/- 3 vs. 96 +/- 2 mm Hg; P less than 0.01) and significantly higher plasma renin activity (16.3 +/- 4.9 vs. 1.8 +/- 0.2 ng.mL-1.h-1; P less than 0.05) and aldosterone level (99 +/- 24 vs. 13 +/- 2 ng/dL; P less than 0.05). Atrial natriuretic peptide produced a similar reduction of arterial pressure in both groups. To investigate whether the blunted natriuretic response to atrial natriuretic peptide in nonresponders was caused by their lower arterial pressure, atrial natriuretic peptide was infused in 7 of these patients after increasing their arterial pressure to the levels of responders with nonrepinephrine. The increase in arterial pressure (from 81 +/- 5 to 95 +/- 5 mm Hg), which was not associated with significant changes in plasma renin activity and aldosterone concentration, did not reverse the blunted renal response to atrial natriuretic peptide in any of these patients. These results indicate that cirrhotic patients with blunted renal response to atrial natriuretic peptide are characterized by low arterial pressure, marked overactivity of the renin-aldosterone system, and severe sodium and water retention. Correction of hypotension without increasing effective blood volume does not restore renal insensitivity to atrial natriuretic peptide.

During the first 18 months of liver transplantation program for adult patients we evaluated 98 potential candidates for this treatment. Forty five patients were refused for transplantation and 53 were accepted. Forty six out of these 53 cases were transplanted. Ten (22%) out of the 46 patients undergoing transplantation had chronic hepatic cholestasis, 31 (67%) chronic hepatic diseases of non biliary origin (3 patients had an associated hepatocarcinoma), and 5 patients (11%) suffered an acute hepatic failure. All transplanted patients with previous chronic hepatic diseases had clinical and biological signs of advanced hepatic failure. There were no operative deaths. During the follow-up period 6 transplanted patients (13%) died. The survival probability among the 46 operated patients was about 84% at 12 months after the transplant. This survival was theoretically higher than that expected to occur without transplantation. The survival probability among the 46 transplanted patients was significantly higher (p = 0.0001) than that recorded in 36 patients with comparable hepatic diseases who were evaluated during the same study period and who were not considered for transplantation due to several reasons. The survival probability at the first year in the later group of 36 patients was 20%.