Initial immunosuppression with or without basiliximab: a comparative study.

BACKGROUND: Following liver transplantation, acute kidney injury (AKI) and chronic kidney disease occur in 20%-50% and 30%-90% of patients, respectively. Basiliximab, a chimeric monoclonal antibody, is highly effective to prevent rejection in organ transplant recipients, particularly among patients with renal dysfunction who benefit from delayed introduction of calcineurin inhibitors. OBJECTIVE: The objective of this study was to measure the immunosuppressive effect of basiliximab and its impact on renal failure, lengths of hospital and intensive care unit (ICU) stays and prevalence of infection. METHODS: From January 2010 through December 2011, we performed a controlled, nonrandomized study comparing two different immunosuppressive regimens: Group I, 36 transplantation on 34 patients, tacrolimus and corticosteroids de novo with mycophenolate mofetil in cases of renal failure; and Group II, 33 transplantation in 33 patients, corticosteriods and mycophenolate mofetil de novo with basiliximab on day 0 and day 4, and inception of tacrolimus on day 3. RESULTS: Basiliximab patients (Group II) showed a significantly lower incidence of renal failure requiring replacement therapy (3.03% vs 25%; P = .014). The incidence of acute cellular rejection episodes treated with corticosteriod boluses was also significantly lower (3.03% vs 25%; P = .014). Bacterial, fungal, and cytomegalovirus infection rates were lower in Group II, although the differences were not significant. Similarly, Group II patients had an insignificantly shorter average stay in the hospital (25.9 vs 40.06 days) and the ICU (5.9 vs 8.17 days). CONCLUSIONS: Basiliximab administration with delayed introduction of calcineurin inhibitors may be an effective strategy to reduce post-liver transplantation AKI requiring renal replacement therapy.

Severe sirolimus-related inflammatory state anemia in an HIV+ liver transplant patient with calcineurin inhibitor renal insufficiency: a case report.

Although multifactorial anemia is common following orthotopic liver transplantation (OLT), the late introduction of sirolimus (SRL) has been associated with high rates of anemia, whose pathogenic mechanisms have not been fully studied. Herein we have described a case of severe anemia in an HIV+ OLT patient who was switched from calcineurin inhibitors (CNI) to SRL due to severe nephrotoxicity. After 22 weeks of SRL, hemoglobin levels dropped 4 g/dL to a nadir of 6.5 g/dL. After discarding other causes for anemia, we concluded that it displayed the features of anemia of a chronic inflammatory state (ACIS): decreased mean corpuscular volume (MCV), low serum iron despite high ferritinemia, and elevated fibrinogen and C-reactive protein (CRP) levels. SRL trough levels were never above the therapeutic range. After blood transfusions and erythropoietin (EPO) use, SRL was maintained within the lower range of therapeutic levels, with significant improvement in renal function. As described among kidney transplant recipients, SRL-related anemia in this HIV+ patient with CNI nephrotoxicity after OLT showed features of ACIS. Blood transfusions and EPO use allowed SRL maintenance.

[The H63D mutation in the HFE gene is related to the risk of hepatocellular carcinoma]. / La mutacion H63D del gen HFE se asocia con un riesgo aumentado de carcinoma hepatocelular .

AIM: To disclose whether mutations in the HFE gene inducing liver iron overload are related to the risk of hepatocellular carcinoma (HCC) in otherwise predisposed patients. PATIENTS AND METHODS: One hundred and ninety-six patients (161 males) diagnosed with HCC and 181 healthy controls were included in the study. All subjects were white Spaniards.C282Y and H63D mutations in the HFE gene were identified in leucocyte genomic DNA using a polymerase chain reaction (PCR) and specific restriction enzymes. RESULTS (CASES/CONTROLS): 1. Genotype distribution: a) C282Y mutation: homozygotes 1/0, heterozygotes 12/23, wild type 183/158 (p = 0.07, non significant); b) H63D mutation: homozygotes 9/5, heterozygotes 85/52, wild type 102/124 (0dds ratio 2.00, 95% C.I. 1.29-3.12, p = 0.002. Four cases and 6 controls were carriers of heterozygous mixed genotypes. 2. Allele frequencies: a) C282Y mutation: wild type allele 378/339, mutated allele 14/23 (p = 0.11, non significant); b) H63D mutation: wild type allele 289/300, mutated allele 103/62 (0dds ratio 1.72, 95% C.I. 1.19-2.50, p = 0.004). Age at diagnosis, gender and etiology of the underlying liver disease do not influence these findings. CONCLUSION: The C282Y mutation in the HFE gene is not related to the risk of HCC in non-hemochromatosis patients. The H63D mutation is associated with a higher risk of HCC in cirrhotic patients irrespective of their underlying liver disease.

Encefalopatía hepática secundaria a la existencia de un shunt portosistémico tratada satisfactoriamente mediante radiología intervencionista / Hepatic encephalopathy secondary to porto-systemic shunt satisfactorily treated with interventionist radiology

La encefalopatía hepática es un estado reversible de alteraciónen la función cognitiva, que puede ocurrir en pacientes con enfermedadhepática aguda o crónica o shunts porto-sistémicos, en elque puede aparecer cualquiera de los signos neurológicos o psiquiátricosconocidos. Las sustancias nitrogenadas procedentes dela digestión intestinal alcanzan el cerebro sin la depuración que suponesu paso por el hígado, debido a las derivaciones porto-sistémicas,y dan lugar a los signos característicos de la encefalopatíahepática. A continuación presentamos dos casos clínicos de pacientescon shunt porto-sistémicos, diagnosticados de encefalopatíahepática crónica recurrente refractaria al tratamiento médicoconvencional, tratados satisfactoriamente con embolización de dichoshunt mediante técnicas de radiología intervencionista

Hepatic encephalopathy is a reversible state of altered cognitionthat may occur in patients with acute or chronic liver diseaseor porto-systemic shunt, and in which known neurological or psychiatricsigns may develop. Nitrogenated substances from intestinaldigestion reach the brain without being cleared by their passagethrough the liver due to the presence of porto-systemicshunt. We report two cases of patients with porto-systemic shuntdiagnosed with recurrent chronic hepatic encephalopathy refractoryto conventional medical treatment. They were satisfactorilytreated with shunt embolization using interventionist radiologytechniques

La mutacion H63D del gen HFE se asocia con un riesgo aumentado de carcinoma hepatocelular / The H63D mutation of the HFE gene is related to the risk of hepatocellular carcinoma

Objetivo: comprobar si las mutaciones del gen HFE, que puedeninducir sobrecarga hepática de hierro, guardan relación conel riesgo de desarrollar carcinoma hepatocelular (CHC) en sujetospredispuestos a sufrir este tumor.Material y métodos: se han incluido 196 pacientes (161 varones)diagnosticados de CHC. Ninguno estaba diagnosticado dehemocromatosis. El grupo control estaba constituido por 181 sujetossanos. Todos los sujetos eran españoles de raza blanca.Las mutaciones C282Y y H63D del gen HFE se identificaronmediante reacción en cadena de polimerasa (PCR) sobre ADN genómicoleucocitario utilizando enzimas de restricción específicas.Resultados (casos/controles): 1. Distribución genotípica:a) mutación C282Y: 1/0 homocigotos, 12/23 heterocigotos,183/158 normales (p = 0,07, n.s.); y b) mutación H63D: 9/5homocigotos, 85/52 heterocigotos, 102/124 normales (odds ratio2,00, IC95% 1,29-3,12, p = 0,002). Cuatro casos y seis controleseran heterocigotos compuestos. 2. Frecuencias alélicas: a)mutación C282Y: normales 378/339, mutados 14/23 (p =0,11, n.s.); b) mutación H63D: normales 289/300; mutados103/62 (odds ratio 1,72, IC95% 1,19-2,50, p = 0,004). No seobservaron diferencias en relación con el sexo, la edad o la etiología(VHC, VHB, etílica o mixta) de la hepatopatía previa.Conclusiones: la mutación C282Y no guarda relación con elriesgo de desarrollar CHC en sujetos sin hemocromatosis conocida.La posesión de la mutación H63D se asocia con un riesgo aumentadode desarrollar CHC independientemente de la etiologíade la hepatopatía crónica subyacente

Aim: to disclose whether mutations in the HFE gene inducingliver iron overload are related to the risk of hepatocellular carcinoma(HCC) in otherwise predisposed patients.Patients and methods: one hundred and ninety-six patients(161 males) diagnosed with HCC and 181 healthy controls wereincluded in the study. All subjects were white Spaniards.C282Y and H63D mutations in the HFE gene were identifiedin leucocyte genomic DNA using a polymerase chain reaction(PCR) and specific restriction enzymes.Results (cases/controls): 1. Genotype distribution: a)C282Y mutation: homozygotes 1/0, heterozygotes 12/23, wildtype 183/158 (p = 0.07, non significant); b) H63D mutation: homozygotes9/5, heterozygotes 85/52, wild type 102/124 (0ddsratio 2.00, 95% C.I. 1.29-3.12, p = 0.002. Four cases and 6controls were carriers of heterozygous mixed genotypes. 2. Allelefrequencies: a) C282Y mutation: wild type allele 378/339, mutatedallele 14/23 (p = 0.11, non significant); b) H63D mutation:wild type allele 289/300, mutated allele 103/62 (0dds ratio1.72, 95% C.I. 1.19-2.50, p = 0.004). Age at diagnosis, genderand etiology of the underlying liver disease do not influence thesefindings.Conclusion: the C282Y mutation in the HFE gene is not relatedto the risk of HCC in non-hemochromatosis patients. TheH63D mutation is associated with a higher risk of HCC in cirrhoticpatients irrespective of their underlying liver disease

[Hepatic encephalopathy secondary to porto-systemic shunt satisfactorily treated with interventionist radiology]. / Encefalopatía hepática secundaria a la existencia de un shunt portosistémico tratada satisfactoriamente mediante radiología intervencionista.

Hepatic encephalopathy is a reversible state of altered cognition that may occur in patients with acute or chronic liver disease or porto-systemic shunt, and in which known neurological or psychiatric signs may develop. Nitrogenated substances from intestinal digestion reach the brain without being cleared by their passage through the liver due to the presence of porto-systemic shunt. We report two cases of patients with porto-systemic shunt diagnosed with recurrent chronic hepatic encephalopathy refractory to conventional medical treatment. They were satisfactorily treated with shunt embolization using interventionist radiology techniques.

Prevention of de novo hepatitis B infection in liver allograft recipients with previous hepatitis B infection or hepatitis B vaccination.

OBJECTIVES: To assess de novo hepatitis B virus (HBV) transmission from liver donors with HBV serum markers (HBM) to their recipients and the need for HBV vaccination before liver transplantation. METHODS: A total of 108 orthotopic liver transplantations for nonviral disease and the risk of developing de novo hepatitis B based on HBMs before transplantation have been studied. Of the 108 patients, 94 met the study criteria and were divided into two groups: 27 who had HBMs before transplantation (from past infection or by previous vaccination) and 67 who had no HBM. Development of de novo hepatitis B was determined by analytical, serological, and histological parameters. RESULTS: No case (0%) of de novo hepatitis B was detected in the pretransplantation HBM group, whereas there were 10 cases (14.5%) in the other group (p < 0.005). CONCLUSIONS: The presence of pretransplantation HBM in liver transplant recipients protects these patients against the development of de novo hepatitis B. This is especially important considering that there is a high prevalence of donors with positive hepatitis B core antibody (especially in some countries), and that these donors transmit HBV infection to recipients without HBM in a significant number of cases. Thus, vaccination against HBV in patients who are candidates for liver transplantation is fundamental to avoid cases of de novo hepatitis B.

Colitis colágena: una entidad con diversas opciones terapéuticas / Collagenous colitis: an entity with different therapeutic options

La colitis colágena es una enfermedad cuya frecuencia ha aumentado progresivamente en los últimos años debido fundamentalmente a la toma rutinaria de biopsias en el estudio de pacientes con diarrea crónica. Se han comunicado buenas respuestas con numerosos tratamientos, aunque hay pocos ensayos clínicos realizados por el escaso número de pacientes con esta patología. Presentamos dos casos de colitis colágena cuyo interés reside en su manejo terapéutico, revisando las distintas alternativas existentes en el tratamiento de esta entidad de creciente importancia en la práctica clínica diaria (AU)

[Collagenous colitis: an entity with diverse therapeutic options]. / Colitis colágena: una entidad con diversas opciones terapéuticas.

Collagenous colitis is a disorder which has been diagnosed with increasing frequency in the last few years, probably due to the routine obtention of colon biopsy specimens in the study of patients with chronic diarrhoea. Good responses have been reported with a number of therapies, although only a scarce number of clinical trials have been performed, partly because of the small number of patients studied. Two cases of collagenous colitis with different therapeutic approaches are here reported. All medical therapy options for this interesting disorder are reviewed.

[Treatment of hepatic and intra-abdominal hydatidosis with mebendazole: prospective comparison of the cyclic and the continuous regimen]. / Tratamiento de la hidatidosis hepática e intraabdominal con mebendazol: comparación prospectiva de las pautas cíclica y contínua.

AIM: To communicate the results of two different schedules (cyclic and continuous) of mebendazole therapy for hepatic and intraabdominal hydatid disease. DESIGN: Prospective and randomized. PATIENTS: 26 cases of abdominal hydatid disease. RESULTS: No significant differences were registered between both groups. CONCLUSION: Cyclic mebendazole therapy does not improve the results of continuous treatment in abdominal hydatid disease.

Randomised controlled trial of efficacy of albendazole in intra-abdominal hydatid disease.

The efficacy of albendazole in hydatid disease is still unclear, because there has been no study that assessed the status of the parasite after treatment. The significance of albendazole-induced echographic changes in the cyst therefore cannot be judged. We did a prospective, controlled, randomised, open study of albendazole in patients with liver hydatid disease, and assessed parasite viability after treatment. 18 patients received no albendazole treatment (controls), 18 received albendazole (10 mg/kg daily) for 1 month (group A), and 19 received the drug for about 3 months (group B). Echography was done before and during treatment; all patients underwent surgery on completion. Parasite (protoscolex viability and development of cysts in mice) and ultrastructure studies were done for all cysts removed. 8 (50%) of cysts in the control group, 13 (72%) in group A, and 16 (94%) in group B were non-viable (p = 0.015). Protoscolex and cyst viability were significantly (p = 0.039 and p = 0.018, respectively) lower in treated patients than in controls. Treatment was also significantly associated with total cyst membrane disintegration. 68% of cysts treated for 3 months showed echographic changes, and only 1 of 20 cysts showing echographic changes during treatment was judged viable. The efficacy of albendazole at a dose of 10 mg/kg daily for 3 months suggests that it is a suitable alternative to surgery in uncomplicated hydatid liver disease, as initial treatment.

Portal vein thrombosis due to Candida albicans associated with hepatic cirrhosis.

A case of portal vein thrombosis due to Candida albicans in a patient with alcoholic hepatic cirrhosis in the absence of hepatocarcinoma is described. Infection is a known cause of portal vein thrombosis but thrombosis by Candida albicans has not to our knowledge been previously reported.

[Prevalence of hepatitis C virus antibody in chronic HBsAg-negative non alcoholic hepatopathy]. / Prevalencia del anticuerpo al virus de hepatitis C en la hepatopatía crónica no alcohólica HBsAg negativa.

The presence of antibody to hepatitis C virus was determined in 316 HBsAg-negative patients with non-alcoholic chronic hepatitis who did not receive any blood transfusion once the diagnosis was made. A titre of antinuclear antibodies of 1/40 or lower was found in 18 patients. Persistent chronic hepatitis was present in 21 patients, active chronic hepatitis in 145, hepatic cirrhosis in 128, and hepatocarcinoma in 22 patients. One hundred and three patients had previously received blood transfusion, 76 had undergone previous surgery without transfusion, a clinical episode of hepatitis could be traced in 14, 13 patients were drug addicts (all of them HIV negative), 1 patient had received multiples injections, another had been treated with acupuncture, and 108 patients were free of any of the above. Anti-HCV was present in 76.6% of patients; a significantly higher proportion (87.4%) was found among patients who had received blood transfusion than in patients with previous surgery (72.4%) (p = 0.012), clinical hepatitis (57.1%), or without previous hepatic disease (70.3%) (p = 0.003). The incidence of anti-HCV was lower among cirrhotics (70.3%) than in patients with active chronic hepatitis (84.1%) (p = 0.006); in contrast, previous blood transfusion was significantly higher (p = 0.001) among the latter (40.7%) than in cirrhotics (21.9%). The incidence of anti-HCV was similar among patients with (78.6%) and without (75.8%) type B infection. Our results suggest that infection with virus C may account for a high proportion of non-alcoholic non-B chronic hepatitis.