[Persistent acute hepatitis in a patient with chronic hepatitis C]. / Hepatitis aguda mantenida en paciente con hepatitis crónica C previa.

We describe the case of a patient with chronic hepatitis C (CHC) who showed a progressive increase in aminotransferase level, reaching values of aspartate aminotransferase 1723 UI/L, alanine aminotransferase 1519 UI/L and gamma-glutamyl-transpeptidase 296 with a bilirubin level of 6 mg/dL and direct bilirubin level of 4.6 mg/dL. One year previously, the patient had been diagnosed with CHC, genotype 1, and had an initial hepatitis C virus RNA load of 249,000 UI/mL. All the specific blood tests performed were negative except for antisoluble liver antigen (anti-SLA) antibodies, which were positive in two different determinations. A diagnosis of overlap syndrome CHC and autoimmune hepatitis was made. Steroid and azathioprine treatment was started with good response. The relationship between CHC and anti-SLA is not well characterized but has been described in these patients. We found no prior reports in the literature of CHC associated with positive anti-SLA in a patient with persistent acute hepatitis.

Hepatitis aguda mantenida en paciente con hepatitis crónica C previa / Persistent acute hepatitis in a patient with chronic hepatitis C

Describimos el caso de un paciente con hepatitis crónica C (HCC) en quien se detectó un incremento progresivo de las transaminasas que alcanzaron valores de aspartato aminotransferasa (AST) de 1.723 U/l, alanina aminotransferasa (ALT) de 1.519 U/l y gammaglutamil transpeptidasa (GGT) de 296 U/l, con un valor de bilirrubina de 6 mg/dl (la bilirrubina directa fue de 4,6 mg/dl). Entre sus antecedentes destaca el diagnóstico previo de una HCC con genotipo 1 y carga viral inicial de 249.000 U/ml. Todas las pruebas analíticas realizadas fueron negativas, a excepción de un antígeno soluble hepático (anti-SLA) positivo en 2 determinaciones consecutivas. Se estableció el diagnóstico de síndrome de superposición HCC y hepatitis autoinmune asociada a anti-SLA, por lo que se inició un tratamiento combinado con esteroides y azatioprina, con buena respuesta clínica y analítica. La relación entre la HCC y la positividad a anti-SLA ha sido escasamente estudiada, pero sí se ha descrito en estos pacientes. Sin embargo, no existe ningún caso en la bibliografía que haya comenzado en forma de hepatitis aguda sobre una HCC ya conocida, como ocurrió en el nuestro

We describe the case of a patient with chronic hepatitis C (CHC) who showed a progressive increase in aminotransferase level, reaching values of aspartate aminotransferase 1723 UI/L, alanine aminotransferase 1519 UI/L and gamma-glutamyl-transpeptidase 296 with a bilirubin level of 6 mg/dL and direct bilirubin level of 4.6 mg/dL. One year previously, the patient had been diagnosed with CHC, genotype 1, and had an initial hepatitis C virus RNA load of 249,000 UI/mL. All the specific blood tests performed were negative except for antisoluble liver antigen (anti-SLA) antibodies, which were positive in two different determinations. A diagnosis of overlap syndrome CHC and autoimmune hepatitis was made. Steroid and azathioprine treatment was started with good response. The relationship between CHC and anti-SLA is not well characterized but has been described in these patients. We found no prior reports in the literature of CHC associated with positive anti-SLA in a patient with persistent acute hepatitis

Mesenteric hyporesponsiveness in cirrhotic rats with ascites: role of cGMP and K+ channels.

The mechanisms that mediate hyporesponsiveness to vasoconstrictors in liver cirrhosis are not completely established. In the present study we have explored the role of NO and potassium channels by studying the pressor response to methoxamine in rats with carbon tetrachloride-induced cirrhosis with ascites. Experiments were performed in the isolated and perfused mesenteric arterial bed of control rats and of cirrhotic rats with ascites. Pressor responses to methoxamine, an alpha-adrenergic agonist, were analysed under basal conditions, after inhibition of guanylate cyclase with Methylene Blue (MB; 10 microM), after inhibition of NO synthesis with N(G)-nitro-L-arginine (L-NNA; 100 microM) and after blockade of potassium channels with tetraethylammonium (TEA; 3 mM). Compared with those from controls, preparations from cirrhotic rats showed a lower pressor response to methoxamine (maximum: controls, 114.4+/-6.8 mmHg; cirrhotic rats, 74.7+/-7.3 mmHg). Pretreatment with MB or L-NNA increased the responses in both groups, but without correcting the lower than normal response of the cirrhotic rats. Pretreatment with TEA alone did not modify the responses as compared with the untreated groups. Pretreatment with TEA plus MB or TEA plus L-NNA also potentiated the responses, and the responses of the cirrhotic animals were greater than those of the groups treated with MB or L-NNA alone. However, no treatment completely normalized the lower response of the mesenteries from cirrhotic animals, suggesting that factors other than NO and potassium channels also participate, although to a lesser degree, in the lower pressor response of the mesenteric arterial bed of animals with cirrhosis. These results confirm that NO and potassium channels are important mediators of the lower vascular pressor response of the mesenteric bed of cirrhotic rats with ascites. This effect seems to be mediated by the NO-dependent formation of cGMP and by the NO-dependent and -independent activation of potassium channels.

Haemodynamic and renal evolution of the bile duct-ligated rat.

In the present study we have characterized the evolution of changes in systemic haemodynamics (thermodilution in conscious animals) and sodium balance (metabolic cages) in a model of liver cirrhosis induced by chronic bile duct ligation (BDL). Mean arterial pressure (BDL, 111.5+/-4.7 mmHg; sham-operated, 122.9+/-3.0 mmHg) and peripheral vascular resistance (BDL, 2.63+/-0.08 units; sham-operated, 2.93+/-0.09 units) were lower in BDL rats from day 12 after surgery and decreased progressively throughout the following days. Portal hypertension was evident earlier in BDL rats and was maintained throughout the study period. Cardiac index (BDL, 58.8+/-3. 9 ml.min(-1).100 g(-1); sham-operated, 43.9+/-1.5 ml.min(-1).100 g(-1)) and stroke volume (BDL, 147.2+/-12.7 ml.beat(-1).100 g(-1); sham-operated, 109.0+/-4.2 ml.beat(-1).100 g(-1)) were significantly elevated in the BDL rats only from day 18 after surgery. There were no significant differences in sodium balance between the groups until day 16 after surgery, at which time BDL animals started to retain significantly more sodium than the controls. Sodium retention increased progressively, and at day 20 BDL rats had retained 0.7 mmol/100 g more than the control animals (accumulated retention: BDL, 2.2+/-0.2 mmol/100 g; sham-operated, 1.5+/-0.2 mmol/100 g). Plasma renin activity and aldosterone concentration were not elevated in the BDL animals at days 12, 16 or 20 after surgery. These data indicate that the BDL rat model shows early portal hypertension, peripheral vasodilation and arterial hypotension, several days before sodium retention is detectable, and in the absence of changes in plasma levels of renin and aldosterone. Overall, these data suggest that, in the BDL rat model, sodium retention is secondary to portal hypertension and peripheral vasodilation.

[Immunologic aspects of chronic diarrhea in relation to inflammatory intestinal disease]. / Aspectos inmunológicos en diarreas crónicas en relación con la enfermedad inflamatoria intestinal.

In a group of patients with chronic diarrhea of unknown origin, a study of cellular and humoral immunity was carried out with in vitro tests and the results are compared to those obtained in a group of patients with ulcerative colitis or Crohn's disease, and to normal controls. In the chronic diarrhea group there was evidence of an immunological deficiency affecting the B and T lymphocytes that had specific characters in relation to IgG, although the IgG deficit was not as important as in intestinal inflammatory disease.

[Course of cellular immunity in patients with chronic inflammatory intestinal disease]. / Evolución de la inmunidad celular en pacientes con enfermedad inflamatoria intestinal crónica.

In a preliminary study of the immunological aspects of intestinal inflammatory disease we found an immunological deficit of T helper lymphocytes, decreased monocytes and chemotaxis and poor response to nonspecific mitogen stimulus. Based on these findings, the study was repeated in the same patients three years later to confirm the evolution of this deficit. Recuperation was observed in the cases in which the disease evolved favorably, suggesting that certain aspects of the immune disorder might be secondary.