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To evaluate the safety and efficacy of transjugular intrahepatic portosystemic shunt (TIPS) in the control of bleeding from ectopic varices.From 1995 to 2004, 24 cirrhotic patients, bleeding from ectopic varices, mean age 54.5 years (range 15-76 years), were treated by TIPS. The etiology of cirrhosis was alcoholic in 13 patients and nonalcoholic in 11 patients. The location of the varices was duodenal (n = 5), stomal (n = 8), ileocolic (n = 6), anorectal (n = 3), umbilical (n = 1), and peritoneal (n = 1).TIPS controlled the bleeding in all patients and induced a decrease in the portacaval gradient from 19.7 +/- 5.4 to 6.4 +/- 3.1 mmHg. Postoperative complications included self-limited intra-abdominal bleeding (n = 2), self-limited hemobilia (n = 1), acute thrombosis of the shunt (n = 1), and bile leak treated by a covered stent (n = 1). Median follow-up was 592 days (range 28-2482 days). Rebleeding occurred in 6 patients. In 2 cases rebleeding was observed despite a post-TIPS portacaval gradient lower than 12 mmHg and was controlled by variceal embolization; 1 patient underwent surgical portacaval shunt and never rebled; in 3 patients rebleeding was related to TIPS stenosis and treated with shunt dilatation with addition of a new stent. The cumulative rate of rebleeding was 23% and 31% at 1 and 2 years, respectively. One- and 2-year survival rates were 80% and 76%, respectively.The present series demonstrates that bleeding from ectopic varices, a challenging clinical problem, can be managed safely by TIPS placement with low rebleeding and good survival rates.

PURPOSE: To evaluate the dimensions of segment 4 of the liver in patients with cirrhosis by using ultrasonography (US). MATERIALS AND METHODS: The transverse diameter of segment 4 was measured in 125 control subjects without liver disease and 167 patients with cirrhosis. The size of segment 4 was measured on oblique subcostal US scans obtained between the left wall of the gallbladder (or the main fissure after cholecystectomy) and the ascending or umbilical portion of the left portal vein at the point where it gives rise to the branch to segment 4. RESULTS: In the control subject group, the mean diameter of segment 4 was 43 mm +/- 8 (standard deviation). In the patient group, the mean diameter of segment 4 was 28 mm +/- 9. The cause or severity of cirrhosis had no influence on the size of segment 4. CONCLUSION: A decreased diameter of segment 4 may be a helpful adjunct sign of cirrhosis in the US investigation of chronic liver disease.

Amongst the potential neurotoxins implicated in the pathogenesis of hepatic encephalopathy, manganese emerges as a new candidate. In patients with chronic liver diseases, manganese accumulates in blood and brain leading to pallidal signal hyperintensity on T1-weighted Magnetic Resonance (MR) Imaging. Direct measurements in globus pallidus obtained at autopsy from cirrhotic patients who died in hepatic coma reveal 2 to 7-fold increases of manganese concentration. The intensity of pallidal MR images correlates with blood manganese and with the presence of extrapyramidal symptoms occurring in a majority of cirrhotic patients. Liver transplantation results in normalization of pallidal MR signals and disappearance of extrapyramidal symptoms whereas transjugular intrahepatic portosystemic shunting induces an increase in pallidal hyperintensity with a concomitant deterioration of neurological dysfunction. These findings suggest that the toxic effects of manganese contribute to extrapyramidal symptoms in patients with chronic liver disease. The mechanisms of manganese neurotoxicity are still speculative, but there is evidence to suggest that manganese deposition in the pallidum may lead to dopaminergic dysfunction. Future studies should be aimed at evaluating the effects of manganese chelation and/or of treatment of the dopaminergic deficit on neurological symptomatology in these patients.

The purpose of this study was to assess liver blood flow and cardiac output in chronic hemodialysis patients (n = 7) before and after a hemodialysis session, and to compare it to normal volunteers (n = 11). We used the hepatic clearance of sorbitol to calculate liver blood flow and echocardiograms to evaluate cardiac output. The latter was higher in hemodialysis patients (predialysis 4.7 +/- 1.8 liters/min, postdialysis 4.5 +/- 0.9 liters/min) compared to normal subjects (3.8 +/- 0.9 liters/min, p = 0.09 and p = 0.05). Hepatic blood clearance of sorbitol was similar in hemodialysis patients before and after dialysis (1,610 +/- 266 and 1,541 +/- 415 ml/min) as well as in normal volunteers (1,565 +/- 313 ml/min). The hepatic extraction ratio of sorbitol is slightly decreased in hemodialysis patients (n = 3) (0.87 +/- 0.03) compared to values reported in the literature for healthy subjects. We conclude that liver blood flow is not significantly altered in hemodialysis patients.

The haemodynamic effects of a meal on the splanchnic and hepatic circulation were evaluated in 30 healthy volunteers, using Doppler ultrasonography. The resistance index (RI) of the superior mesenteric artery and of the left and right intrahepatic arteries, the portal vein blood flow as well as the ratio between maximal velocity in the left and right intrahepatic arteries and the adjacent portal vein were measured initially, then 15, 30, 45, and 60 min after the ingestion of a standard balanced liquid meal. Postprandial haemodynamic changes were maximal 30 min after the meal; at that time, mesenteric artery RI decreased significantly [mean -11% (SEM 14%)] whereas portal vein blood flow increased markedly [mean +79% (SEM 14%)]; a significant increase in hepatic artery RI was observed in both liver lobes. The ratio between maximal velocities of the intrahepatic artery and the intrahepatic portal vein was reduced significantly; this ratio decreased more markedly in the right lobe of the liver. These findings would suggest that there was an adaptation of hepatic artery to portal vein blood flow after a meal. The subsequent increase in intrahepatic portal vein flow velocity was found to be greater in the right lobe of the liver.

Thirty healthy volunteers and 12 liver allograft recipients (two with cirrhotic changes seen at microscopy) were given a standard meal. Doppler sonography of the right and left hepatic arteries, the superior mesenteric artery, and the portal vein was performed. The change in hepatic arterial resistance was evaluated with the resistive index (RI). After the standard meal, portal venous flow increased in both the healthy volunteers and allograft recipients (more so in the latter group). Superior mesenteric arterial RI decreased in all subjects. A postprandial increase in hepatic arterial RI, likely reflecting constriction of the hepatic artery, was seen in both groups. It was absent in the two patients with recurrent transplant cirrhosis. These results show the importance of examining hepatic arterial flow in the fasting subject, since high resistance after a meal may be falsely interpreted as a sign of disease. Absence of a postprandial change in resistance of the hepatic artery could signal abnormal liver function.

Fifty-five of 353 patients with suspected portal hypertension studied with Doppler sonography had a patent paraumbilical vein. Of these 55 patients, 39 had the classic intrahepatic venous circulation found in Cruveilhier-Baumgarten syndrome: hepatopetal flow in all segmental portal veins and hepatofugal flow leaving the liver in a paraumbilical vein in the falciform ligament to join veins of the anterior abdominal wall. Sixteen patients had variants of the classic pattern: Flow in one or more segmental portal veins of the left lobe or the entire liver was hepatofugal. In addition, new venous channels connecting the left portal vein with the extrahepatic paraumbilical vein were found. Assessment of liver function with the Pugh score showed severe impairment in the majority of patients with a patent paraumbilical vein. Patients with the classic intrahepatic circulation had smaller esophageal varices than those with hemodynamic or anatomic variants. The presence of a patent paraumbilical vein did not prevent formation of esophageal varices in the patients studied.

SUMMARY Twenty-two subjects (11 HLA A1 B8 DR3, 11 non-A1 B8 DR3) were tested for the capacity of their lymphocytes to express Tac molecules and interleukin-2 (IL-2) receptors (quantified using radiolabelled IL-2) after mitogen stimulation. Ten of these subjects (five Al B8 DR3 and five non-A1 B8 DR3) were also tested for the ability of their lymphocytes to proliferate under IL-2 stimulation. Al B8 DR3 subjects express a normal number of high-affinity IL-2 receptor sites, but the affinity of these receptors sites is significantly increased. Unexpectedly, Al B8 DR3 lymphoblasts show a lower response to IL-2 than non-Al B8 DR3 for high doses of recombinant IL-2.

Assessment of renal function, namely glomerular filtration rate (GFR), by the renal creatinine clearance, may be problematic and less accurate in cirrhotics; however, it is an essential element in the global evaluation of these patients. In order to better characterize misinterpretation of GFR by the renal creatinine clearance, we compared a group of cirrhotic patients with renal failure (n - 30) to a group of chronic renal failure patients (CRF) without liver disease (n - 5). Inulin and PAH clearances were measured during a 4-hour infusion of inulin and PAH; renal creatinine clearance was measured during a 24-hour urine collection and this, simultaneously with inulin and PAH clearance. We observed that in moderate to severe renal failure (renal inulin clearance 30 +/- 10 ml/min), GFR (i. e. renal inulin clearance) in cirrhotic patients was overestimated by the renal creatinine clearance, similarly to CRF patients (ratio 1.8 +/- 0.7 and 1.6 +/- 0.9 respectively); however cirrhotic patients have a lower serum creatinine (186 +/- 97 vs 133 +/- 62 micromol/l respectively). On the other hand, cirrhotic patients with mild renal dysfunction (renal inulin clearance 74 +/- 15 ml/min) had a renal creatinine clearance of 77 +/- 25 ml/min. Systemic inulin clearance overestimated renal inulin clearance, proportionally to the severity of renal dysfunction. We conclude that it is only the degree of renal failure, irrespective of etiology, that explains the overestimation of the glomerular filtration rate by the renal creatinine clearance in cirrhotic patients; hence, there is no specific alteration in the renal excretion of creatinine in cirrhotic patients.

Ascites becomes refractory to medical treatment in nearly 10% of cirrhotic patients, who then require repeated large-volume paracentesis. In this prospective study we evaluated the use of transjugular intrahepatic portosystemic shunt (TIPS) in 30 patients with refractory ascites. TIPS was successful in all and resulted in a 54% reduction in portacaval gradient (from 22.8 +/- 0.8 to 10.4 +/- 0.6 mm Hg). Ascites became easily controlled with diuretics in 26 patients following TIPS. Ascites recurrence associated with shunt stenosis was observed during follow-up in eight patients; revision could be undertaken in five of them and resulted in good control of ascites. In responders, a marked decrease in plasma aldosterone and renin activity, a reduction in serum creatinine, and a rise in urinary sodium excretion were observed. Creatinine and inulin clearances improved significantly; PAH clearance remained unchanged. However, new-onset or worsening hepatic encephalopathy was seen in 14 patients. Severe disabling chronic encephalopathy occurred in five patients; it could be reversed successfully by balloon occlusion of the shunt in three. The cumulative survival rate was 41 and 34% at 1 and 2 years, respectively. In summary, TIPS can control refractory ascites in a majority of patients but is associated with a high rate of chronic disabling HE. In addition, the survival rate is poor. Randomized trials are needed to evaluate the exact role of TIPS in the management of refractory ascites. It is unlikely to improve survival but can ameliorate quality of life in nontransplant candidates and be useful as a bridge to transplantation, in particular, to improve denutrition associated with longstanding tense ascites.

Refractory ascites worsens the end-stage course of decompensated cirrhosis. Transjugular intrahepatic portasystemic shunt (TIPS) has been proposed to treat this condition with erratic success, inducing controversial reports on the risk-benefit ratio associated to this technique. In order to assess the usefulness of TIPS for this indication, this paper updates some definitions concerning the refractory ascites. We also analyze the main complications of TIPS and review some physiopathological pathways, taking peculiar interest in the Montreal experience.

Hepatorenal syndrome (HRS) is a functional renal failure occurring in advanced liver cirrhosis with ascites. It is due to renal cortical vasoconstriction resulting from complex hemodynamic disturbances related to cirrhosis and portal hypertension. There is no consistently effective therapy except for liver transplantation. We report a case of severe HRS in a patient with advanced liver cirrhosis and portal hypertension. Three sessions of hemodialysis were performed because of severe renal failure (serum urea 83 mg/dl, serum creatinine 6 mg/dl). Creation of an intrahepatic portosystemic shunt reduced the portocaval gradient from 18 to 7 mm Hg. Spectacular improvement of the renal function was observed soon after the procedure, with spontaneous recovery of diuresis and a return of serum urea and creatinine to baseline values. The patient unfortunately died 2 months later from adult respiratory distress syndrome post emergency surgery for a massive bleed related to a duodenal ulcer. Throughout this episode, the renal function remained stable. The postmortem examination showed histologically normal kidneys. We conclude that the intrahepatic portosystemic shunt can improve renal function in cirrhotic patients with HRS; it could be used in patients awaiting liver transplantation to reverse preoperative renal failure.

The purposes of this study were to evaluate the effect of a well-functioning transjugular intrahepatic portosystemic shunt (TIPS) on the splanchnic and intrahepatic circulation, to determine if sonographic measurements can predict shunt dysfunction before clinical manifestations of portal hypertension occur, and to compare Doppler sonographic findings with portocaval gradient measurements before and after shunt revision.Forty-four patients with cirrhosis (n = 43) and myelofibrosis (n = 1) who underwent successful TIPS insertion were included in this prospective study. Indications for TIPS placement were: refractory ascites (24 patients), bleeding esophageal varices (17 patients), portal hypertensive gastropathy (two patients), and bleeding colonic varices (one patient). The portal vein and the inferior vena cava were catheterized; and the portocaval gradient was recorded before TIPS placement, at 2 and 12 months after TIPS placement, and when clinical or Doppler findings suggested shunt dysfunction. Doppler studies were done within 1 week before TIPS placement, within 2 days after TIPS placement, every 2-3 months thereafter, and before and after a TIPS revision. The Doppler studies included flow volume measurements in the portal vein and in the stent, as well as determination of the direction of flow in the segmental branches of the portal vein, in the splanchnic veins, and in portosystemic collaterals. Changes in Doppler findings and in catheter pressure measurements were compared using Spearman's rank correlation test. Significance was set at the .05 level.A marked decrease (-51%) in portocaval gradient was observed after TIPS placement. At Doppler sonography, portal vein velocity and diameter were both higher after TIPS placement, resulting in a marked increase in portal venous flow (170%). Mean flow velocity in the shunt was 55.8 +/- 3.6 cm/sec, and flow volumes in the shunt and in the main portal vein were 1596 ml/min and 1731 ml/min, respectively (p = nonsignificant). Dysfunction of the stent occurred in 27% of the patients. Changes in stent blood flow volume were closely related to changes in the portocaval gradient (r = -0.67, p.001). Reduction of blood flow volume in the stent or change of direction of flow in intrahepatic portal veins or in collateral veins signaled shunt dysfunction (84% sensitivity, 89% specificity).Marked hemodynamic changes in the portal venous system occur soon after a TIPS procedure. Monitoring of shunt function with periodic Doppler sonography, including calculation of shunt blood flow, is useful in detecting shunt dysfunction before clinical signs occur.

Portal vein obstruction with secondary variceal bleeding in the setting of chronic pancreatitis has not been recognized as frequently as splenic vein occlusion. This condition can be difficult to diagnose and treat.A 54-year old man was referred for massive recurrent endoscopy-negative upper-gastrointestinal bleeding. The diagnosis of duodenopancreatic varices was finally made. Direct portography showed a high-grade stenosis of the proximal portal vein that was dilated and stented with a balloon expandable prosthesis.The gradient across the stenosis fell from 9 to 2 mm Hg. Bleeding stopped. After 7 months of follow-up, the patient has experienced no rebleeding, and a Doppler examination is normal.In patients with chronic pancreatitis and upper gastrointestinal tract bleeding of unknown origin, obstruction of one of the major splanchnic veins must be excluded. Portal vein dilatation and stenting appears to be a safe procedure with good short-term results.

Liver transplantation and the intrahepatic shunt have changed the management of variceal hemorrhage and refractory ascites. The purpose of this work is to review the results obtained with intrahepatic shunting. From January 1991 to May 1993, 45 patients underwent a transjugular intrahepatic portosystemic shunt. In 23 patients, liver insufficiency was considered moderate and in 21 severe. Indications for the procedure were: variceal bleeding (23), refractory ascites (19) and portal hypertensive gastritis (3). The portocaval gradient was lowered from 24.2 +/- 5.1 mm Hg to 12.9 +/- 3.9 (-47%). The procedure was effective in 78% of variceal bleeders and in 89% of patients with ascites. Thirty-day mortality was 22%. One-year survival was 39%. Liver failure or severe encephalopathy occurred in 27% of patients. Four patients (9%) presented intra-abdominal bleeding. Four patients developed renal failure. Transjugular intrahepatic portosystemic shunts are effective in lowering portal pressure and controlling complications of portal hypertension. However, important side effects are present and controlled studies are required to evaluate this new treatment.

Introduction Le Fibroscan® est un dispositif mesurant l’elasticite hepatique et permettant le diagnostic de la fibrose. Une nouvelle sonde XL a ete developpee specifiquement pour l’evaluation des patients obeses. Le diabete etant un facteur de risque de la fibrose, un objectif de l’etude est d’explorer l’impact du diabete sur les hepatopathies, chez des patients obeses avec SPMet. Les objectifs complementaires sont d’evaluer les performances de la sonde XL et d’etablir des modeles predictifs de la fibrose. Patients et methodes 90 patients obeses avec SPMet ont ete inclus : 62 % d’hommes, IMC moyen : 34 Kg/m2, âge moyen : 47 ans, 39 % avec diabete de type2 (Diab +). Tous les patients ont eu un examen Fibroscan®, une biopsie hepatique (classification de Brunt-Kleiner) et des tests sanguins. Des regressions logistiques multi-variees ont permis d’etablir des modeles statistiques predictifs de la fibrose. Les performances diagnostiques sont evaluees par l’aire sous la courbe ROC (AUROC). Resultats Les atteintes hepatiques sont plus frequentes chez les Diab + : 94 % avec steatose vs 89 % (Diab-), steato-hepatite 31 % vs 16 % (Diab-), fibrose 83 % vs 51 % (Diab-). Les performances diagnostiques du Fibroscan® (sonde XL) sont respectivement AUROC = 0.82 et 0.86 pour la fibrose significative (F≥2) et severe (F≥3). Le modele statistique optimal predictif de la fibrose combine elasticite, AST, HbA1c ajuste sur le sexe et l’âge. Il donne une AUROC = 0.90 pour (F≥2) et AUROC = 0.96 pour (F≥3). La combinaison entre elasticite et parametres biocliniques ameliore les performances des parametres biocliniques seuls (AST, HbA1c, sexe et âge) : AUROC = 0.78 pour (F2) et AUROC = 0.82 pour (F≥3). Conclusion Le terrain diabetique semble favoriser la survenue des hepatopathies d’ou la necessite d’un diagnostic precoce de la fibrose. La mesure de l’elasticite avec la sonde XL du Fibroscan® permet un diagnostic de bonne precision de la fibrose chez les patients obeses avec SPMet. Ces performances sont ameliorees en combinant l’elasticite et des parametres biocliniques.

The pathogenesis of portal hypertension in patients with lymphoproliferative and myeloproliferative disorders is not fully understood. We investigated 20 patients with myeloproliferative disease and 47 patients with lymphoproliferative disease. Transvenous liver biopsies and hepatic vein pressure gradient measurements were performed in all patients, and portal vein blood flow was measured by pulsed Doppler sonography in 31 of these patients and in 22 normal volunteers. The hepatic vein pressure gradient was significantly higher in patients with hepatic infiltrates, fibrosis or both than in patients without hepatic lesions (8.3 +/- 5.0 mmHg vs. 4.1 +/- 2.3 mmHg; p0.01). Portal vein blood flow was significantly higher in patients with hematological disease than in normal volunteers (31.2 +/- 15.5 ml/min.kg vs. 14.2 +/- 4.6 ml/min.kg;p0.01). In 81.8% of patients with hepatic infiltrates, fibrosis or both and increased portal vein blood flow, the hepatic vein pressure gradient was greater than 6 mm Hg. Although we saw a significant correlation between splenic vein blood flow and portal vein blood flow (n = 20; p0.01), we found no significant correlation between splenic vein blood flow and hepatic vein pressure gradient or spleen size. Hepatic infiltration and fibrosis appear to be major determinants of increased hepatic vein pressure gradient, probably because they increase intrahepatic vascular resistance. The role of increased splenic blood flow is probably not determinant. However, because portal pressure was not measured directly in this study, the incidence of portal hypertension may have been underestimated.

A 28-yr-old male with Rotor's disease was studied with 99mTc-mebrofenin. The scintigraphic pattern was that of a slow liver uptake with unimpaired excretion and persistent visualization of the cardiac blood pool, kidneys and urinary tract up to 6 hr. The gallbladder was visualized at 55 min postinjection.

Variceal bleeding in cirrhotic patients with severe liver failure that is not controllable by endoscopic sclerotherapy is a life-threatening situation. We report the case of a patient with decompensated cirrhosis (Pugh class C) who bled repeatedly from gastric varices despite multiple sessions of sclerotherapy. The portal vein was catheterized by a transjugular approach. A tract between a hepatic vein and the portal vein was created after balloon dilatation, and this opening was stented with an expandable stainless steel Palmaz stent. The portal vein pressure decreased from 35 mm Hg to 19 mm Hg after shunting. Gastric varices also were embolized. Two months later, bleeding had not recurred; the shunt remained opened and the marked decrease in portal pressure still persisted. Endoscopy showed the disappearance of gastric varices. This procedures could become a life-saving therapeutic option for such critically ill cirrhotic patients.

Antibodies directed against the central nervous system were looked for by indirect immunohistochemistry in the sera of 8 patients with paraneoplastic neurological syndrome (group 1), 21 cancer patients without neurological signs, 23 patients with miscellaneous neurological diseases and 63 normal subjects (groups 2 to 4). Four patients in group 1 had very high titres of antibodies. In 2 patients with small-cell lung carcinoma associated with sensory neuropathy the antibody recognized the cytoplasm and nucleus of all neurons. A 37 Kd protein was recognized by Western blot. A woman with cancer of the ovary and cerebellar syndrome exhibited an antibody against Purkinje's cell cytoplasm with a band of about 50-55 Kd at Western blot. In a woman with chronic uveitis and cerebellar atrophy with disappearance of Purkinje's cells the antibody (in blood and CSF) recognized certain layers of the retina as well as glial cells and cells present in the subependymal areas of the brain. Two bands of 46 and 59 Kd were revealed by Western blot. Immunoglobulins were detected in the cytoplasm of white matter cells in the cerebellum and brain stem. Among the other groups, one patient with lung cancer had a moderate titre of neuronal antinuclear antibody. The Western blot test was negative. The relevance of these antibodies for the diagnosis and treatment is discussed.

We report our experience of 36 renal transplanted patients against a current T negative allo-cross-match, but historical T and/or B positive allo-cross-matches, whatever the result of the current B cross-match. Additionally, we have determined the immunoglobulin class of the antibody directed against B and T lymphocytes. The graft survival rate did not differ between the 36 patients forming the study group, and the 229 patients transplanted within the same period with negative T and B, on current and historical sera, cross-matches. Within this study group there was no changes in graft survival rate for the following three subgroups, which were retrospectively defined: historical positive (14 patients) versus negative (22 patients) T cross-match, current positive (15 patients) versus negative (21 patients) B cross-match, and IgM (16 patients) versus IgG (20 patients) against B lymphocytes. In terms of transplant outcome, our policy was thus safe.

In 65 patients with a biopsy-proven diagnosis of membranous glomerulonephritis, the association with HLA class I, class II and class III antigens was studied using classical techniques. We found a highly significant association with the HLA-DR3 (Pc = 8 x 10(-5)) antigen and with the HLA-B8 (Pc = 2 x 10(-4)) antigen in linkage disequilibrium with the former. In addition, there was an excess of null C4 allotypes (C4 AQo or C4 BQo) in patients and a significant decrease of BfS allele. Finally, the most commonly observed phenotype was A1 B8 DR3 BfS C4AQoB1. These results confirm a strong association between major histocompatibility complex and primary membranous glomerulonephritis, raising the possibility of a susceptibility gene being necessary for the development of that disease.

Objectifs Evaluer l’efficacite et l’innocuite de la mise en place de TIPS pour controler les hemorragies digestives survenant sur varices ectopiques chez les patients cirrhotiques. Materiels et methodes De 1995 a 2004, 24 patients cirrhotiques (âge moyen 54,5 ans) saignant de varices ectopiques (duodenales, stomales, ileocoliques, anorectales, ombilicales et periotenales) ont ete traites par TIPS. Resultats Le TIPS a permis le controle de l’hemorragie chez tous les patients avec une baisse du gradient de pression porto-cave de 19,7 ± 5,4 a 6,4 ± 3,1 mmHg. La surveillance etait de 592 jours (28 a 2482 jours). Le taux de recidive hemorragique etait respectivement de 23 % et 31 % a 1 et 2 ans et le taux de survie de 80 % et 76 % a 1 et 2 ans. Une recidive hemorragique a ete observee chez 6 patients dont 2 malgre un gradient porto-cave inferieur a 12 mmHg. Ces recidives ont ete traitees efficacement par reprise de TIPS (3), embolisation de varices (2) et shunt porto-cave chirurgical (1). Conclusion Cette serie demontre que le TIPS est une methode efficace et sure pour le traitement des hemorragies digestive par varices ectopiques, avec un faible taux de recidive et un bon taux de survie.

The blood-brain uptake process for tryptophan and phenylalanine was investigated using the multiple-indicator dilution technique in 13 unanesthetized dogs with and without portacaval shunts. Tracer doses of labeled albumin (extracellular reference) and tryptophan or phenylalanine, prepared in autologous dog plasma, were injected into one carotid artery, and dorsal sagittal sinus dilution curves were obtained. Portacaval shunting was not associated with significant changes in the initial brain uptake ratio U for tryptophan or phenylalanine, despite increases in plasma phenylalanine and tyrosine. In the 13 dogs, U was not significantly correlated with the plasma levels of either the different branched-chain or aromatic amino acids or the molar ratio between these groups. These findings do not support the current hypothesis that the active transport of aromatic amino acids across the blood-brain barrier is increased after portacaval shunt. Our data suggest, instead, that the blood-brain uptake process for aromatic amino acids is linear and increases in shunted animals because their plasma levels are increased.

The t(8;16)(p11;p13) is a recently described new chromosome rearrangement of acute non-lymphocytic leukemia (ANLL). It appears to be specifically associated with acute monoblastic (AML-M5) or unusual myelomonocytic leukemia with prominent erythrophagocytosis in the leukemic cells. A complex t(3;8;17)(q27;p11;q12) is reported in a case of acute monoblastic leukemia with erythrophagocytosis. Sixteen cases of this t(8;16) and two other variant translocations are reviewed. The pathogenetic mechanism of the variant translocations is discussed, suggesting that the der(8) is a consistent recombinant.

Forty-five patients with 46 surgical portosystemic shunts were examined by duplex Doppler sonography, and the results were compared with those of esophageal endoscopy, angiography, surgery, and clinical follow-up. Thirty-eight shunts were patent, and in 33 of these, the shunt was directly visualized and flow was observed with Doppler sonography. Eight shunts were obstructed. After a successful portosystemic shunt procedure, flow in the shunted splanchnic vein was directed toward the shunt and the systemic vein. We studied the intrahepatic portal venous circulation in all of the patients; we found that in the presence of patent portosystemic shunt, portal flow is hepatofugal. This reversal of blood flow occurred in all but four patients. In the end-to-side portacaval shunt, where the portal vein is ligated, blood in intrahepatic portal branches presumably reaches the shunt through perihepatic collaterals. In the presence of a thrombosed shunt, intrahepatic portal venous flow was hepatopetal. To our knowledge, this is the first noninvasive in vivo study of intrahepatic portal circulation after portosystemic shunt surgery. The duplex Doppler evaluation of portosystemic shunts appears to be reliable and should be the method of choice for shunt patency assessment in patients with recurrent signs of portal hypertension. In addition to demonstrating flow at the site of the anastomosis, the Doppler study may yield an easy and reliable sign of shunt patency: reversed flow (hepatofugal flow) in the intrahepatic portal veins probably signals a patent shunt, even if the site of the anastomosis cannot be visualized directly by sonography.

The mechanism of hepatic encephalopathy (HE) is still unknown. A characteristic amino acid pattern in HE has been described: an increased level of plasma free tryptophan, a fall in plasma branched chain amino acids (BCAA) valine, leucine and isoleucine and a rise in plasma aromatic amino acids (AAA) phenylalanine and tyrosine.1 The brain uptake of AAA would increase; the ensuing depletion of brain dopamine and norepinephrine and increase of brain octopamine, which is considered as a false neurotransmitter, would result in perturbation of cerebral neurotransmission.2

The authors have observed 5 cases of cholestatic jaundice with cytolysis during treatment with amineptine, a new tricyclic compound recently made available. The responsibility of the drug was virtually certain for the following reasons: (a) there was no other cause of jaundice, such as viral infection, gallstones, toxic agents or association with other hepatotoxic drugs; (b) clinical and biochemical findings were similar in all patients; (c) in 2 patients, reintroduction of the drug after temporary withdrawal resulted in rapid recurrence of the condition, with the same symptoms and course. The shorter delay (2 and 8 days instead of 11 and 18 days) between absorption of amineptine and reappearance of the symptoms in these two patients is suggestive of an immunoallergic mechanism.