Laparoscopic cholecystectomy in patients with bilharzial portal hypertension.
(41/1000)
OBJECTIVE: The purpose of this study was to evaluate the results of laparoscopic cholecystectomy in patients with bilharzial portal hypertension. METHODS: Patients who had gallstones and bilharzia had ultrasonographic assessment of peri-portal fibrosis, endoscopy, hemagglutination and rectal snip. Operating time, blood loss, hospital stay, time of return to work and operative mortality were recorded. Follow-up was two weeks, six weeks and six months after discharge. RESULTS: Twenty-five out of 450 patients, who had laparoscopic cholecystectomy, suffered from bilharzial portal hypertension. Ten patients had grade 1 varices, 10 had grade 2 varices, and 5 had grade 3 esophageal varices. All patients had varying degrees of peri-portal fibrosis as shown by ultrasound. Rectal snip showed schistosoma mansoni in 5 patients, and a hemagglutination test was positive in all. Two patients had conversion to open cholecystectomy. Mean operating time was 1 hour and 15 minutes. Average blood loss was 50 cc. Mean hospital stay for 23 patients was 48 hours. Average time of return to work was 2 weeks in 23 patients and 6 weeks in the 2 patients who had conversion. Twenty-two patients benefited from the operation. There was no mortality in this series. CONCLUSIONS: Laparoscopic cholecystectomy in patients with bilharzial portal hypertension is feasible and has low morbidity. (+info)
Diagnostic accuracy of abdominal ultrasonography compared to magnetic resonance imaging in siderosis of the spleen.
(42/1000)
A prospective study to compare the diagnostic performance of ultrasonography with magnetic resonance imaging using gradient-recalled echo technique in cases of siderosis of spleen was conducted in 53 cirrhotic patients with endoscopic proof of gastroesophageal varices. Of the 34 patients with splenic siderosis on MR imaging, punctate hyperechoic foci were detected in the spleen on ultrasonography in 24 patients. Using MR imaging as the reference standard for the diagnosis of splenic siderosis, the sensitivity of ultrasonography is 70.6%; specificity is 78.9%; positive predictive value is 85.7%; and negative predictive value is 40%. We conclude that ultrasonography is a fairly accurate technique in the diagnosis of splenic siderosis. (+info)
Base of tongue varices associated with portal hypertension.
(43/1000)
A symptomatic case of tongue base varices in a patient with portal hypertension secondary to liver cirrhosis is presented. There are no previously documented cases in the world literature. Oesophageal varices may not be the only source of expectorated blood in a patient with portal hypertension. (+info)
Hepatic localization of endothelin-1 in patients with idiopathic portal hypertension and cirrhosis of the liver.
(44/1000)
Endothelin-1 (ET-1) may mediate increased resistance to hepatic sinusoidal blood flow. We evaluated the hepatic distribution of ET-1 in patients with idiopathic portal hypertension (IPH), in which liver architecture may be normal, and in patients with cirrhosis, in which distortion of hepatic sinusoidal architecture is prominent. Immunohistochemistry and in situ hybridization were used to localize ET-1 in hepatic tissue of patients with IPH and cirrhosis. ET-1 was measured in plasma from a peripheral vein, the hepatic vein, and the portal vein of patients with cirrhosis of the liver and controls. On immunohistochemistry and in situ hybridization, ET-1 was localized to periportal hepatocytes and sinusoidal cells in patients with IPH and cirrhosis. Minimal positive staining for ET-1 was observed in control livers. Plasma ET-1 levels were significantly greater in patients with cirrhosis than in controls. In patients with cirrhosis, ET-1 was greater in the hepatic vein compared with the portal vein. However, the level of plasma ET-1 in patients with cirrhosis did not correlate with either the presence of ascites or portacaval pressure gradient. We conclude that in IPH, ET-1 is localized to sites in which it can modulate intrahepatic resistance. In late stages of cirrhosis, ET-1 may not modulate resistance. We speculate that vascular resistance in late stages of cirrhosis probably results from distortion of hepatic architecture. (+info)
Liver disease in patients with hereditary hemorrhagic telangiectasia.
(45/1000)
BACKGROUND: Hereditary hemorrhagic telangiectasia, or Rendu-Osler-Weber disease, is an autosomal dominant disorder characterized by angiodysplastic lesions (telangiectases and arteriovenous malformations) that affect many organs. Liver involvement in patients with this disease has not been fully characterized. METHODS: We studied the clinical findings and results of hemodynamic, angiographic, and imaging studies in 19 patients with hereditary hemorrhagic telangiectasia and symptomatic liver involvement. RESULTS: We evaluated 14 women and 5 men who ranged in age from 34 to 74 years. All but one of the patients had a hyperdynamic circulation (cardiac index, 4.2 to 7.3 liters per minute per square meter of body-surface area). In eight patients, the clinical findings were consistent with the presence of high-output heart failure. The cardiac index and pulmonary-capillary wedge pressure were elevated in the six patients in whom these measurements were performed. After a median period of 24 months, the condition of three of the eight patients had improved, four were in stable condition with medical therapy, and one had died. Six patients had manifestations of portal hypertension such as ascites or variceal bleeding. The hepatic sinusoidal pressure was elevated in the four patients in whom it was measured. After a median period of 19 months, the condition of two of the six patients had improved, and the other four had died. Five patients had manifestations of biliary disease, such as an elevated alkaline phosphatase level and abnormalities on bile duct imaging. After a median period of 30 months, the condition of two of the five had improved, the condition of one was unchanged, heart failure had developed in one, and one had died after an unsuccessful attempt at liver transplantation. CONCLUSIONS: In patients with hereditary hemorrhagic telangiectasia and symptomatic liver-involvement, the typical clinical presentations include high-output heart failure, portal hypertension, and biliary disease. (+info)
Portal hypertension induces sodium channel expression in colonocytes from the distal colon of the rat.
(46/1000)
Cellular mechanisms for Na(+) retention in portal hypertension are undefined, but epithelial Na(+) channels (ENaC) may be involved. Under high-salt diet, ENaC are absent from distal colon of rat but can be induced by mineralocorticoids such as aldosterone. Presence of rat ENaC was determined by amiloride inhibition of (22)Na(+) uptake in surface colonocytes 7 and 14 days after partial portal vein ligation (PVL) or sham surgery. At both times, uptake inhibition was significantly increased in PVL rats. Presence of mRNA transcripts, determined by RT-PCR, demonstrated that channel alpha- and gamma-subunits were similarly expressed in both groups but that beta-subunit mRNA was increased in PVL rats. This confirms that there was induction of rat ENaC and indicates that beta-subunit has a regulatory role. Urinary Na(+) was decreased for 3 days after PVL but was not different at other times, and serum aldosterone levels were elevated at 7 days, at a time when urinary Na(+) output was similar to that of sham-operated rats. We conclude that PVL leads to induction of ENaC in rat distal colon. An increase in aldosterone levels may prevent natiuresis and is probably one of several control mechanisms involved in Na(+) retention in portal hypertension. (+info)
Splanchnic hyposensitivity to glypressin in a haemorrhage/transfused rat model of portal hypertension: role of nitric oxide and bradykinin.
(47/1000)
Hyposensitivity to vasopressin is a well documented phenomenon in animals with portal hypertension and patients with cirrhosis subject to haemorrhage. Haemorrhage is associated with the endogenous release of bradykinin, which may subsequently stimulate the formation of nitric oxide (NO). The present study investigated the relative contribution of NO synthase (NOS) isoforms and the role of bradykinin in the pathogenesis of splanchnic hyposensitivity to a long-acting vasopressin analogue, glypressin, in rats with portal hypertension induced by partial portal vein ligation (PVL). At 14 days after the operation, systemic and portal haemodynamics were measured in stable or bleeding PVL rats receiving an intravenous infusion of glypressin (0.07 mg/kg). In the treatment groups, N(G)-nitro-L-arginine methyl ester (L-NAME; a non-selective NOS inhibitor), L-canavanine (a specific inhibitor of inducible NOS) or HOE 140 (a bradykinin B(2) receptor antagonist) was administered 45 min before the infusion of glypressin. In rats with a hypotensive haemorrhage, 4.5 ml of blood was withdrawn and 50% of the withdrawn blood was re-infused before the administration of glypressin or various inhibitors. Splanchnic hyposensitivity to glypressin was demonstrated in the haemorrhage/transfused PVL rats. The infusion of L-NAME elevated the mean arterial pressure in the bleeding PVL rats without the modulation of portal pressure. The addition of L-NAME or HOE 140, but not L-canavanine, significantly and similarly potentiated the portal-hypotensive effects of glypressin. It is concluded that constitutive NOS and bradykinin are responsible, at least partly, for the splanchnic hyposensitivity to glypressin observed in the early stages of the haemorrhage/transfused rat model of portal hypertension. (+info)
Systemic and portal hemodynamic effects of anandamide.
(48/1000)
The endogenous cannabinoid anandamide causes hypotension and mesenteric arteriolar dilation. A detailed analysis of its effects on systemic and portal venous hemodynamics had not yet been performed. We assessed the effects of anandamide (0.4-10 mg/kg) on systemic and portal hemodynamics with and without prior treatment with various antagonists. The specific antagonists used included SR-141716A, N(omega)-nitro-L-arginine methyl ester, indomethacin, and nordihydroguaiaretic acid. Anandamide produced a dose-dependent decrease in mean arterial pressure due to a drop in systemic vascular resistance (SVR) that was accompanied by a compensatory rise in cardiac output. Anandamide also elicited an increase in both portal venous flow and pressure, along with a decline in mesenteric vascular resistance (MVR). Pretreatment with 3 mg/kg SR-141716A, a CB(1) antagonist, prevented the decline of SVR and MVR from the lower dose of anandamide. Antagonism of nitric oxide synthetase, cyclooxygenase, or 5-lipoxygenase did not prevent the systemic nor the portal hemodynamic effects of anandamide. Furthermore, the use of R-methanandamide, a stable analog of anandamide, produced similar hemodynamic effects on the mesenteric vasculature, thereby implying that the effects of anandamide are not related to its breakdown products. Anandamide produced profound, dose-dependent alterations in both the systemic and portal circulations that could be at least partially blocked by pretreatment with SR-141716A. (+info)