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A Albillos

Publications and source records attributed to A Albillos.

85 records · Page 5Linked to original sources

Sequence of morphological and hemodynamic changes of gastric microvessels in portal hypertension.

Changes in gastric microvasculature and blood flow at different phases of portal hypertension were studied in rats 1, 2, 3, 4, and 15 days after induction of portal hypertension or sham operation. Vessel lumen and vessel wall thickness were expressed as a ratio referred to the vessel size. On day 2 after constriction of the portal vein, gastric blood flow was decreased (0.57 +/- 0.06 vs. 0.99 +/- 0.20 mL.min-1.100 g-1; P less than 0.05), and gastric vessels had a distended lumen (0.42 +/- 0.02 vs. 0.28 +/- 0.03; P less than 0.01) and a thin wall (2.11 +/- 0.2 vs. 3.82 +/- 0.4; P less than 0.01). On day 4, the gastric blood flow of portal hypertensive animals was increased (1.15 +/- 0.14 vs. 0.71 +/- 0.07 mL.min-1.100 g-1; P less than 0.05), whereas gastric vessels had a reduced lumen (0.27 +/- 0.02 vs. 0.33 +/- 0.02; P less than 0.01) and a thick wall (4.19 +/- 0.52 vs. 3.16 +/- 0.30; P less than 0.05). By day 15, vessels with the largest lumens (0.45 +/- 0.01 vs. 0.29 +/- 0.01; P less than 0.01) and the thinnest walls (1.78 +/- 0.26 vs. 3.58 +/- 0.62; P less than 0.01) were observed in portal hypertensive animals. In conclusion, the gastric vessels of the 15-day portal vein-ligated rat resemble the structural abnormalities described in human portal hypertensive gastropathy.

Animals↗

Oral administration of clonidine in patients with alcoholic cirrhosis. Hemodynamic and liver function effects.

The effects of long-term oral clonidine treatment on hepatic and systemic hemodynamics and on quantitative liver function tests were investigated in 15 patients with alcoholic cirrhosis. Clonidine was administered at a mean dose of 0.33 +/- 0.1 mg/day (mean +/- SD) for a mean period of 64 +/- 10 days. Oral clonidine induced a significant reduction in the hepatic venous pressure gradient from 18.8 +/- 3.0 mm Hg to 15.9 +/- 3.4 mm Hg (P less than 0.001), which was the result of an increase in the free hepatic venous pressure from 5.1 +/- 4.2 mm Hg to 8.7 +/- 3.8 mm Hg (P less than 0.05). In 10 of the 15 patients (67%), the reduction in the hepatic venous pressure gradient was greater than 10% of baseline values. Hepatic blood flow did not change significantly after clonidine treatment. Additionally, treatment with clonidine decreased mean arterial pressure by 15.5% +/- 6% (P less than 0.001), heart rate by 17.7% +/- 7% (P less than 0.001), and cardiac output by 14.6% +/- 7% (P less than 0.001). However, systemic vascular resistance did not change significantly. There were no adverse effects on liver function, as shown by the nonsignificant changes in galactose-elimination capacity (149 +/- 59 vs. 170 +/- 58 mg/min), hepatic clearance of indocyanine green (0.19 +/- 0.10 vs. 0.17 +/- 0.07 L/min), and hepatic intrinsic clearance of indocyanine green (0.23 +/- 0.14 vs. 0.21 +/- 0.1 L/min) before and after clonidine treatment, respectively. In none of the patients was the drug withdrawn because of side effects, although 12 subjects complained of dry mouths. This study suggests that in patients with alcoholic cirrhosis, long-term oral clonidine administration achieves a reduction in the hepatic venous pressure gradient without adverse effects on hepatic blood flow and liver function.

Administration, Oral↗

Ascitic fluid polymorphonuclear cell count and serum to ascites albumin gradient in the diagnosis of bacterial peritonitis.

The analysis of ascitic fluid has been complicated by several recently reported new tests. To simplify this assessment, we evaluated nine parameters prospectively and simultaneously in blood and ascitic fluid from 285 patients with ascites to determine which were the most reliable for immediate diagnosis of the etiology of the ascites and of its complications. Subjects were first divided into four groups: sterile cirrhotic ascites (n = 201), spontaneous bacterial peritonitis (n = 41), malignant ascites (n = 34), and miscellaneous ascites (n = 9). An ascitic fluid polymorphonuclear count greater than 500/microliters was the test with the greatest accuracy (96%) for the diagnosis of spontaneous bacterial peritonitis. Neither the most precise cutoff values for ascitic fluid pH (less than 7.32) and ascitic fluid lactate (greater than 32 mg/dl), nor their respective blood-ascitic fluid gradients (greater than 0.11 and less than -20 mg/dl) were more reliable indexes of spontaneous bacterial peritonitis, mainly due to the decreased ascitic fluid pH and increased ascitic fluid lactate observed in malignant ascites, tuberculous peritonitis, and pancreatic ascites. A blood-ascitic fluid albumin gradient less than 1.1 g/dl was the most accurate parameter for the diagnosis of malignant ascites (diagnostic efficacy, 93%). Therefore, the etiologic analysis of ascitic fluid might be simplified and the single practice of two tests, ascitic fluid polymorphonuclear cell count and blood-ascitic fluid albumin gradient, provides immediately useful information.

Adult↗

Different HCl and pepsinogen I secretion patterns in anatomically defined gastric ulcer subsets.

Anatomically, functionally, and clinically, peptic ulcer patients are a heterogeneous group of subjects. These patients can be classified according to the anatomic localization of the niche. The functional state of the gastric mucosa was studied in 30 gastric ulcer patients, 25 duodenal ulcer patients, and 10 normal controls. The classification of the first group was based on Johnson's criteria, with the following results: 10 individuals were type I, 10 were type II, and 10 were type III. Pepsinogen I levels and gastric acid secretion were measured in all 65 subjects under basal conditions and after subcutaneous pentagastrin stimulation. Both basal and stimulated serum pepsinogen I values were significantly higher (p less than 0.05) in gastric ulcer type III patients than in the other four groups. These values in gastric ulcer type I were similar to those of the controls. Gastric ulcer type II patients showed an intermediate functional state similar to that of duodenal ulcer patients. In both gastric ulcer type II and duodenal ulcer patients, the basal and stimulated pepsinogen I levels were significantly higher (p less than 0.05) than those found in controls, whereas the basal serum gastrin levels were similar in the five groups. In conclusion, different HCl and pepsinogen I secretory patterns, with functional heterogenicity of the gastric mucosa, are shown here for the anatomically defined gastric ulcer subsets.

Adult↗

Study of the secretion of pepsinogen I in cirrhotic humans with and without portacaval shunt.

Thirty-nine subjects have been studied: 14 with hepatic cirrhosis who had not been subjected to surgery, 13 cirrhotic patients in whom portacaval shunt had been performed, and 12 normal controls. In all of them, we performed serum determinations of pepsinogen I, both basal and after pentagastrin stimulation, and of basal gastrin levels, as well as analyses of basal and stimulated gastric acid secretion (basal acid output and maximal acid output). The values for pepsinogen I, basal or post-stimulation, were higher (p less than 0.001) in patients with cirrhosis who had not undergone surgical shunt than in those in the control group. However, there were no statistically significant differences when these two groups were compared with the patients who had been subjected to portacaval shunt. In this last group of patients, seven had levels similar to those of the controls, and six presented higher values. Likewise, the values for gastric acid secretion were similar in the three groups of patients, and the basal gastrin level was lower (p less than 0.001) among patients with liver cirrhosis, whether or not they had undergone surgery, than among the control population. In conclusion, the functional alterations of the gastric mucosa in patients with hepatic cirrhosis are not significantly different from those found in cirrhotic patients with portacaval shunt.

Adult↗

Arterioportal fistula and hemobilia with associated acute cholecystitis: a complication of percutaneous liver biopsy.

Complications attributable to percutaneous liver biopsy, including hemobilia and arterioportal fistula, are uncommon. In this report, we present the case of a patient who underwent percutaneous liver biopsy and, as a consequence of this procedure, developed an arterioportal fistula and hemobilia with associated acute cholecystitis. The diagnosis of hemobilia was possible with abdominal ultrasound and upper endoscopy, but the patient required cholecystectomy. Hepatic angiography was performed, demonstrating the arterioportal fistula and hemobilia. Transcatheter embolization occluded the fistula, resolving the hemobilia. We recommend ultrasound and upper endoscopy as initial diagnostic procedures, but angiography and selective embolization must not be delayed if arterioportal fistula and/or hemobilia is suspected since these measures may help to prevent further complications.

Acute Disease↗