Biomedical subjects

J Rodés

Publications and source records attributed to J Rodés.

At least 19 recordsLinked to original sources

PubMed1992

[A change in the epidemiologic pattern of hepatitis A in Spain].

BACKGROUND: Seroepidemiologic studies carried out in different countries show that the prevalence of markers for infection by hepatitis A (HVA) is progressively decreasing in relation with improvement in the level of health care. The prevalence of anti-HVA in Catalunya and the factors related with infection by HVA were studied in order to obtain bases for designing prevention strategies adequate for the epidemiology of this infection. METHODS: Anti-HVA was determined by a method of enzyme immunoassay in a randomized sample of the general population in Catalunya. Investigation of the influence of socio/demographic variables in the prevalence of HVA infection was carried out. RESULTS: The global prevalence of anti-HVA was of 36%. In the population from 6 to 14 years of age it was of 13% and that of those over the age of 15 it was 86%. The prevalence of anti-HVA increases with age and is related with the social level of the families, the level of education and the place of birth. The incidence was higher in children of the lowest social class, in adults with the least education and in those born outside Catalunya. These factors constituted independent risk factors of HVA infection. CONCLUSIONS: The present study confirms the association between HVA infection and socio-economic factors and demonstrates that the infection is not commonly found in infancy, an increase in the number of susceptible adults is foreseeable.

Age Factors↗

PubMed1992

[Prognostic value of hepatic clearance of indocyanine green in patients with liver cirrhosis and hemorrhage of esophageal varices].

BACKGROUND: The prognostic value of the quantitative tests of hepatocellular function are not clearly established. Although these tests have significantly correlated with the Child-Pugh classification, it has not been demonstrated that they are better than the same in regards to prognosis. METHODS: The present study was aimed at investigating the prognostic values of hepatic clearance and the intrinsic clearance of indocyanine green (ICG) in 91 cirrhotic patients who had presented hemorrhage due to rupture of the esophageal varices. The clinical and biochemical data, portal pressure determined during suprahepatic vein catheterization, and the clearance, intrinsic clearance, extraction and hepatic blood flow measured during continual infusion of ICG were included in the analysis. All these data were obtained following the stabilization of the patients once over the hemorrhagic episode. RESULTS: The mean survival of the series was 48 months. During follow up (25 +/- 17, interval 1-58 months) 3 of the 32 patients died (9%) of group A of the Child-Pugh classification, 17 of the 52 patients of group B (33%) and 6 of the 7 patients of group C (85%). The Child-Pugh classification was the only variable with an independent predictive value in the multivariate analysis in the Cox model. On exclusion of the 7 patients pertaining to group C, whose survival was clearly inferior to that of the rest of the series, the variables with independent predictive value were, hepatic clearance of less than 240 ml/min and the presence of ascites, while the Child-Pugh classification had no independent predictive value on survival. CONCLUSIONS: The results of the present study indicate that hepatic clearance of ICG and the presence of ascites may have prognostic value in patients of Child-Pugh classification A and B who have recovered from a hemorrhagic episode due to rupture of esophageal varices.

Adult↗

PubMed1992

Pathogenesis of arterial hypotension in cirrhotic rats with ascites: role of endogenous nitric oxide.

Nitric oxide is a vasodilator tonically secreted by endothelial cells that is involved in the regulation of arteriolar tone. This study, which includes two protocols, was performed to investigate whether nitric oxide plays a role in the pathogenesis of arterial hypotension in cirrhosis with ascites. In protocol 1, the administration of increasing doses (25, 50, 250, 500 and 1,000 micrograms.kg-1.min-1) of the nitric oxide biosynthesis inhibitor N omega-nitro-L-arginine to 18 conscious rats with cirrhosis and ascites produced, at each dose tested, a significantly greater increase in arterial pressure than in 17 conscious control rats. At the lowest dose of N omega-nitro-L-arginine, arterial pressure significantly rose in cirrhotic rats but not in controls. In protocol 2, arterial pressure, estimated renal plasma flow, glomerular filtration rate and sodium excretion were measured in 12 cirrhotic rats with ascites and 10 control rats before and during the sequential infusion of previously selected doses of N omega-nitro-L-arginine (25, 50 and 250 micrograms.kg-1.min-1). Changes in arterial pressure reproduced those observed in protocol 1. In control rats, N omega-nitro-L-arginine caused a decrease in estimated renal plasma flow without affecting glomerular filtration rate or sodium excretion. In contrast, N omega-nitro-L-arginine administration to cirrhotic animals did not produce any appreciable renal vasoconstrictor effect, and it increased glomerular filtration rate and sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Nonsyndromic paucity of intrahepatic bile ducts in infancy and idiopathic ductopenia in adulthood: the same syndrome?

Eleven patients with chronic intrahepatic cholestasis in whom a liver biopsy specimen showed unexplained bile duct paucity were investigated. Cholestasis developed during the neonatal period in three, at infancy (before 14 yr) in four and after 14 yr in the remaining four patients. In all patients other conditions characterized by chronic cholestasis associated with ductopenia such as primary biliary cirrhosis, primary sclerosing cholangitis, drug-induced liver disease, sarcoidosis or graft-vs.-host disease were excluded. Cardiovascular abnormalities in the three patients who had neonatal cholestasis permitted diagnosis of Alagille's syndrome. Clinical, biochemical and histological features were similar in the remaining eight patients, independent of the age at which the disease appeared. Idiopathic adulthood ductopenia may be a late-onset form of the nonsyndromic paucity of interlobular bile ducts seen in children, or it may be due to a still-unidentified cause that strikes later in life.

Adolescent↗

PubMed1992

Tumor size determines the efficacy of percutaneous ethanol injection for the treatment of small hepatocellular carcinoma.

This study was aimed at defining the therapeutic value of percutaneous ethanol injection in patients with solitary hepatocellular carcinoma less than 4 cm. Ultrasound-guided ethanol injection was performed in 24 cirrhotic patients (9 Child A, 10 Child B and 5 Child C), with hepatocellular carcinoma not suitable for surgical treatment. Its efficacy was assessed by repeated ultrasound, computed tomography and tumor biopsy during a follow-up ranging between 4 and 41 mo. Ethanol injection did not achieve a complete tumor necrosis in five cases after a minimum of 12 injections. Seven of the remaining 19 cases, with initial success, have shown recurrence during follow-up, thus resulting in 50% success rate, which was significantly related to baseline tumor size. The six patients with nodules less than 2 cm achieved a complete response, whereas this was recorded in 2 of the 7 with tumor size between 2 and 3 cm, and in only 1 of the 11 cases between 3 and 4 cm. The 1- and 2-yr survival of Child's A and B patients was 87% and 70%, respectively. These results indicate that percutaneous ethanol injection is a useful treatment for hepatocellular carcinoma, especially in tumors less than 3 cm. The high survival rate among patients with nonadvanced liver disease suggests that this therapeutic approach can be considered an alternative approach to surgical resection for tumors smaller than 3 cm.

Aged↗

PubMed1992

Incidence and predictive factors of first episode of spontaneous bacterial peritonitis in cirrhosis with ascites: relevance of ascitic fluid protein concentration.

To investigate the long-term probability of the appearance of the first episode of spontaneous bacterial peritonitis in cirrhosis with ascites and to identify predictors of this complication, we closely followed throughout their illness 127 patients consecutively admitted to our unit for the treatment of an episode of ascites without prior spontaneous bacterial peritonitis (follow-up period: 21 +/- 22 mo). Thirteen patients (10%) had the first spontaneous bacterial peritonitis episode during follow-up. The appearance probability of this complication is 11% at 1 yr and 15% at 3 yr. Thirty-three variables obtained at admission (including clinical data, standard liver and kidney function test results, ascitic fluid protein concentrations and hemodynamic parameters) were analyzed in relation to their value in predicting spontaneous bacterial peritonitis development. In univariate analysis (Kaplan-Meier curves) five variables reached statistical significance (p less than 0.05) as predictive factors for the development of the first spontaneous bacterial peritonitis episode. These five variables were poor nutritional status, increased serum bilirubin levels, increased serum AST levels, decreased prothrombin activity and reduced total protein concentration in ascitic fluid. When these five variables were introduced in a multivariate analysis, only the ascitic fluid protein concentration was found to correlate independently with spontaneous bacterial peritonitis development (p = 0.002). The probability of first spontaneous bacterial peritonitis after 3 yr of follow-up was 24% and 4% in patients with ascitic fluid protein content lower than 1 gm/dl and greater than or equal to 1 gm/dl, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Influence of dietary zinc on hepatic collagen and prolyl hydroxylase activity in alcoholic rats.

The effects of dietary zinc on hepatic collagen and prolyl hydroxylase activity in normal and alcoholic rats has been investigated in four groups of pair-fed male Wistar rats given either liquid ethanol or a control diet for 12 wk. Each group of pair-fed animals received a diet with a different zinc concentration (standard diet, 7.6 mg/L; low-zinc diet, 3.4 mg/L; zinc-supplemented diet, 76 mg/L; and zinc-extrasupplemented, 300 mg/L. There were no significant differences in hepatic collagen concentration and prolyl hydroxylase activity between alcoholic and normal rats receiving a standard diet (collagen, 77 +/- 5 and 73 +/- 6 micrograms/mg protein; and prolyl hydroxylase; 37 +/- 26 and 36 +/- 22 cpm/mg protein). Alcoholic rats fed a low-zinc diet showed increased prolyl hydroxylase activity (75 +/- 10 cpm/mg protein, p less than 0.05), although no changes in hepatic collagen (77 +/- 10 micrograms/mg protein) were observed in comparison with rats fed a standard alcoholic diet. By contrast, hepatic collagen was significantly lower in alcoholic rats fed a zinc-supplemented diet (66 +/- 4 and 63 +/- 3 micrograms/mg protein, p less than 0.05 and p less than 0.01, respectively), and hepatic prolyl hydroxylase activity was particularly lower in rats receiving zinc 300 mg/L (18 +/- 20 cpm/mg protein). Similar effects were observed in normal rats. We conclude that dietary zinc influences hepatic prolyl hydroxylase activity and collagen deposition in alcoholic rats, and in consequence, the control of dietary zinc is necessary to assess the effects of alcohol on collagen metabolism in rats.

Alcohol Drinking↗

PubMed1992

S-adenosylmethionine treatment prevents carbon tetrachloride-induced S-adenosylmethionine synthetase inactivation and attenuates liver injury.

Administration of carbon tetrachloride to rats resulted in induction of hepatic fibrosis and a 60% reduction of hepatic S-adenosylmethionine synthetase activity without producing any significant modification of hepatic levels of S-adenosylmethionine synthetase messenger RNA. The reduction of S-adenosylmethionine synthetase activity was corrected by treatment with S-adenosylmethionine (3 mg/kg/day, intramuscularly). Administration of carbon tetrachloride also produced a 45% depletion of liver glutathione (reduced form) that was corrected by S-adenosylmethionine treatment. After the rats received carbon tetrachloride, a 2.3-fold increase in liver collagen was observed; prolyl hydroxylase activity was 2.5 times greater than that seen in controls. These increases were attenuated in animals treated with carbon tetrachloride and S-adenosylmethionine. The attenuation by S-adenosylmethionine treatment of the fibrogenic effect of carbon tetrachloride was associated with a decrease in the number of rats in which cirrhosis developed.

Animals↗

PubMed1992

Prevalence of hepatitis B markers in the population of Catalonia (Spain). Rationale for universal vaccination of adolescents.

The prevalence of hepatitis B markers was determined in a representative sample of the general population of Catalonia (Spain). HBsAg was found in 0.5% of children (less than 15 years of age) and in 1.7% of adults (more than 15 years of age), and anti HBs in 1.6% and 18%, respectively. Age-specific prevalence for both markers showed a low risk for hepatitis B before puberty, and a progressive rise since adolescence, suggesting that perinatal transmission and horizontal transmission in children are relatively uncommon in Spain. Prevalence of hepatitis B markers was significantly higher among subjects with low education level, residing in an urban area and born outside Catalonia, but in the stratified analysis, a statistical significant difference was only maintained in the prevalence of HBV markers between those who live in urban and rural areas, and between those who were born outside Catalonia and in Catalonia. These data may be used as a basis for a strategy of hepatitis B prevention in Spain which include universal vaccination of adolescents, passive-active immunization of newborns to HBsAg positive mothers and vaccination of susceptible adults subjects from high-risk groups.

Adolescent↗

PubMed1992

Lymphocyte beta 2-adrenoceptors and plasma catecholamines in patients with cirrhosis.

The hemodynamic response to propranolol in patients with cirrhosis is heterogeneous. In some patients, there is an expected decrease in portal pressure, whereas in others, portal pressure fails to decrease despite adequate beta-blockade. It has been suggested that this lack of response could be related to down-regulation of beta 2-adrenoceptors, promoted by the increased adrenergic activity frequently found in decompensated cirrhosis. The present study investigated this hypothesis by measuring the density and affinity of lymphocyte beta 2-adrenoceptors (L-beta 2-AR), an established index of beta 2-adrenoceptors in target organs, and the plasma levels of norepinephrine and epinephrine in a group of 32 patients with cirrhosis and portal hypertension. The portal pressure response to propranolol administration (0.1 mg/kg + 2 mg/h) was also investigated (n = 27). Patients with cirrhosis had increased norepinephrine levels (605 +/- 360 vs. 224 +/- 110 pg/mL in controls; P less than 0.001), but plasma epinephrine level was not increased (136 +/- 72 vs. 111 +/- 22 pg/mL in controls; NS). There were no differences between cirrhotic patients and controls in the density of L-beta 2-AR (1398 +/- 489 vs. 1278 +/- 356 receptors/cell; NS). Portal pressure decreased greater than 10% in 12 patients (responders) and less than 10% in the remaining 15 (nonresponders). Contrary to previous suggestions, there were no significant differences between responders and nonresponders in relation to the density of L-beta 2-AR (1362 +/- 527 vs. 1487 +/- 419 receptors/cell; NS), to the affinity of these receptors (0.15 +/- 0.27 vs. 0.13 +/- 0.12 nmol/L; NS), to the plasma levels of norepinephrine (661 +/- 508 vs. 621 +/- 256 pg/mL; NS), and to plasma epinephrine concentration (141 +/- 90 vs. 140 +/- 75 pg/mL; NS). These results show that the response of portal pressure to propranolol administration is neither related to the density and affinity of L-beta 2-AR nor to the plasma levels of norepinephrine and epinephrine. Thus, the determination of these parameters cannot substitute measurements of portal pressure to identify those patients with an adequate portal pressure response to propranolol treatment.

Aged↗

PubMed1992

Effects of long-term rifampicin administration in primary biliary cirrhosis.

The effects of rifampicin treatment (10 mg.kg-1.day-1) on pruritus and cholestasis were evaluated in 16 patients with primary biliary cirrhosis and pruritus followed up for 2-24 months. Assessment of pruritus severity, liver tests, aminopyrine breath test, and bile acids was done at 2 weeks and every 3 months after the beginning of the study. Two patients (12.5%) were withdrawn after 2 months of treatment because they had hepatitis caused by rifampicin. Four patients were withdrawn after 4 months because of liver transplantation (3 cases) and the development of leg edema associated with administration of rifampicin. The remaining 10 patients received therapy for 14.4 +/- 0.7 months and did not experience side effects. Pruritus improved in all patients and disappeared in 11 patients (79%) after 3 months of treatment. Moreover, all patients followed up for more than 1 year were free of pruritus. The alkaline phosphatase level decreased significantly, and the aminopyrine breath test results increased significantly after 2 weeks of treatment (P less than 0.001) and did not change thereafter. In the 9 patients treated for 15 months, alkaline phosphatase levels decreased to 63% of the basal levels and aminopyrine breath test results increased to 153% of baseline values. Transaminases, gamma-glutamyltransferase, and total bile salt levels decreased significantly after 2 weeks of treatment but returned to baseline after 3 months. No changes in bilirubin and cholesterol levels were observed. It is concluded that long-term rifampicin treatment is effective for relieving pruritus in primary biliary cirrhosis, but liver enzymes should be monitored to detect drug-induced hepatitis.

Bile Acids and Salts↗

PubMed1992

Effects of somatostatin on renal function in cirrhosis.

To investigate the renal effects of somatostatin in cirrhosis, renal function and plasma and urinary levels of endogenous neurohumoral vasoactive substances were measured in conditions of intravenous water overload (20 mL/kg body wt with 5% glucose) before and during the intravenous infusion of somatostatin (250-500 micrograms/h) in 6 cirrhotic patients without ascites and 17 nonazotemic cirrhotic patients with ascites. Somatostatin induced a significant reduction of renal plasma flow, glomerular filtration rate, and free water clearance in both groups of patients. In patients with ascites, somatostatin also reduced urinary sodium excretion. Changes in renal function were significantly more marked in patients with ascites than in those without ascites and occurred in the absence of changes in mean arterial pressure and plasma levels of renin, aldosterone, norepinephrine, antidiuretic hormone, and atrial natriuretic peptide. Somatostatin induced a significant reduction in the plasma concentration of glucagon and urinary excretion of prostaglandin E2 that was not related to changes in renal function. These findings indicate that somatostatin administration induces renal vasoconstriction and impairs glomerular filtration rate, free water clearance, and sodium excretion in cirrhosis by a mechanism unrelated to systemic hemodynamics and endogenous neurohumoral vasoactive systems.

Dinoprostone↗

PubMed1992

Increased gastric mucosal perfusion in cirrhotic patients with portal hypertensive gastropathy.

To characterize gastric mucosal perfusion in cirrhotic patients with portal hypertensive gastropathy, 34 cirrhotics with this lesion and 24 noncirrhotics were studied by reflectance spectrophotometry and laser-Doppler flowmetry during endoscopy. A significant correlation was observed between the hemoglobin content of the gastric mucosa, measured by reflectance spectrophotometry, and the serum hemoglobin concentration both in cirrhotics (r = 0.72) and in noncirrhotics (r = 0.87). IHb ratio (hemoglobin content of gastric mucosa divided by blood hemoglobin concentration) was higher in cirrhotics with portal hypertensive gastropathy than in noncirrhotics (P < 0.001), whereas the oxygen content of the gastric mucosa was similar in both groups. This pattern indicates that cirrhotics with portal hypertensive gastropathy have increased gastric perfusion without congestion. Gastric blood flow estimated by laser-Doppler was significantly higher in cirrhotics with portal hypertensive gastropathy than in noncirrhotics (P < 0.001). In cirrhotic patients, gastric areas with cherry red spots showed a significantly higher IHb ratio than areas with a mosaic or scarlatina pattern (P < 0.05). The magnitude of changes in gastric perfusion and the endoscopic severity of portal hypertensive gastropathy had no relationship with the degree of portal hypertension or the azygos blood flow.

Female↗

PubMed1992

Modulation of the hyperdynamic circulation of cirrhotic rats by nitric oxide inhibition.

The effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) biosynthesis on the splanchnic and systemic circulation, were investigated in rats with cirrhosis induced by carbon tetrachloride. Portal hypertension in these rats was accompanied by decreased arterial blood pressure and peripheral vascular resistance as well as by splanchnic vasodilation with increased portal venous inflow and decreased splanchnic resistance. Intravenous bolus administration of L-NMMA (25 mg/kg) significantly increased systemic blood pressure and decreased cardiac output. L-NMMA also significantly increased systemic and splanchnic vascular resistance; whereas blood flow to the stomach, small intestine, colon, pancreas, mesentery, spleen, and kidney was decreased significantly. L-NMMA did not alter the portal pressure or portosystemic shunting in these cirrhotic rats, yet portal vascular resistance increased, suggesting effects on the intrahepatic and collateral circulation. Pretreatment with L-arginine (300 mg/kg) prevented the hemodynamic changes induced by L-NMMA. These findings support the concept that local excess formation of NO contributes to changes in splanchnic circulation associated with portal hypertension in cirrhosis.

Animals↗

PubMed1992

Renal insensitivity to atrial natriuretic peptide in patients with cirrhosis and ascites. Effect of increasing systemic arterial pressure.

The IV infusion of pharmacological doses (0.05 microgram.kg-1.min-1) of atrial natriuretic peptide to 16 patients with cirrhosis and ascites induced a significant increase in sodium excretion (65 +/- 23 to 517 +/- 231 mu Eq/min), urine volume (10.7 +/- 2.3 to 15.7 +/- 3.7 mL/min), and glomerular filtration rate (89 +/- 4 to 110 +/- 4 mL/min) in only 5 patients (responders). No significant changes in these parameters (15 +/- 6 to 11 +/- 4 mu Eq/min, 5.5 +/- 1.0 to 4.2 +/- 1.1 mL/min, and 81 +/- 5 to 79 +/- 6 mL/min, respectively) were observed in the remaining patients (nonresponders). Compared with responders, nonresponders had significantly lower baseline sodium excretion (P less than 0.02), urine flow (P less than 0.05), free water clearance (2.5 +/- 0.9 vs. 6.9 +/- 2.1 mL/min; P less than 0.05), and mean arterial pressure (82 +/- 3 vs. 96 +/- 2 mm Hg; P less than 0.01) and significantly higher plasma renin activity (16.3 +/- 4.9 vs. 1.8 +/- 0.2 ng.mL-1.h-1; P less than 0.05) and aldosterone level (99 +/- 24 vs. 13 +/- 2 ng/dL; P less than 0.05). Atrial natriuretic peptide produced a similar reduction of arterial pressure in both groups. To investigate whether the blunted natriuretic response to atrial natriuretic peptide in nonresponders was caused by their lower arterial pressure, atrial natriuretic peptide was infused in 7 of these patients after increasing their arterial pressure to the levels of responders with nonrepinephrine. The increase in arterial pressure (from 81 +/- 5 to 95 +/- 5 mm Hg), which was not associated with significant changes in plasma renin activity and aldosterone concentration, did not reverse the blunted renal response to atrial natriuretic peptide in any of these patients. These results indicate that cirrhotic patients with blunted renal response to atrial natriuretic peptide are characterized by low arterial pressure, marked overactivity of the renin-aldosterone system, and severe sodium and water retention. Correction of hypotension without increasing effective blood volume does not restore renal insensitivity to atrial natriuretic peptide.

Atrial Natriuretic Factor↗

PubMed1992

Assessment of the renin-angiotensin system in cirrhotic patients. Comparison between plasma renin activity and direct measurement of immunoreactive renin.

The renin-angiotensin system plays an important physiological role and has prognostic significance in cirrhotics with ascites. The degree of stimulation of this system is usually estimated by measuring plasma renin activity after incubation periods of 2-3 h. Recent investigations showed that the direct measurement of immunoreactive renin also estimates the degree of activity of the system. In this study, immunoreactive renin and plasma renin activity (measured at incubation periods of 10, 20, 50 and 180 min) were determined in ten healthy subjects, five hyperreninemic non-hepatic patients and 47 cirrhotics with ascites. Cirrhotic patients showed significantly higher plasma renin activity (5.1 +/- 0.9 ng/ml per h, p less than 0.05) and immunoreactive renin (145.4 +/- 24.4 pg/ml, p less than 0.01) than healthy subjects (1.2 +/- 0.15 ng/ml per h and 25.1 +/- 1.1 pg/ml, respectively). The angiotensin I generation rate was constant during the 3-h incubation in 22 cirrhotics and a close relationship (r = 0.956, p less than 0.001) between plasma renin activity (3.5 +/- 1.6 ng/ml per h) and immunoreactive renin (71 +/- 25 pg/ml) was observed in these patients. In the remaining 25 cirrhotics the generation rate of angiotensin I declined with time and the calculated plasma renin activity at 180 min was lower than the activity calculated at 10 min by 50.7%.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

PubMed1992

Sodium fluoride prevents bone loss in primary biliary cirrhosis.

Low-bone-turnover osteoporosis is a common complication of primary biliary cirrhosis (PBC). Since sodium fluoride stimulates bone formation we assessed the effect of this drug on bone mass in a 2-year, prospective, double-blind trial including 22 women with PBC who were randomly assigned to receive sodium fluoride (50 mg/day) or placebo. All received calcium supplements and low doses of vitamin D. Bone mineral density of the lumbar spine was measured by dual-photon absorptiometry initially and every 6 months. Vertebral fractures were evaluated in thoracic and lumbar spine initially, and after 1 and 2 years. Seven patients in the fluoride group and eight in the placebo group completed the trial. In the fluoride group, bone mineral density did not change after 2 years (initial 1.05 +/- 0.07, final 1.07 +/- 0.06 g/cm2; p = n.s.). In the placebo group, however, bone mineral density decreased significantly (initial 1.00 +/- 0.07, final 0.93 +/- 0.06 g/cm2; p = 0.03). Moreover, in the fluoride group bone mineral density increased by 2.9 +/- 3.6%, and in the placebo group decreased by 6.6 +/- 2.6% (p = 0.04). None of the patients developed new vertebral or non-vertebral fractures. Treatment with sodium fluoride did not impair liver function or cholestasis in PBC. These results indicate that sodium fluoride prevents bone loss in PBC and therefore might be considered as a possible therapeutic agent for osteoporosis associated with this liver disease. Since a small number of patients completed the trial, further studies are required.

Absorptiometry, Photon↗

PubMed1992

Surgical resection and survival in Western patients with hepatocellular carcinoma.

In a retrospective study the survival of 28 patients with hepatocellular carcinoma, 25 of them with underlying cirrhosis, submitted to surgical resection was compared with the survival of 28 untreated patients, matched for variables known to bear independent prognostic value and therefore sharing the same baseline prognosis. Diagnosis was made in the same time period for both groups of patients. In addition, to further evaluate the effects of tumor resection on survival, the outcome of operated patients was also compared to their expected survival. This was derived from a mathematical model which takes into account the regression coefficients of the variables previously shown to be independently related to the survival of untreated patients with hepatocellular carcinoma. The median survival for resected patients was 27.1 months, which was significantly better than untreated controls (12.4 months; p less than 0.003). Median survival for patients submitted to resection and with tumors smaller than 5 cm was 35.8 months, while the median survival for untreated cases was 14.6 months p less than 0.0005. The comparison of observed survival (82% at one year and 73% at two years) and statistically expected survival (58% and 34%, respectively) further indicated that surgical resection effectively improves prognosis in Western patients with hepatocellular carcinoma. Thus, early detection of small tumors in the population at risk appears to be justified.

Aged↗