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J Bosch

Publications and source records attributed to J Bosch.

At least 253 records · Page 14Linked to original sources
PubMed1991

High grade atrioventricular heart block in 2 adults with systemic lupus erythematosus.

We describe 2 patients with systemic lupus erythematosus (SLE) and high grade atrioventricular (AV) block. In one patient anti-Ro antibodies were positive. This antibody has been associated with congenital complete heart block in children of mothers with SLE; however, its role in adult high grade AV block is not clear. We reviewed the 8 published cases of adults with SLE and high grade AV block. The possible mechanisms that could be implicated in the pathology of high grade AV block are discussed.

Adult↗
PubMed1991

[Haemophilus influenzae and genital infection].

We report nine cases of H. influenzae genital infections in women. Six patients had a total of 7 episodes of Bartholin glands abscess. One patient developed a post-caesarean endomyometritis on the 16th post-delivery day. The remaining patient developed an amniotic fluid infection in the 32nd week of pregnancy. All the nine H. influenzae strains were sensitive to ampicillin. We assess the rising importance of H. influenzae as an etiologic agent of female genital tract infections.

Abscess↗
PubMed1991

[Symptomatic chronic subdural hematoma. Analysis of 68 cases treated surgically with small craniotomy and placement of a closed drainage system].

Sixty eight cases of chronic subdural hematoma (CSDH) surgically treated (December 1984-December 1988) with twist drill craniostomy (3-4 mm) and application of a closed drainage system (CDS) are reviewed. The patients were distributed in four groups depending on the density of the hematoma: hypodense (36 cases), isodense (6 cases), of mixed density (22 cases) and hyperdense (4 cases). In about one third of patients (25 cases) the duration of symptoms was shorter than one week, in 21 cases it was between one week and one month, and in 22 patients it was longer than one month. 77.95% of cases had a preceding head injury. Headache and motor deficits were the leading symptoms, being present in 43 (63.2%) and 42 (61.7%) cases, respectively. Twelve patients (17.6%) were comatose on admission. Twelve patients required reoperation. Six patients died (8.8%). The preoperative neurological status and associated systemic diseases influenced the outcome. We think that limited craniostomy with CDS is the therapy of choice for symptomatic CSDH.

Aged↗
PubMed1991

Cancer antigen 125 in serum and ascitic fluid of patients with liver diseases.

Serum concentrations of cancer antigen 125 (CA 125) were determined for 373 patients with various liver diseases: 57 with acute hepatitis, 57 with chronic hepatitis, 244 with liver cirrhosis (86 compensated and 158 decompensated), and 15 with primary liver cancer. The antigen was measured simultaneously in the serum and ascitic fluid of 46 of the patients with liver cirrhosis and sequentially in the serum and ascitic fluid of another 25 cirrhotics treated with paracentesis and (or) diuretics. Abnormal results for CA 125 were detected in sera from 4% of the patients with acute or chronic hepatitis, 60% of the patients with liver cirrhosis, and 67% of the patients with primary liver cancer. The main factor associated with abnormal serum concentrations of this antigen was the presence of ascites, with pathological CA 125 values in 94% of patients with ascites without jaundice (mean 566 +/- 528 arb. units/mL), compared with only 40% of patients with jaundice and without ascites (mean 40.1 +/- 28.5 arb. units/mL) (P less than 0.001). High concentrations of CA 125 were mainly associated with spontaneous bacterial peritonitis. The serum concentration of CA 125 decreased after treatment with paracentesis, but increased in patients treated with diuretics rather than paracentesis. The release of this antigen in liver cirrhosis appears to be independent of the liver disorder and, rather, results from peritoneal synthesis of this antigen.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed1991

Effects of ritanserin, a selective and specific S2-serotonergic antagonist, on portal pressure and splanchnic hemodynamics in portal hypertensive rats.

Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-serotonergic antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 +/- 0.8 mm Hg to 9.4 +/- 0.6 mm Hg; p less than 0.05). This was associated with lower portocollateral resistance (1.8 +/- 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 +/- 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 +/- 0.7 ml/min 100 gm vs. 5.4 +/- 0.5 ml/min 100 gm), mean arterial pressure (95.9 +/- 3.5 mm Hg vs. 94.0 +/- 4.0 mm Hg) and cardiac index (31.9 +/- 3.5 ml/min 100 gm vs. 28.5 +/- 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension.

Animals↗
PubMed1991

Propranolol in the prevention of the first hemorrhage from esophagogastric varices: A multicenter, randomized clinical trial. The Boston-New Haven-Barcelona Portal Hypertension Study Group.

To assess the effectiveness of propranolol in the prevention of initial variceal hemorrhage, a double-blind, randomized trial was carried out in three centers. Patients with cirrhosis (78% alcoholic), hepatic venous pressure gradients greater than 12 mm Hg and endoscopically proven esophageal varices were randomly assigned to propranolol (51 patients) or placebo (51 patients). Of the 102 patients, 58% were Child's class A, 34% were Child's class B and 8% were Child's class C. Daily dosage was determined by the administration of progressively increasing doses of propranolol with the hepatic vein catheter in place to achieve a 25% decrease in hepatic venous pressure gradient, a decrease in hepatic venous pressure gradient to less than 12 mm Hg or a decrease in resting heart rate to less than 55 beats/min. During a mean follow-up period of 16.3 mo, 11 patients in the placebo group (22%) bled from esophageal varices compared with 2 in the propranolol group (4%) during a mean period of 17.1 mo (p less than 0.01). Three additional patients (6%) in the placebo group bled from portal hypertensive gastropathy compared with none in the propranolol group. Propranolol appeared effective in preventing bleeding from large varices. Eleven deaths (22%) occurred in the placebo group compared with eight deaths (16%) in the propranolol group (NS). The mean dose of propranolol was 132 mg/day, and the median dose was 80 mg/day. Using a compliance index (pill count, clinic attendance, alcohol and propranolol levels and alcohol history), 81% of the propranolol patients and 77% of the placebo patients were considered compliant. Complications severe enough to require cessation of therapy occurred in eight patients (16%) in the propranolol group and four in the placebo group (8%) (NS). We conclude that propranolol effectively prevents the first variceal hemorrhage in patients with alcoholic cirrhosis and large esophageal varices but does not improve survival.

Blood Pressure↗
PubMed1991

Double-blind investigation of the effects of propranolol and placebo on the pressure of esophageal varices in patients with portal hypertension.

This study was aimed at investigating the effects of propranolol on esophageal variceal pressure in patients with portal hypertension. Variceal pressure was measured at endoscopy using a miniature pressure-sensitive gauge in 20 patients with portal hypertension. Measurements were obtained under baseline conditions and 20 min after double-blind administration of propranolol (0.15 mg/kg; n = 10) or an identical amount of placebo (normal saline, 0.3 ml/kg; n = 10). Under baseline conditions, variceal pressure was similar in propranolol and placebo groups (14.1 +/- 5 mm Hg vs. 14.9 +/- 6.6 mm Hg, respectively; not significant). Placebo had no significant effect on variceal pressure (baseline = 14.9 +/- 6.6 mm Hg; placebo = 15.5 +/- 6.6 mm Hg; not significant), and values after placebo administration were closely correlated with baseline values (r = 0.98; y = 1.1 + 0.97 x; p less than 0.0001). In contrast, propranolol caused a significant decrease in the pressure of esophageal varices (from 14.1 +/- 5 mm Hg to 11.3 +/- 4.4 mm Hg; p less than 0.0002). No significant changes in the size of esophageal varices were observed after propranolol or placebo administration. This study shows (a) the endoscopic pressure-gauge technique has a low variability and may be used to assess acute drug-induced changes in variceal pressure; and (b) propranolol causes significant decreases in variceal pressure in patients with portal hypertension and esophageal varices.

Adult↗
PubMed1990

Enhancement of portal pressure reduction by the association of isosorbide-5-mononitrate to propranolol administration in patients with cirrhosis.

This study investigated whether oral doses of isosorbide-5-mononitrate, a preferential venous dilator that decreases portal pressure, could enhance the effects of propranolol on portal hypertension. Taking part in the study were 28 patients with cirrhosis and portal hypertension. Twenty patients (group 1) had hemodynamic measurements in baseline conditions after beta-blockade by intravenous administration of propranolol and after receiving oral doses of isosorbide-5-mononitrate. The remaining eight patients (group 2) were given oral isosorbide-5-mononitrate while receiving chronic propranolol therapy. In group 1, propranolol significantly reduced portal pressure (estimated as the gradient between wedged and free hepatic venous pressures) from 21.5 +/- 3.9 to 18.6 +/- 4.2 mm Hg (-13.7%, p less than 0.001), azygos blood flow (-38%, p less than 0.001), hepatic blood flow (-12.8%, p less than 0.05), cardiac output (-24.5%, p less than 0.001) and heart rate (-18.4%, p less than 0.001) without significant changes in mean arterial pressure. Addition of oral isosorbide-5-mononitrate caused a further and marked fall in portal pressure (to 15.7 +/- 3.1 mm Hg, p less than 0.001), without additional changes in azygos blood flow but with significant additional reductions in hepatic blood flow (-15.5%, p less than 0.05), cardiac output (-11.5%, p less than 0.001) and mean arterial pressure (-22%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Hemodynamic effects of glucagon in portal hypertension.

It has been suggested that glucagon contributes to the pathogenesis of portal hypertension by increasing portal blood flow. This study examined this issue by assessing the hemodynamic effects of a pharmacological dose of glucagon (1 mg, intravenously) in patients with cirrhosis and portal hypertension (n = 10) and in subjects without significant liver disease (controls = n = 5). Patients with cirrhosis had much higher glucagon levels than control subjects (875 +/- 167 vs. 186 +/- 25 pg/ml, p less than 0.01) and showed blunted hemodynamic responses after glucagon administration. This occurred despite greater circulating glucagon levels, probably because of a significant prolongation of the plasma half-life of exogenously administered glucagon (4.9 +/- 0.4 vs. 2.7 +/- 0.1 min, p less than 0.1). Control subjects had marked increases in heart rate (+ 19% +/- 4%, p less than 0.01), cardiac index (+ 16% +/- 4%, p = 0.01) and arterial pressure (+ 10% +/- 3%, p less than 0.05), but corresponding changes in patients with cirrhosis (+ 7% +/- 1%, + 6% +/- 1%, and + 6% +/- 2%, respectively) were significantly less pronounced (p = 0.05), and there was a negative correlation between basal glucagon levels and the response of heart rate to glucagon injection (r = -0.804, p less than 0.001). Resistance to the systemic effects of glucagon in cirrhosis may thus be caused by a down-regulation of vascular glucagon receptors. In addition, glucagon administration caused a significant increase in portal pressure (from 18.1 +/- 1.1 to 19.0 +/- 1.2 mm Hg, p less than 0.01), as well as in azygos blood flow (from 0.54 +/- 0.03 to 0.64 +/- 0.04 L/min, + 19% +/- 4%, p less than 0.02), reflecting increased portocollateral blood flow. These findings are consistent with the hypothesis that glucagon is one of the factors contributing to the splanchnic vasodilatation and increased portal pressure of cirrhosis.

Azygos Vein↗
PubMed1990

Vasopressin/nitroglycerin infusion vs. esophageal tamponade in the treatment of acute variceal bleeding: a randomized controlled trial.

Vasopressin infusion and esophageal tamponade are still widely used to arrest variceal bleeding, but no objective evidence exists on the superiority of either of the two procedures. In this study, 108 cirrhotic patients bleeding from varices were included in a prospective, randomized trial to investigate the comparative effectiveness and safety of balloon tamponade (using the Sengstaken-Blakemore tube for esophageal varices and the Linton-Nachlas tube for gastric varices) (n = 52) and intravenous vasopressin infusion (0.4 to 0.8 mu/min) plus intravenous nitroglycerin infusion (40 to 400 micrograms/min) (n = 56). Both treatments were maintained for 24-hr. The hemostatic efficacy according to the intention to treat was 86.5% for tamponade and 66% for pharmacological therapy (p less than 0.01). No significant differences were found with respect to rebleeding during the first 72 hr after treatment, mortality rate or side effects. These results suggest that esophageal tamponade is more effective than vasopressin/nitroglycerin infusion in the treatment of variceal bleeding in cirrhotic patients.

Acute Disease↗
PubMed1990

Effects of propranolol on gastric microcirculation and acid secretion in portal hypertensive rats.

Rats with chronic portal hypertension have an increased gastric mucosal blood flow and an impaired acid secretory response to pentagastrin stimulation. This study investigated the effects of propranolol, a drug widely used in the treatment of portal hypertension, on gastric mucosal blood flow and acid secretion in portal hypertensive rats with partial portal vein occlusion. In study I, gastric mucosal blood flow, measured by hydrogen gas clearance, and acid output were determined in basal conditions and after the administration of propranolol (0.3 mg/kg/min) or vehicle infusion in portal hypertensive and sham-operated rats. Gastric mucosal blood flow was significantly higher (p less than 0.005) in portal hypertensive rats than in sham-operated rats, and it was significantly reduced (p less than 0.05) after propranolol infusion in portal hypertensive rats (39 +/- 2 vs. 35 +/- 3 ml/min/100 gm). Basal acid output was not significantly modified with propranolol infusion, either in portal hypertensive or sham-operated animals. In study II, acid output was measured in portal hypertensive rats in basal conditions, during pentagastrin (20 micrograms/kg/hr) infusion and after the combined infusion of pentagastrin and propranolol (or vehicle). Pentagastrin infusion significantly increased (p less than 0.001) acid output, but propranolol did not modify stimulated gastric acid secretion. In conclusion, propranolol induced a slight but significant reduction in gastric mucosal blood flow and did not change basal or stimulated gastric acid secretion.

Animals↗
PubMed1990

Hemodynamic events in a prospective randomized trial of propranolol versus placebo in the prevention of a first variceal hemorrhage.

In a double-blind randomized trial, the hemodynamic events following the administration of propranolol (n = 51) or a placebo (n = 51) were prospectively studied in cirrhotic patients with esophageal varices. The hepatic venous pressure gradient, heart rate, and variceal size were determined at the baseline and 3, 12, and 24 months after the beginning of therapy. Baseline values were similar in both groups. At 3 months, the hepatic venous pressure gradient decreased significantly in propranolol-treated patients (from 18.1 +/- 4.2 to 15.7 +/- 3.4 mm Hg; P less than 0.05) but not in patients receiving the placebo (19.6 +/- 6.8 to 17.5 +/- 5.3 mm Hg; NS). At subsequent time intervals this gradient decreased significantly from the baseline value in both groups. Heart rate decreased significantly in the propranolol-treated group at all times (P less than 0.001). Variceal hemorrhage occurred in 13 patients (11 placebo-, 2 propranolol-treated; P less than 0.01), all of whom had a hepatic venous pressure gradient greater than 12 mm Hg. In 21 patients (14 propranolol-, 7 placebo-treated) the hepatic venous pressure gradient decreased to less than or equal to 12 mm Hg; none of them bled from esophageal varices, and their mortality rate also decreased. Because most of the bleeding events occurred during the first year (10 placebo-, 1 propranolol-treated; P less than 0.01), propranolol seems to have its protective effect during the period associated with the largest reduction in the hepatic venous pressure gradient. Because a reduction in the hepatic venous pressure gradient to less than 12 mm Hg protects from variceal bleeding and increases the rate of survival, this should be the aim of the pharmacological therapy of portal hypertension.

Adult↗
PubMed1990

The lung in patients with cirrhosis.

To summarize, nowadays it seems clear that in patients with cirrhosis: (a) the pulmonary circulation is usually markedly dilated. (b) This vasodilation is due to a loss of vascular tone and it is characterized by a poor (or even absent) vascular reactivity in front of the hypoxic stimulus. (c) This abnormal behaviour of the pulmonary circulation results in VA/Q mismatching (basically perfusion of low VA/Q units) independently of airway disease, and may lower arterial PO2. (d) In the most severe cases, shunt (and perhaps O2 diffusion limitation) is becoming progressively more important. (e) The high cardiac output and minute ventilation of these patients minimize or prevent the appearance of arterial hypoxemia at rest. (f) The fall in arterial PO2 during exercise is not due to a deterioration of the degree of VA/Q mismatching seen at rest nor to any limitation in the diffusion of oxygen. It is caused by the relative 'normalization' (with respect to the metabolic demands) of the haemodynamic and ventilatory status of the patient. This may not apply to patients with severe resting arterial hypoxemia in whom the mechanisms modulating pulmonary gas exchange during exercise have not yet been addressed. What remains to be elucidated at the present time? (a) Which is (are) the precise biochemical mediator(s) of this low pulmonary vascular tone and, presumably, failure of hypoxic pulmonary vasoconstriction? It might be either a substance(s) that the failing liver fails to produce or detoxify. Thus, the ultimate biochemical basis of these physiological abnormalities must still necessarily remain speculative while awaiting future studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1990

Long-term haemodynamic effects of isosorbide 5-mononitrate in patients with cirrhosis and portal hypertension.

Since it is well known that pharmacological tolerance may rapidly occur on continuous administration of organic nitrates, in this study we attempted to investigate whether isosorbide 5-mononitrate (Is-5-Mn), a long-acting vasodilator that decreases portal pressure in acute haemodynamic studies, causes a significant reduction in portal pressure following long-term oral administration. Eleven patients with cirrhosis and portal hypertension were studied prior to and following 3 months of continuous administration of Is-5-Mn, 40 mg b.i.d. The hepatic venous pressure gradient decreased significantly following long-term Is-5-Mn treatment (from 18.6 +/- 3.4 to 17.2 +/- 3.1 mmHg; p less than 0.01). This was associated with a moderate increase in hepatic blood flow. Azygos blood flow and portal blood flow did not change. There were significant decreases in mean arterial pressure (from 89.4 +/- 13.7 to 82.6 +/- 10.8 mmHg; p less than 0.05) and heart rate (from 77 +/- 10 to 73 +/- 10 b.p.m.; p less than 0.05). In contrast, there were no changes in portal pressure or hepatic and systemic haemodynamics in a control group of 17 patients receiving placebo. Repeated nitroglycerin cross-tolerance studies in five patients receiving Is-5-Mn indicated the development of a partial pharmacological tolerance (as shown by blunted haemodynamic response to nitroglycerin after long-term Is-5-Mn administration). This study shows that Is-5-Mn continues to cause a significant decrease in portal pressure during long-term therapy, with only partial pharmacological tolerance to this compound.

Administration, Oral↗
PubMed1990

Prolonged remission after cyclosporine therapy in pemphigus vulgaris: report of two young siblings.

We report the clinical evolution of two young siblings with severe pemphigus vulgaris treated with cyclosporine for 30 and 12 months, respectively. One was resistant to treatment with high-dose corticosteroids and azathioprine. A good clinical response was achieved in both cases. No major side effects were observed. The patients have remained disease free for more than 20 months after stopping cyclosporine therapy.

Child↗
PubMed1990

Decreased systemic vascular sensitivity to norepinephrine in portal hypertensive rats: role of hyperglucagonism.

This study examined whether hyperglucagonism may promote an altered sensitivity to norepinephrine (NE) and contribute to systemic vasodilation in rats with portal hypertension due to portal vein stenosis. Three groups of male Sprague-Dawley rats were studied, portal hypertensive, normal controls, and hyperglucagonemic controls. Systemic vascular reactivity was studied by constructing dose-response curves of systemic vascular resistance (SVR) during infusions of increasing doses of NE and calculating NE ED50, the dose of NE that caused 50% of the maximal increase in SVR. Measurement of SVR was based on simultaneous measurements of arterial pressure and cardiac output (CO). Repeated measurements of CO were performed by indicator dilution curves of indocyanine green by means of a fiber-optic catheter placed in the carotid artery. Portal hypertensive rats had a decreased systemic sensitivity to NE, shown by a significant increase in NE ED50 compared with normal controls (60 +/- 8 micrograms vs. 25 +/- 3 micrograms; P less than 0.001). Glucagon levels were markedly increased in the portal hypertensive group (332 +/- 51 pg/ml vs. 176 +/- 22 pg/ml in controls; P less than 0.005). Glucagon infusion in normal rats achieved levels similar to those observed in portal hypertension (305 +/- 48 pg/ml; NS). Systemic vascular sensitivity to NE was also impaired in these hyperglucagonemic normal animals, as shown by an abnormal NE ED50 (69 +/- 16 micrograms; P less than 0.001 vs. controls) that was almost identical to that observed in portal hypertension. These results are consistent with the hypothesis that a reduced sensitivity to NE can contribute to systemic vasodilation in portal hypertension and suggest that hyperglucagonism can play a key role in its pathogenesis.

Animals↗