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J Quiroga

Publications and source records attributed to J Quiroga.

At least 73 records · Page 4Linked to original sources
PubMed1994

Recurrent Trichosporon beigelii endocarditis after aortic valve replacement.

Fungal endocarditis of the bioprosthetic heart valve, implanted in a patient without evidence of impaired immunity, is reported. Clinical manifestations of endocarditis appeared 7 years after aortic valve replacement for rheumatic disease and included embolization into the popliteal artery. Trichosporon beigelii was isolated from the cultured fragments of the embolus. Two valve replacements were performed because of recurrent infection during the following 4 years. In spite of prolonged antifungal therapy, the patient died from multiorgan septic involvement.

Adult↗
PubMed1993

Arteriovenous shunting, hemodynamic changes, and renal sodium retention in liver cirrhosis.

BACKGROUND: Arterial vasodilation has been postulated to initiate sodium retention in cirrhosis. This work was designed to analyze whether arteriovenous shunting underlies vasodilation and influences renal function in cirrhosis. METHODS: The femoral arteriovenous difference in oxygen content (Ca-VO2) was measured in 10 healthy subjects (control group) and 31 cirrhotic patients: 9 without ascites (group 1), 10 with ascites and a urinary sodium excretion rate (UNaV) of > 10 mEq/24 h (group 2), and 12 with ascites and UNaV of < or = 10 mEq/24 h (group 3). In 8 subjects from each group, femoral blood flow and the cardiac output were determined by duplex-Doppler ultrasonography. In 9 cases arteriovenous shunting in the femoral territory was estimated using 30 +/- 5-microns radiolabeled microspheres. RESULTS: Ca-VO2 was lower in group 3 than in controls or group 1. Ca-VO2 correlated inversely with femoral blood flow, plasma renin activity, plasma aldosterone concentration, and degree of shunting measured by microspheres. Ca-VO2 correlated directly with systemic vascular resistance and prothrombin index. CONCLUSIONS: In decompensated cirrhotic patients, there is an increased arteriovenous shunt for oxygen in the lower extremities that is associated with increased arterial blood flow, decreased systemic vascular resistance, and worsening of liver function. This shunt is due partly to opening of arteriovenous precapillary connections.

Aldosterone↗
PubMed1993

Liver cytoprotection by prostaglandins.

During the last decade intensive work on the relationships between the liver and the arachidonic acid cascade has greatly expanded our knowledge of this area of research. The liver has emerged as the major organ participating in the degradation and elimination of arachidonate products of systemic origin. The synthesis in the liver of arachidonate products derived from the cyclooxygenase, lipoxygenase and cytochrome P450 system pathways has been demonstrated. The participation of leukotriene B4 and cysteinyl-leukotrienes as mediators of liver damage and the possible therapeutic usefulness of prostaglandins (PGs) in acute liver injury has attracted the interest of clinicians. This article reviews the essential features regarding the role of arachidonate metabolites in liver disease and specially focuses on the cytoprotective effects on the liver displayed by PGE2, PGE1, PGI2 and synthetic PG analogs in experimental models of liver damage induced by ischemia-reperfusion injury, carbon tetrachloride, bacterial lipopolysaccharide and viral hepatitis and on the possible mechanisms underlying liver cytoprotection in these experimental models. The therapeutic usefulness of PGs in clinical practice is critically analyzed on the basis of available evidence in patients with fulminant hepatic failure and primary graft nonfunction following liver transplantation.

Animals↗
PubMed1993

Graft-versus-host disease after liver transplantation.

We describe a case of graft-versus-host disease that developed in the recipient of an orthotopic liver transplant. A maculopapular eruption developed on postoperative day 25. After the diagnosis of graft-versus-host disease was made aggressive therapy was instituted, which resulted in a complete recovery.

Exanthema↗
PubMed1993

Partial splenic embolization for the treatment of hypersplenism in cirrhosis.

Hypersplenism is of great relevance in the management of cirrhosis because of the widespread use of myelodepressant drugs such as interferon or antineoplastic agents. Because no standard therapy exists for this complication, we have evaluated the efficacy and risks of splenic embolization in the treatment of hypersplenism in cirrhosis. Partial splenic embolization was performed in 40 consecutive patients with the following indications: 25 patients with active viral cirrhosis before interferon therapy, 8 patients with unresectable hepatocellular carcinoma before anti-neoplastic chemotherapy and 7 patients with thrombocytopenia associated with spontaneous bleeding events, with high risk of central nervous system hemorrhage or facing major surgery. After selective catheterization of the splenic artery, partial splenic embolization was performed by means of repeated injections of gelatin sponge until a 40% to 60% reduction in the splenic blood flow was achieved. After partial splenic embolization a significant and sustained increase in platelet and white blood cell count was observed during the follow-up period (mean = 13.9 +/- 2.2 mo; range = 1 to 36 mo). The goal of partial splenic embolization was achieved in all but two patients in whom a dose reduction of interferon was needed. Hypersplenism relapsed in only seven patients, and all of them exhibited an embolization of less than 50% of the splenic mass. Postembolization syndrome was the main side effect, but no life-threatening complications were detected. In conclusion, partial splenic embolization is a safe and effective therapy of hypersplenism in cirrhosis.

Adult↗
PubMed1992

Neurological complications after liver retransplantation.

Postoperative neurological complications in 185 patients who underwent two or more orthotopic liver transplantations were reviewed. The most common neurological complications were alteration of mental status (84%), seizures (33%) and focal motor deficits (15%). The frequency of neurological complications after a second orthotopic liver transplantation was significantly greater than that after a single orthotopic liver transplantation. However, neurological complications were more frequent after a second orthotopic liver transplantation than after a third transplant. Significantly more neurological complications occurred in patients who did not survive a year than in those who did, regardless of the number of transplants they underwent. These findings indicate that the risk of neurological complications among patients with multiple orthotopic liver transplantations is greater in those who require a second transplant; this risk appears to diminish after a third transplant. Importantly, the presence of neurological complications is associated with increased post-orthotopic liver transplantation mortality rate.

Adult↗
PubMed1992

Role of leukotrienes B4 and C4 in liver allograft rejection.

Previous studies have shown that eicosanoids may act in vitro as immunoregulatory substances. In this study, the concentrations of leukotriene B4 (LTB4) and leukotriene C4 (LTC4) were measured in a model of allograft rejection. Six orthotopic allotransplants of the liver were performed in dogs without the administration of immunosuppressives. LTB4 levels showed an increase coinciding with the start of rejection, significant differences being present between the basal levels and those measured 24 h post-revascularization (P < 0.05), and every day from the 3rd postoperative day (P < 0.01). LTB4 rose before the parameters generally used in evaluating rejection. LTC4 levels increased significantly (P < 0.001) in the first 24 h, and experienced no further variations. LTB4 may play an important role in the mechanisms which bring about the response to the allograft. This substance could be a specific and early marker for rejection.

Animals↗
PubMed1991

Concordance for dyslipidemic hypertension in male twins.

Sixty cases of dyslipidemic hypertension were identified in the 1028 middle-aged, white, male twin participants in the first examination of the National Heart, Lung, and Blood Institute Twin Study (1969 to 1973). The prevalence of dyslipidemic hypertension was similar by zygosity but proband concordance was three times greater in monozygotic than dizygotic twins (0.44 [seven concordant and 18 discordant pairs] vs 0.14 [two concordant and 24 discordant pairs]), suggesting a genetic effect on the condition. Low high-density lipoprotein cholesterol level was the most common lipid abnormality in concordant pairs. Mortality from ischemic heart disease was significantly higher in individuals with dyslipidemic hypertension. Obesity and glucose intolerance were closely associated with the syndrome. Moreover, within the 18 discordant monozygotic twin pairs, the twins with dyslipidemic hypertension had gained significantly more weight as adults and were significantly heavier than their unaffected cotwins. Thus, although genetic factors may influence development of dyslipidemic hypertension, nongenetic, potentially modifiable aspects of obesity are also closely related to expression of this clinically important syndrome.

Adult↗
PubMed1991

Inhibitors of the lipoxygenase arachidonic acid pathway impair glycocholate efflux in isolated rat hepatocytes.

Lipoxygenase arachidonic acid metabolites mediate secretory processes in several tissues, but their possible involvement in liver transport functions is still unknown. This study evaluated the influence of the lipoxygenase inhibitor nordihydroguayaretic acid (NDGA), the cyclooxygenase inhibitor indomethacin (INDO), and the dual cyclo and lipoxygenase inhibitors 3-amino-1-[m-(trifluoromethyl)-phenyl]-2-pyrazoline (BW 755c) and eicosatetraynoic acid (ETYA) on the handling of glycocholic acid (GC) by isolated rat hepatocytes. No drug modified cell viability or oxygen consumption in hepatocytes. In 30-min incubations with 50 microM GC the initial rate of GC uptake (V0) in control hepatocytes was 1.15 +/- 0.09 nmol.mg protein-1.min-1. The cellular GC content remained constant from 10 to 30 min (steady-state phase), the 30-min value being 6.63 +/- 0.35 nmol.mg protein-1. NDGA (10-50 microM), BW 755c (25-200 microM) and ETYA (5-100 microM), prevented the steady-state phase occurring, thus determining a progressive accumulation of GC in cells with time. As compared to controls, 50 microM NDGA (+37%, p less than 0.01), 200 microM BW 755c (+39%, p less than 0.01) and 5 microM ETYA (+19%, p less than 0.05) induced the highest increases in the amount of GC in cells at 30 min, in all cases V0 being unchanged. Concentrations of BW 755c and ETYA above those indicated also decreased V0. Both V0 and the amount of cellular GC in the steady-state phase were proportionally decreased by high INDO concentrations (25-100 microM) which did not modify the morphology of the uptake curve. Since experiments with dual and lipoxygenase inhibitors suggested an impairment of GC efflux, the initial rate of GC efflux (V0ef) was measured in hepatocytes preloaded with 50 microM GC and transferred to a GC-free medium. In controls, V0ef was 1.12 +/- 0.12 nmol.mg protein-1.min-1. BW 755c (200 microM) and NDGA (50 microM) reduced V0ef by 45 and 38%, respectively. The kinetic analysis of the effect of 200 microM BW 755c on the efflux process using hepatocytes preloaded with GC from 5 to 200 microM disclosed a non-competitive inhibition. Vmax was reduced from 1.37 +/- 0.15 to 0.89 +/- 0.10 (p less than 0.01), whereas Km was unchanged (3.79 +/- 0.33 vs. 4.25 +/- 0.54, N.S.). In summary, inhibitors of the lipoxygenase arachidonic acid pathway impaired the efflux of GC from isolated rat hepatocytes. The hypothesis is raised that oxidized metabolites of arachidonic acid may participate on the secretion of bile salts in these cells.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1991

Renal prostacyclin influences renal function in non-azotemic cirrhotic patients treated with furosemide.

The influence of prostaglandins on renal function changes induced by furosemide was analyzed in 21 non-azotemic cirrhotic patients with ascites. Patients were studied in two periods of 120 min immediately before and after furosemide infusion (20 mg, ev). Furosemide caused an increase in creatinine clearance in 15 patients (group A: 99 +/- 7 vs. 129 +/- 5 ml/min; mean +/- S.E.) and a reduction in the remaining six (group B: 102 +/- 13 vs. 71 +/- 9 ml/min). Parallel changes were observed in the urinary excretion of 6-Keto-prostaglandin-F1 alpha (metabolite of renal prostacyclin) which augmented after furosemide in 14 of the 15 patients from group A (478 +/- 107 vs. 1034 +/- 159 pg/min, p less than 0.001) and decreased in all patients from group B (1032 +/- 240 vs. 548 +/- 136 pg/min, p less than 0.05). In contrast, the urinary excretion of prostaglandin E2 was stimulated by furosemide in all patients (group A, 92 +/- 19 vs. 448 +/- 60 pg/min, p less than 0.001; and group B, 209 +/- 63 vs. 361 +/- 25 pg/min, p less than 0.05). In all of the patients furosemide-induced changes (post- minus pre-furosemide values) in creatinine clearance were closely correlated in a direct and linear fashion with those in 6-Keto-prostaglandin-F1 alpha (r = 0.74; p less than 0.001). These changes were associated with a higher furosemide-induced natriuresis in group A than in group B (641 +/- 68 vs. 302 +/- 46 mumol/min, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Concordance of ischemic heart disease in the NHLBI twin study after 14-18 years of follow-up.

Morbidity and mortality were assessed in the NHLBI twin study at the end of 1987. Deaths were greater in DZ twins (58/520, 11.2%) than MZ twins (38/508, 7.5%). Ischemic heart disease concordances were 2.3 times higher in MZ pairs and 2.8 times higher in DZ pairs than expected based on the prevalence of ischemic heart disease in the cohort. Family history scores for heart disease, calculated 14-18 years earlier at entry to the study, were significantly higher in DZ pairs where one or both members later developed ischemic heart disease and in corcordant MZ pairs than in twin-pairs without any subsequent heart disease. Concordance rates were not significantly different between MZ and DZ pairs. The results agree with previous suggestions that selection at enlistment into the armed services over 40 years ago, as well as later volunteering for the NHLBI twin study, resulted in a decline in the number of concordant MZ pairs.

Cause of Death↗
PubMed1991

Liver changes in patients with hyperthyroidism.

We studied liver changes in the hepatic biopsies of five patients with hyperthyroidism. A characteristic histopathologic picture consisting of mild to moderate intrahepatocytic cholestasis, lobular inflammatory infiltrate with some eosinophils, and Kupffer cell hyperplasia was found in all cases. We discuss the specificity, clinicopathological correlations and the possible pathophysiology of these lesions.

Biopsy↗
PubMed1991

Enhanced responsiveness to CNS-induced natriuresis in anesthetized nonascitic cirrhotic rats.

Central nervous system (CNS)-induced natriuresis was investigated in nonascitic rats with CCl4-induced cirrhosis (CTC rats) under pentobarbital anesthesia. At baseline, urine sodium output (UNa+V, in mumol.min-1.100 g body wt-1) (-30%, P less than 0.01) and mean arterial pressure (MAP, in mmHg) (-12%, P less than 0.001) were significantly reduced in CTC rats (n = 32) compared with matched controls (n = 34). In response to intracerebroventricular infusion of sodium-rich (349 mM) artificial cerebrospinal fluid (Na(+)-CSF infusion), UNa+V was significantly higher in CTC rats (2.8 +/- 0.3; n = 15) than in controls (1.7 +/- 0.2; n = 17; P less than 0.01); no differences were found in pressor changes (24 +/- 3 vs. 19 +/- 2). A similar but normal sodium CSF (150 mM) infusion did not influence UNa+V or MAP in any group (n = 12, both). In contrast, CTC rats (n = 5) showed, compared with controls (n = 5), significantly reduced natriuretic (UNa+V, 6.9 +/- 0.5 vs. 12.4 +/- 0.9; P less than 0.001) and pressor (+16 +/- 3 vs. +31 +/- 2; P less than 0.01) responses to an intravenous hypertonic sodium overload. Natriuresis induced by Na(+)-CSF infusion was related to increases in creatinine clearance (similar in both groups) and in fractional sodium excretion, which was significantly higher in CTC rats (5.90 +/- 0.15%) than in controls (3.65 +/- 0.14%; P less than 0.01). In summary, CNS-dependent efferent natriuretic mechanisms were preserved in CTC rats and were able to reverse renal tubular sodium retention in these animals. It is proposed that Na(+)-CSF infusion may be a useful tool for the study of renal sodium retention in experimental liver cirrhosis.

Animals↗
PubMed1991

[The treatment of primary biliary cirrhosis with ursodeoxycholic acid. The short- and median-term results and their relation to the study of the disease].

We present the results of the treatment with ursodeoxycholic acid (UDCA, 7-9 mg/kg body weight daily) of 17 patients with primary biliary cirrhosis (8 in stages I-II; 9 in stages III-IV). At two months the mean values of alkaline phosphatase, gammaglutamiltranspeptidase, alanine and aspartate aminotransferase were reduced (p less than 0.001, p less than 0.001, p less than 0.01 and p less than 0.01 respectively). This improvement persisted without increase during the first year. At two months the total bilirubin value was reduced (p less than 0.01) associated with a reduction in the conjugated fraction (p less than 0.05). Cholesterol and gammaglobulin mean values also decreased at two months (p less than 0.05). We found no changes in IgM levels and antimitochondrial antibody titers. The improvement was similar in both groups (early I-II and advanced III-IV stages) and the treatment showed no undesirable effects either in early or advanced stages. Almost all the patients with pruritus (6 out of 7) improved with the treatment and the use of cholestyramine was reduced in all.

Administration, Oral↗
PubMed1991

Cause and timing of first allograft failure in orthotopic liver transplantation: a study of 177 consecutive patients.

The cause and timing of first liver allograft failure was evaluated in 177 patients who underwent a second liver transplant between January 1984 and December 1988. The population studied consisted of 94 men and 83 women with a mean age 41.3 +/- 1.0 yr (mean +/- S.E.M.). Mean first-graft survival was 130.6 +/- 22.9 days (range = 0 to 2,073 days). Sixty-eight percent of the grafts failed in the first postoperative month, 26% failed between the second and twelfth month and only 6% failed beyond the twelfth month from the date of the initial transplant. Six principal causes of graft failure were identified. Early allograft losses occurred as a result of four major problems: primary graft nonfunction (30.0% of all grafts; mean graft survival = 3.4 +/- 0.3 days); ischemic injury of the graft without overt vascular injury (9.6%; mean graft survival = 17.5 +/- 1.9 days); acute rejection (10.7%; mean graft survival = 30.4 +/- 6.4 days); and overt vascular complications (26.6%; mean graft survival = 59.6 +/- 24.1 days). Late graft failures were the result of either chronic rejection (11.3%; mean graft survival = 496.3 +/- 136.0 days) or recurrence of the primary liver disease (6.8%; mean graft survival = 550.5 +/- 172.1 days). Graft failure occurred as a result of a variety of miscellaneous causes in 5% of the cases (mean graft survival in this group = 300.0 +/- 110.6 days). Overall 6-mo patient survival after a second liver transplant was 46.3%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗