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Biomedical subjects

P Marchetti

Publications and source records attributed to P Marchetti.

At least 91 records · Page 5Linked to original sources
PubMed1999

Plasma membrane potential in thymocyte apoptosis.

Apoptosis is accompanied by major changes in ion compartmentalization and transmembrane potentials. Thymocyte apoptosis is characterized by an early dissipation of the mitochondrial transmembrane potential, with transient mitochondrial swelling and a subsequent loss of plasma membrane potential (DeltaP sip) related to the loss of cytosolic K+, cellular shrinkage, and DNA fragmentation. Thus, a gross perturbation of DeltaPsip occurs at the postmitochondrial stage of apoptosis. Unexpectedly, we found that blockade of plasma membrane K+ channels by tetrapentylammonium (TPA), which leads to a DeltaP sip collapse, can prevent the thymocyte apoptosis induced by exposure to the glucocorticoid receptor agonist dexamethasone, the topoisomerase inhibitor etoposide, gamma-irradiation, or ceramide. The TPA-mediated protective effect extends to all features of apoptosis, including dissipation of the mitochondrial transmembrane potential, loss of cytosolic K+, phosphatidylserine exposure on the cell surface, chromatin condensation, as well as caspase and endonuclease activation. In strict contrast, TPA is an ineffective inhibitor when cell death is induced by the potassium ionophore valinomycin, the specific mitochondrial benzodiazepine ligand PK11195, or by primary caspase activation by Fas/CD95 cross-linking. These results underline the importance of K+ channels for the regulation of some but not all pathways leading to thymocyte apoptosis.

Animals↗
PubMed1999

Effects of acute or prolonged exposure to human leptin on isolated human islet function.

The adipocyte-derived hormone leptin has been reported to inhibit, have no effect, or potentiate insulin secretion in-vitro; these effects mainly depend on the species considered, the concentrations used, and the length of exposure. We investigated the direct effects of recombinant human leptin (HL) on human pancreatic beta cell function by studying insulin secretion (IS), hexokinase and glucokinase activity and Km, and potassium channel permeability in purified human islets (HI). In acute experiments, no effect of 1, 5, 20, or 50 ng/ml HL on glucose or arginine stimulated insulin release was found, whereas 500 ng/ml HL caused a significant decrease of glucose induced IS. After 24h pre-culture with either 20 or 500 ng/ml HL, a significant reduction of glucose (but not arginine) stimulated IS was observed. Exposure to leptin caused a significant increase of potassium channel permeability, whereas hexokinase and glucokinase activity and Km remained unchanged. These results suggest that physiological human leptin concentration is able to importantly affect glucose (but not arginine) stimulated insulin release from human islets only after prolonged exposure. This effect is probably mediated by changes of potassium channel permeability, and is not accompanied by modifications of glucose phosphorylating enzymes properties.

Adult↗
PubMed1999

Differential roles of N- and C-terminal immunoreceptor tyrosine-based inhibition motifs during inhibition of cell activation by killer cell inhibitory receptors.

Killer cell inhibitory receptors (KIRs) inhibit NK and T cell cytotoxicity when recognizing MHC class I molecules on target cells. They possess two tandem intracytoplasmic immunoreceptor tyrosine-based inhibition motifs (ITIMs) that, when phosphorylated, each bind to the two Src homology 2 domain-bearing protein tyrosine phosphatases SHP-1 and SHP-2 in vitro. Using chimeric receptors having an intact intracytoplasmic KIR domain bearing both ITIMs (N + C-KIR), a deleted domain containing the N-terminal ITIM only (N-KIR), or a deleted domain containing the C-terminal ITIM only (C-KIR), we examined the respective contributions of the two ITIMs in the inhibition of cell activation in two experimental models (a rat mast cell and a mouse B cell line) that have been widely used to analyze KIR functions. We found that the two KIR ITIMs play distinct roles. When coaggregated with immunoreceptor tyrosine-based activation motif-bearing receptors such as high-affinity IgE receptors or B cell receptors, the N + C-KIR and the N-KIR chimeras, but not the C-KIR chimera, inhibited mast cell and B cell activation, became tyrosyl-phosphorylated, and recruited phosphatases in vivo. The N + C-KIR chimera recruited SHP-1 as expected, but also SHP-2. Surprisingly, the N-KIR chimera failed to recruit SHP-1; however, it did recruit SHP-2. Consequently, the N-terminal ITIM is sufficient to recruit SHP-2 and to inhibit cell activation, whereas the N-terminal and the C-terminal ITIMs are both necessary to recruit SHP-1. The two KIR ITIMs, therefore, are neither mandatory for inhibition nor redundant. Rather than simply amplifying inhibitory signals, they differentially contribute to the recruitment of distinct phosphatases that may cooperate to inhibit cell activation.

Animals↗
PubMed1999

The biguanide compound metformin prevents desensitization of human pancreatic islets induced by high glucose.

Pancreatic islet desensitization by high glucose concentrations is a temporary and reversible state of beta-cell refractoriness to glucose (and possibly other secretagogues), due to repeated or prolonged pre-exposure to increased glucose concentrations. We evaluated whether the oral antidiabetic agent metformin affects this phenomenon in isolated, human pancreatic islets, and whether the possible effects of the biguanide are influenced by the presence of a sulphonylurea, glyburide. Islets prepared from five human pancreases were incubated for 24 h in M199 culture medium containing either 5.5 or 22.2 mmol/l glucose, with or without a therapeutic concentration (2.4 microg/ml) of metformin. Then, the islets were challenged with either 3.3 mmol/l glucose, 16.7 mmol/l glucose, or 3.3 mmol/l glucose + 10 mmol/l arginine, and insulin release was measured. After incubation in the absence of metformin, the human islets exposed to 22.2 mmol/l glucose showed no significant increase in insulin release when challenged with 16.7 mmol/l glucose (confirming that hyperglycemia desensitizes pancreatic beta-cells). In the presence of metformin, the islets fully maintained the ability to significantly increase their insulin release in response to glucose, even when previously exposed to 22.2 mmol/l glucose. No major effect on arginine-induced insulin release was observed, whatever the culture conditions. The protective action of metformin was observed also when glyburide was present in the incubation medium, whereas the sulphonylurea alone did not affect insulin release from the islets previously exposed to high glucose concentrations. These in vitro results suggest that metformin can prevent the desensitization of human pancreatic islets induced by prolonged exposure to increased glucose concentrations.

Adolescent↗
PubMed1999

Clinical features and survivial of cirrhotic patients with subclinical cognitive alterations detected by the number connection test and computerized psychometric tests.

The prevalence and the clinical implications of subclinical cognitive alterations in cirrhotic patients have not been well defined as yet. Therefore, we performed a study to assess the clinical features and the survival of cirrhotic patients with cognitive alterations detected by the number connection test (NCT) and a set of computerized psychometric tests (Scan, Choice1, and Choice2) measuring the reaction times and the percentage of errors in performing specific tasks. Ninety-four cirrhotic patients (aged 58 +/- 9 years) without overt hepatic encephalopathy and 80 controls (aged 53 +/- 15 years) were consecutively enrolled. The median follow-up in cirrhotic patients was 426 days (lower quartile = 213 days; upper quartile = 718 days). Results of the NCT, Scan test, and Choice2 test were significantly worse in cirrhotic patients, whereas Choice1 did not differ significantly from the controls. In cirrhotic patients, the prevalence of altered psychometric tests was 21% (CI95% = 14%-31%) by NCT, 23% (CI95% =15%-33%) by Scan test, and 20% (CI95% =16%-30%) by Choice2 test. The alterations of NCT, Scan, and Choice2 were found to be related to the severity of liver disease, independently of its etiology. Increased risk of death was found to be associated with altered Scan test (hazard ratio = 2.4; CI95% =1. 1-5.3), or altered Choice2 test (hazard ratio = 2.8; CI95% = 1.2-6. 3). Multivariate regression showed that Scan and Choice2 tests had prognostic value on survival, in addition to Child-Pugh classes in the first year of follow-up.

Cognition↗
PubMed1999

A comparison of preconstituted, fixed combinations of low-dose glyburide plus metformin versus high-dose glyburide alone in the treatment of type 2 diabetic patients.

In the present study we assessed and compared the effectiveness and safety of preconstituted, fixed, combinations of low-dose glyburide plus metformin with higher-dose glyburide monotherapy in patients with type 2 diabetes. This randomized, double-blind, cross-over study comprised 40 patients. After a 30-day run-in period of dietary treatment, patients received combined glyburide (5, 7.5 or 10 mg/day) and metformin (800, 1,200 or 1,600 mg/day) as preconstitued, fixed combinations, or glyburide alone (5, 10 or 15 mg/day). The dose was increased stepwise so as to have 1 (T1), 2 (T2) and 3 (T3) months of treatment for any given regimen (6 months in total). After 2 weeks of washout (T4), the groups were then crossed over (T5, T6, T7 periods). Body weight, fasting plasma glucose, HbA(1c), blood lactate, total cholesterol and HDL-cholesterol, and triglycerides were measured at the beginning and end of T1 and T5, and end of T2, T3, T6 and T7; postprandial plasma glucose, fasting and postprandial plasma insulin and C-peptide were evaluated at the beginning of T1 and T5, and end of T3 and T7. At these latter time points additional assessments included routine clinical chemistry measurements, ECG, and ophthalmoscopic examination. Statistical analysis was performed by the paired Student's t-test and analysis of variance for cross-over studies. Thirty-three patients completed the study. Fasting plasma glucose, postprandial plasma glucose and HbA(1c) levels improved significantly during combined treatment with glyburide at lower doses plus metformin. This effect was achieved without any major change of insulin and C-peptide concentrations. Circulating lactate concentrations increased during the regimen including metformin, but they remained well within the reference values for normal subjects. Plasma total cholesterol and triglycerides levels remained substantielly unchanged throughout the study, whereas HDL-cholesterol concentrations increased slightly, but significantly, with glyburide plus metformin therapy. Routine clinical chemistry measurements, ECG and ophthalmoscopic examinations did not change during the study. These results demonstrate that improved metabolic control can be achieved with preconstituted, fixed combinations of low-dose glyburide plus metformin in patients with type 2 diabetes, compared to higher doses of the sulphonylurea alone.

Blood Glucose↗
PubMed1999

Spectral versus visual EEG analysis in mild hepatic encephalopathy.

OBJECTIVE: Spectral EEG analysis has been claimed to reduce subjective variability in EEG assessment of hepatic encephalopathy and to allow the detection of mild encephalopathy. METHOD: To test such assumptions, 43 digital EEG were recorded in 32 cirrhotics without overt encephalopathy or with grade 1 overt encephalopathy; 7 patients were re-tested (2-5 times) in their follow up. All patients underwent psychometric assessment. Nineteen controls were considered. EEG were blindly evaluated by two electroencephalographers and by spectral EEG analysis performed according to 3 different techniques. RESULTS: The reliability of the classification based on spectral analysis (biparietal technique) was higher than that based on a three-degree qualitative visual reading (concordance/discordance = 58/4 versus 46/16 P < 0.01) and comparable with that of semiquantitative visual assessment based on posterior basic rhythm (concordance/discordance = 55/7 P = 0.5). The accuracy of spectral EEG analysis was higher than that of qualitative visual EEG readings alone (90 versus 75%) and comparable to semi-quantitative visual assessment (87%), however, statistical significance was not reached. In the follow-up, the variations of theta and delta relative power were found to be significantly correlated with psychometric variations. CONCLUSIONS: In conclusion, spectral EEG analysis may improve the assessment of mild hepatic encephalopathy by decreasing inter-operator variability and providing reliable parameters correlated with mental status.

Adult↗
PubMed1999

Chemotactic activity of culture supernatants of free and encapsulated pancreatic rat islets towards peritoneal macrophages.

Longterm efficiency of encapsulated pancreatic islet transplantation is limited by macrophagic reaction at the surface of biocompatible membrane. The aim of this work was to investigate the influence of soluble factors released by free and encapsulated islets on macrophage chemotaxis. The culture mediums conditioned for 6 days by free and encapsulated rat islets were incubated with peritoneal murine, rat allo and syngenic macrophages to study their migration. Culture supernatants of rat fibroblasts and acinar cells, glucose-stimulated free rat islets and supernatants of free rat islets treated by heat and proteinase K were also tested for their chemotactic activity. Islets encapsulation decreased the chemotactic activity of culture medium conditioned for 6 days by free rat islets on murine (1.66 +/- 0.20 vs. 3.10 +/- 0.23; p < 0.001, n = 5) and rat allogenic macrophages (1.63 +/- 0.21 vs. 4.70 +/- 0.36; p < 0.001, n = 9). There was no migration of rat macrophages towards syngenic islets. Fibroblasts exhibited a very strong chemotactic effect as compared to acinar cells. Insulin was not involved in macrophage migration. Proteinase K treatment of culture supernatant of free rat islets totally inhibited the chemotactic activity. After heating at 56 degrees C and 100 degrees C, this activity was reduced to 41 +/- 7% and 32 +/- 5% of the initial activity, respectively. In conclusion, pancreatic islet stimulated macrophage migration by release of immunological specific proteins partly retained by macroencapsulation.

Animals↗
PubMed1999

Identification of IgG-specific oligoclonal banding in serum and cerebrospinal fluid by isoelectric focusing: description of a simplified method for the diagnosis of neurological disorders.

Clinical laboratory procedures using cerebrospinal fluid (CSF) to assist in the diagnosis of multiple sclerosis (MS) are based essentially on the determination of oligoclonal bands (OB) in CSF and not in serum. To date, the techniques using isoelectric focusing (IEF) have represented one of the most efficient methods for detecting supernumerary bands in CSF but unfortunately were not always compatible with a routine use. Here, we describe a revised method of IEF suitable for the diagnosis of neurological disorders. The kit-based technique was simplified and the present procedure allowed an easier execution, reduced the overall analysis time and permitted an uncomplicated intepretation of oligoclonal profiles. Moreover, the technique developed was very sensitive and specific for the diagnosis of MS diagnosis. In conclusion, the IEF protocol described in this report is suitable for OB detection in any laboratory.

Central Nervous System Diseases↗
PubMed1999

Autoantibodies to CD38 (ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase) in Caucasian patients with diabetes: effects on insulin release from human islets.

The type II transmembrane glycoprotein CD38 (ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase) has been proposed as a mediator of insulin secretion from pancreatic beta-cells and as a candidate for autoimmune reactions in type 2 diabetes. We evaluated the presence of anti-CD38 autoantibodies in Caucasian patients with diabetes and investigated the effect of these antibodies on insulin secretion from isolated human pancreatic islets. The presence of anti-CD38 autoantibodies was evaluated by using Western blot analysis in 236 patients with type 2 diabetes (mean age 63 years), in 160 patients with type 1 diabetes (mean age 38 years), and in 159 nondiabetic subjects. Anti-CD38 autoantibody titers at least 3 SD above the mean value of the control group were found in 9.7% of type 2 diabetic patients and in 13.1% of type 1 diabetic patients (chi2 = 15.9, P = 0.0003 vs. 1.3% of control subjects). No significant differences were observed in sex distribution, current age, age at diabetes onset, BMI, fasting serum glucose, or glycemic control between anti-CD38+ and anti-CD38-diabetic patients in either the type 2 or type 1 diabetic groups. The effect of 23 anti-CD38- and 13 anti-CD38+ sera on insulin secretion at low (3.3 mmol/l) or high (16.7 mmol/l) medium glucose concentrations was evaluated in isolated human pancreatic islets. Data are medians (interquartile range). The anti-CD38+ sera potentiated insulin release both at low [95 (64) vs. 23 (12) microU/ml of control incubations, respectively, P < 0.0001] and high [271 (336) vs. a control of 55 (37) microU/ml, respectively, P = 0.001] medium glucose concentrations, whereas the anti-CD38- sera did not. Furthermore, in the pooled data from all 36 tested sera, insulin levels in the islet incubation medium were directly related to the anti-CD38 antibody titer. We conclude that autoantibodies to CD38 are associated with both type 1 and type 2 diabetes in Caucasian subjects. These autoantibodies exert a stimulatory effect on insulin secretion by cultured human islets. The role of this autoimmune reaction in the pathogenesis of diabetes remains to be elucidated.

ADP-ribosyl Cyclase↗
PubMed1998

Characterization of sulfonylurea receptors in isolated human pancreatic islets.

Current information on pancreatic islet sulfonylurea receptors has been obtained with laboratory animal pancreatic beta cells or stable beta-cell lines. In the present study, we evaluated the properties of sulfonylurea receptors of human islets of Langherans, prepared by collagenase digestion and density-gradient purification. The binding characteristics of labeled glibenclamide to pancreatic islet membrane preparations were analyzed, displacement studies with several oral hypoglycemic agents were performed, and these latter compounds were tested as for their insulinotropic action on intact human islets. [3H]glibenclamide saturable binding was shown to be linear at < or =0.25 mg/ml protein; it was both temperature and time dependent. Scatchard analysis of the equilibrium binding data at 25 degrees C indicated the presence of a single class of saturable, high-affinity binding sites with a Kd value of 1.0+/-0.07 nM and a Bmax value of 657+/-48 fmol/mg of proteins. The displacement experiments showed the following rank order of potency of the oral hypoglycemic agents we tested: glibenclamide = glimepiride > tolbutamide > chlorpropamide >> metformin. This binding potency order was parallel with the insulinotropic potency of the evaluated compounds.

ATP-Binding Cassette Transporters↗
PubMed1998

PK11195, a ligand of the mitochondrial benzodiazepine receptor, facilitates the induction of apoptosis and reverses Bcl-2-mediated cytoprotection.

One critical step of the apoptotic process is the opening of the mitochondrial permeability transition (PT) pore leading to the disruption of mitochondrial membrane integrity and to the dissipation of the inner transmembrane proton gradient (Delta Psim). The mitochondrial PT pore is a polyprotein structure which is inhibited by the apoptosis-inhibitory oncoprotein Bcl-2 and which is closely associated with the mitochondrial benzodiazepine receptor (mBzR). Here we show that PK11195, a prototypic ligand of the 18-kDa mBzR, facilitates the induction of Delta Psim disruption and subsequent apoptosis by a number of different agents,including agonists of the glucocorticoid receptor,chemotherapeutic agents (etoposide, doxorubicin),gamma irradiation, and the proapoptotic second messenger ceramide. Whereas PK11195 itself has no cytotoxic effect, it enhances apoptosis induction by these agents. This effect is not observed for benzodiazepine diazepam, whose binding site in the mBzR differs from PK11195. PK11195 partially reverses Bcl-2 mediated inhibition of apoptosis in two different cell lines. Thus, transfection-enforced Bcl-2 overexpression confers protection against glucocorticoids and chemotherapeutic agents, and this protection is largely reversed by the addition of PK11195. This effect is observed at the level of Delta Psim dissipation as well as at the level of nuclear apoptosis. To gain insights into the site of action of PK11195, we performed experiments on isolated organelles. PK11195 reverses the Bcl-2-mediated mitochondrial retention of apoptogenic factors which cause isolated nuclei to undergo apoptosis in a cell-free system. Mitochondria from control cells, but not mitochondria from Bcl-2-overexpressing cells, readily release such apoptogenic factors in response to atractyloside, a ligand of the adenine nucleotide translocator. However, control and Bcl-2-overexpressing mitochondria respond equally well to a combination of atractyloside and PK11195. Altogether, these findings indicate that PK11195 abolishes apoptosis inhibition by Bcl-2 via a direct effect on mitochondria. Moreover, they suggest a novel strategy for enhancing the susceptibility of cells to apoptosis induction and, concomitantly, for reversing Bcl-2-mediated cytoprotection.

Animals↗
PubMed1998

The thiol crosslinking agent diamide overcomes the apoptosis-inhibitory effect of Bcl-2 by enforcing mitochondrial permeability transition.

In several different cell lines, Bcl-2 prevents the induction of apoptosis (DNA fragmentation, PARP cleavage, phosphatidylserine exposure) by the pro-oxidant ter-butylhydroperoxide (t-BHP) but has no cytoprotective effect when apoptosis is induced by the thiol crosslinking agent diazenedicarboxylic acid his 5N,N-dimethylamide (diamide). Both t-BHP and diamide cause a disruption of the mitochondrial transmembrane potential delta psi(m) that is not inhibited by the broad spectrum caspase inhibitor z-VAD.fmk, although z-VAD.fmk does prevent nuclear DNA fragmentation and poly(ADP-ribose) polymerase cleavage in these models. Bcl-2 stabilizes the delta psi(m) of t-BHP-treated cells but has no inhibitory effect on the delta psi(m) collapse induced by diamide. As compared to normal controls, isolated mitochondria from Bcl-2 overexpressing cells are relatively resistant to the induction of delta psi(m) disruption by t-BHP in vitro. Such Bcl-2 overexpressing mitochondria also fail to release apoptosis-inducing factor (AIF) and cytochrome c from the intermembrane space, whereas control mitochondria not overexpressing Bcl-2 do liberate AIF and cytochrome c in response to t-BHP. In contrast, Bcl-2 does not confer protection against diamide-triggered delta psi(m) collapse and the release of AIF and cytochrome c. This indicates that Bcl-2 suppresses the permeability transition (PT) and the associated release of intermembrane proteins induced by t-BHP but not by diamide. To further investigate the mode of action of Bcl-2, semi-purified PT pore complexes were reconstituted in liposomes in a cell-free, organelle-free system. Recombinant Bcl-2 or Bcl-X(L) proteins augment the resistance of reconstituted PT pore complexes to pore opening induced by t-BHP. In contrast, mutated Bcl-2 proteins which have lost their cytoprotective potential also lose their PT-modulatory capacity. Again, Bcl-2 fails to confer protection against diamide in this experimental system. The reconstituted PT pore complex itself cannot release cytochrome c encapsulated into liposomes. Altogether these data suggest that pro-oxidants, thiol-reactive agents, and Bcl-2 can regulate the PT pore complex in a direct fashion, independently from their effects on cytochrome c. Furthermore, our results suggest a strategy for inducing apoptosis in cells overexpressing apoptosis-inhibitory Bcl-2 analogs.

Apoptosis↗
PubMed1998

Evoked potential abnormality scores are a useful measure of disease burden in relapsing-remitting multiple sclerosis.

Fifty patients with relapsing-remitting multiple sclerosis were examined and studied with serial evoked potential and magnetic resonance imaging (MRI) measurements as part of a clinical trial. An evoked potential abnormality score (EPAS) for each testing session was calculated consisting of the total number of abnormal tests. The EPAS correlated well with Expanded Disability Status Scale (EDSS) at years 0, 1, and 2, with Spearman correlation coefficient scores of 0.68, 0.66, and 0.72, respectively. MRI lesion volume correlations ranged from 0.27 to 0.34 for the EDSS. EPAS are a potentially useful surrogate measure of clinical disability in relapsing-remitting multiple sclerosis.

Disability Evaluation↗
PubMed1998

Visual attention in cirrhotic patients: a study on covert visual attention orienting.

Attentional dysfunction, which influences overall cognitive productivity, is not well characterized in cirrhotic patients. The aim of this study was to clarify the features of covert visual attention orienting in cirrhotics without overt hepatic encephalopathy. One hundred consecutive cirrhotic patients and 40 controls were enrolled. Visual covert attention orienting was assessed by the Posner test, which evaluates the effect of a cue on visual reaction times. Patients were characterized by the number connection test (NCT) and electroencephalographic (EEG) spectral analysis. The severity of liver disease was graded using standard laboratory parameters and the Child-Pugh's classification. Fifty-five psychometric and EEG evaluations were performed in the follow-up of 17 patients to assess the relationship between the variations of psychometric and neurophysiological findings. NCT and quantified-EEG parameters (altered in 19% and 40% of cirrhotic patients, respectively) were linked to each other and to the severity of liver disease. The Posner test showed a delay of visual reaction times in class B-C cirrhotic patients. Reaction times were correlated with ammonia and EEG parameters. The effect of the cue was higher in cirrhotic patients than in controls, particularly in the invalid position. This study suggests that cirrhotic patients have a reduced activity rate and reduced capacity to disengage attention previously focused on a cue. Such alterations are linked to NCT and EEG findings.

Adult↗
PubMed1998

Gastroesophageal reflux in neurologically impaired children: partial or total fundoplication?

BACKGROUND: It is difficult to give guidelines when approaching gastroesophageal disease in neurologically impaired children. Indication for surgery has been increasing over recent years, but there is no consensus on the surgical technique of choice. Nothing has been written specifically comparing the results of different procedures in these patients, so far. STUDY DESIGN: We retrospectively compare the short- and long-term results of two different types of fundoplication in a series of children operated on for documented gastroesophageal reflux disease at our institution. RESULTS: One group (group A) of 27 patients, operated on between 1977 and 1993, underwent Nissen fundoplication, the other (group B), formed of 20 patients all of whom were operated on between 1993 and 1995, underwent Thai fundoplication. We compared the results in terms of positive outcome (recovery) and negative outcome (minor and major complication), computing the relative odds of group A versus group B in terms of risk of complication, and we compared the mean operative time and the length of hospital stay by means of a student's t-test analysis. CONCLUSIONS: Our results show that there is no statistical difference between the two procedures in terms of relative risk of complication and success rate. The duration of surgery and hospital stay were significantly shorter in group B. The Thal procedure can, therefore, be proposed as first choice in the management of these patients.

Adolescent↗
PubMed1998

Stenting for caustic strictures: esophageal replacement replaced.

METHODS: From 1983 to 1996, 31 children with caustic esophageal strictures were seen at Bambino Gesù Children's Hospital; they were all treated conservatively except for two cases complicated by tracheoesophageal fistula. The remaining 29 patients were divided into three groups depending on the treatment, which was modified over the years. Group A (1983 to 1987) consisted of seven patients treated by periodic dilatations; group B (1988 to 1992) consisted of 10 children treated by 40 days of esophageal stenting plus dexamethasone, 0.5 mg/kg/d plus ranitidine plus no oral feeding for 7 to 10 days; group C (1993 to 1996) consisted of 12 cases treated by 40 days of esophageal stenting plus dexamethasone, 1 mg/kg/d plus omeprazole plus early oral feeding resumption. RESULTS: No differences were observed between the three groups of patients with regard to the mean age and to the ingested substance, whereas a significant difference (P = .007) was observed in the mean length of the stricture between group A and C (3.4+/-1.3 and 5.6+/-1.6 cm, respectively). In all but one of the patients (96.5%) complete healing of the stenosis was achieved by conservative treatment, with definitive relief of dysphagia. One patient in group C did not improve after a repeated stenting procedure and was surgically treated. However, in group A, resolution of the stricture was obtained after an average of 19.9+/-14.8 dilatations in a mean period of 25.3+/-17.2 months. In group B, a mean of 12+/-11.3 dilatations were required in a mean period of treatment of 14.1+/-10.6 months. In patients in group C, a mean of 3.5+/-3.2 dilatations were necessary in a mean of 5.8+/-4.8 months. A statistically significant difference was observed both with regard to the number of dilatations and to the duration of treatment, between group A and group C (P = .002) and group B and C (P = .03). CONCLUSION: Esophageal replacement should be considered only in cases complicated by tracheoesophageal fistula or in the rare patients who do not respond to repeated esophageal stenting.

Anti-Bacterial Agents↗