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P Puri

Publications and source records attributed to P Puri.

At least 145 records · Page 8Linked to original sources
PubMed1998

Morphometric aspects of the submucous plexus in whole-mount preparations of normal human distal colon.

BACKGROUND/PURPOSE: The diagnosis of intestinal neuronal dysplasia (IND) has traditionally been based on the finding of hyperplasia of the submucous plexus and increased acetylcholinesterase activity in parasympathetic nerve fibers in the lamina propria. However, recently it has been suggested that proposed diagnostic criteria relating to nerve cell density may overlap with age-related changes and that the finding of giant ganglia (ganglia containing more than seven ganglion cells) is the most relevant diagnostic parameter of IND. Ganglion cell counting is usually performed on conventional histological sections, whereas the topology of whole ganglia has been poorly studied. The aim of this study was to define the number of ganglion cells per ganglion and the ganglion cell density (the number of ganglion cells per surface area) in submucous whole-mount preparations of normal human colon. METHODS: Specimens from distal colon were obtained during postmortem examination from 14 patients who died of nongastrointestinal disease. The submucous layer was prepared as a whole mount and stained for NADPH diaphorase (a nitrergic neurotransmitter marker) and cuprolinic blue (a general neuronal marker). Ganglion cell density was estimated by counting at least 10 mm2. The number of ganglion cells per ganglion was counted in at least 20 ganglia per case. RESULTS: Ganglion cell density (NADPH diaphorase) fell markedly during the first 5 to 6 years of life (r = -0.60, P < .05). Most ganglion cells formed ganglia of 3 to 64 cuprolinic blue staining cells. The mean number of ganglion cells per ganglion did not vary with age. CONCLUSIONS: The density of NADPH diaphorase-positive ganglion cells in the submucous plexus of human distal colon decreases markedly with age. However, the number of ganglion cells per ganglion remains constant. These findings indicate that the age of the patient has crucial importance for the histolopathologic evaluation of enteric nervous system disorders.

Adolescent↗
PubMed1998

Increased insulin-like growth factor and platelet-derived growth factor system in the pyloric muscle in infantile hypertrophic pyloric stenosis.

BACKGROUND: Infantile hypertrophic pyloric stenosis (IHPS) is characterized by hypertrophy of the pyloric muscle. The etiology of IHPS is unknown. The growth of smooth muscle cells (SMC) is regulated by several growth factors. Insulin-like growth factor (IGF) and platelet-derived growth factor (PDGF) act synergistically to stimulate SMC proliferation. The effects of IGF-I and PDGF are mediated via their receptors. METHODS: Full-thickness muscle biopsy specimens were obtained from eight IHPS patients (age range, 14 to 46 days) at pyloromyotomy and from eight age-matched controls without gastrointestinal disease at autopsy performed within 4 hours after death. Indirect three-step immunohistochemistry was performed using anti-IGF-I, IGF-I receptor alpha (IGF-IR alpha), IGF-IR beta, PDGF-BB and PDGF receptor (PDGF-R) antibodies and visualized by peroxidase staining. RESULTS: The most striking difference between tissues from IHPS patients and controls was the marked increase in IGF-I, IGF-IR alpha, IGF-IR beta and PDGF-R in the hypertrophic circular muscle layer, and, to a lesser degree, in the longitudinal muscle in pyloric stenosis. CONCLUSION: The findings suggest that the upregulated local IGF and PDGF systems may play a role in the development of pyloric muscle hypertrophy in IHPS.

Becaplermin↗
PubMed1998

Adventitial changes in pulmonary vasculature in congenital diaphragmatic hernia complicated by pulmonary hypertension.

PURPOSE: The purpose of this study was to characterize structural changes in the pulmonary vasculature in congenital diaphragmatic hernia (CDH) complicated by persistent pulmonary hypertension (PPH) with particular emphasis on adventitial thickness. METHODS: Victorian blue Van Gieson (VVG) staining and immunostaining with antialpha smooth muscle actin (ASMA) were performed on lung tissues obtained at autopsy from 23 patients with CDH complicated by PPH and 11 age-matched control tissues of sudden infant death syndrome patients (SIDS). The degree of medial and adventitial thickening was measured in pulmonary arteries with an external diameter (ED) of less than 75 microm, 75 to 100 microm, 100 to 150 microm, 150 to 250 microm, 250 to 500 microm, and greater than 500 microm by IPS-4.01 image analyzer and compared statistically. The degree of medial thickening and adventitial thickening was also measured in pulmonary veins with an ED of less than 100 microm, 100 to 200 microm, and greater than 200 microm. To determine whether the characteristic structural changes were size related, each was related to ED. The area of adventitia and media of the pulmonary arteries and veins was measured using image analyzer. RESULTS: There was a significant increase in medial and adventitial thickness in arteries of all sizes in CDH patients compared with controls (P < .01). The degree of adventitial area was significantly increased for arteries of all sizes (P < .01) and the degree of medial area was significantly increased only for arteries less than 100 microm size (P < .05) in CDH patients compared with controls. Calculation of the areas of the various components in the wall of each artery showed that for small arteries (<100 microm ED), the area of the lumen was smaller, and the areas of the media and adventitia were larger in CDH patients compared with controls (P < .01). There was a significant increase in adventitial thickness and area in veins of all sizes in CDH patients compared with controls (P < .01). The adventitial thickness of pulmonary veins were ED of less than 100 microm: CDH, 13.5 microm +/- 3.5; control, 9.21 microm +/- 2.0; ED 100 to 200 microm: CDH, 21.3 microm +/- 7.5; control, 13.0 microm +/- 4.8; ED greater than 200 microm: CDH, 34.4 microm +/- 12.5; control, 22.3 microm +/- 4.2. CONCLUSIONS: The present study provides the first quantitative demonstration of structural alterations in pulmonary veins in addition to pulmonary arteries in CDH complicated by PPH. The structural remodeling of the pulmonary vein is perhaps as a result of an increase in transvascular pressure in PPH.

Actins↗
PubMed1998

Altered insulin-like growth factor I mRNA expression in human hypoplastic lung in congenital diaphragmatic hernia.

BACKGROUND/PURPOSE: Insulin-like growth factor I (IGF-I) is a peptide growth factor that is synthesized in many organs during human development and plays a role in the growth and differentiation of tissue. IGF-I has been shown to be produced in rat and human fetal lung and to be an important mitogen involved in lung growth and development. The cells responsible for the synthesis of IGF-I in lung in vivo have been demonstrated to be type II pneumocytes, alveolar macrophages, and mesenchymal cells. Recent studies have shown that IGF-I mRNA expression in the lung is predominant during fetal life and decreases before birth, becoming barely detectable in the neonatal lung. The aim of this study was to investigate IGF-I mRNA expression in CDH lung to understand the basis of pulmonary hypoplasia in newborns with CDH. METHODS: Lung tissue samples were obtained during autopsy from 13 patients with CDH. Nine were full-term newborns (mean age, 3.8 days), and four were stillborns. Normal lung tissue from eight sudden infant death syndrome infants (mean age, 15.3 days) acted as controls. In situ hybridization was performed on frozen sections using IGF-I-specific and digoxigenin-labeled oligonucleotide probe and visualized by nitro blue tetrazolium staining. RESULTS: In control lung, IGF-I mRNA expression was absent or weak in type II pneumocytes and alveolar macrophages. In contrast, there was strong IGF-I mRNA expression in type II pneumocytes and alveolar macrophages in hypoplastic CDH lung in newborns as well as stillborns. CONCLUSION: The findings of strong IGF-I mRNA expression in the hypoplastic lung suggest that lung hypoplasia in CDH is a persistence of fetal stage of lung development.

Hernia, Diaphragmatic↗
PubMed1998

Administration of antenatal glucocorticoids prevents pulmonary artery structural changes in nitrofen-induced congenital diaphragmatic hernia in rats.

BACKGROUND/PURPOSE: The aim of this study was to investigate whether maternal administration of dexamethasone has any effect on pulmonary vasculature in nitrofen-induced experimental congenital diaphragmatic hernia (CDH) in a rat model. METHODS: A CDH model was induced in pregnant rats after administration of 100 mg nitrofen on day 9.5 of gestation. Antenatal dexamethasone, 0.25 mg/kg was given intraperitoneally on day 18.5 and 19.5 of gestation. The fetuses were divided into three groups: group I (n = 10), normal controls; group II (n = 10), nitrofen-induced CDH; group III (n = 10), nitrofen-induced CDH with maternal antenatal dexamethasone treatment. The fetuses were killed by cesarean section at term. Victorian blue van Gieson staining and immunostaining with antialpha smooth muscle actin (ASMA) were performed on lung tissue. The degree of adventitial thickness and area, and medial thickness and area were measured in pulmonary arteries by image analyzer and analyzed statistically. RESULTS: There was a significant increase in adventitial thickness and area in group II compared with group I and III (P < .01). There was also a significant increase in medial thickness in group II compared with group I and III (P < .01). The degree of adventitial thickness and area and degree of medial thickness and area were similar in controls and maternal dexamethasone-treated CDH group. CONCLUSION: This study demonstrates that antenatal maternal dexamethasone treatment prevents pulmonary artery structural changes in nitrofen-induced CDH in rats.

Animals↗
PubMed1998

Reduced glial cell line-derived neurotrophic factor level in aganglionic bowel in Hirschsprung's disease.

BACKGROUND/PURPOSE: Glial cell line-derived neurotrophic factor (GDNF) is suggested to be essential for the development of the enteric nervous system. The aim of this study was to investigate GDNF protein expression in human aganglionic (AG) bowel in Hirschsprung's disease (HD) using immunofluorescence and enzyme-linked immunosorbent assay (ELISA) analysis, to further understand the pathophysiology of HD. METHODS: Colonic specimens were obtained from eight patients with HD (aged 7 days to 14 months) at the time of definite pull-through surgery, including both normoganglionic (NG) and aganglionic (AG) segments. Immunofluorescence was performed using anti-GDNF polyclonal antibody and FITC-conjugated secondary antibody on the formalin-fixed and paraffin-embedded specimens. For ELISA analysis, specimens were homogenized by adding 10 volumes of 10-mmol/L phosphate-buffered saline containing proteinase inhibitors. Centrifuged supernatant was used for the quantitative analysis using sandwich-type ELISA for human GDNF. RESULTS: There was strong GDNF immunoreactivity in the mucosal epithelium, submucosal and myenteric plexuses, and hypertrophic nerve trunks. In the mucosa in AG bowel, the number of GDNF immunoreactive epithelial cells was significantly reduced compared with NG bowel (mean +/- SD, AG/NG = 227.2 +/- 73.1/310.8 +/- 80.5 GDNF immunoreactive cells per 100 crypts, P < .05). Using ELISA, the level of GDNF in full-thickness bowel was reduced significantly in AG bowel compared with NG bowel (mean +/- SD, AG/NG = 860.2 +/- 309.8/1777.5 +/- 271.4 pg/g wet tissue, P < .001). CONCLUSION: Because GDNF is essential for the development of the enteric nervous system, our findings of reduced level of GDNF in AG bowel as well as reduced number of GDNF immunoreactive cells in the mucosa of AG bowel suggest that GDNF may play an important role in the pathogenesis of HD.

Colon↗
PubMed1998

CNS location of uterine-related neurons revealed by trans-synaptic tracing with pseudorabies virus and their relation to estrogen receptor-immunoreactive neurons.

Retrograde, transneuronal tracing with Bartha's strain of pseudorabies virus was used in rats to identify spinal cord, brainstem and hypothalamic loci of uterine-related neurons that could function in the regulation of uterine activity. Based on the premise that estrogen might influence such uterine-related neurons, the existence of estrogen receptors in neurons in these same loci was examined. Viral injections were made into the uterine cervix, body and cervical end of the uterine horns, and the rats allowed to survive for four to six days. After four days, mainly the spinal cord, medulla and pons contained virus-infected neurons. After longer survival times, progressively higher levels of the neuraxis contained viral-labeled neurons, so that by six days hypothalamic uterine-related neurons were identified. First-order virus-infected neurons were visualized by immunohistochemistry in the pelvic paracervical parasympathetic ganglia and in inferior mesenteric sympathetic ganglia. Preganglionic and putative interneurons were labeled in the lumbosacral spinal cord and thoracic spinal cord mainly in the lateral horn area (sacral parasympathetic nucleus and intermediolateral nucleus), lateral aspect of the dorsal horn, intermediate gray, lamina X and dorsal gray commissural area. In the brainstem, labeling was most evident and consistent in the nucleus tractus solitarius, ventrolateral medulla, raphe magnus and pallidus nuclei, parapyramidal area, A5 cell group, Barrington's nucleus of the pons and periaqueductal gray of the midbrain. In the hypothalamus, virus-infected neurons were most marked in the paraventricular nucleus, with fewer in the medial preoptic area and ventromedial hypothalamic nucleus. Estrogen receptor-immunoreactive neurons were most often present among the virus-labeled uterine-related neurons of the spinal cord, nucleus tractus solitarius, ventrolateral medulla, periaqueductal gray, medial preoptic area and ventromedial hypothalamic nucleus. These results identify a multisynaptic pathway of neurons whose eventual output is involved in uterine functions, whose distribution is similar to that revealed by pseudorabies virus tracing from other visceral organs, and which are often mixed among estrogen-responsive neurons.

Afferent Pathways↗
PubMed1998

Hirschsprung's disease: a search for etiology.

In 1967, Okamoto et al suggested that the absence of ganglion cells in Hirschsprung's disease (HD) was attributable to failure of migration of neural crest cells. The earlier the arrest of migration, the longer the aganglionic segment. Since then, this hypothesis generally has been accepted. However, subsequent experiments using mouse models of intestinal aganglionosis indicate that nerve cells may reach the correct position but then fail to develop or survive. An alternative hypothesis has been proposed that the aganglionosis may be caused by failure of differentiation as a result of microenvironmental changes after the migration has occurred. Extracellular matrix proteins are recognized as important microenvironmental factors. It has been shown that enteric neurogenesis is dependent on extracellular matrices, which provide a migration pathway for neural crest-derived cells and promote the maturation of settled neural crest-derived cells. Altered distributions of extracellular matrices have been shown in human HD cases and murine HD models, suggesting the role of extracellular matrices in the pathogenesis of HD. Recent studies suggest that intestinal smooth muscle cells, target cells of enteric neurons, play an important role in guiding and influencing its own innervation. Normal maturation was inhibited in neurons cultured with smooth muscle cells of aganglionic colon in comparison to normal colon. Furthermore, it was demonstrated that levels of neurotrophic factors, crucial in the development and survival of enteric neurons, are decreased in circular muscle layers of aganglionic colon in comparison to normoganglionic colon. The smooth muscle cells of the aganglionic colon may represent an unfavorable microenvironment for neuronal development compared with the normally innervated region. Recently, markedly increased immunoreactivity of major histocompatibility complex (MHC) class II antigens and ICAM-1 was demonstrated in aganglionic bowel, suggesting the immunological mechanisms may be involved in the etiology of HD. Genetic factors have been implicated in the etiology of this condition because HD is known to occur in families and in association with some chromosomal abnormalities. Recent expansion of molecular genetics identified multiple susceptibility genes of HD, including the RET gene, the glial cell line-derived neurotrophic factor gene, the endothelin-B receptor gene, and endothelin-3 gene. Of these, inactivating mutations of the RET gene are the most frequent, occurring in 50% of familial and 15% to 20% of sporadic cases of HD. To date, despite extensive research, the exact etiology of this condition remains poorly understood. The present report describes the authors' current understanding of and recent progress in the etiology of HD.

Animals↗
PubMed1998

Genetic aspects of Hirschsprung's disease.

Hirschsprung's disease (HD) is a relatively common cause of intestinal obstruction in the newborn, characterized by the absence of autonomic ganglion cells in the terminal bowel. Existence of familial cases indicates that genetic factors may be involved in the etiology of some cases of HD. Different inheritance patterns observed in subsets of HD families or kindreds, and the detection of different chromosome aberrations in some HD patients, suggest genetic heterogeneity of HD. Recent expansion of molecular genetics has identified multiple susceptibility genes of HD. These include the RET gene, the glial cell-derived neurotrophic factor gene, the endothelin-B receptor gene, and endothelin-3 gene. Furthermore, some other genes or genetic factors are speculated to be implicated in the development of HD, and it is believed that multiple factors play a role in disease development in some cases. Taken together, these data suggest and may explain the complexity of the etiology of HD. This review focuses on recent advances in our understanding of the genetic aspects of HD.

Drosophila Proteins↗
PubMed1998

Intestinal neuronal dysplasia.

Intestinal neuronal dysplasia (IND) is a disorder of the enteric nervous system that was first described by Meier-Ruge in 1971. IND may be associated with Hirschsprung's disease or may occur as an isolated disorder. The incidence of isolated IND varies from 0.3% to 40% of suction rectal biopsies. The uncertainty regarding the incidence of IND has resulted from considerable confusion concerning essential diagnostic criteria. The diagnostic difficulties reflect the wide variability in the literature in terms of diagnostic criteria, biopsy procedures, staining techniques, and patient age. The recent application of histochemical and immunohistochemical techniques indicates that IND is a distinct histopathologic entity. The majority of patients with IND can be treated conservatively with laxatives and enemas. If bowel symptoms persist after at least 6 months of conservative treatment, internal sphincter myectomy should be considered.

Hirschsprung Disease↗
PubMed1998

Ischemic retinitis as a result of acute episodic blood loss.

Acute episodic blood loss leads to a sudden change in the haemodynamics leading to a number of ocular and systemic effects. Occurrence of ischemic retinitis secondary to acute blood loss is of a very rare occurrence. This communication presents a case of infarction of the nerve fibre layer secondary to acute blood loss in a 55-year-old male.

Acute Disease↗
PubMed1998

Medical management of orbital myocysticercosis: a pilot study.

PURPOSE: To evaluate the efficacy of albendazole in the management of orbital myocysticercosis. METHOD: Twenty-one consecutive patients diagnosed as having orbital myocysticercosis by ultrasonography, supported by computed tomography (CT)/magnetic resonance imaging (MRI), were included in the study. All patients received oral albendazole at a dosage of 30 mg/kg for 15 days with a low-dose steroid cover (5-10 mg per day). The patients were followed on day 2 at 2 weeks, 1 month, 3 months, 6 months and 9 months, and finally at 1 year. Orbital sonography was performed at 2 weeks, 3 months, 6 months, 9 months and 1 year. CT scan was performed at 6 months and 1 year. RESULTS: Orbital sonography revealed a well-defined cystic lesion with clear contents and a hyperechoic area suggestive of a scolex in all the patients. CT or MRI provided additional supportive evidence. The size of the cysts measured before treatment ranged from 6.2 to 13.4 mm (mean 11.4 mm). Medial rectus was involved in 10 cases, superior rectus in 7 cases and lateral rectus in 4 cases. Serial ultrasonography revealed a gradual reduction in the cyst size in 20 patients. A mild obscuration of the cyst wall, followed by collapse of the cyst cavity and obscuration of the scolex, were progressively seen as the cyst reduced in size. Complete resolution of the cyst was seen in all cases at 6 months. A CT scan performed at 1 year supported the ultrasonographic findings. No systemic side effects were noted. CONCLUSION: Oral albendazole appears to be highly efficacious in the management of orbital myocysticercosis.

Adolescent↗
PubMed1998

Management of choroidal metastasis: a report.

Cancers metastatic to the eye are the most common intraocular malignancy, the choroid being the most common site of affection. Breast and lung cancers are the two most common malignancies metastatic to the eye. Patients usually present with diminished visual acuity of field loss. Management of these cases is very gratifying with a large majority of patients showing resolution and maintenance of useful vision in the involved eye. This communication presents our experience in management of a case of choroidal metastasis from a breast primary. A combination of radiotherapy and chemotherapy lead to complete resolution of the lesion with no recurrences in a follow-up of over 6 months.

Angiography↗
PubMed1998

Multicenter survey of endoscopic treatment of vesicoureteral reflux using polytetrafluoroethylene.

PURPOSE: Endoscopic subureteral polytetrafluoroethylene (Teflon) injection has been used successfully to treat primary and secondary vesicoureteral reflux in children. We review the results of subureteral polytetrafluoroethylene injection in terms of its effectiveness, long-term followup and morbidity. MATERIALS AND METHODS: A total of 53 pediatric urologists and/or pediatric surgeons at 41 centers worldwide answered an inquiry regarding experience with subureteral polytetrafluoroethylene injection in vesicoureteral reflux. Data were collected from a completed standard questionnaire. From 1984 to 1996, 1,921 boys and 6,411 girls with a mean age of 4.5 years (12,251 refluxing ureters) were treated endoscopically with subureteral polytetrafluoroethylene injection. Reflux was grades I to V in 407 (3.3%), 3,832 (31.2%), 5,213 (42.5%), 2,218 (18.1%) and 581 (4.7%) ureters, respectively. In the majority of patients subureteral polytetrafluoroethylene injection was performed on an outpatient basis. Most urologists monitored patients with voiding cystourethrography and renal ultrasound at 3 months, 1 year and 3 years. All patients were followed 1 to 13 years. RESULTS: Reflux resolved in 9,226 ureters (75.3%) after 1 polytetrafluoroethylene injection, in 1,478 (12%) after 2 and in 250 (2%) after 3 or 4. Vesicoureteral reflux improved to grade I after 1 or 2 injections in 743 (6%) ureters, which needed no further treatment. Subureteral injection failed to correct reflux in 554 ureters (4.5%), which were then treated with ureteral reimplantation. Vesicoureteral junction obstruction requiring ureteral reimplantation developed in 41 ureters (0.33%). More than 90% of patients have been followed for more than 2 years. At followup reflux recurred in 326 (2.8%) endoscopically corrected refluxing ureters. No clinically untoward effects were reported in any patient due to the use of polytetrafluoroethylene as an injectable material. CONCLUSIONS: The results of this multicenter survey confirm that endoscopic subureteral polytetrafluoroethylene injection is a simple, safe and effective outpatient procedure for treating all grades of vesicoureteral reflux.

Adolescent↗
PubMed1998

Urinary tract infection and renal damage in sibling vesicoureteral reflux.

PURPOSE: Siblings of index patients with vesicoureteral reflux are known to have an increased incidence of reflux. Previously reported studies have evaluated vesicoureteral reflux in asymptomatic siblings of children who were previously proved to have reflux. We determine the incidence and nature of vesicoureteral reflux in symptomatic siblings of children with documented vesicoureteral reflux. MATERIALS AND METHODS: Between January 1990 and December 1996, 624 patients were diagnosed with vesicoureteral reflux during the investigation of documented urinary tract infections. All patients were evaluated for reflux by contrast voiding cystourethrography and reflux was graded according to the international reflux study. 99mTechnetium dimercapto-succinic acid nuclear renal scans were performed to detect renal scarring. The medical records and voiding cystourethrograms of the 624 consecutive patients with vesicoureteral reflux were retrospectively reviewed to identify siblings with vesicoureteral reflux. RESULTS: Vesicoureteral reflux was noted in 85 siblings (134 refluxing ureters) of the 624 index patients (13.6%), including 1 and 2 siblings of 38 and 3 patients, respectively. Mean age at presentation of the 37 boys and 48 girls was 2.5 years. Reflux was unilateral in 36 siblings and bilateral in 49. Reflux was grades I to V in 8, 9, 51, 55 and 11 ureters, respectively. Nuclear scan revealed reflux nephropathy in 22 of the 77 tested siblings (28.5%). CONCLUSIONS: When vesicoureteral reflux is discovered in symptomatic siblings, it is usually high grade and associated with a higher incidence of reflux nephropathy. Of further interest are the findings that refluxing symptomatic siblings of index patients are usually younger and boys are as commonly affected as girls. Screening for vesicoureteral reflux in asymptomatic siblings is recommended to decrease the incidence of reflux nephropathy.

Child↗
PubMed1998

Endoscopic correction of vesicoureteric reflux in failed reimplanted ureters.

PURPOSE: Persistent vesicoureteral reflux (VUR) after reimplantation of ureters requiring reoperation has been reported in up to 7.5% of cases. We report our experience with endoscopic subureteric Teflon injection (STING) in the treatment of VUR after failure of reimplantation of ureters. MATERIALS AND METHODS: Between 1985 and 1995, 31 children (18 male, 13 female) with persistent high-grade VUR after failure of reimplantation of ureters were referred to our hospital for endoscopic correction of VUR. The reflux was unilateral in 22 and bilateral in 9 (40 refluxing units). The ages at the time of STING ranged from 2 to 14 years. Ultrasound and voiding cystourethrography was performed in all patients at 3 months, 1 year and 3 years after STING procedure. Patients were followed-up for periods ranging from 1 to 11 years. RESULTS: VUR was successfully corrected in 27 ureters after a single injection. Seven ureters required two injections and 4 ureters three injections for the correction of reflux. Failure to correct reflux was noted in 2 ureters and these were corrected by reoperation. CONCLUSIONS: STING is a simple and effective day care procedure for the correction of VUR after failure of reimplantation of ureters.

Adolescent↗
PubMed1998

Absence of brain parenchymal damage following intravascular injection of polytetrafluoroethylene paste.

OBJECTIVE: Polytetrafluoroethylene (PTFE) paste has been used for over 30 years to treat urinary incontinence and for 14 years to treat vesicoureteral reflux with little reported morbidity. Some investigators have been concerned by the use of PTFE as the implanted substance, because migration of PTFE particles from the site of injection in the periurethral and periureteral regions to the lungs and brain has been reported in animal studies. We injected PTFE paste intravascularly in dogs in order to investigate its effect on brain parenchyma. METHODS: A total of 12 mongrel dogs, weighing 11.5-17.5 kg, were divided into four groups. Group 1 (n = 3): injection of 0.5 ml of PTFE paste suspended in 50 ml of saline into a peripheral vein once a week for 4 weeks. Group 2 (n = 3): injection of 50 ml of saline into a peripheral vein once a week for 4 weeks as controls. Group 3 (n = 3): one injection of 0.1 ml of PTFE paste suspended in 20 ml of saline into the right carotid artery. Group 4 (n = 3): one injection of 20 ml of saline into the right carotid artery as controls. After an interval of 6 months, all animals were sacrificed and the lungs and brain removed. Brain from 1 animal in each group was dissolved in sodium hypochlorite solution, the resulting organ suspension was centrifuged, and the smear preparations of the precipitate examined by polarized light microscopy, scanning electron microscopy, and X-ray microanalysis. Brains from 2 animals in each group were fixed in formalin solutions, 6-micrometer sections were cut and stained with haematoxylin and eosin, Cajal stain for Purkinje fibre, and Luxol fast blue stain for myelin, and glial fibrillary acidic protein immunohistochemistry was carried for astrocytes using monoclonal mouse anti-GFAP (glial fibrillary acidic protein) at a dilution of 1:50 with an avidin-biotin-peroxidase complex method. RESULTS: PTFE particles were seen in the cerebral vessels in only those animals who had PTFE injected into the right carotid artery. The haematoxylin and eosin staining showed PTFE particles in vessels with focal foreign-body reaction, but no infarction. Luxol fast blue staining showed no demyelination around vessels containing the particles and the parenchyma. Cajal staining demonstrated no abnormality of nerve fibres, and there was no astrocytosis using GFAP immunohistochemical staining. CONCLUSIONS: Our findings indicate that following intravenous injection, there was no evidence of migration of PTFE to the brain. Small quantities of PTFE injected into the carotid arteries were associated with local foreign-body reaction, but no brain parenchymal tissue damage was found.

Animals↗