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1.
Int J Surg ; 109(5): 1430-1438, 2023 May 01.
Artículo en Inglés | MEDLINE | ID: mdl-36974676

RESUMEN

BACKGROUND: Oral medications, onabotulinumtoxinA injections, and transcutaneous tibial nerve stimulation (TTNS) are recommended by the American Urological Association/Society of Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction guidelines as non or minimally invasive treatments for patients with neurogenic detrusor overactivity (NDO) without treatment hierarchy. OBJECTIVE: The objective was to compare and rank the effectiveness and safety of oral medications, three doses of onabotulinumtoxinA, and TTNS on improving urodynamic outcomes in patient-reported outcomes and safety outcomes in patients with NDO. METHODS: The authors searched PubMed, EMBASE, MEDLINE, Cochrane Library, Medicine, and clinicaltrials.gov, from their inception to October 2022 and included randomized controlled studies on the drug, onabotulinumtoxinA, and TTNS for the treatment of patients with NDO. Outcomes included urodynamic parameters, voiding diary, quality of life changes, adverse event rate and postvoid residual. RESULTS: A total of 26 articles and 2938 patients were included in the statistics. Regarding effectiveness, all interventions except TTNS and α-blockers were statistically different for the placebo group. The urodynamic outcome and patient-reported outcome suggested that onabotulinumtoxinA injection (urodynamic outcome: onabotulinumtoxinA 200 U, the mean surface under the cumulative ranking curve (SUCRA): 87.4; patient-reported outcome: onabotulinumtoxinA 100 U, mean SUCRA: 89.8) was the most effective treatment, and the safety outcome suggested that TTNS (SUCRA: 83.3) was the safest. Cluster analysis found that antimuscarinics and ß3-adrenoceptor-agonists possessed good effectiveness and safety. CONCLUSION: OnabotulinumtoxinA injection is probably the most effective way to treat patients with NDO, with increasing effectiveness but decreasing safety as the dose rises. The effectiveness of α-blockers and TTNS was not statistically different from the placebo group. Antimuscarinics and ß3-adrenoceptor-agonists have good effectiveness and safety.


Asunto(s)
Toxinas Botulínicas Tipo A , Vejiga Urinaria Neurogénica , Vejiga Urinaria Hiperactiva , Humanos , Adulto , Femenino , Toxinas Botulínicas Tipo A/efectos adversos , Calidad de Vida , Metaanálisis en Red , Antagonistas Muscarínicos/uso terapéutico , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria Neurogénica/tratamiento farmacológico , Vejiga Urinaria Hiperactiva/tratamiento farmacológico , Vejiga Urinaria Hiperactiva/inducido químicamente , Resultado del Tratamiento , Receptores Adrenérgicos/uso terapéutico , Nervio Tibial
2.
Am J Ther ; 29(5): e507-e511, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35731251

RESUMEN

BACKGROUND: Neurogenic detrusor overactivity (NDO) is treated with antimuscarinics as first-line treatment. For patients with contraindications or unresponsive, intradetrusor injections with botulinum toxin (BoNT) are a safe and effective but expensive option. STUDY QUESTION: Our study evaluated whether adding solifenacin to the intradetrusor injection of BoNT A could boost the effect of BoNT in patients with NDO due to multiple sclerosis or spinal cord injury refractory to antimuscarinics alone and/or lead to less frequent injections. STUDY DESIGN: We performed a prospective study on 49 patients assigned alternatively to group A, undergoing BoNT injections, and group B, adding solifenacin. MEASURES AND OUTCOMES: We gathered data from urodynamic testing and questionnaire assessments before and 3 months after injections and reinjections. We analyzed 39 patients who achieved total continence and a minimum 24-month follow-up period. RESULTS: After treatment, both groups had statistically significant improvement of overactive bladder questionnaire (OABq) score, post void residue (PVR), and peak detrusor pressure (Pdet). Reinjection was needed after a mean 8.2 months for group A and 11.7 months for group B. We analyzed the improvement rate of parameters compared between the 2 groups-group B had greater OABq score improvement (A = 17.25 ± 5.07, B = 20.44 ± 4.51, P = 0.0485), as well as for maximum bladder capacity (A = 11.05 ± 7.04 mL, B = 19.39 ± 6.43 mL, P = 0.0005); differences in Pdet change (A = 51.72 ± 16.57 cmH 2 O, B = 50.80 ± 16.33 cmH 2 O, P = 0.7635) and PVR change (A = 17.67 ± 12.63 mL, B = 12.30 ± 8.32 mL, P = 0.126) were not statistically significant. CONCLUSIONS: Our study shows that adding solifenacin improves patient satisfaction, increases the interval between reinjections, thus lowering costs, and improves maximum bladder capacity. Pdet was kept in safe ranges, but no statistically significant conclusions could be drawn regarding Pdet and PVR decrease related to adding solifenacin. Although our study is limited by the small series of patients and lack of randomization and placebo control group, the BoNT-solifenacin combination could be considered in NDO in terms of cost-effectiveness. Further studies would be beneficial.


Asunto(s)
Toxinas Botulínicas Tipo A , Vejiga Urinaria Neurogénica , Vejiga Urinaria Hiperactiva , Toxinas Botulínicas Tipo A/efectos adversos , Humanos , Antagonistas Muscarínicos/uso terapéutico , Estudios Prospectivos , Succinato de Solifenacina , Resultado del Tratamiento , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria Neurogénica/tratamiento farmacológico , Vejiga Urinaria Hiperactiva/tratamiento farmacológico
3.
Minerva Urol Nephrol ; 74(5): 625-635, 2022 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-33769020

RESUMEN

BACKGROUND: A randomized, double-blind, non-inferiority clinical study was performed on the efficacy and tolerability of IncobotulinumtoxinA (Incobot/A) vs. OnabotulinumtoxinA (OnabotA) intradetrusor injections in patients with refractory neurogenic detrusor overactivity incontinence performing intermittent catheterization. METHODS: Sixty-four patients with spinal cord injury (SCI) or multiple sclerosis were randomized to receive 30 intradetrusor injections of Incobot/A or OnabotA 200 U; 28 patients in incobotulinumtoxinA group and 29 in onabotulinumtoxinA group completed the study. Primary outcome measure was the non-inferior variation from baseline in daily urinary incontinence episodes (week 12), with a non-inferiority margin of one episode/day. Secondary outcomes measures were changes in Incontinence- Quality of Life questionnaire, Visual Analog Scale Score (bother of symptoms on Quality of Life), urodynamic parameters, occurrence of adverse effects and related costs (week 12). RESULTS: At week 12, mean value of difference in urinary incontinence episodes/day between the two groups was -0.2 (95% two-sided CI: -1; 0.7); the difference in incontinence episodes/day between the two groups was -0.4 with a higher limit of one-sided 95% CI of 0.2 episodes/day which was much lower than the non-inferiority margin of one episode/day. Total score and subscores of Incontinence- Quality of Life questionnaire, Visual Analog Scale scores and urodynamics did not show differences between the two groups. Adverse effects were similar for both treatments, with urinary tract infection being the most frequent, localised effect. Minor costs were observed following Incobot/A. CONCLUSIONS: In patients with refractory neurogenic incontinence due to SCI or multiple sclerosis, incobotulinumtoxinA was not inferior to onabotulinumtoxinA in improving clinical and urodynamic findings in the short-term follow-up, with comparable adverse effects but minor costs.


Asunto(s)
Toxinas Botulínicas Tipo A , Esclerosis Múltiple , Traumatismos de la Médula Espinal , Vejiga Urinaria Neurogénica , Vejiga Urinaria Hiperactiva , Incontinencia Urinaria , Toxinas Botulínicas Tipo A/efectos adversos , Humanos , Inyecciones Intramusculares , Esclerosis Múltiple/inducido químicamente , Esclerosis Múltiple/complicaciones , Calidad de Vida , Traumatismos de la Médula Espinal/inducido químicamente , Traumatismos de la Médula Espinal/complicaciones , Resultado del Tratamiento , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria Neurogénica/etiología , Vejiga Urinaria Hiperactiva/tratamiento farmacológico , Incontinencia Urinaria/tratamiento farmacológico , Incontinencia Urinaria/etiología
4.
J Pharmacol Exp Ther ; 335(1): 239-48, 2010 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-20624991

RESUMEN

We investigate the role of M(2)-muscarinic receptors in maintaining neurogenic bladder contraction during hyperglycemia. Mice were injected with a single dose of streptozotocin (125 mg/kg), and neurogenic contraction of urinary bladder from wild type and M(2)-muscarinic receptor knockout (M(2) KO) mice was measured at 8 to 24 weeks after treatment. In wild-type bladder lacking urothelium, the summation of the cholinergic (64%) and purinergic (56%) components of the electrical-field-stimulated response exceeded 100%, indicating a reserve capacity. Although the cholinergic component was slightly less in the M(2) KO mouse, the total electrical-field-stimulated contraction was the same as wild type. The cholinergic and purinergic components of contraction in wild-type bladder were minimally affected by streptozotocin treatment. In M(2) KO bladder, streptozotocin treatment reduced both the cholinergic (after 8-9 and 20-24 weeks) and purinergic (after 20-24 weeks only) components. The loss of function was approximately 50 to 70%. Similar results were observed in bladder with intact urothelium. M(2) KO bladder was more sensitive to the relaxant effect of isoproterenol compared with wild type, and this difference significantly increased at the early and late time points after streptozotocin treatment. In the presence of urothelium, however, this difference in isoproterenol sensitivity was smaller with streptozotocin treatment, but this trend reversed over time. Our results show that M(2) receptors oppose urinary bladder distension in wild-type bladder and inhibit streptozotocin-induced neuropathy.


Asunto(s)
Antibióticos Antineoplásicos , Antagonistas Muscarínicos/farmacología , Receptor Muscarínico M2/efectos de los fármacos , Estreptozocina , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria Neurogénica/prevención & control , Adenosina Trifosfato/análogos & derivados , Adenosina Trifosfato/farmacología , Agonistas Adrenérgicos beta/farmacología , Algoritmos , Animales , Glucemia/metabolismo , Peso Corporal/efectos de los fármacos , Estimulación Eléctrica , Hiperglucemia/inducido químicamente , Hiperglucemia/patología , Técnicas In Vitro , Isoproterenol/farmacología , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Contracción Muscular/efectos de los fármacos , Contracción Muscular/fisiología , Músculo Liso/efectos de los fármacos , Tamaño de los Órganos/efectos de los fármacos , Receptor Muscarínico M2/genética
5.
Pain Med ; 10(8): 1389-94, 2009 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-19863744

RESUMEN

OBJECTIVE: To present two case reports of a rare but devastating injury after image-guided, lumbar transforaminal injection of steroids, and to explore features in common with previously reported cases. BACKGROUND: Image (fluoroscopic and computed tomography [CT])-guided, lumbar transforaminal injections of corticosteroids have been adopted as a treatment for radicular pain. Complications associated with these procedures are rare, but can be severe. CASE REPORTS: An 83-year-old woman underwent a fluoroscopically guided, left L3-L4, transforaminal injection of betamethasone (Celestone Soluspan). A 79-year-old man underwent a CT-guided, right L3-L4, transforaminal injection of methylprednisolone (DepoMedrol). Both patients developed bilateral lower extremity paralysis, with neurogenic bowel and bladder, immediately after the procedures. Magnetic resonance imaging scans were consistent with spinal cord infarction. There was no evidence of intraspinal mass or hematoma. CONCLUSION: These cases consolidate a pattern emerging in the literature. Distal cord and conus injury can occur following transforaminal injections at lumbar levels, whether injection is on the left or right. This conforms with the probability of radicular-medullary arteries forming an arteria radicularis magna at lumbar levels. All cases used particulate corticosteroids, which promotes embolization in a radicular artery as the likely mechanism of injury. The risk of this complication can be reduced, and potentially eliminated, by the utilization of particulate free steroids, testing for intra-arterial injection with digital subtraction angiography, and a preliminary injection of local anesthetic.


Asunto(s)
Fluoroscopía/métodos , Dolor de la Región Lumbar/tratamiento farmacológico , Vértebras Lumbares/cirugía , Paraplejía/inducido químicamente , Radiculopatía/tratamiento farmacológico , Esteroides/efectos adversos , Anciano , Anciano de 80 o más Años , Arterias/lesiones , Arterias/patología , Arterias/fisiopatología , Embolia/inducido químicamente , Embolia/patología , Embolia/fisiopatología , Femenino , Humanos , Enfermedad Iatrogénica/prevención & control , Infarto/inducido químicamente , Infarto/patología , Infarto/fisiopatología , Inyecciones Epidurales/efectos adversos , Inyecciones Epidurales/métodos , Pierna/inervación , Pierna/fisiopatología , Dolor de la Región Lumbar/fisiopatología , Vértebras Lumbares/diagnóstico por imagen , Vértebras Lumbares/patología , Imagen por Resonancia Magnética , Masculino , Metilprednisolona/administración & dosificación , Metilprednisolona/efectos adversos , Paraplejía/fisiopatología , Complicaciones Posoperatorias/etiología , Complicaciones Posoperatorias/fisiopatología , Complicaciones Posoperatorias/prevención & control , Radiculopatía/fisiopatología , Traumatismos de la Médula Espinal/inducido químicamente , Traumatismos de la Médula Espinal/patología , Traumatismos de la Médula Espinal/fisiopatología , Esteroides/administración & dosificación , Esteroides/química , Cirugía Asistida por Computador/efectos adversos , Cirugía Asistida por Computador/métodos , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria Neurogénica/fisiopatología , Articulación Cigapofisaria/efectos de los fármacos , Articulación Cigapofisaria/fisiopatología
8.
J Med Toxicol ; 4(2): 106-8, 2008 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-18570171

RESUMEN

INTRODUCTION: The use of 3,4-methylenedioxymethamphetamine (MDMA, known as "ecstasy"), a synthetic amphetamine and "club drug," has been associated with acute, transient urinary retention. We report a case of neurogenic bladder and chronic urinary retention associated with MDMA abuse. CASE REPORT: A 21-year-old male presented to the emergency department (ED) because he had abdominal pain and difficulty urinating. He had experienced difficulty in initiating urination over the past 1.5 months, with periods of 24 to 36 hours between voids and large volumes of urine. The patient had a chronic pattern of MDMA use, taking 4 tablets/day for 3 months. Two weeks before coming to the ED, he had been admitted to an inpatient drug rehabilitation center. During the time since that admission, the patient had visited EDs repeatedly for insertion and removal of Foley catheters to relieve the urinary retention until he could be admitted to a urologic service. Cystometrogram was abnormal, finding no sensation of bladder fullness after instillation of 350 mL of saline and inability to generate a voluntary voiding pressure. Cystoscopy revealed no outlet obstruction. The findings were consistent with neurogenic bladder. The patient was given prescriptions for bethanecol and phenazopyridine, and told to continue a 10-day course of sulfamethoxazole/trimethoprim for urinary tract infection. He was discharged with a Foley catheter in place. Symptoms of urinary retention persisted at 1-year follow-up, despite self-catheterization and complete cessation of MDMA use. CONCLUSION: Chronic MDMA use may lead to neurogenic bladder and chronic urinary retention.


Asunto(s)
Trastornos Relacionados con Anfetaminas/complicaciones , Estimulantes del Sistema Nervioso Central/efectos adversos , N-Metil-3,4-metilenodioxianfetamina/efectos adversos , Vejiga Urinaria Neurogénica/inducido químicamente , Retención Urinaria/inducido químicamente , Adulto , Antiinfecciosos Urinarios/uso terapéutico , Betanecol/uso terapéutico , Enfermedad Crónica , Cistoscopía , Humanos , Masculino , Agonistas Muscarínicos/uso terapéutico , Fenazopiridina/uso terapéutico , Resultado del Tratamiento , Combinación Trimetoprim y Sulfametoxazol/uso terapéutico , Vejiga Urinaria Neurogénica/patología , Vejiga Urinaria Neurogénica/terapia , Cateterismo Urinario , Retención Urinaria/patología , Retención Urinaria/terapia
10.
J Neurol Sci ; 267(1-2): 158-61, 2008 Apr 15.
Artículo en Inglés | MEDLINE | ID: mdl-17949753

RESUMEN

Transient paraparesis has been reported with intrathecal chemotherapy agents and the most common cause is an incomplete inflammatory myelopathy. We report a case of a 30-year-old man diagnosed with acute lymphoblastic leukaemia who developed subacute anterior lumbosacral polyradiculopathy following intrathecal methotrexate, an unusual complication of intrathecal chemotherapy in adults. Spinal magnetic resonance discarded myelopathy. Cerebrospinal fluid exam showed elevation of protein, mononuclear pleocytosis and immunoglobulin synthesis. Electrodiagnostic study showed alterations of sensory and motor conductions only in lower limbs, consistent with multilevel radiculopathy. Differential diagnosis included toxic and neoplastic polyradiculopathy, and axonal variant of acute inflammatory demyelinating polyradiculoneuropathy. The authors review possible pathogenic mechanisms and propose several therapeutic and preventive options.


Asunto(s)
Plexo Lumbosacro/efectos de los fármacos , Metotrexato/efectos adversos , Paraparesia/inducido químicamente , Polirradiculopatía/inducido químicamente , Raíces Nerviosas Espinales/efectos de los fármacos , Adulto , Antimetabolitos Antineoplásicos/administración & dosificación , Antimetabolitos Antineoplásicos/efectos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Interacciones Farmacológicas/fisiología , Resultado Fatal , Humanos , Hidrocortisona/administración & dosificación , Inyecciones Espinales/efectos adversos , Pierna/inervación , Pierna/fisiopatología , Plexo Lumbosacro/patología , Plexo Lumbosacro/fisiopatología , Masculino , Metotrexato/administración & dosificación , Neuronas Motoras/patología , Músculo Esquelético/inervación , Músculo Esquelético/fisiopatología , Conducción Nerviosa/fisiología , Parálisis/inducido químicamente , Paraparesia/patología , Paraparesia/fisiopatología , Polirradiculopatía/patología , Polirradiculopatía/fisiopatología , Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamiento farmacológico , Leucemia-Linfoma Linfoblástico de Células Precursoras/genética , Infecciones del Sistema Respiratorio , Sepsis , Raíces Nerviosas Espinales/patología , Raíces Nerviosas Espinales/fisiopatología , Vejiga Urinaria Neurogénica/inducido químicamente
11.
Hong Kong Med J ; 13(4): 311-3, 2007 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-17592176

RESUMEN

Ten young ketamine abusers presented with lower urinary tract symptoms to two regional hospitals in Hong Kong. Investigations demonstrated contracted bladders and other urinary tract abnormalities. These types of findings have never been reported before in ketamine abusers. The possible aetiology is also discussed.


Asunto(s)
Ketamina/envenenamiento , Trastornos Relacionados con Sustancias/complicaciones , Vejiga Urinaria Neurogénica/inducido químicamente , Adulto , Femenino , Humanos , Masculino , Vejiga Urinaria Neurogénica/diagnóstico
12.
Neurology ; 68(18): 1455-9, 2007 May 01.
Artículo en Inglés | MEDLINE | ID: mdl-17470746

RESUMEN

OBJECTIVE: To compare acute and chronic effects of l-dopa on bladder function in levodopa-naive Parkinson disease (PD) patients who had urinary urgency. METHODS: We evaluated 26 l-dopa-naive PD patients at a university-based PD center with a first urodynamic session with a double examination: in the off treatment condition and 1 hour after acute challenge with carbidopa/l-dopa 50/200 mg; then, a chronic l-dopa monotherapy was administered (mean dose 300 +/- 150 mg). Two months later, patients underwent a second urodynamic session with a single evaluation 1 hour after the acute carbidopa/l-dopa challenge. RESULTS: The first acute l-dopa challenge significantly worsened bladder overactivity (neurogenic overactive detrusor contractions threshold [NDOC-t; 32% of worsening] and bladder capacity [BC; 22% of worsening]); on the contrary, l-dopa challenge during chronic administration ameliorated the first sensation of bladder filling (FS; 120% of improvement), NDOCT-t (93% improvement), and BC (33% of improvement) vs the values obtained with acute administration. An 86% significant improvement of FS in comparison with the basal value was observed. CONCLUSIONS: The acute and chronic l-dopa effects may be due to the different synaptic concentrations or to the activation of postsynaptic mechanisms obtained by chronic administration.


Asunto(s)
Levodopa/administración & dosificación , Levodopa/efectos adversos , Enfermedad de Parkinson/complicaciones , Enfermedad de Parkinson/tratamiento farmacológico , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria Neurogénica/tratamiento farmacológico , Enfermedad Aguda/terapia , Carbidopa/administración & dosificación , Carbidopa/efectos adversos , Enfermedad Crónica/terapia , Dopaminérgicos/administración & dosificación , Dopaminérgicos/efectos adversos , Relación Dosis-Respuesta a Droga , Esquema de Medicación , Quimioterapia Combinada , Femenino , Humanos , Plexo Hipogástrico/efectos de los fármacos , Plexo Hipogástrico/fisiopatología , Masculino , Persona de Mediana Edad , Fibras Parasimpáticas Posganglionares/efectos de los fármacos , Fibras Parasimpáticas Posganglionares/fisiopatología , Enfermedad de Parkinson/fisiopatología , Transmisión Sináptica/efectos de los fármacos , Transmisión Sináptica/fisiología , Resultado del Tratamiento , Vejiga Urinaria/efectos de los fármacos , Vejiga Urinaria/inervación , Vejiga Urinaria/fisiopatología , Vejiga Urinaria Neurogénica/fisiopatología , Trastornos Urinarios/inducido químicamente , Trastornos Urinarios/tratamiento farmacológico , Trastornos Urinarios/fisiopatología
13.
Spinal Cord ; 43(7): 448-9, 2005 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-15741977

RESUMEN

OBJECTIVE: To present complications and pitfalls in voiding cystourethrography (VCUG) and introduce a guideline for performing VCUG in a long-term spinal cord injury (SCI) patient with neurogenic bladder dysfunction (NBD) and contracted bladder. STUDY DESIGN: A case report. SETTING: Maharaj Nakorn Chiang Mai Hospital, Chiang Mai, Thailand. METHOD: We describe a chronic C(5) tetraplegic man with NBD and contracted bladder, who developed autonomic dysreflexia (AD), gross hematuria and extravasation of contrast median during VCUG. RESULT: A foley catheter was retained after VCUG. AD was resolved and urine cleared after a week of continuous bladder irrigation. CONCLUSION: VCUG should be performed with caution in a long-term SCI patient with NBD and contracted bladder. Forceful pushing of the contrast media by the hand-injection method caused abrupt distention of the contracted bladder, damaged bladder mucosa and aggrevated AD. We suggest a guideline as follows: report bladder capacity and AD, if present, in an X-ray requisition form; use the gravity-drip method, stop the drip and drain the contrast media if a sudden headache and rising of blood pressure (BP) develop; observe urine colour, and report if bleeding or AD occurs.


Asunto(s)
Medios de Contraste/efectos adversos , Extravasación de Materiales Terapéuticos y Diagnósticos/diagnóstico , Extravasación de Materiales Terapéuticos y Diagnósticos/prevención & control , Cuadriplejía/diagnóstico por imagen , Traumatismos de la Médula Espinal/diagnóstico por imagen , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria Neurogénica/diagnóstico , Enfermedad Crónica , Extravasación de Materiales Terapéuticos y Diagnósticos/etiología , Humanos , Masculino , Persona de Mediana Edad , Cuadriplejía/complicaciones , Radiografía , Traumatismos de la Médula Espinal/complicaciones , Uretra/diagnóstico por imagen , Vejiga Urinaria/diagnóstico por imagen , Vejiga Urinaria Neurogénica/prevención & control
14.
Eur J Neurosci ; 20(2): 474-82, 2004 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-15233756

RESUMEN

In order to clarify the functional role of the isolectin B4 (IB4)-binding afferent pathway in the micturition reflex, we investigated the effects on bladder activity of intrathecal application of the IB4-saporin conjugate, a targeting cytotoxin that destroys neurons binding IB4. In rats, IB4-saporin (2.5 micro m) or vehicle was administered through an intrathecal catheter implanted at the level of the L6-S1 spinal cord. Three weeks after IB4-saporin administration, cystometry in conscious animals revealed a reduction in bladder overactive responses induced by intravesical capsaicin or ATP infusion without affecting normal voiding function. In histochemical studies, double staining for IB4 and saporin was detected in L6 dorsal root ganglia (DRG) neurons 2 days after the treatment. Three weeks after the treatment, the area in lamina II of the L6 spinal cord stained with IB4 was significantly reduced compared with the area stained in control rats. The staining in the L1 spinal cord was not affected. The percentage of neurons in the L6 DRG intensely labeled with IB4 was also reduced in IB4-saporin-treated rats. These results indicate that intrathecal treatment with the IB4-saporin conjugate at the level of L6-S1 spinal cord, which reduces IB4 afferent nerve terminal staining in lamina II of the L6 spinal cord as well as the number of IB4-binding neurons in L6 DRG, suppressed bladder overactivity induced by bladder irritation without affecting normal micturition. Thus targeting IB4-binding, non-peptidergic afferent pathways sensitive to capsaicin and adenosine 5'-triphosphate may be an effective treatment for overactivity and/or pain responses in the bladder.


Asunto(s)
Inmunotoxinas/toxicidad , Lectinas/toxicidad , N-Glicosil Hidrolasas/toxicidad , Proteínas de Plantas/toxicidad , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria/efectos de los fármacos , Adenosina Trifosfato/farmacología , Animales , Capsaicina/farmacología , Citotoxinas/toxicidad , Interacciones Farmacológicas , Femenino , Citometría de Flujo/métodos , Técnicas Histológicas , Inmunotoxinas/metabolismo , N-Glicosil Hidrolasas/metabolismo , Proteínas de Plantas/metabolismo , Células del Asta Posterior/efectos de los fármacos , Células del Asta Posterior/fisiopatología , Ratas , Ratas Sprague-Dawley , Proteínas Inactivadoras de Ribosomas Tipo 1 , Saporinas , Médula Espinal/citología , Médula Espinal/efectos de los fármacos , Vejiga Urinaria/efectos de la radiación
15.
Urologe A ; 42(12): 1588-93, 2003 Dec.
Artículo en Alemán | MEDLINE | ID: mdl-14668986

RESUMEN

Bladder dysfunction can result from pathological changes in the bladder itself, of its central neurological regulation, (BPS), or of non-urological diseases such as diabetes or heart failure. Medication-induced bladder dysfunction can mostly be treated by simple changes in the pharmacological therapy. Bladder dysfunction can be induced pharmacologically by activating or inhibitory influences on adrenergic, sympathetic, beta-receptor-induced relaxation of the detrusor, alpha-receptor-induced contraction of the bladder neck, or cholinergic, parasympathetic, muscarinic receptor-induced contraction of the detrusor. Diuretics can increase urine production, thus possibly leading to incontinence. If incontinence occurs in patients, treatment should be stopped if possible and additional pharmacological therapy should not be started before medication-induced bladder dysfunction is excluded.


Asunto(s)
Composición de Medicamentos/efectos adversos , Enfermedades de la Vejiga Urinaria/inducido químicamente , Enfermedades de la Vejiga Urinaria/terapia , Vejiga Urinaria Neurogénica/inducido químicamente , Vejiga Urinaria Neurogénica/terapia , Vejiga Urinaria/efectos de los fármacos , Vejiga Urinaria/inervación , Incontinencia Urinaria/inducido químicamente , Incontinencia Urinaria/terapia , Diagnóstico Diferencial , Diuréticos/efectos adversos , Enfermedades de la Vejiga Urinaria/diagnóstico , Enfermedades de la Vejiga Urinaria/prevención & control , Vejiga Urinaria Neurogénica/diagnóstico , Vejiga Urinaria Neurogénica/prevención & control , Incontinencia Urinaria/prevención & control
17.
Br J Pharmacol ; 124(1): 190-6, 1998 May.
Artículo en Inglés | MEDLINE | ID: mdl-9630359

RESUMEN

1. We have developed and characterized a model of immediate hypersensitivity/inflammation of the urinary bladder in vivo induced by local application of ovalbumin (OA) in OA- sensitive female rats. Two parameters of the inflammatory response were assessed following OA challenge: plasma protein extravasation (PPE) and changes in smooth muscle reactivity. The former was estimated by measurement of Evans blue extravasation at 0.5, 2, 4, 8 and 24 h time point following in vivo challenge. Changes in reactivity were determined by measurement of isotonic tension responses of urinary bladder strips following OA challenge in vitro. 2. Acute in vivo intravesical OA challenge (10 mg in 0.3 ml saline) in actively sensitized female Wistar rats caused a time-dependent PPE in the urinary bladder which was biphasic with peak responses at 2-4 and 24 h. 3. The PPE response to acute OA challenge, above base-line, at 2 h was abolished by systemic capsaicin pretreatment (50 mg kg(-1), s.c., 4 days before use) (P < 0.05) whilst the response at 24 h was unaffected. The 2 h time point was then used for further studies. 4. Degranulation of mast cells, achieved by pretreatment with compound 48/80 (5 mg kg(-1), s.c. for 3 consecutive days), completely abolished the PPE response to OA challenge at the 2 h time point. 5. The tachykinin NK1 receptor antagonist, SR 140333 (0.1 micromol kg(-1), i.v.), abolished the 2 h PPE response whilst the tachykinin NK2 receptor antagonist MEN 11420 (0.1 micromol kg(-1), i.v.) appeared to reduce the response by approximately 50% but this did not reach significance. The bradykinin B2 receptor antagonist, Hoe 140 (0.1 micromol kg(-1), i.v.), similarly to SR 140333, blocked the 2 h PPE response to OA, whereas the selective B1 receptor antagonist B 9858 (0.1 micromol kg(-1), i.v.) had no significant effect. Inhibition of cyclo-oxygenase (COX) achieved by pretreatment with the COX inhibitor dexketoprofen (5.3 micromol kg(-1), i.v.) also blocked the PPE response, whilst the leukotriene receptor antagonist ONO 1078 (1 micromol kg(-1), i.v.) significantly reduced PPE by about 80%. 6. In the rat isolated urinary bladder OA (1 mg ml(-1)) challenge produced a biphasic response with a rapidly achieved maximal contraction followed by a sustained contraction for approximately 25 min. In vitro capsaicin pretreatment (10 microM for 15 min) significantly attenuated the duration of the sustained contraction whilst having no effect on the maximum contractile response achieved. In vivo pretreatment of animals with compound 48/80 significantly attenuated (42%) the maximum contractile response. Combination of both treatments almost completely abolished the response. In vitro treatment with Hoe 140 (1 microM) had no significant effect on the response to OA and neither did ONO 1078 (1 microM). 7. These results show that both the early inflammatory response and alterations in smooth muscle reactivity to OA challenge in actively sensitized animals are dependent on mast cell degranulation and the activation of sensory C-fibres. Furthermore this model of allergic cystitis may be useful for investigating both the processes involved and potential novel therapies in the treatment of interstitial cystitis.


Asunto(s)
Cistitis/inducido químicamente , Ovalbúmina/farmacología , Vejiga Urinaria Neurogénica/inducido químicamente , Animales , Proteínas Sanguíneas/metabolismo , Cistitis/metabolismo , Cistitis/fisiopatología , Modelos Animales de Enfermedad , Femenino , Técnicas In Vitro , Músculo Liso/fisiopatología , Ratas , Ratas Wistar , Vejiga Urinaria Neurogénica/metabolismo , Vejiga Urinaria Neurogénica/fisiopatología
18.
Am J Ind Med ; 30(1): 56-61, 1996 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-8837683

RESUMEN

Of 60 cases of neurotoxicity related to occupational exposures of workers at plants producing acrylamide monomers, cases involving neurotoxicity related to jobs using polymers with acrylamide monomer contamination have not been widely reported. In 1992, two patients were referred to the Division of Occupational and Environmental Health, Department of Family and Community Health, Marshall University School of Medicine, in Huntington, West Virginia for evaluation. The patients had worked in different coal preparation plants in southern West Virginia for over 10 years and had exposure to an acrylamide polymer flocculent contaminated with acrylamide monomer. Both patients had no instruction on proper use of, or the dangers of, acrylamide and were not given adequate safety equipment. Patient A developed Parkinsonism and Patient B peripheral neuropathies with a neurogenic bladder. These two case reports highlight the need to reemphasize the basic tenets of occupational health and safety. Many chemicals are being introduced into mining operations and awareness of potential toxic exposures and new diseases not previously reported in the mining industry must become part of the surveillance system by mine management and labor safety committees. Further studies on the extent of acrylamide neurotoxicity in the mining industry is encouraged.


Asunto(s)
Acrilamidas/efectos adversos , Minas de Carbón , Enfermedades Profesionales/inducido químicamente , Enfermedad de Parkinson Secundaria/inducido químicamente , Enfermedades del Sistema Nervioso Periférico/inducido químicamente , Vejiga Urinaria Neurogénica/inducido químicamente , Floculación , Humanos , Masculino , Persona de Mediana Edad , Exposición Profesional , Salud Laboral , Vigilancia de la Población , Seguridad , West Virginia
19.
Med Pediatr Oncol ; 24(1): 61-2, 1995 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-7968797

RESUMEN

Inadvertent intrathecal administration of vincristine results in severe neurotoxicity. Motor and sensory bladder dysfunction have been reported but the long-term urologic consequences are unknown due to the associated high mortality. We report a case of accidental intrathecal vincristine administration with patient survival and follow-up of 24 months. The child developed a lower motor neuron neuropathic bladder requiring intermittent self-catheterization of the bladder. Urinary tract management of these children should be based on the urodynamic findings.


Asunto(s)
Errores de Medicación , Vejiga Urinaria Neurogénica/inducido químicamente , Vincristina/toxicidad , Niño , Humanos , Inyecciones Espinales , Masculino
20.
Spine (Phila Pa 1976) ; 19(6): 719-20, 1994 Mar 15.
Artículo en Inglés | MEDLINE | ID: mdl-8009339

RESUMEN

Reversible complication of intrathecal morphine delivered by an implanted pump is described in one patient. The patient was evaluated initially using a contrast CT of the thoracic spine as well as urodynamics studies. After decreasing the intrathecally administered morphine from 2 mg/24 hr to .5 mg/24 hr, the patient's neurogenic bladder reversed within 4 days. Implanted pumps to deliver intrathecal narcotic medications are being used currently to treat intractable pain. This is a case report of reversible urinary retention secondary to the intrathecal narcotic.


Asunto(s)
Morfina/efectos adversos , Retención Urinaria/inducido químicamente , Anciano , Relación Dosis-Respuesta a Droga , Falla de Equipo , Humanos , Bombas de Infusión Implantables , Inyecciones Espinales , Masculino , Morfina/administración & dosificación , Columna Vertebral/diagnóstico por imagen , Tórax , Tomografía Computarizada por Rayos X , Vejiga Urinaria Neurogénica/inducido químicamente , Urodinámica
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