Síntomas de tramo urinario inferior y síndrome de apnea obstructiva del sueño: evolución urodinámica antes y después de un año de tratamiento con presión continua positiva de la vía aérea / Lower urinary tract symptoms and obstructive sleep apnea syndrome: Urodynamic evolution before and after one year of treatment with continuous positive airway pressure

Objetivo: Demostrar el potencial impacto urodinámico que puede tener el uso adecuado de presión continua positiva de la vía aérea (CPAP) en pacientes con síndrome de apnea-hipopnea obstructiva del sueño y observar si la posible mejoría de los síntomas de tramo urinario inferior es debida a alguna modificación urodinámica. Métodos: Estudio prospectivo con pacientes recientemente diagnosticados de síndrome de apnea-hipopnea obstructiva del sueño mediante poligrafía del sueño. Se estudian desde el punto de vista urológico para descartar importantes patologías urológicas. Se utilizan cuestionarios validados IPSS y OAB-V8, diarios miccionales de 3 días y estudios urodinámicos invasivos, todos ellos antes de comenzar con CPAP y tras un año de su uso adecuado. Resultados: Se llevan a cabo 84 estudios urodinámicos en 43 pacientes. La puntuación IPSS disminuye 3,58 puntos. La puntuación OAB-V8 disminuye 2,87 puntos. Los episodios de nicturia disminuyen más de uno por noche. El porcentaje de pacientes con poliuria nocturna disminuye un 26%. La acomodación vesical significativamente aumenta (97,39 vs. 200,40 ml/cm H2O). Disminuye la presencia de detrusor hiperactivo en el estudio urodinámico de 11 (antes de CPAP) a 5 pacientes (tras CPAP). Conclusión: Tras el tratamiento apropiado con CPAP se observa una mejoría estadística y clínica de distintos síntomas de tramo urinario inferior con escasa repercusión urodinámica

Objective: To report the clinical evolution and the urodynamic behaviour of several lower tract urinary symptoms in patients with obstructive sleep apnea syndrome before and after the treatment with continuous positive airway pressure (CPAP) devices. Methods: A prospective study was performed; patients with recent diagnosis of sleep apnea confirmed by nocturnal sleep polygraphy and absence of medical urological past history. In order to discard important lower urinary tract conditions, urological examinations were previously performed. Urinary symptoms were evaluated using the IPSS and OAB-V8 validated questionnaires, three-day Bladder Diary and invasive urodynamic examinations with a gap of one year before and one year after using the CPAP. Results: 84 urodynamic studies were carried out in 43 patients. The IPSS score decreased by 3.58 points. The OAB-V8 score decreased by 2.87 points. Nocturia episodes decreased to one per night. The percentage of patients with nocturnal polyuria went down to 26%. The bladder compliance significantly increased (97.39 vs 200.40ml/cm H2O). The presence of detrusor overactivity decreased from 11 (before CPAP) to 5 patients (after CPAP). Conclusion: The proper treatment with CPAP showed a statistical and clinical improvement of several LUTS with limited urodynamic modifications

Lower urinary tract symptoms and obstructive sleep apnea syndrome: Urodynamic evolution before and after one year of treatment with continuous positive airway pressure. / Síntomas de tramo urinario inferior y síndrome de apnea obstructiva del sueño: evolución urodinámica antes y después de un año de tratamiento con presión continua positiva de la vía aérea.

OBJECTIVE: To report the clinical evolution and the urodynamic behaviour of several lower tract urinary symptoms in patients with obstructive sleep apnea syndrome before and after the treatment with continuous positive airway pressure (CPAP) devices. METHODS: A prospective study was performed; patients with recent diagnosis of sleep apnea confirmed by nocturnal sleep polygraphy and absence of medical urological past history. In order to discard important lower urinary tract conditions, urological examinations were previously performed. Urinary symptoms were evaluated using the IPSS and OAB-V8 validated questionnaires, three-day Bladder Diary and invasive urodynamic examinations with a gap of one year before and one year after using the CPAP. RESULTS: 84 urodynamic studies were carried out in 43 patients. The IPSS score decreased by 3.58 points. The OAB-V8 score decreased by 2.87 points. Nocturia episodes decreased to one per night. The percentage of patients with nocturnal polyuria went down to 26%. The bladder compliance significantly increased (97.39 vs 200.40ml/cm H2O). The presence of detrusor overactivity decreased from 11 (before CPAP) to 5 patients (after CPAP). CONCLUSION: The proper treatment with CPAP showed a statistical and clinical improvement of several LUTS with limited urodynamic modifications.

[Neurogenic etiology in patients with erectile dysfunction]. / Etiología neurógena en pacientes con disfunción eréctil.

OBJECTIVES: Erectile dysfunction (ED) is a disorder with a high prevalence that increases with age. It is estimated that 18.9% of men's between 25 and 70 years suffer it in Spain. Most cases have a multifactorial origin and it is admitted the influence on its pathogenesis of systemic diseases, different kind of drugs, psychogenic factors, cardiovascular, endocrinological and neurological diseases. Neurologic cause erectile dysfunction may have its origin in the central or peripheral nervous system. Among possible process of neurogenic erectile dysfunction of central origin would be tumors, cerebral vascular accidents, encephalitis, Parkinson disease, multiple sclerosis and other demyelinization diseases, dementias, olivopontocerebellar degeneration and epilepsy. Myelopathies of any etiology may be, depending on their localization and extension, cause of erectile dysfunction. At the peripheral level, disorders of the sensitive tracts constituting the afferent limb of the erection spinal reflex, and the efferent vegetative or somatic tracts mediating arterial vasodilatation, cavernous smooth muscle relaxation or pelvic floor striated muscle contraction. The aim of this work is to review in detail the most relevant causes of neurogenic erectile dysfunction, their etiopathogenic mechanisms and therapeutic approaches currently considered more adequate for each particular case. CONCLUSIONS: The correct diagnostic approach to patients with erectile dysfunction passes through identification, if possible, of the etiopathogenic factors implied. Regarding this, detection and identification of a possible neurogenic risk factor will contribute to a better understanding of the physiopathologic mechanisms, and more adequate diagnostic, prognostic and therapeutic approaches, mainly in those patients refractory to first line therapy.

Etiología neurógena en pacientes con disfunción eréctil / Neurogenic etiology in patients with erectile dysfunction

Objetivo: La disfunción eréctil (DE) es una alteración cuya prevalencia es elevada y aumenta con la edad. Se estima que en España afecta al 18,9% de los varones de 25 a 70 años. En la mayor parte de los casos es de origen multifactorial y en su patogenia se admite la influencia de enfermedades sistémicas, fármacos de diferentes tipos, factores psicógenos, patologías cardiovasculares, endocrinopatías y alteraciones neurológicas. La disfunción eréctil de causa neurológica puede tener su origen a nivel del Sistema Nervioso Central o Periférico. Entre las posibles causas de disfunción eréctil neurógena de origen central estarían tumores, accidentes cerebrovasculares, encefalitis, Enfermedad de Parkinson, Esclerosis Múltiple y otras enfermedades desmielinizantes, demencias, degeneración olivo pontocerebelosa y epilepsia. Las mielopatías de cualquier etiología, pueden ser dependiendo de su localización o extensión, causas de disfunción eréctil. A nivel periférico pueden ser causa de DE las alteraciones de las vías sensitivas que constituyen el brazo aferente del reflejo espinal de la erección y las de las vías eferentes vegetativas o somáticas que median en la vasodilatación arterial, la relajación del músculo liso cavernoso o la contracción de la musculatura estriada del suelo de la pelvis. La finalidad de este trabajo es revisar detalladamente las causas más relevantes de DE de origen neurógeno, sus mecanismos etiopatogénicos y los abordajes terapéuticos que en la actualidad se consideran más adecuados para cada caso particular. Conclusión: La correcta aproximación diagnóstica al paciente con DE pasa por identificar, en la medida de lo posible, los factores etiopatogénicos implicados su origen. En este sentido, la detección e identificación, de la posible presencia del factor de riesgo neurógeno, contribuirá a un mejor entendimiento de sus mecanismos fisiopatológicos y con ello a una aproximación diagnóstica, pronóstica y terapéutica más adecuada especialmente en aquellos pacientes refractarios a la terapia de primera línea (AU)

Objectives: Erectile dysfunction (ED) is a disorder with a high prevalence that increases with age. It is estimated that 18.9% of men’s between 25 and 70 years suffer it in Spain. Most cases have a multifactorial origin and it is admitted the influence on its pathogenesis of systemic diseases, different kind of drugs, psychogenic factors, cardiovascular, endocrinological and neurological diseases. Neurologic cause erectile dysfunction may have its origin in the central or peripheral nervous system. Among possible process of neurogenic erectile dysfunction of central origin would be tumors, cerebral vascular accidents, encephalitis, Parkinson disease, multiple sclerosis and other demyelinization diseases, dementias, olivopontocerebellar degeneration and epilepsy. Myelopathies of any etiology may be, depending on their localization and extension, cause of erectile dysfunction. At the peripheral level, disorders of the sensitive tracts constituting the afferent limb of the erection spinal reflex, and the efferent vegetative or somatic tracts mediating arterial vasodilatation, cavernous smooth muscle relaxation or pelvic floor striated muscle contraction. The aim of this work is to review in detail the most relevant causes of neurogenic erectile dysfunction, their etiopathogenic mechanisms and therapeutic approaches currently considered more adequate for each particular case. Conclusions: The correct diagnostic approach to patients with erectile dysfunction passes through identification, if possible, of the etiopathogenic factors implied. Regarding this, detection and identification of a possible neurogenic risk factor will contribute to a better understanding of the physiopathology mechanisms, and more adequate diagnostic, prognostic and therapeutic approaches, mainly in those patients refractory to first line therapy (AU)

Expression of p75(LNGFR) and Trk neurotrophin receptors in normal and neoplastic human prostate.

OBJECTIVE: To analyse the occurrence and cell distribution of p75(LNGFR) and Trk neurotrophin receptors in normal prostate, benign prostatic hypertrophy (BPH) and prostate carcinoma, and to determine the effect of androgen suppression on the expression of these proteins in prostate cancer samples. MATERIALS AND METHODS: The study comprised formalin-fixed and paraffin-embedded material, obtained during surgery and from cadavers during removal of organs for transplantation. Light microscopy immunohistochemistry was carried out using polyclonal antibodies against Trks, and a monoclonal antibody against p75(LNGFR). General markers for epithelial and endocrine cells were assessed in parallel. RESULTS: TrkA immunoreactivity (IR) was restricted to the basal epithelial cells in some acini (37%). This pattern remained unchanged or IR extended to the whole acini in BPH, and varied widely in prostate cancer. In normal tissue and BPH, TrkC IR was detected exclusively in the stroma. Nevertheless, it progressively increased in the epithelial cells of well-differentiated to moderately differentiated prostate carcinoma, whereas in stromal cells there were no substantial changes. TrkB IR was absent in all the samples. There was weak p75(LNGFR) IR in normal epithelial cells, which increased in prostate cancer and to a lesser extent in BPH. Androgen suppression was ineffective in reversing TrkA modifications, whereas it caused a decrease in the expression of TrkC and p75(LNGFR). CONCLUSION: The abnormal growth of prostatic epithelium is accompanied by increased TrkA expression and the induction of TrkC expression in epithelial cells. These results suggest that neurotrophins could be involved in the abnormal growth of the human prostate, acting through specific Trk signal-transducing receptors whose expression is regulated by androgens.

Neurotrophins and neurotrophin receptors in some neural crest-derived tumours (ganglioneuroma, phaeochromocytoma and paraganglioma).

AIM: This study analyses the occurrence and distribution of neurotrophins and their receptors in some types of tumours of neural-crest derived cells. METHODS AND RESULTS: Light microscopy immunohistochemistry associated with quantitative image analysis was used to study the expression of neurotrophins (nerve growth factor, brain-derived neurotrophic factor and neurotrophin (NT)-3) and their cognate receptors (p75(LNGFR), TrkA, TrkB and TrkC) in histologically defined ganglioneuroma, phaeochromocytoma and paraganglioma. The material was fixed in 10% formaldehyde, paraffin-embedded and processed for indirect peroxidase immunohistochemistry using a battery of poly- and monoclonal antibodies to detect neurotrophins and their receptors, as well as some neuronal, endocrine and glial cell markers. A subpopulation of cells in phaeochromocytomas and ganglioneuromas expressed NT-3, but not other neurotrophins, while in paragangliomas no neurotrophins were detected. Regarding neurotrophin receptors, all tumours lacked p75(LNGFR), except for the ganglionic part of a case of mixed phaeochromocytoma, whereas they displayed TrkA (two of two ganglioneuromas, six of nine phaeochomocytomas and three of four paragangliomas). Furthermore, TrkC was regularly detected in a neuronal subpopulation in ganglioneuroma. Interestingly, the percentage of neurones expressing TrkA and TrkC was increased with respect to normal tissues in ganglioneuromas, as well as the percentage of the area occupied by TrkA-immunoreactive cells in the phaeochromocytomas. CONCLUSION: The pattern of expression of neurotrophins and neurotrophin receptors in the analysed tumours basically matches that of sympathetic neurones, adrenal chromaffin cells and paraganglionic cells, and suggests responsiveness of these cells to neurotrophins. Nevertheless, the function of TrkA and TrkC in regulating the biology of these tumours, if any, remains to be elucidated.

[Primary leiomyosarcoma. A rare tumor of the adrenal gland]. / Leiomiosarcoma primario. Un raro tumor de la glándula suprarrenal.

OBJECTIVE: To report on a rare case of primary leiomyosarcoma of the adrenal. To our knowledge, this is the fourth case reported in the literature. METHODS: A patient with primary leiomyosarcoma of the adrenal gland is presented. The clinical features are described, and the diagnostic and therapeutic aspects of this rare primary mesenchymal tumor are discussed. RESULTS/CONCLUSIONS: The aggressive nature and the poor prognosis of this rare tumor type are emphasized.

Neuroendocrine cells in benign prostatic hyperplasia and prostatic carcinoma: effect of hormonal treatment.

The present study was undertaken to analyze the changes in neuroendocrine cells of the human prostate induced by neoplasms and the effect of hormonal treatment. Samples of human prostate (n = 47) were obtained during surgery or removal of organs for transplantation. The cases analyzed represent normal prostates (n = 4); benign prostatic hyperplasias (n = 10; prostatic carcinomas with Gleason scores of 2-4 (n = 5), 5-7 (n = 10), and 8-10 (n = 3), and prostatic carcinomas treated with hormonal therapy (n = 15). Immunohistochemistry for chromogranin A was performed, and the density of neuroendocrine cells as well as the intensity of the immunostaining within their cytoplasms were evaluated using image analysis. Neuroendocrine cells showing chromogranin A immunoreactivity were identified in all cases studied. They were localized scattered in the acini, and no differences in their morphology were observed among groups. Interestingly, chromogranin A immunoreactivity was also present in typical epithelial cells of prostatic cancer with Gleason scores ranging from 8 to 10. The density of chromogranin A immunoreactive cells was higher in neoplastic tissue with respect to the normal prostate, reaching maximal values in prostatic carcinomas with Gleason scores of 8-10 which were hormonally treated. Regarding the intensity of immunostaining in the prostatic carcinomas with Gleason scores of 8-10 only, a significant increase in relation to the other groups was found. The present results demonstrate that the neuroendocrine cells have similar morphological features and distribution in normal prostate, benign prostatic hyperplasia, and prostatic carcinoma. Their density in prostatic cancer increases following hormonal therapy and varies in relation to the tumoral degree or histological evaluation, suggesting a role of neuroendocrine cells in human prostatic cancer.

[Squamous cell carcinoma of the prostate. Presentation of a case and review of the literature]. / Carcinoma de próstata de células escamosas. Presentación de un caso y revision de la literatura.

Presentation of one case report of squamous cells prostate carcinoma. This type of prostate tumour accounts for 0.5-1% of all prostate neoplasias and presents clinical and evolutive aspects that are different from those of prostate adenocarcinoma with a poor response to any therapy and a very poor prognosis relative to adenocarcinoma. A literature review is included.

[Epididymal leiomyoma. Report of 2 cases]. / Leiomioma de epidídimo. Presentación de dos casos.

At present, the paratesticular tumors are not frequent, but when they appear, the most common location is on spermatic cord and epididymis. Within the epididymal tumors the most frequent (75%) are benign tumors, been the second one the leiomyoma after the adenomatoid tumor. We want to show two clinical cases about epididymal leiomyoma in patients who had different ages. We achieve the definitive diagnostic after the tumor removed by histological analysis. We also checked the medical literature.

Dopamine D1 and D2 receptors in the human ureter and urinary bladder: a radioligand binding and autoradiographic study.

OBJECTIVE: To analyse the pharmacological profile and the anatomical localization of the dopamine D1 and D2 receptors in sections of the pelvic part of the ureter and of the fundus of the urinary bladder. PATIENTS, MATERIALS AND METHODS: Samples of the pelvic part of the ureter and of the fundus of the urinary bladder were taken in men (age range 61 +/- 4 years) who were undergoing lower urinary tract surgery. Biochemical characterization and autoradiographical techniques were used on frozen sections of the ureter or the urinary bladder. [3H]-SCH 23390 was used as a ligand of dopamine D1 receptors and [3H]-spiroperidol as a ligand of dopamine D2 receptors. RESULTS: [3H]-SCH 23390 and [3H]-spiroperidol were bound by specific sections of the ureter and of the urinary bladder. The pharmacological profile of the binding was consistent with the labelling of D1 and D2 receptors respectively. Light microscope analysis of the localization of D1 and D2 receptors revealed the accumulation of the two radioligands in the tunica muscularis of the ureter or of the urinary bladder. CONCLUSION: A possible role of the dopaminergic system in the control of urine flow and of some dysfunctions of the lower urinary tract is suggested.

Autoradiographic localization of dopamine D1 receptors in the human kidney.

The pharmacological profile and the anatomical localization of the selective D1-receptor antagonist [3H][R]-(+)-8-chloro-2,3,4,5-tetrahydro-5-phenyl-1H-3-benzazepin-7 -al- hemimaleate ([3H]SCH 23390) were studied in frozen sections of human kidney by using combined in vitro radioreceptor binding and autoradiographic techniques. [3H]SCH 23390 was bound by sections of human kidney in a manner consistent with the labeling of D1 sites, with a Kd value of 3.87 nM and with a Bmax value of 143 fmol/mg protein. Light microscope autoradiography revealed the highest density of [3H]SCH 23390 binding sites within the macula densa and the proximal tubules followed in descending order by the ascending limb of the loop of Henle, the distal tubules and the descending limb of the loop of Henle. No specific binding was noticeable within the glomeruli or within the epithelium of collecting tubules. [3H]SCH 23390 binding sites were also observed within the medial layer of intrarenal artery branches. These findings show that dopamine D1 receptor sites in the human kidney have a localization similar to that described in laboratory mammals with a higher density of tubular than of vascular receptors. The above data account for the vascular, diuretic and natriuretic effects elicited by D1 receptor stimulation in man.