PubMed Health⌕ Search

Biomedical subjects

J M Rodríguez-Vallejo

Publications and source records attributed to J M Rodríguez-Vallejo.

6 recordsLinked to original sources
PubMed2000

[Morphologic course of prostatic hyperplasia].

OBJECTIVE: To find a morphologic model of the development of prostate hyperplasia. METHODS: Study of the transitional zone in 60 patients (30 with infravesical obstruction, 30 with no obstructive symptoms) and quantification of the involved surface, number of pure stromal and glandular-stromal nodes, node area for each of them, and non-nodular area of the transitional zone, correlating each parameter to age based on clinical status. RESULTS: The greater transitional zone area is seen in patients with obstruction: 1376.83 +/- 408.17 mm2 vs 321.39 +/- 151.49 mm2 in asymptomatic patients, mainly due to a higher number of glandular-stromal nodes (17 vs 2.2) and their size, with a correlation to age (p = 0.03). Moderate increases of non-nodular areas are also found. CONCLUSIONS: These findings suggest that onset of prostate hyperplasia may be due to a consistent increase of the transitional area, and that in some patients, probably because of local factors, nodular development occurs as a result of both an increase in nodes number and size.

Aged↗
PubMed1999

Expression of basic fibroblast growth factor and its receptors FGFR1 and FGFR2 in human benign prostatic hyperplasia treated with finasteride.

BACKGROUND: The development of benign prostatic hyperplasia (BPH) is an androgen-dependent process which may be mediated by a number of locally produced growth factors. One of these, the basic fibroblast growth factor (bFGF or FGF2), has a mitogenic effect on prostatic stroma. High expression levels of bFGF have been reported in BPH. FGFR1 and FGFR2 receptors, that exhibit affinity for bFGF, have been identified in normal and hyperplastic prostate. Finasteride, a 5alpha-reductase inhibitor, is an effective drug in the treatment of BPH, inducing regressive changes in the prostate of treated patients, even though its mechanisms of action are not yet completely elucidated. This study was designed to assess the effects of finasteride on the expression levels of bFGF, FGFR1, and FGFR2 in patients with BPH. METHODS: The expression levels of bFGF, FGFR1, and FGFR2 in 9 patients with prostatic hyperplasia treated with finasteride were assessed by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis of mRNA expression and were compared with those of 9 control patients with untreated BPH. RESULTS: Immunohistochemistry showed strong bFGF immunoreactivity in the prostatic stroma of untreated patients, this being somewhat weaker in the epithelium. In treated patients, epithelial immunoreactivity was practically negative, and a considerable reduction in stromal immunoreactivity was seen. These findings were also confirmed by RT-PCR. FGFR1 showed a weak immunoreactivity in the stroma and in basal epithelial cells. FGFR1 showed a weak immunoreactivity in the stroma and in basal epithelial cells. FGFR2 exhibited strong stromal immunoreactivity, becoming weaker in the basal epithelium. No differences were seen in the expression of both receptors between the groups of treated and untreated patients. CONCLUSIONS: A marked reduction in bFGF levels is seen in BPH treated with finasteride in comparison to untreated BPH. In our opinion, finasteride may act as a negative regulator of bFGF expression, counteracting the role of bFGF in the development of BPH.

5-alpha Reductase Inhibitors↗
PubMed1999

In vivo proton magnetic resonance spectroscopy of diseased prostate: spectroscopic features of malignant versus benign pathology.

In vivo Proton Magnetic Resonance Spectroscopy appears potentially useful for non-invasive discrimination between benign prostatic hyperplasia (BPH) and prostate carcinoma (PC). Aiming to delimit the range within which spectra from one or the other pathology should occur, and establish extreme spectroscopic features of malignant versus benign prostate disease, we performed endorectal proton MR spectroscopy on 20 patients severely affected of either benign prostatic hyperplasia (BPH) (n = 10) or prostate cancer (PC) (n = 10). They were selected on the basis of the large volume and homogeneity of their lesions, which were histologically confirmed after spectroscopy. Consequently, high-quality short-TE proton spectra with well-resolved metabolite signals, and practically free of volume averaging issues were obtained in all cases. Apart from the typical citrate, creatine, and choline signals of prostate spectra, both BPH and PC spectra showed a peak centered at 3.6 ppm which was assigned to myo-inositol. The intensity of this contribution was found significantly increased in PC cases compared to BPH. Possible relationships between neoplastic transformation and the metabolic pathways in which myo-inositol participates are discussed. Average spectroscopic profiles were calculated for both advanced pathologies, and showed obvious differentiated features. In quantitative terms, the ratio of citrate to choline peak areas as well as that of creatine to myo-inositol appeared as the most convenient to discriminate between advanced PC cases (both ratios below 1.0) and advanced BPH cases (both ratios above 1.0).

Aged↗
PubMed1998

Regressive changes in finasteride-treated human hyperplastic prostates correlate with an upregulation of TGF-beta receptor expression.

BACKGROUND: Prostatic atrophy has been documented histologically as a consequence of finasteride action on human hyperplastic prostates. An increase in apoptotic rates has also been reported in androgen-deprived hyperplastic prostates. Transforming growth factor beta (TGF-beta) signaling is implicated in apoptotic cell death. TGF-betas have been detected in normal and diseased human prostate. In the normal prostate, TGF-beta acts as a predominantly negative growth regulator. TGF-beta signaling receptors TbetaRI and TbetaRII have been shown to be negatively regulated by androgens. METHODS: We studied the histological changes in 9 selected finasteride-treated patients with benign prostatic hyperplasia (BPH), and analyzed the levels of expression and localization of TGF-beta receptor types TbetaRI and TbetaRII in these patients as compared to selected BPH controls. RESULTS: The prostatic epithelial compartment seemed to be a primary target site for finasteride action, since we observed moderate to severe glandular atrophy after 4-6 months of treatment. TGF-beta receptors were upregulated in treated cases. We assessed a twofold increase in TbetaRII mRNA levels in treated cases as compared to controls. An increase in both TbetaRI and TbetaRII at the protein level by immunostaining was observed, which also provided a helpful means for detecting glands undergoing regression. CONCLUSIONS: We conclude that finasteride may modulate the TGF-beta signaling system to promote changes leading to apoptosis of epithelial cells and prostatic glandular atrophy.

Apoptosis↗
PubMed1997

[Relationship of prostatic carcinoma of the peripheral zone with glandular atrophy and prostatic intraepithelial neoplasia].

The study of the prostate's peripheral area in 32 patients, with age ranging between 48 to 75 years (mean, 61.4 +/- 6.7), demonstrates the frequency of certain morphological changes such as glandular atrophy (46.8%), which are neither related to age (p = 0.8) or the carcinoma (p = 0.8). A very different issue is the prostatic intraepithelial neoplasia, which although not statistically related to age in this series (p = 0.3) (probably due to the absence of young adults), appears to develop in earlier stages than cancer, is associated in 88.8% carcinomas (p = 0.03) and has a close topographic correlation to latent microscopic foci of adenocarcinoma of the prostate's peripheral area, anatomic proximity of both lesions occurring in 55.5% cases.

Adenocarcinoma↗