65-month testosterone replacement therapy for androgen deficiency-induced ED: a case report and review of the literature / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the mechanism of erectile dysfunction (ED) with testosterone deficiency and discuss the feasibility of long-term testosterone replacement therapy (TRT) by observing a case of ED with testosterone deficiency treated by TRT for 65 months.</p><p><b>METHODS</b>We treated an ED patient with testosterone deficiency by TST for 65 months, and evaluated the therapeutic effects by analyzing his IIEF-5 score, dynamic changes in testosterone, PSA, hemoglobin and red blood cell count, and adverse events.</p><p><b>RESULTS</b>The patient was a 46-year-old man, with an IIEF-5 score of 7, baseline serum total testosterone (TT) of 2.79 ng/ml, and no response to phosphodiesterases-5 inhibitors (PDE5i). He was diagnosed with late-onset hypogonadism (LOH) and treated by TRT: testosterone undecanoate at 80 mg bid po for the first 2 weeks and then at 40 mg bid po. Two months after medication, the TT level was increased to normal (3.45 ng/ml), and physical fitness and anxiety symptoms were markedly improved, with no significant improvement in sexual function. Then we administered PDE5i on demand in addition, which elevated his IIEF-5 score to > 21. The combined medication of TRT and on-demand PDE5i lasted for 45 months followed by TRT alone for another 18 months. The patient was restored to normal penile erection and sexual satisfaction, with the IIEF-5 score remaining at > 21. Regular follow-up revealed no significant abnormalities in the testosterone level, PSA, and routine blood tests.</p><p><b>CONCLUSION</b>TRT enhances the effect of PDE5i in the treatment of androgen deficiency-induced ED, and long-term TRT is safe and effective for androgen deficiency.</p>

Pituitary prolactinoma with severe erectile dysfunction as the initial symptom: diagnosis and treatment of 4 cases / 中华男科学杂志

<p><b>OBJECTIVE</b>Pituitary prolactinoma with severe erectile dysfunction (ED) as the initial symptom is often misdiagnosed. This article explores the diagnosis and treatment of severe ED caused by pituitary prolactinoma.</p><p><b>METHODS</b>We retrospectively analyzed the diagnosis and treatment of 4 cases of pituitary prolactinoma with severe ED (IIEF-5 score 5 - 7) as the initial clinical symptom confirmed by MRI.</p><p><b>RESULTS</b>The 4 cases of pituitary prolactinoma-induced severe ED, with serum prolactin 10 times above the maximum normal level, were misdiagnosed for 2 years. All failed to respond to the PDE5 inhibitor therapy, and then 3 of them underwent transnasal hypophysectomy. Twenty-four months of follow-up found the level of prolactin restored to normal in 1 case (IIEF-5 = 19), and reduced to 600 and 768 IU/L respectively (IIEF-5 = 15) in the other 2. Then administration of the PDE5 inhibitor was followed, which produced satisfactory efficacy. One case was treated with oral bromocriptine, which restored the prolactin level to normal at 12 months (IIEF-5 > 21).</p><p><b>CONCLUSION</b>Prolactin detection and brain MRI can help to confirm pituitary prolactinoma with severe ED at the onset. As for its treatment, in case of an extremely high level of prolactin, simple administration of the PDE5 inhibitor is ineffective. When the prolactin level is reduced after surgery or medication, the symptom of ED can be improved and, in case of no obvious relief, administration of the PDE5 inhibitor can be followed, which may achieve satisfactory results.</p>

Arsenic trioxide induces the apoptosis of prostate cancer PC-3 cells via the P38 signaling pathway / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the role of the P38 signaling pathway in the apoptosis of arsenic trioxide (As2 O3)-induced androgen-independent prostate cancer PC-3 cells.</p><p><b>METHODS</b>Androgen-independent prostate cancer PC-3 cells were treated with different concentrations of As2 O3 for 24, 48 and 72 hours. The inhibitory effect of As2 O3 on the cell growth was measured by MTT, the expression of p- P38 detected by Western blot, and the rate of cell apoptosis determined by Annexin V and PI double staining before and after interfering the P38 signaling pathway by SB203580, a highly selective P38 inhibitor.</p><p><b>RESULTS</b>As2 O3 inhibited the proliferation of PC-3 cells in a concentration- and time-dependent manner, and quickly activated P38 phosphorylation, thus giving full play to its biological activities. After 24 hours of treatment with As2 O3 at the concentrations of 2, 10 and 20 micromol/L, the apoptosis rates of the PC-3 cells were (18.9 +/- 0.43), (24.7 +/- 0.29) and (49.7 +/- 1.79)%, respectively, which were reduced to (14.8 +/- 0.81), (22.1 +/- 0.51) and (39.6 +/- 1.74)% after interfering the P38 pathway with SB203580. Inhibition of the P38 pathway significantly reduced the apoptosis of the PC-3 cells induced by As2 O3 (P < 0.05).</p><p><b>CONCLUSION</b>As2 O3 can induce the apoptosis of prostate cancer PC-3 cells by activating the P38 signaling pathway, and interfering the P38 signaling pathway can reduce their apoptosis, which suggests that the P38 signaling pathway is involved in the apoptosis of As2 O3-induced androgen-independent prostate cancer PC-3 cells.</p>