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Androgen deficiency is a physical disorder that not only affects adults but can also jeopardize children's health. Because there are many disadvantages to using traditional androgen replacement therapy, we have herein attempted to explore the use of human umbilical cord mesenchymal stem cells for the treatment of androgen deficiency. We transplanted CM-Dil-labeled human umbilical cord mesenchymal stem cells into the testes of an ethane dimethanesulfonate (EDS)-induced male rat hypogonadism model. Twenty-one days after transplantation, we found that blood testosterone levels in the therapy group were higher than that of the control group (P = 0.037), and using immunohistochemistry and flow cytometry, we observed that some of the CM-Dil-labeled cells expressed Leydig cell markers for cytochrome P450, family 11, subfamily A, polypeptide 1, and 3-β-hydroxysteroid dehydrogenase. We then recovered these cells and observed that they were still able to proliferate in vitro. The present study shows that mesenchymal stem cells from human umbilical cord may constitute a promising therapeutic modality for the treatment of male hypogonadism patients.

Purpose: To investigate a possible relation between penile Doppler ultrasound examination (PDUE) parameters and efficacy of chronic therapy with tadalafil (TAD) combined with a protocol of aerobic physical activity (PA) in patients with late onset hypogonadism (LOH)., Methods: The study evaluated 30 patients consecutively enrolled with LOH and erectile dysfunction which present contraindication to hormonal replacement therapy for concomitant prostate disease. These patients were subjected to a combined protocol with phosphodiesterase V selective inhibitors (TAD 5 mg daily) and aerobic PA., Results: After three months, we observed significant improvements in erectile function [IIEF-5, median (IQR) = 13.0 (7.0-18.0) versus 6.0 (5.0-6.75); p < 0.01] and of the main metabolic [homeostatic model assessment index, median (IQR) = 2.5 (1.62-3.37) versus 3.0 (2.0-3.75); p < 0.01; body mass index, median (IQR) = 27.0 (24.0-28.75) versus 27.5 (24.0-29.5)] and vascular parameters [peak systolic velocity, median (IQR) = 29.5 (24.25-31.0) versus 28.0 (23.0-24.25); acceleration time, median (IQR) = 114 (105.25-134.0) versus 115.0 (106.5-134.0)], assessed by PDUE., Conclusion: PA in association with phosphodiesterase V inhibitors could compensate the effects of hypogonadism on erectile function and facilitate the clinical response to these drugs even in the absence of adequate serum concentrations of total testosterone.

We present the case of a 39-year-old man who reported to the primary care physician for low back pain. Pain persisted despite extensive assessment and therapy. During the course, bilateral femoral neck fractures occurred and due to multiple enrichments in scintigraphy chronic multifocal (sterile) osteomyelitis was suspected. In the further follow-up the appropriate diagnosis of osteomalacia was established in bone biopsy and adequate treatment with Vitamin D was initiated. During therapy, the patient was free of pain or discomfort.

The primary function of Leydig cells is to secrete testosterone, which is critical in the regulation of male reproduction and development. Low levels of testosterone will lead to male hypogonadism. Stem cell-derived Leydig cell transplantation may be a promising alternative therapy for male hypogonadism. Thus far, others have reported that Leydig-like cells can be derived from mesenchymal stem cells, embryonic stem cells (ESCs), and induced pluripotent stem cells. However, the efficiency of the differentiating Leydig cells remains low, and progress toward generating functional adult Leydig cells (ALCs) is limited. Herein, we describe a robust method of directing differentiation of mouse embryonic stem cells (mESCs) into Leydig-like cells in vitro by overexpression of the transcription factor steroidogenic factor-1 (SF-1) and treatment with a combination of 8-Bromoadenosine-3',5'-cyclic monophosphate and forskolin. These differentiated cells express mRNA encoding the steroidogenic enzymes and produce progesterone and testosterone. Importantly, when transplanted into male rats that had their original Leydig cells selectively eliminated by ethylene dimethanesulfonate, these in vitro-derived Leydig-like cells further developed into functional ALCs that rescued serum testosterone levels. These data provide evidence that mESCs can be induced to differentiate into Leydig-like cells in vitro, which can develop in the in vivo microenvironment.

Objectives: To review the controversial issues of the Testosterone Deficiency Syndrome (TDS) with an emphasis on the concerns about the diagnosis., Design and Methods: The relevant literature was reviewed with particular attention to matters related to the clinical manifestations of the syndrome, the need for biochemical assessment and questions of biological and analytical variation that have to be taken into account. Therapeutic options were also appraised., Results: There are numerous difficulties with the clinical diagnosis of TDS due to the lack of specificity and subtlety of the manifestations when the degree of deficiency is not severe. Confirmation of the clinical impression requires laboratory evaluation but the choice of assays remains an unsettled issue although there is a general consensus that both free testosterone and bioavailable testosterone best reflect the degree of androgenicity. The laboratory diagnosis enjoys a great deal of credibility among clinicians but shortcomings in the interpretation of the assays need to be reiterated and the need for close collaboration between the clinician and the clinical biochemist is important for diagnostic accuracy. Even when the clinical picture is convincing, the laboratory may produce inconclusive results. The option of a therapeutic trial should be contemplated in this situation. Treatment options should be decided between the physician and the patient considering issues of availability, tolerance, efficacy and cost., Conclusions: TDS is a prevalent condition but a matter of persistent controversy due to the vagaries of the clinical and laboratory diagnosis. Symptomatic men with documented T deficiency deserve treatment to improve their quality of life., (Copyright © 2013 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)

The authors prove congenital anorchism by operative way as they recommend to think of congenital anomaly of testes--anorchism in all patients with lacking testis in the scrotum and inguinal canal. This anomaly is established in three patients. They propose a double hormonal stimulation with choriongonadotropin according to a fixed scheme as a basic diagnostic method in men with congenital anorchism. It is necessary to begin timely substitutive androgenic therapy in men with established anomaly. Usage of testicular prosthesis for correction of the cosmetic defect is one of the therapeutic stages of this congenital state. The prosthesis is of great psychological advantage in men with anorchism. Transplantation of testes is a future therapeutic method in patients with anorchism.