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Azoospermia clinical trials

View clinical trials related to Azoospermia.

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NCT ID: NCT01509482 Completed - Insulin Resistance Clinical Trials

Insulin Resistance in Idiopathic Oligospermia and Azoospermia

Start date: January 2012
Phase: N/A
Study type: Interventional

Insulin resistance in men can be the underlying major factor in reproductive abnormalities ( chronic hypospermatogenesis ) as well as metabolic abnormalities similar to polycystic ovarian syndrome ( PCOS ) in women.

NCT ID: NCT01375062 Completed - Azoospermia Clinical Trials

Obtaining Undifferentiated Cells From Testis Biopsy

Start date: May 2009
Phase: N/A
Study type: Interventional

The purpose of this study is to isolate and culture stem cell from adult human testicular biopsies for future transplantation in fertility preservation.

NCT ID: NCT01206270 Completed - Clinical trials for Klinefelter Syndrome

Androgen for Leydig Cell Proliferation

ALCeP
Start date: June 2009
Phase: Phase 2/Phase 3
Study type: Interventional

Patients with infertility often presents alterations at ultrasonographic examination of the testis. These alterations include a much higher incidence of small, multiple, non-palpable hypoechoic micro-nodules that can show internal vascularization. This finding often create alarm and anxiety, because it has to be placed in a differential diagnosis versus low-stage malignant germ cell tumors. Nevertheless, explorative surgery reveal that a consistent number of these lesion are benign, due to Leydig cell hyperplasia or Leydig cell tumours. The purpose of this study is to evaluate the effects of androgen therapy on the size and number of non-palpable hypoechoic micro-nodules in patients with elevated gonadotropin levels.

NCT ID: NCT00548977 Completed - Male Infertility Clinical Trials

Genetic Studies Spermatogenic Failure

Start date: January 2001
Phase: N/A
Study type: Observational

The proposed study is designed to test the following hypotheses: 1. Mouse autosomal or X-linked genes which are exclusively expressed in mouse spermatogonia are also spermatogonia-specific in human. 2. Severe spermatogenic defect, especially hypospermatogenesis or SCOS, is caused by an intrinsic defect in germ line stem cell or speramtogenia. 3. Spermatogonia-specific genes are caudate genes for human spermatogenic defect, especially for hypospermatogenesis or SCOS. 4. For a significant fraction of cases with severe spermatogenic defect, the sterile genes are transmitted via multifactorial inheritance mode. 5. For some cases with severe spermatogenic defect, mutations of spermatogonia- specific genes may be transmitted in the X-linked recessive, autosomal recessive, or autosomal dominant mode.

NCT ID: NCT00484081 Completed - Infertility Clinical Trials

Microdissection Testicular Sperm Extraction (MicroTESE) and IVF-ICSI Outcome in Non-Obstructive Azoospermia (NOA)

Start date: June 2005
Phase: N/A
Study type: Interventional

We evaluated the application of surgical testicular exploration with the aid of a microscope (MictoTESE) to increase the chances of obtaining sperm in men with impaired sperm production, a condition known as non-obstructive azoospermia. We also evaluated the outcomes of these couples when the sperm obtained were used in ICSI (Intracytoplasmic Sperm Injection) during assisted reproductive technology treatment. We believe that excellent results may be obtained with the use of the following techniques in the treatment of couples where non-obstructive azoospermia is a significant cause.

NCT ID: NCT00044369 Completed - Male Infertility Clinical Trials

Role of the Toxic Metal Cadmium in the Mechanism Producing Infertility With a Varicocele

Start date: May 2000
Phase: N/A
Study type: Observational

Varicose veins in the scrotum (varicocele) are responsible for >20% of male infertility in the US. Varicocele are associated with decreased sperm number and markedly reduced sperm fertilizing ability. Surgical repair or removal of varicocele restores fertility in only 1/3 of cases. The goal of this study is to identify markers that predict the outcome of variocele correction. This would offer considerable health cost savings. Based on preliminary findings, we will obtain testis biopsies and semen specimens from infertile men with varicocele and prospectively examining the levels of cadmium, a toxic metal, and expression of genes required for normal sperm function. The semen and biopsies will be obtained during clinically dictated procedures. Cadmium and gene expression will be compared with response to varicocele repair (i.e., increased sperm production; pregnancy).