PubMed · 13693003
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W S CHIANG. 1961-01-28. Surgically correctable azoospermia.. https://pubmed.ncbi.nlm.nih.gov/13693003/
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OBJECTIVE: To investigate 2 polymorphism sites in exon 3 and intron 2 of FKBP6 in Chinese population, while screening the gene mutations and polymorphisms in exons 3, 4 of FKBP6, and the association of these polymorphisms with azoospermia. METHODS: Possible variations of exons 3, 4 and genotypes and frequencies of 2 polymorphic loci were examined by denaturing high-performance liquid chromatography(DHPLC) and PCR-restriction fragment length polymorphism(PCR-RFLP) technique in 177 azoospermia patients and 231 control individuals. RESULTS: The observed allele frequencies conformed well to Hardy-Weinberg equilibrium. The frequency of 278A allele was significantly higher in controls than that in patients (P<0.05). C/T(s7797242) polymorphism was not found in either group and variations in exons 3, 4 were not detected. CONCLUSION: 278A polymorphism of FKBP6 gene was associated with idiopathic azoospermia, while C/T, 370G/A, 430G/C, 467T/C, 468G/A polymorphisms might be very rare in Chinese population.
OBJECTIVE: To investigate the genetic causes of azoospermia and severe oligozoospermia. METHODS: Cytogenetic analysis and multiplex polymerase chain reaction(PCR) analysis were done on the 148 patients with azoospermia and serious oligozoospermia. RESULTS: Eleven of the 148(7.4%) cases showed microdeletion of at least one STS. In fifteen STS of AZFa, AZFb,AZFd, AZFc, thirteen STS, eleven STS,two STS and one STS microdeletion were found in each case respectively, including two with 12 STS, five with 5 STS microdeletion.Seven cases had chromosomal morphologic changes(4.7%),four had deletion and one had deletion with translocation of long arm on Y chromosome. One had enlarged region one band two(q12) on long arm of Y chromosome and one had reciprocal translocation of autosomes. CONCLUSION: The findings indicated that AZF microdeletion and chromosomal abnormality should be important causes of male infertility.
Azoospermia may occur because of reproductive tract obstruction (obstructive azoospermia) or inadequate production of spermatozoa, such that spermatozoa do not appear in the ejaculate (non-obstructive azoospermia). Azoospermia is diagnosed based on the absence of spermatozoa after centrifugation of complete semen specimens using microscopic analysis. History and physical examination and hormonal analysis (FSH, testosterone) are undertaken to define the cause of azoospermia. Together, these factors provide a >90% prediction of the type of azoospermia (obstructive v. non-obstructive). Full definition of the type of azoospermia is provided based on diagnostic testicular biopsy. Obstructive azoospermia may be congenital (congenital absence of the vas deferens, idiopathic epididymal obstruction) or acquired (from infections, vasectomy, or other iatrogenic injuries to the male reproductive tract). Couples in whom the man has congenital reproductive tract obstruction should have cystic fibrosis (CF) gene mutation analysis for the female partner because of the high risk of the male being a CF carrier. Patients with acquired obstruction of the male reproductive tract may be treated using microsurgical reconstruction or transurethral resection of the ejaculatory ducts, depending on the level of obstruction. Alternatively, sperm retrieval with assisted reproduction may be used to effect pregnancies, with success rates of 25-65% reported by different centres. Non-obstructive azoospermia may be treated by defining the cause of low sperm production and initiating treatment. Genetic evaluation with Y-chromosome microdeletion analysis and karyotype testing provides prognostic information in these men. For men who have had any factors potentially affecting sperm production treated and remain azoospermic, sperm retrieval from the testis may be effective in 30-70% of cases. Once sperm are found, pregnancy rates of 20-50% may be obtained at different centres with in vitro fertilisation and intracytoplasmic sperm injection.