Outcome of microsurgical testicular sperm extraction in familial idiopathic nonobstructive azoospermia

Arafa, Mohamed; Elbardisi, Haitham; Alsaid, Sami; Majzoub, Ahmad; Al-Malki, Ahmad H.; ElRobi, I.; Al‐Ansari, Abdulla

doi:10.1111/and.12378

Cited by 9 publications

(7 citation statements)

References 24 publications

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“…[2][3][4] Together, these analyses explain the cause of only ~30% of cases of NOA. [5][6][7] It is generally assumed that many of the remaining idiopathic cases have genetic causes, but although variants in ~55 genes have been associated with NOA in humans 8,9 and variants in hundreds of genes are known to impair spermatogenesis in mouse models, [10][11][12] there has been limited prospective, point-of-care, next-generation sequencing assessment of males with idiopathic NOA to determine the fraction with genetic causes. 13 The challenge in identifying genetic variants in idiopathic males is that the high prevalence of NOA, despite the detrimental effect on reproductive fitness, suggests that high genetic heterogeneity underlies this condition.…”

Section: Introductionmentioning

confidence: 99%

Point-of-care whole-exome sequencing of idiopathic male infertility

Fakhro

Elbardisi

Arafa

et al. 2018

Genetics in Medicine

127

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Section: Introductionmentioning

confidence: 99%

Point-of-care whole-exome sequencing of idiopathic male infertility

Fakhro

Elbardisi

Arafa

et al. 2018

Genetics in Medicine

127

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“…We found that parameters to forecast testicular SRR have become the particular focus of research over recent years. Researchers have considered several parameters which could act as predictors, including age, testicular volume, histopathology (hypospermatogenesis and Johnsen score), serum FSH, INH-B, TT levels, Y chromosomal microdeletions and family history [ 8 , 14 , 24 , 25 ]. However, other researchers have some that parameters could not be treated as predicators, including age, testicular volume, histopathology (hypospermatogenesis), previous negative TESE, serum FSH, LH, INH-B levels, seminal plasma INH-B, and anti-Müllerian hormone [ 7 , 16 , 21 , 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…The two patients in Group A with successful sperm retrieval belonged to one family. The histopathological diagnosis was the same in the brothers for each family [ 25 ]. The associated use of multiple parameters thus increased predicted value.…”

Section: Discussionmentioning

confidence: 99%

A clinical trial on the consistency of bilateral testicular tissue histopathology and Johnsen score: single side or bilateral side biopsy?

et al. 2018

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To evaluate and compare left and right testicular tissue histopathology and Johnsen score, and to investigate the necessity for bilateral testicular biopsy. We recruited180 patients with non-obstructiveazoospermia (NOA) on testicular biopsy who had undergonetesticular sperm aspiration (TESA). Pathological sections of testicular tissue were diagnosed by specially-assigned doctors, who evaluated pathological findings, determined the Johnsen score and confirmed for the presence or absence of sperm. Sperm positive rates for left and right testicular histopathology were 55.0% and 51.7% respectively, and the proportion of Johnsen scores≥8 for left and right testes were 53.3% and 50.0%, respectively. Cohen kappa values revealed that the identification of sperm in bilateral testicular samples was not consistent and was related to random effects; Optimized cut-off value for bilateral testicular volume was 11ml (Johnsen score ≥8), and optimized cut-off values of E2 on left and right testes were 144.5pmol/L and 133.5 pmol/L (Johnsen score≤7). However, age, serum prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH) and total testosterone (TT) levels were not accurate predictors for the existence of testicular sperm. There was nostatistical significance between left and right testicular histopathology in terms of sperm positive rates or Johnsen score; the Johnsen score were caused entirely by random effects and a score from one side could not represent the other side. Therefore, we recommend that both testes need to undergo surgery when NOA patients undergo testicular biopsy or sperm retrieval.

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“…According to testicular spermatogenic function, azoospermia can be classified as obstructive‐azoospermia (OA) and non‐obstructive‐azoospermia (NOA) (Wosnitzer et al ., ). Although some NOA patients have been identified with sperm in the testis (Arafa et al ., ; Ragab et al ., ), there are negligible possibilities for microsurgical extraction for the part of NOA cases, including those patients with deletion of azoospermia factor a or b (AZFa or AZFb) (Krausz et al ., ). Therefore, screening the AZF regions of the Y chromosome is of great importance to predict the prognosis of management in patients with azoospermia (Krausz & Casamonti, ).…”

Section: Introductionmentioning

confidence: 99%

Normal fertility with deletion of sY84 and sY86 in AZFa region

Tang

Liu

et al. 2019

Andrology

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Background Entire deletion of the azoospermia factor a (AZFa) region commonly results in non‐obstructive‐azoospermia (NOA). Although sY84 and sY86 are recommended as the first choice of sequence‐tagged sites (STSs) primers in AZFa region, and their deletions suggest a very high probability of complete deletion of AZFa, extension analysis is now compulsory to identify the deletion pattern. Objectives We aim to verify that extension analysis is relevant in assessing the deletion pattern of AZF by reporting a family in which two normal fertile men were confirmed to have a deletion of sY84 and sY86. Materials and methods According to the EAA/EMQN recommendation, AZF evaluation was detected by multiplex polymerase chain reaction (PCR) with six STSs, and extension analysis was performed to identify the deletion pattern due to the deletions of sY84 and sY86. And the further exploration was conducted to map the breakpoints of deleted DNA fragment. Results Deletion of sY84 and sY86 was found in the case with coinstantaneous normal semen analysis. An identically partial deletion pattern of AZFa region with the absence of an hg38Y fragment (12470437~12690385, 219949 bp in total) was found in both the case and his father, which includes three pseudogenes and one non‐coding‐RNA gene. Discussion and conclusion The extension analysis has permitted the diagnosis of a partial AZFa deletion and confirmed the importance of the extension analysis in order to provide a more accurate prediction for the testis phenotype.

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Outcome of microsurgical testicular sperm extraction in familial idiopathic nonobstructive azoospermia

Cited by 9 publications

References 24 publications

Point-of-care whole-exome sequencing of idiopathic male infertility

Point-of-care whole-exome sequencing of idiopathic male infertility

A clinical trial on the consistency of bilateral testicular tissue histopathology and Johnsen score: single side or bilateral side biopsy?

Normal fertility with deletion of sY84 and sY86 in AZFa region

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