Evidence map›Paper›PMID 40231331›Full record

ArticleThe Journal of clinical endocrinology and metabolism2025

Unraveling a Subgroup of Men With Unexplained Male Infertility-Men With Normogonadotropic Nonobstructive Azoospermia.

Vanessa Schwarzkopf, Joachim Wistuba, Reinhild Sandhowe-Klaverkamp, Sabine Kliesch, Jörg Gromoll, Maria Schubert

Abstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. GutFrontiers in cellular and infection microbiology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Vanessa SchwarzkopfCentre of Reproductive Medicine and Andrology, Institute of Reproductive and Regenerative Biology, University of Münster, Münster 48149, Germany.
Joachim WistubaCentre of Reproductive Medicine and Andrology, Institute of Reproductive and Regenerative Biology, University of Münster, Münster 48149, Germany.
Reinhild Sandhowe-KlaverkampCentre of Reproductive Medicine and Andrology, Institute of Reproductive and Regenerative Biology, University of Münster, Münster 48149, Germany.
Sabine KlieschCentre of Reproductive Medicine and Andrology, Department of Clinical and Surgical Andrology, University of Münster, EAA Training Center, Münster 48149, Germany.
Jörg GromollCentre of Reproductive Medicine and Andrology, Institute of Reproductive and Regenerative Biology, University of Münster, Münster 48149, Germany.ORCID 0000-0002-7788-8138
Maria SchubertCentre of Reproductive Medicine and Andrology, Department of Clinical and Surgical Andrology, University of Münster, EAA Training Center, Münster 48149, Germany.ORCID 0000-0001-8548-9551

Funding

Clinical Research Unit 329621271Clinical Research Unit CRU326Deutsche ForschungsgemeinschaftGerman Society of AndrologyUniversity of Münster SC112316
6 · The paper itself

Abstract

contextNonobstructive azoospermia (NOA) constitutes male infertility with complete absence of sperm in the ejaculate. NOA can originate in testicular malfunction or in endocrine dysregulation. Elevated follicle-stimulating hormone (FSH) levels are diagnostically valuable for NOA.

objectiveAn azoospermic patient cohort comprising 79 men and exhibiting no obstruction but normal FSH levels was identified. Focusing on this normogonadotropic nonobstructive azoospermic (NNOA) group, the study aimed to characterize these patients in depth.

methodsWhether the missing FSH upregulation in patients with NNOA is due to testicular or pituitary/hypothalamic malfunctions was examined by analyzing somatic, endocrine, and testicular parameters compared with 87 men with hypergonadotropic NOA and 88 normozoospermic men.

resultsTesticular phenotypes of patients with NNOA and NOA were compared in histologically stratified subgroups (most advanced germ cell type). Using flow cytometry, the samples were evaluated for testicular cell composition by ploidy analysis. Concerning the distinct histological classification (hypospermatogenesis, spermatogenic arrest, Sertoli cell only, tubular atrophy) NNOA men produced more elongated spermatids and showed higher sperm retrieval. Testicular tissue composition between patients with NNOA and patients with NOA only differed after meiosis.

conclusionThe missing FSH upregulation in NNOA might be due to a testicular malfunction, as both FSH and testosterone were normal and NNOA spermatogenesis differed only after meiosis. Two explanations are possible: NNOA represents a phenotype in which spermatogenesis fails-different from NOA-only at the postmeiotic level, leaving FSH regulation unaffected, or the same mechanism underlies both NNOA and NOA, but the groups are at different stages of progression of the same disorder.

Indexed as

AzoospermiaInfertility, MaleTestisAdultCohort StudiesFollicle Stimulating HormoneHumansMaleSpermatogenesisFollicle Stimulating Hormonefollicle-stimulating hormone (FSH)nonobstructive azoospermiaspermatogenesisunexplained infertility

Identifiers

PMID40231331
PMCPMC12623054

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.