ArticleEndocrine pathology2005
The pituitary in klinefelter syndrome.
Article in Endocrine pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Hypopituitarism and Rathke's cleft cyst in 48,XXYY Syndrome: new insights into sex chromosome aneuploidies.Einstein (Sao Paulo, Brazil) · 2025Article
- Mixed hypogonadism: a neglected combined form of hypogonadism.Endocrine · 2024Article
- Article
- Central hypogonadism in Klinefelter syndrome: report of two cases and review of the literature.Journal of endocrinological investigation · 2021Review
- Pituitary hyperplasia with Sertoli cell-only and 47,XYY syndromes: an uncommon triad.BMJ case reports · 2020Article
- Macrogonadotropinoma, a venous thromboembolic event and asymptomatic extensive periventricular white matter changes in a patient with Klinefelter syndrome.Clinical case reports · 2020Article
- Pituitary Hyperplasia in Severe Primary Hypothyroidism: A Case Report and Review of the Literature.Case reports in endocrinology · 2019Article
- Article
- Pituitary hyperplasia: case series and literature review of an under-recognised and heterogeneous condition.Endocrinology, diabetes & metabolism case reports · 2015Article
- Tumefactive postmenopausal gonadotroph cell hyperplasia.Endocrine pathology · 2012Article
- Consensus statement on diagnosis and clinical management of Klinefelter syndrome.Journal of endocrinological investigation · 2010Review
- Gonadotropin-positive pituitary tumors accompanied by ovarian tumors in aging female ERbeta-/- mice.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Diagnosis and treatment difficulties of psychiatric symptoms in Klinefelter syndrome: a case report.BMJ case reports · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKlinefelter syndrome is a genetically determined primary gonadal defect characterized by the XXY karyotype. The testes are small, blood testosterone levels are low, and blood gonadotropin levels are elevated. Pituitary changes in patients with Klinefelter syndrome have not been evaluated in detail.
designThe first patient, a 76-yr-old man, was operated for a large sellar mass. The second and third patients, a 62- and a 52-yr-old man, respectively, died of cardiac failure. Both the latter pituitaries were normal-sized and removed at autopsy. The diagnosis of Klinefelter syndrome was confirmed by genetic testing in all three cases. The formalin-fixed and paraffin-embedded pituitaries of three patients were evaluated for adenohypophysial hormone immunoreactivity. For immunohistochemistry, the streptavidin- biotin-peroxidase (ABC) complex method was applied.
resultsIn case 1, histology and immunohistochemistry revealed an oncocytic gonadotroph macroadenoma immunoreactive for FSH and alpha subunit. No pituitary gland was evident. The pituitary of case 2 featured hyperplasia of gonadotrophs, some with features of "gonadal deficiency cells," and a microadenoma immunoreactive for GH. The pituitary of case 3 similarly showed hyperplasia of gonadotrophs and the formation of gonadal deficiency cells.
conclusionProtracted stimulation of gonadotrophs due to lack of androgen feedback might have been a factor in the formation of the gonadotroph adenoma in case 1 and in the development of gonadotroph hyperplasia in cases 2 and 3. The clinically silent GH microadenoma of case 2 was regarded as an incidental finding.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.