ArticleFrontiers in endocrinology2026
Stress-associated transient enlargement of pre-existing adrenal hyperplasia in 21-hydroxylase deficiency: a case report.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The adrenal gland plays a pivotal role in the stress response via the hypothalamic-pituitary-adrenal (HPA) axis and the sympatho-adrenomedullary system (SAMS). Congenital adrenal hyperplasia (CAH) results from pathogenic variants in genes encoding adrenal steroidogenic enzymes. The most common form, 21-hydroxylase deficiency, impairs cortisol biosynthesis, leading to compensatory overproduction of adrenocorticotropic hormone (ACTH) and chronic adrenal hyperplasia. Case presentation: A 40-year-old man was referred for incidentally detected bilateral adrenal lesions on abdominal computed tomography (CT). CT revealed marked bilateral adrenal enlargement with clear contours. One month before admission, he had an acute upper respiratory tract infection and recovered after treatment with a cephalosporin. On admission, physical examination showed hyperpigmentation of the nipples region, lips, gums, and buccal mucosa. Superficial lymph nodes were palpable. He reported a history of infertility and suspected precocious puberty. Endocrinology markers demonstrated an elevated ACTH level (180 ng/L; reference range 5.0-78.0 ng/L) with a cortisol level of 174 nmol/L (reference range 133.0-537.0 nmol/L). Luteinizing hormone and follicle-stimulating hormone levels were both low, whereas dehydroepiandrosterone sulfate was elevated. Markedly elevated 17α-hydroxyprogesterone levels and a blunted cortisol response were observed under ACTH-stimulated conditions. Based on the clinical phenotype and biochemical findings, CAH due to 21-hydroxylase deficiency was diagnosed and considered consistent with the simple virilizing form, which was subsequently genetically supported by the CYP21A2 I172N homozygous mutation in exon 4. Remarkably, without any specific treatment, adrenal volume decreased substantially within one month, from 61.06 cm Conclusions: In patients with 21-OHD and residual enzymatic activity, infectious stress may trigger transient enlargement of pre-existing adrenal hyperplasia, potentially as a compensatory response to increased cortisol demand, followed by partial regression after stress resolution.
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.