Evidence map›Paper›PMID 35399924›Full record

ArticleFrontiers in endocrinology2022

Case Report: Primary Aldosteronism Due to Bilateral Aldosterone-Producing Micronodules With HISTALDO Classical and Contralateral Non-Classical Pathology.

Yi-Ju Chen, Kang-Yung Peng, Jeff S Chueh, Hung-Wei Liao, Tsung-Yi Hsieh, Vin-Cent Wu, Shuo-Meng Wang

Open access · goldAbstract readCase Reports
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 26% of its field
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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Primary Aldosteronism: State-of-the-Art Review.American journal of hypertension · 2022
    Article
  5. Review
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

7 authors at 2 institutions in 1 country.

Yi-Ju ChenDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Kang-Yung PengDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Jeff S ChuehDepartment of Urology, National Taiwan University, National Taiwan University Hospital, Taipei, Taiwan.
Hung-Wei LiaoDivision of Nephrology, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Tsung-Yi HsiehDepartment of Urology, National Taiwan University, National Taiwan University Hospital, Taipei, Taiwan.
Vin-Cent WuDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Shuo-Meng WangDepartment of Urology, National Taiwan University, National Taiwan University Hospital, Taipei, Taiwan.
National Taiwan University Hospital · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Non-classical multiple aldosterone-producing micronodules/nodules (mAPM/mAPN) could be the pathogenesis of primary aldosteronism (PA). The co-existence of mAPM with adenomas harboring somatic mutations has not previously been reported. Methods: We presented a PA patient with bilateral mAPM and concomitant autonomous cortisol secretion (ACS). Results: A 46-year-old Taiwanese woman presented with hypertension, hypokalemia, and bilateral adrenal adenomas. A 1 mg low-dose dexamethasone suppression test showed elevated morning serum cortisol. An adrenal vein sampling (AVS) suggested a left-sided lateralization of hyperaldosteronism. A right partial adrenalectomy and a left total adrenalectomy were performed. The patient showed biochemical and hypertension remission after the operation. This patient had bilateral mAPM with concomitant ACS, a right histopathologically classical PA adenoma, and a left non-classical PA adenoma. The right adrenal adenoma showed CYP11B1-negative and CYP11B2-positive staining and harbored the Conclusion: In a PA patient with concomitant ACS, bilateral APM could coexist with both histopathologically classical and non-classical PA adenomas, each with different somatic mutations. The presence of ACS could lead to the misinterpretation of AVS results.

Indexed as

AdenomaAdrenocortical AdenomaHyperaldosteronismHypertensionAldosteroneCytochrome P-450 CYP11B2FemaleG Protein-Coupled Inwardly-Rectifying Potassium ChannelsHumansHydrocortisoneMiddle AgedSteroid 11-beta-HydroxylaseAldosteroneCytochrome P-450 CYP11B2G Protein-Coupled Inwardly-Rectifying Potassium ChannelsHydrocortisoneKCNJ5 protein, humanSteroid 11-beta-Hydroxylasealdosterone-producing adenoma (APA)aldosterone-producing micronodule (APM)autonomous cortisol secretion (ACS)KCNJ5 mutationprimary aldosteronismPRKACA mutations

Identifiers

PMID35399924
PMCPMC8989467
OpenAlexW4221086573

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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.