Evidence map›Paper›PMID 35854271›Full record

ArticleBMC endocrine disorders2022

Ectopic ACTH-producing neuroendocrine tumor occurring with large recurrent metastatic pheochromocytoma: a case report.

Fumi Saishouji, Sarie Maeda, Hideaki Hamada, Noriko Kimura, Ai Tamanoi, Saiko Nishida, Masaji Sakaguchi, Motoyuki Igata, Kiho Yokoo, Fumi Kawakami and 2 more

Open access · goldAbstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC endocrine disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 28% 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, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Ectopic ACTH Syndrome Caused by Pheochromocytoma: A Case Report and Systematic Review.Endocrine, metabolic & immune disorders drug targets · 2026
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
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

12 authors at 3 institutions in 1 country.

Fumi Saishouji *Department of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Sarie Maeda *Department of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Hideaki Hamada *Department of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Noriko KimuraDepartment of Diagnostic Pathology, Department of Clinical Research, National Hospital Organization, Hakodate Hospital, 16-18 Kawahara, Hakodate, Hokkaido, 041-8512, Japan.
Ai TamanoiDepartment of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Saiko NishidaDepartment of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Masaji SakaguchiDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Motoyuki IgataDepartment of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Kiho YokooDepartment of Diagnostic Pathology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Fumi KawakamiDepartment of Diagnostic Pathology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Eiichi ArakiDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan.
Tatsuya KondoDepartment of Diabetes, Metabolism and Endocrinology, Kumamoto University Hospital, 1-1-1 Honjo, Chuo-Ward, Kumamoto, 860-8556, Japan. t-kondo@gpo.kumamoto-u.ac.jp.ORCID http://orcid.org/0000-0003-4830-8955
Kumamoto University Hospital · JPKumamoto University · JPNational Hospital Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEctopic ACTH-dependent Cushing syndrome is rarely caused by pheochromocytoma (PCC). Glucocorticoid-regulated positive feedback loops in ACTH and catecholamines were proposed in some similar cases. CASE PRESENTATION: We present here an 80-year-old man who had previously undergone surgery for a left adrenal PCC and newly developed severe hypertension, hypokalemia, and typical Cushingoid manifestations. Investigations revealed hyperglycemia, hypokalemia, and extremely high catecholamines and their metabolites, ACTH and cortisol. Imaging modalities showed a recurrent large left adrenal mass positively visualized with

conclusionsWe experienced a case of severe ectopic ACTH producing the largest reported recurrent malignant left PCC with liver metastases that presented positive feedback loops in the ACTH/cortisol and catecholamine/cortisol axes. Clinicians should be aware of the paradoxical response of ACTH on metyrapone treatment and possible steroid-induced catecholamine crisis.

Indexed as

ACTH Syndrome, EctopicAdrenal Gland NeoplasmsHypokalemiaNeuroendocrine TumorsPheochromocytomaAdrenocorticotropic HormoneAged, 80 and overCatecholaminesHumansHydrocortisoneMaleMetyraponeNeoplasm Recurrence, LocalAdrenocorticotropic HormoneCatecholaminesHydrocortisoneMetyraponeCatecholamine,CortisolEctopic ACTH-producing tumorPositive feedback loopRecurrent metastatic pheochromocytoma,

Identifiers

PMID35854271
PMCPMC9297627
OpenAlexW4286219563

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.