Evidence map›Paper›PMID 32309131›Full record

ArticleRespiratory medicine case reports2020

A case report of pulmonary amyloidosis recognized by detection of AA amyloid exclusively in alveolar macrophages.

Thiyaphat Laohawetwanit, Kei Tanaka, Yoshiaki Zaizen, Kazuhiro Tabata, Kouji Ando, Hiroshi Ishimoto, Hiroshi Mukae, Yasushi Miyazaki, Andrey Bychkov, Junya Fukuoka

Open access · goldAbstract readCase Reports
In one paragraph

Article in Respiratory medicine case reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 57% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

10 authors at 2 institutions in 2 countries.

Thiyaphat LaohawetwanitChulabhorn International College of Medicine, Thammasat University, Pathumthani, Thailand.
Kei TanakaDepartment of Pathology, Nagasaki University Hospital, Nagasaki, Japan.
Yoshiaki ZaizenDepartment of Pathology, Nagasaki University Hospital, Nagasaki, Japan.
Kazuhiro TabataDepartment of Pathology, Nagasaki University Hospital, Nagasaki, Japan.
Kouji AndoDepartment of Hematology, Atomic Bomb Disease and Hibakusha Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Hiroshi IshimotoSecond Department of Internal Medicine, Nagasaki University Hospital, Nagasaki, Japan.
Hiroshi MukaeSecond Department of Internal Medicine, Nagasaki University Hospital, Nagasaki, Japan.
Yasushi MiyazakiDepartment of Hematology, Atomic Bomb Disease and Hibakusha Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Andrey BychkovDepartment of Pathology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Junya FukuokaDepartment of Pathology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Nagasaki University · JPNagasaki University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloidosis is a rare condition in which tissue deposits of inert fibrillar protein result in organ damage and dysfunction. There are several types of amyloid fibrils. Some of the most common forms are AL (amyloid light chain) protein and AA (amyloid-associated) type of amyloid fibril protein. Pulmonary amyloidosis is relatively common but is usually asymptomatic. Thus, the diagnosis may be easily overlooked. A 78-year-old male with a history of multiple myeloma followed by systemic amyloidosis presented with abnormal chest CT showing diffuse interlobular thickening in the whole lung field with bilateral pleural effusion. Bronchoalveolar lavage and transbronchial biopsy were performed. Due to the patient's poor condition and hemorrhage, only one fragment was available from forceps biopsy. Histologically, there was no amyloid deposition in the lung parenchyma; however, some histiocytes showed eosinophilic granular contents which prompted us to perform additional staining. The cytoplasmic material turned to be positive with direct fast scarlet (DFS) staining and AA amyloid immunostaining. Similar macrophages with AA amyloid were also found in the bronchoalveolar fluid. We experienced a case with AA amyloidosis affecting the lung diagnosed by the presence of intracytoplasmic amyloid in alveolar macrophages. The microscopic changes were so subtle that they may be overlooked. Recognition of amyloid deposition in alveolar macrophages may be an important clue to diagnose pulmonary amyloidosis. Such finding is of particular significance in the small-sized specimens, such as biopsies and cytologic smears.

Indexed as

Bronchoalveolar lavageMultiple myelomaPathologyPulmonary amyloidosisSystemic AA amyloidosis

Identifiers

PMID32309131
PMCPMC7155221
OpenAlexW3015231472

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LicenceCC BY-NC-ND
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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.