Evidence map›Paper›PMID 31572323›Full record

ArticleFrontiers in microbiology2019

Cerebrospinal Fluid CXCL10 as a Candidate Surrogate Marker for HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis.

Keiko Tamaki, Tomoo Sato, Jun Tsugawa, Shinsuke Fujioka, Naoko Yagishita, Natsumi Araya, Junji Yamauchi, Ariella L G Coler-Reilly, Misako Nagasaka, Yasuhiro Hasegawa and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

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  17. Pathogenesis of HTLV-1 infection and progression biomarkers: An overview.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
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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 2 institutions in 2 countries.

Keiko TamakiDepartment of Neurology, Fukuoka University, Fukuoka, Japan.
Tomoo SatoDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Jun TsugawaDepartment of Neurology, Fukuoka University, Fukuoka, Japan.
Shinsuke FujiokaDepartment of Neurology, Fukuoka University, Fukuoka, Japan.
Naoko YagishitaDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Natsumi ArayaDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Junji YamauchiDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Ariella L G Coler-ReillyDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Misako NagasakaDepartment of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, United States.
Yasuhiro HasegawaDepartment of Neurology, St. Marianna University School of Medicine, Kawasaki, Japan.
Yoshihisa YamanoDepartment of Rare Diseases Research, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Yoshio TsuboiDepartment of Neurology, Fukuoka University, Fukuoka, Japan.
St. Marianna University School of Medicine · JPFukuoka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human T-cell leukemia virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a debilitating, progressive disease without effective treatment; therefore, development of disease modifying therapy that improves long-term functional outcomes is an unmet need for patients. However, it is virtually impossible to consider this as a primary endpoint in clinical trials owing to the prolonged disease course. Therefore, development of surrogate markers that help predict the effectiveness of new interventions is essential. Currently, several candidate surrogate markers have been identified for HAM/TSP. Cerebrospinal fluid (CSF) C-X-C motif chemokine 10 (CXCL10) is involved in the pathogenesis of HAM/TSP and was shown to correlate with disease progression. However, it remains unclear whether changes in CSF CXCL10 levels are observed in response to treatment and whether these correlate with prognosis. Here we investigated several markers, including CSF CXCL10, in this respect. Data pertaining to patient characteristics and results of motor function evaluation and CSF examination of 13 HAM/TSP patients who received steroid treatment were retrospectively analyzed. Osame motor disability scores (OMDS), 10 m walking time, and CSF levels of CXCL10, neopterin, total protein, cell counts, and anti-HTLV-1 antibody titer were compared before and after steroid therapy. Levels of all CSF markers, with the exception of cell count, were significantly decreased after treatment. Nine of the 13 patients (69.2%) showed improvement in OMDS and were considered responders. Pre-treatment CSF levels of CXCL10 and anti-HTLV-1 antibody titer in responders were higher than those in non-responders (

Indexed as

biomarkercerebrospinal fluidCXCL10HAM/TSPHTLV-1neopterin

Identifiers

PMID31572323
PMCPMC6749079
OpenAlexW2971002404

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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.