Evidence map›Paper›PMID 39533305›Full record

ReviewThrombosis journal2024

Laboratory and clinical haemostatic aberrations in primary dermatologic disease: A review.

Divya Sharma, Sierra Thomas, Trace B Moody, Mitchell Taylor, Bianca Ituarte, Corey J Georgeson, Christopher D Barrett, Erin X Wei

Abstract readReview
In one paragraph

Review in Thrombosis journal, 2024. 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
–field-weighted citation impact
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.

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

8 authors.

Divya Sharma *Department of Dermatology, University of Nebraska Medical Center, 985645, Omaha, NE, 68198-5645, USA.
Sierra Thomas *Department of Dermatology, University of Nebraska Medical Center, 985645, Omaha, NE, 68198-5645, USA.
Trace B Moody *Division of Acute Care Surgery, Department of Surgery, University of Nebraska Medical Center, Omaha, NE, USA.
Mitchell TaylorDepartment of Dermatology, University of Nebraska Medical Center, 985645, Omaha, NE, 68198-5645, USA.
Bianca ItuarteDepartment of Dermatology, University of Nebraska Medical Center, 985645, Omaha, NE, 68198-5645, USA.
Corey J GeorgesonDepartment of Dermatology, University of Nebraska Medical Center, 985645, Omaha, NE, 68198-5645, USA.
Christopher D BarrettDivision of Acute Care Surgery, Department of Surgery, University of Nebraska Medical Center, Omaha, NE, USA.
Erin X WeiDepartment of Dermatology, University of Nebraska Medical Center, 985645, Omaha, NE, 68198-5645, USA.

Funding

Using Patient-Reported Outcomes, Inflammatory Profiles, and Cardiovascular Phenogroups to Expand the Definition of Heart Failure with Preserved Ejection FractionP20GM152326 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Rebekah L. Gundry · 2024 to 2026
$10.3M
Mechanisms of Complement Activation in Traumatic InjuryK08HL171936 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Christopher David Barrett · 2024 to 2026
$500k
National Heart, Lung and Blood Institutes K08-HL171936Nebraska Research Initiative Award R01AI165666NHLBI NIH HHS K08 HL171936NIGMS NIH HHS P20 GM152326NIGMS NIH HHS P20-GM152326
6 · The paper itself

Abstract

Inflammatory dermatologic diseases have long been viewed as a "skin limited" disease process. Current literature on inflammatory dermatologic diseases investigates their relationship and influence on thromboembolic states and thromboembolic complications and the understanding of their pathophysiology and molecular mechanisms.Studies specifically discuss known inflammatory skin diseases including alopecia areata, vitiligo, psoriasis, hidradenitis suppurativa, atopic dermatitis, chronic spontaneous urticaria, and autoimmune bullous diseases, and their effects on systemic inflammation, associated cardiovascular comorbidities, and thromboembolic or hypercoagulable states. The limited current literature shows potential for links between inflammatory skin diseases and hypercoagulable states. Biomarkers such as F1 + 2, D-dimer, eosinophilic cationic protein, and PAI-1 are currently being studied to outline the mechanisms connecting inflammatory skin disease to the coagulation system. Further study and larger amounts of data are needed to draw definitive conclusions, especially when interpreting biomarkers alone such as PAI-1.The mechanisms, rates of systemic inflammation, and clinical outcomes of traditionally "skin limited" inflammatory diseases remain chronically understudied in dermatology. Many organ systems have well established connections between inflammatory disease and hypercoagulable states, but there are significant gaps in the literature regarding skin diseases. There is a significant need for comprehensive investigation of molecular mechanisms behind inflammatory dermatologic disease and hypercoagulability, how hypercoagulability effects clinical outcomes, and proper intervention to optimize patient outcomes.

Indexed as

Alopecia AreataAtopic dermatitisBullous Pemphigoid, PemphigusChronic spontaneous UrticariaCoagulationD-DimerDermatitis HerpetiformisHidradenitis SuppurativaHypercoagulableProthrombinPsoriasisVitiligo

Identifiers

PMID39533305
PMCPMC11558853

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.