Evidence map›Paper›PMID 26843560›Full record

ArticleNeurology2016

Cutaneous adverse events in multiple sclerosis patients treated with daclizumab.

Irene Cortese, Joan Ohayon, Kaylan Fenton, Chyi-Chia Lee, Mark Raffeld, Edward W Cowen, John J DiGiovanna, Bibiana Bielekova

Registry-linked trialOpen access · greenAbstract readClinical Trial, Phase I
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01143441 (Investigating Mechanism of Action of DAC HYP in the Treatment of High-Inflammatory Multiple Sclerosis), which is not on this map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.7field-weighted citation impact, top 5% 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.

NCT01143441 phase1completednot on this map

Investigating Mechanism of Action of DAC HYP in the Treatment of High-Inflammatory Multiple Sclerosis (MS)

TypeinterventionalSponsorNational Institute of Neurological Disorders and Stroke (NINDS)Ran2010 to 2017Enrolled48ConditionsMultiple Sclerosis, Multiple Sclerosis, Relapsing-RemittingArmsDAC-HYP
3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Natural killer cells in the central nervous system.Cell communication and signaling : CCS · 2023
    Review
  3. Article
  4. Monoclonal Antibodies as Neurological Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  5. Article
  6. Review
  7. Daclizumab Therapy for Multiple Sclerosis.Cold Spring Harbor perspectives in medicine · 2019
    Review
  8. Review
  9. Review
  10. A comprehensive review on the treatment approaches of multiple sclerosis: currently and in the future.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  11. Review
  12. Review
  13. Daclizumab: Development, Clinical Trials, and Practical Aspects of Use in Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Daclizumab.Hospital pharmacy · 2016
    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

8 authors at 1 institution in 1 country.

Irene CorteseFrom the Neuroimmunology Clinic (I.C., J.O.) and the Neuroimmunological Diseases Unit (B.B.), National Institute of Neurological Disorders and Stroke, and the Laboratory of Pathology (C.-C.L., M.R.) and the Dermatology Branch (E.W.C., J.J.D.), Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda; and Department of Neurology (K.F.), Johns Hopkins School of Medicine, Baltimore, MD.
Joan OhayonFrom the Neuroimmunology Clinic (I.C., J.O.) and the Neuroimmunological Diseases Unit (B.B.), National Institute of Neurological Disorders and Stroke, and the Laboratory of Pathology (C.-C.L., M.R.) and the Dermatology Branch (E.W.C., J.J.D.), Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda; and Department of Neurology (K.F.), Johns Hopkins School of Medicine, Baltimore, MD.
Kaylan FentonFrom the Neuroimmunology Clinic (I.C., J.O.) and the Neuroimmunological Diseases Unit (B.B.), National Institute of Neurological Disorders and Stroke, and the Laboratory of Pathology (C.-C.L., M.R.) and the Dermatology Branch (E.W.C., J.J.D.), Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda; and Department of Neurology (K.F.), Johns Hopkins School of Medicine, Baltimore, MD.
Chyi-Chia LeeFrom the Neuroimmunology Clinic (I.C., J.O.) and the Neuroimmunological Diseases Unit (B.B.), National Institute of Neurological Disorders and Stroke, and the Laboratory of Pathology (C.-C.L., M.R.) and the Dermatology Branch (E.W.C., J.J.D.), Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda; and Department of Neurology (K.F.), Johns Hopkins School of Medicine, Baltimore, MD.
Mark RaffeldFrom the Neuroimmunology Clinic (I.C., J.O.) and the Neuroimmunological Diseases Unit (B.B.), National Institute of Neurological Disorders and Stroke, and the Laboratory of Pathology (C.-C.L., M.R.) and the Dermatology Branch (E.W.C., J.J.D.), Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda; and Department of Neurology (K.F.), Johns Hopkins School of Medicine, Baltimore, MD.
Edward W CowenFrom the Neuroimmunology Clinic (I.C., J.O.) and the Neuroimmunological Diseases Unit (B.B.), National Institute of Neurological Disorders and Stroke, and the Laboratory of Pathology (C.-C.L., M.R.) and the Dermatology Branch (E.W.C., J.J.D.), Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda; and Department of Neurology (K.F.), Johns Hopkins School of Medicine, Baltimore, MD.
John J DiGiovannaFrom the Neuroimmunology Clinic (I.C., J.O.) and the Neuroimmunological Diseases Unit (B.B.), National Institute of Neurological Disorders and Stroke, and the Laboratory of Pathology (C.-C.L., M.R.) and the Dermatology Branch (E.W.C., J.J.D.), Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda; and Department of Neurology (K.F.), Johns Hopkins School of Medicine, Baltimore, MD.
Bibiana BielekovaFrom the Neuroimmunology Clinic (I.C., J.O.) and the Neuroimmunological Diseases Unit (B.B.), National Institute of Neurological Disorders and Stroke, and the Laboratory of Pathology (C.-C.L., M.R.) and the Dermatology Branch (E.W.C., J.J.D.), Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda; and Department of Neurology (K.F.), Johns Hopkins School of Medicine, Baltimore, MD. bibi.bielekova@nih.gov.
Johns Hopkins University · US

Funding

Molecular Diagnostics Core LaboratoryZICBC011079 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI XI, LIQIANG · 2009 to 2025
$33.8M
From therapeutic mechanisms to unraveling the pathophysiology of MSZIANS003056 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI BIELEKOVA, BIBIANA · 2009 to 2018
$14.5M
Dermatology Consultation ServiceZIDBC011317 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI COWEN, EDWARD · 2010 to 2021
$6.4M
Intramural NIH HHS
6 · The paper itself

Abstract

objectiveTo analyze the spectrum and mechanisms of cutaneous adverse events (AEs) in patients with multiple sclerosis treated with daclizumab high-yield process (DAC-HYP).

methodsA total of 31 participants in an institutional review board-approved open-label phase I study of DAC-HYP (NCT01143441) were prospectively evaluated over 42 months for development of cutaneous AEs. Participants provided written informed consent. Fifteen participants were naive to anti-CD25 therapy (cohort B), while 16 had received daclizumab (Zenapax; Hoffmann-La Roche) IV for 4-9 years (mean 5.8 years) prior to enrollment (cohort A). Immunohistochemistry was performed on pretreatment and posttreatment skin biopsies of normal-appearing skin (cohort B only) and on lesional biopsies in participants presenting with rash (both cohorts).

resultsCutaneous AEs occurred in 77% of patients, the majority presenting with patches of eczema requiring no treatment. Moderate to severe rash developed in 6 participants (19%) and required discontinuation of DAC-HYP in 4 (13%). More severe rashes presented psoriasiform phenotype, but lesional biopsies lacked features of either psoriasis or drug hypersensitivity eruptions. Instead, irrespective of clinical severity, lesional biopsies showed nonspecific features of eczematous dermatitis, but with prominent CD56+ lymphocytic infiltrates. Pretreatment and posttreatment biopsies of normal-appearing skin demonstrated no histopathologic changes.

conclusionsObserved cutaneous AEs are likely related to the immunomodulatory effects DAC-HYP exerts on innate lymphoid cells, including natural killer cells. Vigilance and timely management of skin reactions may prevent treatment discontinuation in participants with severe rash.

Indexed as

AdultAntibodies, Monoclonal, HumanizedDaclizumabDrug EruptionsFemaleHumansImmunoglobulin GImmunosuppressive AgentsMaleMultiple SclerosisTreatment OutcomeAntibodies, Monoclonal, HumanizedDaclizumabImmunoglobulin GImmunosuppressive Agents

Identifiers

PMID26843560
PMCPMC4793779
OpenAlexW2317258215

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.