Evidence map›Paper›PMID 37207448›Full record

ReviewThe Journal of clinical endocrinology and metabolism2023

New-Onset Diabetes After COVID-19.

Sun H Kim, Ipsa Arora, Daniel S Hsia, William C Knowler, Erin LeBlanc, Eleftherios Mylonakis, Richard Pratley, Anastassios G Pittas

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of clinical endocrinology and metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 4 pooled it
9.5field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 4 syntheses or guidelines pooled it, 49 citations in OpenAlex.

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  7. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
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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

8 authors at 7 institutions in 1 country.

Sun H KimDivision of Endocrinology, Gerontology and Metabolism, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0003-0895-7491
Ipsa AroraDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, Tufts Medical Center, Boston, MA 02111, USA.
Daniel S HsiaPennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA.ORCID 0000-0003-2832-3429
William C KnowlerNational Institute of Diabetes and Digestive and Kidney Diseases, Phoenix, AZ 85016, USA.ORCID 0000-0002-7004-5197
Erin LeBlancCenter for Health Research, Kaiser Permanente, Portland, OR 97227, USA.ORCID 0000-0002-4067-3432
Eleftherios MylonakisDepartment of Medicine, Houston Methodist Hospital, Houston, TX 77030, USA.ORCID 0000-0002-4624-0777
Richard PratleyAdventHealth Translational Research Institute, Orlando, FL 32804, USA.ORCID 0000-0002-2912-1389
Anastassios G PittasDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, Tufts Medical Center, Boston, MA 02111, USA.ORCID 0000-0002-0124-7174
Tufts Medical Center · USKaiser Permanente Center for Health Research · USMethodist Hospital · USNational Institute of Diabetes and Digestive and Kidney Diseases · USPennington Biomedical Research Center · USStanford University · USTranslational Research Institute for Metabolism and Diabetes · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is evidence suggesting that infection with SARS-CoV-2 can lead to several long-term sequelae including diabetes. This mini-review examines the rapidly evolving and conflicting literature on new-onset diabetes after COVID-19, which we term NODAC. We searched PubMed, MEDLINE, and medRxiv from inception until December 1, 2022, using Medical Subject Headings (MeSH) terms and free text words including "COVID-19," "SARS-CoV-2," "diabetes," "hyperglycemia," "insulin resistance," and "pancreatic β-cell." We also supplemented searches by examining reference lists from retrieved articles. Current evidence suggests that COVID-19 increases the risk of developing diabetes, but the attributable risk is uncertain because of limitations of study designs and the evolving nature of the pandemic, including new variants, widespread population exposure to the virus, diagnostic options for COVID-19, and vaccination status. The etiology of diabetes after COVID-19 is likely multifactorial and includes factors associated with host characteristics (eg, age), social determinants of health (eg, deprivation index), and pandemic-related effects both at the personal (eg, psychosocial stress) and the societal-community level (eg, containment measures). COVID-19 may have direct and indirect effects on pancreatic β-cell function and insulin sensitivity related to the acute infection and its treatment (eg, glucocorticoids); autoimmunity; persistent viral residency in multiple organs including adipose tissue; endothelial dysfunction; and hyperinflammatory state. While our understanding of NODAC continues to evolve, consideration should be given for diabetes to be classified as a post-COVID syndrome, in addition to traditional classifications of diabetes (eg, type 1 or type 2), so that the pathophysiology, natural history, and optimal management can be studied.

Indexed as

COVID-19Diabetes MellitusHyperglycemiaInsulin ResistanceHumansRisk FactorsSARS-CoV-2COVID-19diabetes mellitushyperglycemiainsulin resistancepancreatic β-cellSARS-CoV-2

Identifiers

PMID37207448
PMCPMC11009784
OpenAlexW4377115592

What OpenQuestion holds

Textmetadata
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.