Evidence map›Paper›PMID 35197086›Full record

ArticleItalian journal of pediatrics2022

SARS-CoV-2 infection as possible downstream disease precipitator in autoantibody-positive insulin-dependent diabetes mellitus: a case report.

Riccardo Schiaffini, Andrea Campana, Annalisa Deodati, Emanuela Peschiaroli, Maria Francesca Lanzillotta, Alessandra Fierabracci

Open access · goldAbstract readCase Reports
In one paragraph

Article in Italian journal of pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
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  4. 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

6 authors at 2 institutions in 1 country.

Riccardo SchiaffiniDiabetes and Growth Disorders Unit, Academic Department of Pediatrics, Bambino Gesù Children's Hospital IRCCS, Rome, Italy. riccardo.schiaffini@opbg.net.
Andrea CampanaMultispecialistic Pediatric Unit, Emergency Acceptance and General Pediatrics Department, Bambino Gesù Children's Hospital, Rome, Italy.
Annalisa DeodatiDiabetes and Growth Disorders Unit, Academic Department of Pediatrics, Bambino Gesù Children's Hospital IRCCS, Rome, Italy.
Emanuela PeschiaroliMultispecialistic Pediatric Unit, Emergency Acceptance and General Pediatrics Department, Bambino Gesù Children's Hospital, Rome, Italy.
Maria Francesca LanzillottaInfectivology and Clinical Trials Research Department, Bambino Gesù Children's Hospital IRCCS, Rome, Italy.
Alessandra FierabracciInfectivology and Clinical Trials Research Department, Bambino Gesù Children's Hospital IRCCS, Rome, Italy. alessandra.fierabracci@opbg.net.
Bambino Gesù Children's Hospital · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSARS-CoV-2 causes lesions, in addition to lung, in endocrine organs such as the pancreas through ACE2 receptor. Recently the relationship between SARS-CoV-2 exposition and the incidence or evolution of clinical autoimmune diabetes has attracted the attention of diabetologists. CASE PRESENTATION: We report the analysis of the clinical history of a child diagnosed for insulin-dependent diabetes mellitus (Type 1 diabetes) at the time a paucisymptomatic COVID-19 infection occurred, followed by well-controlled metabolic status. As opposite to previous findings SARS-CoV2 did not cause ketosis and ketoacidosis. Polydipsia was reported a few months and weight loss 4 weeks before SARS- CoV-2 infection suggesting that SARS-CoV-2 could not be the trigger of Type 1 diabetes in this patient.

conclusionsSARS-CoV-2 in this patient was an unexpected event in the course of disease. We advance the hypothesis that the SARS-CoV-2 infection, even if paucisymptomatic could have acted in the present case report as a hypothetical downstream precipitating factor; whilst the inciting triggering event of the autoimmune disease, as confirmed by the presence of circulating autoantibodies, could have occurred even before, as generally assumed for this category of disorders. The precipitating mechanism could have been the acute interaction between virus and the ACE receptor on the beta cells, at the time that hyperglycemia and glycosuria were ascertained, and HbA1c levels confirmed a metabolic dysregulation over the previous 3 months in absence of ketoacidosis.

Indexed as

COVID-19Diabetes Mellitus, Type 1AutoantibodiesHumansRNA, ViralSARS-CoV-2AutoantibodiesRNA, ViralCOVID-19Disease etiopathogenesisManagementType 1 diabetes

Identifiers

PMID35197086
PMCPMC8864604
OpenAlexW4212886856

What OpenQuestion holds

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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.