Evidence map›Paper›PMID 31637182›Full record

ArticleJournal of translational internal medicine2019

Elevated Lactic Acid During Ketoacidosis: Pathophysiology and Management.

Hamda Houssein Ahmed, David De Bels, Rachid Attou, Patrick M Honore, Sebastien Redant

Open access · hybridAbstract read
In one paragraph

Article in Journal of translational internal medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Hamda Houssein AhmedIntensive Care Unit, CHU Brugmann, Free University of Brussels ULB (ULB), Brussels, Belgium.
David De BelsIntensive Care Unit, CHU Brugmann, Free University of Brussels ULB (ULB), Brussels, Belgium.
Rachid AttouIntensive Care Unit, CHU Brugmann, Free University of Brussels ULB (ULB), Brussels, Belgium.
Patrick M HonoreIntensive Care Unit, CHU Brugmann, Free University of Brussels ULB (ULB), Brussels, Belgium.
Sebastien RedantIntensive Care Unit, CHU Brugmann, Free University of Brussels ULB (ULB), Brussels, Belgium.
Centre Hospitalier Universitaire Brugmann · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lactic acidosis results from an acid-base balance disorder of the body due to an excess of lactic acid. It is frequently found in critically ill patients admitted to the intensive care. The most common cause is type A, found in pathologies such as cardiogenic, septic and hypovolemic shock, trauma and severe hypoxemia. The type B is less common and arises without evidence of tissue hypoperfusion or shock. Divers etiologies have been described for this type of hyperlactatemia: Grand Mal seizures, liver failure, hematologic malignancies, congenital enzyme deficiencies, thiamine deficiencies and diabetes mellitus and also alcohol abuse, which may induce a lactic acid under-use or an increased production. The authors describe a rare complication of type 1 Diabetes Mellitus (T1DM), leading to a major and persistent expression of a type B lactic acidosis during ketoacidosis.

Indexed as

glycogenic hepatopathyketoacidosislactic acidosisMauriac syndrome

Identifiers

PMID31637182
PMCPMC6795052
OpenAlexW2979874768

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.