Evidence map›Paper›PMID 28844079›Full record

ReviewCurrent rheumatology reports2017

Gout and Metabolic Syndrome: a Tangled Web.

Gabrielle E Thottam, Svetlana Krasnokutsky, Michael H Pillinger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 5 pooled it
6.9field-weighted citation impact, top 2% 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

77 citing papers in PubMed, 5 syntheses or guidelines pooled it, 148 citations in OpenAlex.

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17 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 1 country.

Gabrielle E ThottamDepartment of Medicine, Roger Williams Medical Center, Providence, RI, USA.
Svetlana KrasnokutskyCrystal Diseases Study Group, Division of Rheumatology, Department of Medicine, New York University School of Medicine, 301 East 17th Street, Suite 1410, New York, NY, 10003, USA.
Michael H PillingerCrystal Diseases Study Group, Division of Rheumatology, Department of Medicine, New York University School of Medicine, 301 East 17th Street, Suite 1410, New York, NY, 10003, USA. michael.pillinger@nyumc.org.
New York University · USProvidence College · USVA NY Harbor Healthcare System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThe complexity of gout continues to unravel with each new investigation. Gout sits at the intersection of multiple intrinsically complex processes, and its prevalence, impact on healthcare costs, and association with important co-morbidities make it increasingly relevant. The association between gout and type 2 diabetes, hypertension, hyperlipidemia, cardiovascular disease, renal disease, and obesity suggest that either gout, or its necessary precursor hyperuricemia, may play an important role in the manifestations of the metabolic syndrome. In this review, we analyze the complex interconnections between gout and metabolic syndrome, by reviewing gout's physiologic and epidemiologic relationships with its major co-morbidities. RECENT

findingsIncreasing evidence supports gout's association with metabolic syndrome. More specifically, both human studies and animal models suggest that hyperuricemia may play a role in promoting inflammation, hypertension and cardiovascular disease, adipogenesis and lipogenesis, insulin and glucose dysregulation, and liver disease. Fructose ingestion is associated with increased rates of hypertension, weight gain, impaired glucose tolerance, and dyslipidemia and is a key driver of urate biosynthesis. AMP kinase (AMPK) is a central regulator of processes that tend to mitigate against the metabolic syndrome. Within hepatocytes, leukocytes, and other cells, a fructose/urate metabolic loop drives key inhibitors of AMPK, including AMP deaminase and fructokinase, that may tilt the balance toward metabolic syndrome progression. Preliminary evidence suggests that agents that block the intracellular synthesis of urate may restore AMPK activity and help maintain metabolic homeostasis. Gout is both an inflammatory and a metabolic disease. With further investigation of urate's role, the possibility of proper gout management additionally mitigating metabolic syndrome is an evolving and important question.

Indexed as

Cardiovascular DiseasesComorbidityDiabetes Mellitus, Type 2FructoseGoutHumansHyperlipidemiasHyperuricemiaInflammationMetabolic SyndromeObesityUric AcidFructoseUric AcidDiabetesFructoseGoutHypertensionMetabolic syndromeUric acid

Identifiers

PMID28844079
OpenAlexW2746891072

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.