Evidence map›Paper›PMID 30476128›Full record

ArticleThe Journal of clinical endocrinology and metabolism2019

Postmortem Findings in a Young Man With Congenital Generalized Lipodystrophy, Type 4 Due to CAVIN1 Mutations.

Nivedita Patni, Frank Vuitch, Abhimanyu Garg

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. A new mutation in theFrontiers in endocrinology · 2023
    Review
  6. Caveolar dysfunction and lipodystrophies.European journal of endocrinology · 2022
    Article
  7. Article
  8. Article
  9. Caveolae as Potential Hijackable Gates in Cell Communication.Frontiers in cell and developmental biology · 2020
    Review
  10. Review
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 1 institution in 1 country.

Nivedita PatniDivision of Pediatric Endocrinology, Department of Pediatrics and Center for Human Nutrition, UT Southwestern Medical Center, Dallas, Texas.
Frank VuitchDepartment of Pathology, UT Southwestern Medical Center, Dallas, Texas.
Abhimanyu GargDivision of Nutrition and Metabolic Diseases, Department of Internal Medicine and the Center for Human Nutrition; UT Southwestern Medical Center, Dallas, Texas.
Southwestern Medical Center · US

Funding

Genetic and Metabolic Basis of Familial LipodystrophiesR01DK105448 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Abhimanyu Garg · 2015 to 2026
$6.5M
NIDDK NIH HHS R01 DK105448
6 · The paper itself

Abstract

Context: Congenital generalized lipodystrophy, type 4 (CGL4) is a rare autosomal recessive disorder caused by mutations in caveolae-associated protein 1. Patients with CGL4 also have myopathy and cardiomyopathy with a predisposition for sudden death due to ventricular arrhythmias. However, the underlying pathology for these morbidities remains unknown. Therefore, we report on an autopsy of a Hispanic boy with CGL4. Case Description: Our patient had early-onset generalized lipodystrophy, feeding difficulties, myopathy, atlanto-axial dislocation, and learning disabilities. He was diagnosed with catecholaminergic polymorphic ventricular tachycardia (CPVT) at age 8 years, had poor compliance with medications, and died suddenly at age 15.3 years. Autopsy showed marked loss of subcutaneous and omental fat with no inflammatory cells in adipose tissue and normal adipocytes in the parathyroid glands. There were adipocytes interdigitating cardiac muscle fibers, with fibro-fatty infiltration in the right ventricle, near coronary sinus, and atrioventricular node. There was no evidence of coronary heart disease. The quadriceps femoris muscle did not show adipocyte infiltration, inflammation, or fibrosis. The muscularis mucosa layer was thickened in the esophagus and at the gastro-duodenal junction, and the esophagus had prominent, large nerves in the subserosa. The liver weighed 3000 g, with minimal chronic inflammation and steatosis in 40% of parenchyma, primarily in zones 2 and 3. There was no spermatogenesis in the spermatic tubules. Conclusions: Our data suggest that fibro-fatty infiltration of the right ventricle may contribute to CPVT in patients with CGL4. Thick muscularis mucosa and large nerves in the esophagus likely contributed to dysphagia and dysmotility. A lack of spermatids suggests infertility in affected male patients.

Indexed as

AdolescentHumansLipodystrophy, Congenital GeneralizedMaleMutationRNA-Binding ProteinsCAVIN1 protein, humanRNA-Binding Proteins

Identifiers

PMID30476128
PMCPMC6364506
OpenAlexW2900655319

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.