ArticleThe Journal of clinical endocrinology and metabolism2019
Postmortem Findings in a Young Man With Congenital Generalized Lipodystrophy, Type 4 Due to CAVIN1 Mutations.
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.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Plasma membrane remodeling determines adipocyte expansion and mechanical adaptability.Nature communications · 2024Article
- Metabolic and other morbid complications in congenital generalized lipodystrophy type 4.American journal of medical genetics. Part A · 2024Article
- Challenges and opportunities in obesity: the role of adipocytes during tissue fibrosis.Frontiers in endocrinology · 2024Review
- A deep learning-based tool for the automated detection and analysis of caveolae in transmission electron microscopy images.Computational and structural biotechnology journal · 2023Article
- A new mutation in theFrontiers in endocrinology · 2023Review
- Caveolar dysfunction and lipodystrophies.European journal of endocrinology · 2022Article
- Approach to Diagnosing a Pediatric Patient With Severe Insulin Resistance in Low- or Middle-income Countries.The Journal of clinical endocrinology and metabolism · 2021Article
- Unusual clinical features associated with congenital generalized lipodystrophy type 4 in a patient with a novel E211XClinical diabetes and endocrinology · 2020Article
- Caveolae as Potential Hijackable Gates in Cell Communication.Frontiers in cell and developmental biology · 2020Review
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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.
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