Lipodystrophies, dyslipidaemias and atherosclerotic cardiovascular disease.
Lipodystrophy
acquired generalised lipodystrophy
acquired partial lipodystrophy
congenital generalised lipodystrophy
familial partial lipodystrophy
metreleptin
Journal
Pathology
ISSN: 1465-3931
Titre abrégé: Pathology
Pays: England
ID NLM: 0175411
Informations de publication
Date de publication:
Feb 2019
Feb 2019
Historique:
received:
15
10
2018
revised:
01
11
2018
accepted:
04
11
2018
pubmed:
1
1
2019
medline:
26
2
2019
entrez:
1
1
2019
Statut:
ppublish
Résumé
Lipodystrophies are rare, heterogeneous, genetic or acquired, disorders characterised by varying degrees of body fat loss and associated metabolic complications, including insulin resistance, dyslipidaemias, hepatic steatosis and predisposition to atherosclerotic cardiovascular disease (ASCVD). The four main types of lipodystrophy, excluding antiretroviral therapy-induced lipodystrophy in HIV-infected patients, are congenital generalised lipodystrophy (CGL), familial partial lipodystrophy (FPLD), acquired generalised lipodystrophy (AGL) and acquired partial lipodystrophy (APL). This paper reviews the literature related to the prevalence of dyslipidaemias and ASCVD in patients with lipodystrophies. Patients with CGL, AGL and FPLD have increased prevalence of dyslipidaemia but those with APL do not. Patients with CGL as well as AGL present in childhood, and have severe dyslipidaemias (mainly hypertriglyceridaemia) and early onset diabetes mellitus as a consequence of extreme fat loss. However, only a few patients with CGL and AGL have been reported to develop coronary heart disease. In contrast, data from some small cohorts of FPLD patients reveal increased prevalence of ASCVD especially among women. Patients with APL have a relatively low prevalence of hypertriglyceridaemia and diabetes mellitus. Overall, patients with lipodystrophies appear to be at high risk of ASCVD due to increased prevalence of dyslipidaemia and diabetes and efforts should be made to manage these metabolic complications aggressively to prevent ASCVD.
Identifiants
pubmed: 30595509
pii: S0031-3025(18)30527-0
doi: 10.1016/j.pathol.2018.11.004
pmc: PMC6402807
mid: NIHMS1517551
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
202-212Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK105448
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR024982
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001105
Pays : United States
Informations de copyright
Published by Elsevier B.V.
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