SynthesisThe Journal of clinical endocrinology and metabolism2026
Bone phenotype of patients with genetic forms of lipodystrophy: a systematic review of literature.
Synthesis in The Journal of clinical endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Bone phenotype of patients with genetic forms of lipodystrophy: a systematic review of literature.The Journal of clinical endocrinology and metabolism · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCongenital lipodystrophies (LDs), including congenital generalized LD (CGL) and familial partial LD (FPLD), are rare disorders characterized by absent or abnormal adipose tissue distribution, leading to clinical, hormonal, and metabolic complications. Although these systemic features are well described, data on bone involvement are limited. This literature review summarizes current evidence on bone manifestations in genetic LDs and potential underlying mechanisms.
methodsA systematic search was performed in PubMed, EMBASE, and the Cochrane Library using terms related to LD and bone outcomes. No restrictions on date, language, or study design were applied. Studies reporting bone-related outcomes in genetic LD in humans were included. Study quality was assessed using PRISMA guidelines and the JBI checklist.
resultsOf 2632 studies identified, 15 met the inclusion criteria. Most focused on CGL1 and CGL2; no studies were found on CGL3 or CGL4. Reported bone abnormalities in CGL1 and CGL2 included osteolytic lesions, bone cysts, osteosclerosis, and pseudo-osteopoikilosis, predominantly in long bones. Bone mineral density (BMD) was generally normal to high at trabecular sites. In contrast, FPLD2 was characterized by reduced BMD at cortical sites and lower trabecular bone score, suggesting impaired bone quality. Proposed mechanisms include reduced bone marrow adipose tissue, disrupted marrow fat conversion, and altered endocrine signaling.
conclusionBone abnormalities are characteristic yet often underrecognized features of genetic LDs, particularly CGL1 and CGL2. Current evidence underlines the broad skeletal impact of adipose dysfunction and highlights the need for standardized, genetically stratified studies to clarify bone risk and guide clinical management in congenital LD.
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