Abstract | BACKGROUND: CASE REPORT: We report a 24-year-old patient with FPLD caused by a mutation in the LMNA gene (R482W) treated with 12 months of rosiglitazone. Subcutaneous fat increased following rosiglitazone treatment as demonstrated by a 29% generalised increase in skin-fold thickness. Leptin levels increased from 5.8 to 11.2 ng/ml. Compared with treatment on Metformin, there was an increase in insulin sensitivity (HOMA S% 17.2-31.6) but no change in glycaemic control. The lipid profile worsened during the follow-up period. CONCLUSION: This initial case suggests that, for modification of cardiovascular risk factors, there are no clear advantages in treating patients with FPLD with rosiglitazone despite increases in subcutaneous adipose tissue. Larger series will be needed to identify moderate beneficial effects and treatment may be more effective in patients with generalised forms of lipodystrophy.
|
Authors | Katharine R Owen, Mollie Donohoe, Sian Ellard, Andrew T Hattersley |
Journal | Diabetic medicine : a journal of the British Diabetic Association
(Diabet Med)
Vol. 20
Issue 10
Pg. 823-7
(Oct 2003)
ISSN: 0742-3071 [Print] England |
PMID | 14510863
(Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't)
|
Chemical References |
- Blood Glucose
- Glycated Hemoglobin A
- Hypoglycemic Agents
- Lamin Type A
- Leptin
- Receptors, Cytoplasmic and Nuclear
- Thiazolidinediones
- Transcription Factors
- lamin C
- Rosiglitazone
|
Topics |
- Adult
- Blood Glucose
(analysis)
- Diabetes Mellitus, Lipoatrophic
(blood, drug therapy, genetics)
- Female
- Follow-Up Studies
- Glycated Hemoglobin
(analysis)
- Humans
- Hypoglycemic Agents
(therapeutic use)
- Insulin Resistance
- Lamin Type A
(genetics)
- Leptin
(blood)
- Mutation
- Receptors, Cytoplasmic and Nuclear
(antagonists & inhibitors)
- Rosiglitazone
- Skinfold Thickness
- Thiazolidinediones
(therapeutic use)
- Transcription Factors
(antagonists & inhibitors)
|