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Intradermal Microdialysis: An Approach to Investigating Novel Mechanisms of Microvascular Dysfunction in Humans
Published on: July 21, 2023
Altered skin microcirculation in patients with systemic lupus erythematosus
O Bongard1, P A Miescher, H Bounameaux
1Division of Angiology and Hemostasis, University Hospital of Geneva, Switzerland.
International Journal of Microcirculation, Clinical and Experimental
|July 1, 1997
Summary
Systemic lupus erythematosus (SLE) patients show impaired nutritional skin blood flow, but total skin microcirculation remains normal. This suggests distinct mechanisms cause microvascular damage in SLE.
Area of Science:
- Rheumatology
- Dermatology
- Vascular Biology
Background:
- Microvasculitis is a common manifestation of systemic lupus erythematosus (SLE).
- Hemodynamic data for skin microcirculation in SLE patients are lacking.
- Understanding microcirculatory dysfunction is crucial for managing SLE complications.
Purpose of the Study:
- To evaluate skin microcirculation hemodynamics in SLE patients.
- To differentiate between nutritional and total skin microcirculation.
- To investigate potential correlations with clinical and serological markers.
Main Methods:
- Simultaneous use of dynamic capillaroscopy (capillary blood cell velocity - CBV) and laser Doppler fluxmetry (LDF).
- Assessment of finger skin microcirculation in 24 SLE patients and healthy controls.
- Measurements taken at rest and during postocclusive reactive hyperemia.
Main Results:
- Nutritional skin flow (CBV) was significantly reduced in SLE patients versus controls at rest and during hyperemia (p < 0.01).
- Total skin microcirculation (LDF) showed no significant difference between groups.
- No significant correlation found between hemodynamic parameters and Raynaud's phenomenon, capillary changes, or anticardiolipin antibodies.
Conclusions:
- SLE patients exhibit impaired nutritional skin microcirculation.
- Total skin microcirculation is preserved, indicating selective hemodynamic alterations.
- Microvascular damage in SLE may involve diverse pathophysiological mechanisms beyond morphological changes.
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