Rheumatology Advance Access published online on May 16, 2006
Rheumatology, doi:10.1093/rheumatology/kel116
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1 Inserm ESPRI HP2 Laboratory, EA 3745, Grenoble Medical School, Grenoble, France; Inserm Clinical Research Center 03, Grenoble, France
* To whom correspondence should be addressed. Objectives. Thermal hyperaemia is impaired in patients with systemic sclerosis (SSc). The objective of these studies was to determine whether this was consecutive to skin fibrosis, microangiopathy or macroangiopathy. Methods. Using laser Doppler flowmetry, we first compared the thermal hyperaemia on the third left finger pad and on the left forearm in 21 patients with non-diffuse systemic sclerosis (SSc), in comparison with primary Raynaud's phenomenon and healthy volunteers. Second, we tested whether the altered thermal hyperaemia correlated to the digital pressure index at baseline, and following the thermal challenge. Results. In the first study, thermal hyperaemia of the finger pad was impaired in terms of both amplitude and kinetics, but not on the forearm in patients with SSc. In the seven SSc patients without cutaneous fibrosis, the response was similarly altered in terms of amplitude and kinetics. In the second study, we observed a weak correlation between the digital systolic blood pressure index. However, in the 15 SSc patients tested at 44°C, the median digital systolic blood pressure index was 1.04 (0.84-1.24) at baseline vs 1.08 (0.87-1.29) at 44°C (NS), while seven of them had an abnormal response in terms of kinetic. Furthermore, only one patient showed a clear-cut decrease in digital systolic blood pressure at 44°C. Conclusion. In patients with SSc, digital thermal hyperaemia is impaired, but does not relate to the skin fibrosis or to an associated macroangiopathy in most cases. Further studies are required to determine whether its impairment reflects a functional or structural microvascular damage.
Received January 9, 2006
Accepted February 28, 2006
Original Papers
Digital thermal hyperaemia impairment does not relate to skin fibrosis or macrovascular disease in systemic sclerosis
M. Salvat-Melis 1,
P. H. Carpentier 2,
C. T. Minson 3,
A. Boignard 4,
G. R. McCord 3,
A. Paris 1,
A. Moreau-Gaudry 5,
and
J.-L. Cracowski 1 *
2 Vascular Medicine Department, Grenoble University Hospital, Grenoble, France
3 Department of Human Physiology, University of Oregon, Eugene, OR, USA
4 Inserm ESPRI HP2 Laboratory, EA 3745, Grenoble Medical School, Grenoble, France
5 Inserm Clinical Research Center 03, Grenoble, France
J.-L. Cracowski, E-mail: Jean-Luc.Cracowski{at}ujf-grenoble.fr
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