[2009] [SAT0227] LIDOCAINE FOR THE TREATMENT OF SYSTEMIC SCLEROSIS – A RANDOMISED CLINICAL TRIAL

R. Riera, L.E.C. Andrade, A.W.S. Souza, C. Kayser, E.M. Yanagita, V.F.M. Trevisani Internal Medicine and Rheumatology Post-Graduation Programs, Universidade Federal de Sao Paulo, Sao Paulo, Brazil

Background: Excessive deposits of collagen in tissue and vascular damage are central indicators of scleroderma pathogenesis, responsible for the majority of disease clinical manifestations, disease development and prognosis, in addition to being the most common targets for treatment attempts.¹ Lidocaine reduces the activity of prolyl-hydroxylase, the enzyme which catalyses the biosynthesis of collagen and which has increased activity in sceroderma.^2,3 A series of cases involving lidocaine were published in medical literature and subjectively demonstrated improvements vis-à-vis skin thickness after the use of intravenous lidocaine, without severe adverse effects reported.⁴ Given the absence of effective treatments for the skin manifestations of scleroderma, lidocaine has been used as a therapeutic option.
Objectives: To evaluate the effectiveness and safety of lidocaine in the treatment of scleroderma patients.
Methods: A double-blind randomised clinical trial. Twenty-six patients (sample size: alpha = 0.05, power = 90%, n = 12) diagnosed within the last five years with scleroderma, according to the criteria established by the American College of Rheumatology, were randomised in two groups: a) lidocaine 2% without vasoconstrictor; b) placebo. The drug and placebo were administered intravenously for four hours, with 20mL administered in the first five days of treatment and 30mL in the last five days of treatment, in three cycles of ten days each, with a one-month interval between treatments. Outcomes: improvement in skin thickening (m-Rodnan score), microvascular abnormalities (nailfold capillaroscopy) and quality of life (Heath Assessment Questionnaire- HAQ). The study was approved by the Ethics Committee of Universidade Federal de São Paulo. Clinical Trial Registration: NCT00740285
Results: There was no statistically significant difference between the groups on the m-Rodnan skin score after the treatment, taken into account both the mean score (p=0.695) as well as the percentage of patients who showed at least a 30% score reduction (p=0.408). There was no difference on the capillaroscopy, considering the enlarged capillaries mean (p=0.416) and drop-out capillaries mean (p=0.385) as well as the percentage of patients who showed a minimum of 30% reduction in the number of enlarged capillaries (p=0.346) and in the number of drop-out capillaries (p=1). There was no difference on the HAQ mean (p=0.807) neither in the percentage of patients who showed at least a 30% HAQ improvement (p=0.386).
There were no serious adverse effects. Although there was no difference in the outcome between the groups, moreover, and rather interestingly, upon responding to the subjective questionnaire anonymously, all patients referred to an improvement in terms of skin thickening and discoloration, expressing their desire to continue with the treatment.
Conclusion: Intravenous lidocaine does not appear to improve the total skin thickening, the main capillaroscopy abnormalities and the quality of life in scleroderma patients.
References:

1. Jimenes AS, Hitraya E, Varga J. Pathogenesis of scleroderma: Collagen. In: Rheumatic Diseases Clinics of North America Scleroderma. 1996; 22(4): 647.
2. Flickman PH, Jefrey JJ, Eifen V. A sensitivity microassay for prolyl-hydroxylase activity in normal and psoriatic skin. Journal of Investigate Dermatology. 1973; 60(1):46-52.
3. Keiser HR, Stein HD, Sjoerdsma A. Increased protocollagen proline hydroxylase activity in sclerodermatous skin. Arch Derm.1971;104:57-60
4. Atra E, Goldenberg J, Sasso WS. Proposição de um novo tratamento para esclerodermia utilizando o cloridrato de dietilamino 2,6 dimetilacetanilida. Revista Brasileira de Reumatologia. 1977; 3:75-80.