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eISSN: 2084-9893
ISSN: 0033-2526
Dermatology Review/Przegląd Dermatologiczny
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3/2014
vol. 101
 
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abstract:
Original paper

Does inflammation play a role in development of necrobiosis lipoidica?

Iwona Słowik-Kwiatkowska
,
Aleksandra Lesiak
,
Anna Woźniacka
,
Anna Sysa-Jędrzejowska
,
Joanna Narbutt

Przegl Dermatol 2014, 101, 187–191
Online publish date: 2014/06/27
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Introduction. Necrobiosis lipoidica (NL) is a granulomatous skin disease of still only partially known pathogenesis. Microangiopathy is considered as one of the most important processes in NL, and vascular endothelial growth factor (VEGF) and endothelin-1 are strongly involved in it. Recent studies have demonstrated the beneficial therapeutic effect of tumor necrosis factor α (TNF-α) inhibitors in treatment of recalcitrant cases of NL, which is due to the important role of TNF-α in development of inflammation and granulomas in the course of NL.

Objective. To assess the serum levels of VEGF, endothelin-1 and TNF-α in NL patients.

Material and methods. The study group consisted of 17 patients with NL (mean age 48.22 ±15.99 years), 37 patients with diabetes mellitus (mean age 52.11 ±17.41 years) and 23 healthy volunteers (mean age 44.13 ±9.33 years) as a control group. Serum concentrations of TNF-α, VEGF and endothelin-1 were assessed in all patients with the ELISA test.

Results. The TNF-α concentration was statistically lower in the controls when compared to the NL patients and diabetic patients (p < 0.05 for all comparisons). There were no differences in VEGF serum levels between all the examined groups (p > 0.05 for all comparisons). Endothelin-1 serum values were under the tested values in most cases; however, statistically more frequently these values were found in the controls than in the NL group (p < 0.05).

Conclusions. The results of our study suggest that inflammation with enhanced synthesis of TNF-α in NL patients is the primary pathological effect, followed by local impairment of angiogenesis.
keywords:

necrobiosis lipoidica, TNF-α, angiogenesis, inflammation



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