PDF hosted at the Radboud Repository of the Radboud University Nijmegen The following full text is a publisher's version. For additional information about this publication click this link. http://hdl.handle.net/2066/24245 Please be advised that this information was generated on 2015-01-23 and may be subject to change. British Journal of Dermatology 1996; 134: 915-918. Leucocytoclastic vasculitis induced by prolonged exercise M.PRINS, J.C.J.M.VERAART, A.H.M.VERMEULEN,* R.-F.I-I.J.HULSMANS AND H.A.M.NEUMANN Departments o f Dermatology and *Pathology, Acadmusch Ziekenhuls, Maastricht, P. Debeyelaan 25, Postbus 5800, 6 2 0 2 A7j Maastricht, the Netherlands Accepted for publication 16 August 1995 Summary Many people develop skin symptoms after long-distance walks, but little is known aetiology of these. In this study we took 11 biopsies from 10 long-distance walkers who walked 80 km. All biopsies originated from purpuric lesions on the lower legs, which had appeared during walking. In all 1 1 specimens, signs of a leucocytoclastic vasculitis were present with leucocytoclasis, exocytosis of erythrocytes and a granulocyte/mononuclear perivascular infiltrate. Immunofluores cence investigations showed deposition of C3c in many specimens and immunoglobulin M in some. The occurrence of a leucocytoclastic vasculitis after prolonged exercise may be explained by the existence of an exercise altered cutaneous microcirculation, complement activation and an altered immune function. Worldwide there is a growing interest in sports and sports medicine. We have seen a patient who developed erythema, purpura and an histological proven leucocy toclastic vasculitis on the lower legs, which only occurred after walking at least 30 km. There have been several reports of exercise-induced purpura and urticarial lesions.1“ These were mostly attributed to local pressure from shoes or clothing, or solar influ ences. However, purpura of the legs, in particular the lower leg region in association with sport, has not been we visited the finish of a long-distance walk to investi gate the prevalence of skin symptoms such as erythema, urticaria and purpura, and to study venous function. is known to venous 9'5 ± standard error 5-6 s; normal > 25 s) as an i of of we report venous system In this í zs in ; c ical lì a long walk. Irom wt ■f Patients and methods Fifty-eight long-distance walkers (40 males, 16 females, sex in two not registered) were evaluated within 1 h following an 80 km m arch (Kennedy mars, Someren, the Netherlands). The participants were gave verbal informed consent. Their legs were exam•: H .A .M .N eum ann. «') 1 9 9 6 British A ssociation of Dertru ined for erythema, urticaria, purpura and chronic venous insufficiency (CVI). Skin changes due to CVI were staged according to Widmer et ah and classified as either absent, or present in a mild or severe form, four participants were evaluated for venous ini dency by light reflection rheography using a Laumann r 1000 Rheograph (Selb, Germany).1 None of the volun teers was examined before the walk and no data on medical history or medication were known. a, urticaria and purpura were described as as a transient or present. E 2ma was local redness of the skin, disappearing after local pres sure. Purpura was distinguished from erythema when failed to blanch the lesion, in 10 participants, two 4 mm punch biopsy specimens were taken from a representative purpuric lesion on the lower leg; in one participant, two series of biopsies were obtained, one series of biopsies from each leg. No biopsies from other sites of the body nor from controls were taken. One of the two specimens was snap-frozen in liquid nitrogen and stored at ~70"C. Cryostat cut 4 /mi sections were stained with fluorescein-conjugated rabbit anti-human I in A (IgA), IgC) ies to Clq, C3c, immunog up, Denmark). The and IgM and fibrin (Dako, ( I specimen was paraffin and stained with haematoxylin and eosin. Both specimens were evaluated by one pathologist and one dermatologist. To standardize the histological features of leucocytoclastic vasculitis, grading criteria were uf : epidermal changes, specially '* 1 915 916 M . P R I N S et al. Table 1. D istribution of oedem a, varicose veins, skin ch an g es as sign of chronic venous insufficiency (CVI), e ry th e m a and p u rp u ra after w alking 8 0 km in 58 v o lu n teers A bsent P resen t Oedem a 24 Varicose veins 30 Skin ch an g es as sign of CVI 45 E rythem a P u rp u ra P u rp u r a and e ry th e m a U rticaria 33 48 52 50 M oderate in 2 2 Distinct in 12 M inor in 19 Stem in 9 Mild in 9 Severe in 4 25 10 6 8 necrosis; exocytosis of erythrocytes; depth of infiltrate; vessel wall invasion by neutrophils; amount of leucocytoclasis and amount of fibrinoid necrosis. All criteria were graded as absent, marginal or distinct. Results In 41 of the 58 volunteers erythema and/or purpura was seen (Table 1). Coexisting urticarial lesions were observed in eight cases. According to the volunteers, all lesions had appeared during the walk, and were pain less. Some were palpable. The purpura were signifi cantly more frequent in participants who had distinct oedema, saphenous vein varicosity, and/or severe skin changes due to CVI. The occurrence of the purpura and erythema was more frequent in females, but the skin symptoms of CVI showed no sex difference. All 11 biopsies showed leucocytoclastic vasculitis Biopsy n u m b er 1 2 3 4 5 (y 7 8 9 10 11 Histological LCV + + M |A M H" 1 ■ ii‘|■i + I m m u n o g lo b u lin s C3c IgM + --- -, I*|™ ’ “1“ IgM-b — --- Discussion Leucocytoclastic vasculitis (syn: allergic vasculitis, leu cocytoclastic angiitis) is characterized by palpable purpura due to deposition of immune complexes in postcapillary venules, primarily of the legs.8 Any other organ, apart from the skin, can be involved. Several factors influence the disease activity, including the concentration of circulating immune complexes, the half-life of the complex and of the antibodies which form the complexes. In many cases the disease is self-limiting, and only confined to the skin. Leucocytoclastic vasculitis can be triggered by many factors including bacterial infection, drugs, immune complexes, blood stasis and systemic Prolonged exercise can now be added to this list. P u rp u ra E rythem a Table 2. H istological and im m u n o fluorescence results, in com bination with the clinical a p p e a ra n c e of the lesion + IgM + — C lq (Table 2), with a mild to severe leucocytoclasis, granu locytes and mononuclear cells invading the vessels 11), marginal exocytosis of erythrocytes (n 3 ) , (n and exocytosis of the infiltrate into epidermis (n = 2 ) (Fig. 1). Fibrinoid necrosis, epidermal necrosis or fibrin thrombus formation were not found. On immunofluor escence, all but one specimen revealed C3c deposition in the subepidermal capillaries. In one case, granular C3c was stretched out along the basement membrane. In another, it was also found in the papillary dermis. Clq was found, in two specimens, in the mid-dermis. igM distribution was seen in four; three times in the capil lary loop and once mid-dermal. One biopsy was nega tive for all antibodies. The infiltrate varied in depth from being superficial and perivascular, i mainly the papillary dermis, to involving the subcutaneous fat with vessel wall invasion by neutrophils. + + + «■| t‘i^|‘.V — ++ - H—b _H_ — W l'l'H « H—h -- f + "I" "I“ 4" 1»|H — .— LCV, leucocytoclastic vasculitis; p u r p u r a a n d ery th em a: absent, -|- = present; im m bulins, C îc and C lq : absent, + = m a rg in a l, + + = distinct. 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