Levels of sVCAM-1 and sICAM-1 in patients with lyme disease.

200 IntroductIon Lyme borreliosis (Lyme disease) is a tick‐borne disease presenting as a wide spec‐ trum of clinical manifestations affecting the skin, joints, nervous system, and heart. The character‐ istic skin manifestation of the disease is erythe‐ ma migrans (EM).1‐3 Lyme borreliosis is caused by the spirochete Borrelia burgdorferi (Bb), which in Poland are transmitted to humans and an‐ imals by tick species Ixodes ricinus and Ixodes persulcatus.1‐5 Clinical presentations of borreliosis are diverse and depend on the stage of the disease and affect‐ ed organs. In the majority of cases, the disease presents as EM within 3–30 days, up to 3 months from the tick bite. In some patients signs and symptoms may first appear after many months, or even years since the infection.2,3 The universally accepted Asbrink‐Hovmark classification involves early (localized and disseminated) and late (chron‐ ic) disease.6,7 Apart from EM, patients with ear‐ ly disseminated disease may also develop borre‐ lial lymphocytoma of the skin. Manifestations of the early disseminated disease include multi‐ ple EM, early Lyme neuroborreliosis, Lyme arthri‐ tis, and sometimes Lyme carditis. Manifestations of late Lyme disease are acrodermatitis chronica atrophicans and neuro logical and rheumatic dis‐ orders of >12 months’ duration.2,3,8 The diagnosis of Lyme borreliosis is based on clinical presentation and results of laborato‐ ry tests. A two‐step diagnostic approach is man‐ datory, with the initial immunoglobulin M (IgM) and immunoglobluin G (IgG) enzyme‐linked im‐ munosorbent assays (ELISA) and if their results orIGInAL ArtIcLE