Abstract | Brojni dokazi potvrđuju autoimunosnu hipotezu aterogeneze, prema kojoj je upala, koja zahvaća intimu aterosklerotski promijenjenih arterija, autoimunog porijekla. Sustavne autoimunosne bolesti i ateroskleroza dijele brojne patogenetske sličnosti, a kronična upala i endotelna disfunkcija čine poveznicu između dvije, na prvi pogled, različite grupe bolesti. U posljednjem desetljeću postalo je očito da bolesnici sa sustavnim autoimunosnim bolestima (sustavni eritemski lupus, reumatoidni artritis i antifosfolipidni sindrom) razvijaju rane i ozbiljne krvožilne aterosklerotske promjene, a vodeći uzrok smrtnosti, u ovoj grupi bolesnika, su akutne kardiovaskularne bolesti. Dosadašnje studije su pokazale da kombinacija tzv. „tradicionalni“ i „netradicionalnih“ čimbenika rizika ima važnu ulogu u patogenezi ubrzane ateroskleroze. Sjoegrenov sindrom (SS) je jedna od najučestalijih sustavnih autoimunosnih bolesti koja primarno zahvaća egzokrine žlijezde. Iako SS dijeli brojna klinička i serološka obilježja sa tzv. „klasičnim“ autoimunosnim bolestima, jedna od karakteristika SS-a je kronični, srednje jaki stupanj upalne reakcije. Za razliku od drugih autoimunosnih bolesti, podatci o povezanosti ateroskleroze i SS-a su manjkavi, a rezultati istraživanja oprečni. Čini se da i mehanizam oštećenja arterijske stijenke, različit između pojedinih autoimunosnih bolesti, određuje brzinu razvoja aterosklerotskih lezija. Prema nekim se studijama znakovi ubrzane i generalizirane ateroskleroze, u bolesnika sa SS-om, povezuju s metaboličkim abnormalnostima, dislipidemijom, hiperuricemijom i šećernom bolešću, dok drugi negiraju prethodno spomenutu povezanost. Potrebne su daljnje epidemiološke studije, s duljim vremenskim periodom praćenja, koje bi razjasnile mehanizam povezanosti između te dvije bolesti. Iako mišljenja nisu usuglašena jedno je sigurno, osim liječenja osnovne bolesti, liječenje bolesnika sa SS-om treba usmjeriti i prema primarnoj i sekundarnoj prevenciji kardiovaskularnih bolesti. |
Abstract (english) | There is considerable evidence to support the autoimmune hypothesis of atherogenesis by which the inflammation that affects the tunica intima of atherosclerotic altered arteries has an autoimmune origin. Systemic autoimmune diseases and atherosclerosis share a number of similarities in pathology. Although they seem like two different diseases, chronic inflammation and endothelial dysfunction make a link between the two, at first sight, different groups of diseases. Over the last decade, it has become obvious that patients with systemic autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis and antiphospholipid syndrome) develop early and severe atherosclerotic vascular changes, and that the leading cause of mortality, in this group of patients, are acute cardiovascular diseases. Previous studies have shown that a combination of the so-called "traditional" and "nontraditional" risk factors play an important role in the pathogenesis of accelerated atherosclerosis. Sjögren's syndrome (SS) is one of the most common systemic autoimmune disease that primarily affects the exocrine glands. Although SS shares many clinical and serological characteristics of the so-called "classical" autoimmune diseases, one of the characteristics of the SS is a chronic, medium high inflammatory response. Unlike other autoimmune diseases, linkage between atherosclerosis and SS is deficient and research results are contradictory. It seems that the mechanism of damage to the arterial wall determines the speed of development of atherosclerotic lesions that differs between certain autoimmune diseases. According to some studies, signs of accelerated and generalized atherosclerosis in patients with SS are associated with metabolic abnormalities, dyslipidemia, hyperuricemia and diabetes, while others deny the previously mentioned relationship. There is a need for further epidemiological studies with long-term follow-up, in order to clarify the mechanism of the association between these two diseases. Although opinions are not harmonized, it is certain, that except treating the primary disease, the treatment of patients with SS should be directed toward primary and secondary prevention of cardiovascular disease. |