C-reactive protein in gallbladder diseases: diagnostic and therapeutic insights

The gallbladder is an important component of the hepatobiliary system whose primary function is to aid in digestion of foodstuffs, excretion of drugs and facilitate removal of waste products from the body. The gall bladder is principally a storage organ for bile, chemically modified salts and acids of cholesterol which are synthesized in the liver and which function as surfactants to solubilize fatty substances of limited aqueous solubility. Any disruption in the amount or activity of bile surfactant can lead to an accumulation of insoluble molecular clumps (e.g., gallstones) that deposit in and obstruct fluid movement within the gallbladder, and which can lead to pathological congestion and tissue damage. The natural host defense response to any event that causes tissue damage is to stimulate inflammation, which non-specifically but aggressively reacts to the stimuli so to remove the cause and repair damaged tissues. The C-reactive protein (CRP) is a primarily hepatically produced serum protein whose blood levels increase within 6–10 h of any tissue-damaging event. The extent with which it increases correlates with the level of tissue damage and associated inflammation. CRP levels are reported to be of value in diagnosing acute cholecystitis severity, in predicting the outcome and prognosis of cancer-associated gallbladder resection, and in helping identify cystic structures during emergency laparoscopic cholecystectomies. As an understanding of distinctive CRP structural isoforms is evolving, its role not only as a biomarker but as regulator of both physiologic and pathophysiologic processes of inflammation may be relevant in the understanding of and treatment approaches for gallbladder-associated disease.