Bile infarct

Morphology The morphologist uses the term cholestasis to describe the presence of bile in the hepatocytes as well as in hypertrophic Kupffer cells (= cellular bilirubino-stasis), particularly in the form of inspissated bile droplets and copper within the more or less dilated canaliculi (= canalicular bilirubinostasis). In extrahepatic cholestasis, bile is additionally found within the likewise mostly dilated interlobular bile ducts (= ductular bilirubinostasis) as well as in the parenchyma in the form of bile infarcts" or bile lakes . 

Eosinophilic infiltrations in the portal fields generally point to intrahepatic cholestasis. By contrast, ductular changes with bile cylinders, ballooning, acidophilia of the liver cells at the lobular centres, bile infarcts, increase in the copper content, etc. are usually signs of extrahepatic cholestasis, (s. fig. 13.5) (s. tab. 13.10)... 

Fickert, P. et al. (2002) Ursodeoxycholic add aggravates bile infarcts in bile duct-ligated and Mdr2 knockout mice via... 

Since her admission to the hospital for an acute myocardial infarction, Ann ] Jeina has been taking the bile salt sequestrant cholestyramine and the HMG-CoA rednctase inhibitor pravastatin to lower her blood cholesterol levels (see Chapter 34). She also takes 160 mg acetylsalicylic acid (ASA aspirin) each day. At her most recent visit to her cardiologist, she asked whether she shonld... 

All HMGRIs are approved for the treatment of primary hypercholesterolemia and familial combined hyperlipidemia (Fredrickson s type Ha and lib) (Table 30.2) In patients who have not responded to diet, exercise, and other non pharmacological methods (Table 30.6) (15,21). They may be used either alone or In combination with bile acid sequestrants, ezetimibe, or niacin. As previously mentioned, they should be administered at least 1 hour before or 4 to 6 hours after bile acid sequestrants when this combination Is desired. Fluvastatin, lovastatin, pravastatin, and simvastatin have been specifically Indicated to reduce the mortality of CHD and stroke. By reducing plasma LDL levels, these compounds slow the progression of atherosclerosis and reduce the risk of myocardial Infarction and other ramifications of vascular occlusion. Atorvastatin, rosuvastatin, and simvastatin have been shown to be effective In homozygous familial hyperlipidemia and are Indicated for this use. Additionally, atorvastatin, pravastatin, and simvastatin are Indicated for primary dysbetallpoprotelnemla (Fredrickson s type III) (Table 30.2). Finally, atorvastatin, pravastatin, rosuvastatin, and simvastatin are Indicated for the treatment of hypertriglyceridemia. 

Hyperlipidemia is known to be one of the most potent factor associated with the premature development of atheromatous arterial disease. Thus an increased serum cholesterol level is frequently found in patients with ischemic heart disease and myocardial infarction, and hypercholesterolemic patients have a high incidence of coronary artery disease. Therefore, because cholesterol is partially eliminated from the body as bile acids (see Section VB), it would be important to know the role of bile acid metabolism in the development of different types of hypercholesterolemia. 

The largest cause of morbidity and mortality comes from involvement of the vascular system, particularly from thromboembolic events which can occur in both arteries and veins and in all sizes of vessels [6], Thrombophlebitis and pulmonary embolism are the most frequent vascular accidents, whereas thromboses of large and medium arteries, especially carotid and renal arteries, are frequent causes of death [7]. Ischemic heart disease is less common. Nenroimaging may demonstrate evidence of infarction or thrombosis. Association with other genotypes linked to increased risk of vascular disease, such as factor V Leiden and thermola-bile methylenetetrahydrofolate reductase, may increase the risk of thrombosis in individuals with homocystinuria [17, 18]. 

A spectrum of end-organ ischemic complications can occur with embolotherapy. Bowel infarction can complicate splanchnic embolization targeting bleeding or could result from inadvertent non-target embolization from an upstream source [88]. Gallbladder infarction or bile duct necrosis can complicate hepatic artery embolization or che-moembolization [89, 90]. Splenic abscess and overwhelming sepsis can occurs following splenic embolization [91]. Skin necrosis and nerve injury have been reported as a result of ethanol embolization of vascular malformations [53, 54]. Buttock muscular necrosis, buttock claudication and sexual dysfunction can occur as a result of internal iliac branch embolization, especially when distal or bilateral [92-95]. 

Two important lipoproteins are the LDL and HDL, which transport cholesterol. The LDL carries cholesterol to the tissues where it can be used for the synthesis of cell membranes and steroid hormones. When the LDL exceeds the amount of cholesterol needed by the tissues, the LDL deposits cholesterol in the arteries (plaque), which can restrict blood flow and increase the risk of developing heart disease and / or myocardial infarctions (heart attacks). This is why LDL is called bad cholesterol. The HDL picks up cholesterol from the tissues and carries it to the liver, where it can be converted to bile salts, which are eliminated from the body. This is why HDL is called good cholesterol. Other lipoproteins include chylomicrons that carry triacylglycerols from the intestines to the... 

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