Biomedical subjects

C Del Piano

Publications and source records attributed to C Del Piano.

5 recordsLinked to original sources

PubMed1999

Enhancement of fatty acid and cholesterol synthesis accompanied by enhanced biliary but not very-low-density lipoprotein lipid secretion following sustained pravastatin blockade of hydroxymethyl glutaryl coenzyme A reductase in rat liver.

A 3-week treatment of rats with pravastatin (PV) augmented biliary cholesterol and phospholipid output 3.6- and 2.2-fold over controls, while bile acid (BA) output and kinetics were unchanged. No major changes were detected in hepatic and serum cholesterol concentrations despite the PV inhibitory property on hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase. To evaluate the mechanisms of this adaptive phenomenon, several parameters of hepatic lipid homeostasis were assessed. Biliary cholesterol changes could not be attributed to an increased influx of lipoprotein cholesterol to the liver and bile. Hepatic low-density lipoprotein (LDL) receptor content, as inferred from Western blot analysis, was unchanged, as was the biliary excretion of labeled cholesterol derived from chylomicron remnants. In vivo 3H2O-incorporation studies showed an 80% increase in hepatic cholesterol synthesis, evidence for bypass of the PV block. Remarkably, fatty acid synthesis was also stimulated twofold, providing substrate for hepatic triglycerides, which were slightly enhanced. However, serum triglycerides decreased 52% associated with a 22% decrease in hepatic very-low-density lipoprotein (VLDL) secretion. Thus, the biochemical adaptation following PV treatment produces complex alterations in hepatic lipid metabolism. An enhanced supply of newly synthesized cholesterol and fatty acids in association with a limited VLDL secretion rate augments the biliary lipid secretion pathway in this experimental model.

Animals↗

PubMed1992

Capillary blood flow to the skin of forearm in cirrhosis.

In liver cirrhosis a hyperkinetic circulatory state is frequently observed as a consequence of an arterial or even a venous peripheral vasodilatation with secondary increase in cardiac output. Indirect evidence suggests that, in liver disease, the manifestation of warm hands, capillary pulsation, or palmar erythema may also relate to such a state by way of an increased skin blood flow. The purpose of the present study has been to directly assess capillary skin blood flow in liver disease through the clearance of a locally injected radioactive substance. The study was performed in 24 patients with different liver diseases, including 14 Child class II cirrhotics, and in 9 control subjects. A small volume of Na 131I solution was injected at the volar surface of the forearm, and radioactive counts were recorded continuously for ten seconds every minute for up to twenty minutes. The best fit line of the disappearance rate was determined by the least square method, and both its T/2 and an estimated blood flow parameter were calculated. The T/2 of isotope disappearance rate was 4.54 +/- 0.71 and 4.38 +/- 0.68 minutes in cirrhotics and controls, respectively. Similarly, estimates of skin blood flow (mL/min/100 g tissue) were 7.82 +/- 1.28 in the cirrhotic patients, not significantly different from those in both patients with mixed liver diseases (7.6 +/- 2.86) and control subjects (8.06 +/- 1.04). Parameters of skin blood flow were also invariant in respect to the various etiologies of liver disease. Thus, the present findings indicate that capillary skin blood flow is not affected by the hyperdynamic circulatory changes occurring in liver cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

[Pancreatic pseudocysts. An important surgical problem].

The pancreatic pseudocyst is a serious complication of acute or chronic pancreatitis. Surgical internal anastomosis can be an adequate solution to this problem. Sixty patients with pancreatic pseudocyst have been referred to our institution in the last 15 years; 47 of them were operated upon. Different techniques were employed according to differences in the pseudocyst wall status and the presence or absence of infection.

Acute Disease↗

PubMed1991

Effect of cholestyramine treatment on biliary lipid secretion rates in normolipidaemic men.

This study was designed to clarify the effect of bile acid sequestrant treatment on the total biliary output rates of cholesterol, phospholipids and bile acids in man, and to correlate these changes with the alterations in plasma lipoprotein levels. For this purpose nine healthy, normolipidaemic men were treated with 16 g of cholestyramine daily over a period of 4 weeks, and the biliary secretion rates were measured by a duodenal perfusion technique. Resin therapy, which profoundly increases de novo synthesis of bile acids, resulted in a lowering of total plasma cholesterol levels, mainly due to a 35% reduction in low density lipoprotein (LDL) cholesterol, and in a 33% increase in plasma triglyceride levels, reflecting enhanced very low density lipoprotein (VLDL) triglyceride concentrations; high density lipoprotein (HDL) levels did not change. However, these lipoprotein changes did not correlate with any alterations in biliary lipid output. Total hepatic secretion rates of the biliary lipids remained generally unchanged during treatment, with a tendency towards lower cholesterol output, resulting in a lower molar percentage of cholesterol in hepatic bile, 3.4 +/- 0.4 vs. 2.9 +/- 0.2 mol %. This is probably due to an increased rate of conversion of cholesterol to bile acids in the hepatocyte. It is concluded that, in man, the liver may adapt well to changes in the enterohepatic circulation of bile acids, thereby maintaining output rates of biliary lipids at a relatively constant level.

Adult↗

PubMedDate not supplied

[Physiopathology of iron metabolism and hemochromatosis: interrelationships, assessment and pathogenesis of iron overload, screening].

Fundamental aspects of iron metabolism relate to the dynamic processes of metal plasma transport as well as cell storage and efflux. Transferrin not only carries iron in the plasma but also delivers it to the various cells by binding to a diffuse specific cell receptor; it also acts by chelating cell iron. Ferritin co-operates by storing iron in the cell. By a still unknown regulatory mechanism, iron, from the ferritin pool, is redistributed in the cell to a cytosolic, easily chelatable, "transit" pool or to a degradative lysosomal hemosiderin pool from which it is slowly released outside the cell. Iron overload, such as that typical of hyperhemolysis or hemochromatosis, profoundly impairs its metabolism by saturating and/or altering transferrin and ferritin, by freeing iron from any regulated transport, thus allowing parenchymal deposition and damage. An important aspect still awaiting clarification relates to the different storage of excess iron in the parenchymal cells, as in hemochromatosis, or in the reticuloendothelial system such as in hemosiderosis. Studies using cellular models attempt to evaluate such differences in terms of altered properties of the iron proteins or their cell receptors, and of the different cell responsivity to non-transferrin iron. In the expectation of better knowledge, attention should be concentrated, from a clinical standpoint, on precise assessment of iron deposits in the tissues with the aim of preventing its excessive accumulation and parenchymal damage. In hemochromatosis, the risk of iron overload is evaluated by HLA typing.

HLA Antigens↗