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Biomedical subjects

A Piccoli

Publications and source records attributed to A Piccoli.

At least 91 records · Page 5Linked to original sources
PubMed1992

Evaluation of surgical risk in palliation and resection of pancreatic cancer. Perspective study and tables to calculate the risk.

High morbidity and mortality rates are reported for bypass and resective surgery of pancreatic cancer. In a retrospective study we correctly predicted the postoperative course in 88% of the patients who underwent bypass surgery and 83% of those who had a resection for pancreatic cancer. Before starting with clinical application of this scoring system, we undertook a prospective study to confirm its predictive value. Sixty-seven consecutive patients with pancreatic cancer were included: 42 patients underwent bypass surgery and 25 pancreatic resections. The operative mortality was 14% for palliative surgery and 0% for resective surgery. Surgical team and nurses were totally unaware of the predicted risk. The preoperative forecast proved to be correct in 81% of bypass surgery and in 88% of resective surgery, although surgical mortality had decreased from 21 to 14% for bypass surgery and from 17 to 0% for resective surgery. Tables are included to calculate the surgical risk for each of 162 combinations of the risk factors considered in the predictive model (81 for bypass surgery and 81 for resective surgery). Calculation of surgical risk is important when evaluating different treatments for pancreatic cancer are available.

Adult↗
PubMed1992

Alteration of plasma proteinase-antiproteinase system in type 1 diabetic patients. Influence of sex and relationship with metabolic control.

The aim of the present study was to investigate whether or not alterations of the plasma proteinase-antiproteinase system were present in type 1 (insulin-dependent) diabetic patients and, if so, whether or not they were related to sex, age at onset and duration of the disease as well as to short- and long-term diabetic control. The plasma concentration of trypsin-like activity and two of the most important plasma serine proteinase inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, were determined in 95 type 1 diabetic and 67 control subjects. The plasma concentration of alpha 1 antitrypsin was found to be markedly decreased (P < 0.001), whereas plasma alpha 2-macroglobulin and trypsin-like activity were increased in diabetics compared to controls (P = 0.009 and < 0.001, respectively). Sex also influenced the values of both proteinase inhibitors in diabetics, women showing higher values of plasma alpha 1-antitrypsin (P = 0.004) than men. In women, HbA1c was also positively correlated with blood glucose (P < 0.001), daily insulin dosage (P < 0.001), and trypsin-like activity of plasma (P = 0.02). On the contrary, in men, HbA1c appeared to be negatively correlated with plasma alpha 2-macroglobulin (P = 0.02). In addition to sex, age at onset (but not duration) of the disease revealed differences in plasma alpha 1-antitrypsin among diabetics, the lowest mean value of this inhibitor being present in men with age at onset below 15 years, who also showed a significant negative correlation between this inhibitor and HbA1c (P = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Glycosaminoglycans prevent morphological renal alterations and albuminuria in diabetic rats.

Abnormal glycosaminoglycan metabolism is involved in the onset of anatomo-functional derangements in diabetic nephropathy, and determines the loss of glomerular basement membrane anionic charges leading to albuminuria. Glycosaminoglycan administration was shown to increase the negative electrical potential of the vessel wall, inhibit mesangial cell proliferation, which is an anatomical hallmark of diabetic nephropathy, and slow down the progression to uremia in subtotally nephrectomized rats, a model that shares some pathogenetic key events with diabetic nephropathy. Based on these considerations, we verified the effect of exogenous glycosaminoglycans on renal involvement in streptozotocin diabetic rats. Long-term administration of two glycosaminoglycans (low-molecular weight heparin and dermatan sulphate) prevented glomerular basement membrane thickening, glomerular anionic charge reduction, as well as the onset of albuminuria without affecting glomerular filtration rate and metabolic control of the disease. Our data demonstrate that the long-term administration of glycosaminoglycans has a favorable effect on morphological and functional renal abnormalities in diabetic rats.

Albuminuria↗
PubMed1991

Plasma insulin levels do not change during atrial natriuretic factor infusion in human essential hypertensives.

In order to evaluate the effects of atrial natriuretic factor (ANF) infusion on plasma insulin (IRI) in hypertension, 32 essential hypertensives (aged 40 to 62 years) were studied. After 1 week of pharmacologic washout under normal sodium intake (120 mEq of Na+/day), patients were randomly assigned to receive either ANF (0.04 micrograms/kg/min) or its vehicle (50 mL of isotonic saline) over a 60-min period in supine position. Plasma IRI and glucose were measured at -60, 0, 20, 40, 60, 120, 180, and 240 min (infusion time: from 0 to 60 min). Plasma levels of IRI and glucose did not change significantly during ANF infusion. On the contrary, after ANF discontinuation plasma IRI rose from levels of 13.5 +/- 6.4 microU/mL at 60 min to values of 20.1 +/- 11.3 microU/mL at 240 min (P less than .0001 v time 0). Plasma glucose showed a similar behavior, increasing from values of 100.4 +/- 5.0 mg/dL at 60 min to values of 120.0 +/- 5.1 mg/dL at 240 min (P less than .02 v time 0). Our findings suggest that ANF did not influence insulin release in hypertensives. The increase of plasma glucose and IRI observed after ANF discontinuation could be due to the relapse of sympathetic activity, suppressed during ANF infusion.

Adult↗
PubMed1991

Role of local and systemic factors in increasing serum glycoprotein markers of pancreatic cancer.

This study was performed in order to evaluate the role of various local and systemic alterations in influencing serum glycoproteic markers in patients with pancreatic cancer, and in healthy and diseased controls. Cancer antigen 19-9 (CA 19-9), carcinoembryonic antigen (CEA), and ferritin were determined in the sera of 23 control subjects, 30 patients with pancreatic cancer, 27 with chronic pancreatitis, and 27 with extra-pancreatic diseases mainly of gastrointestinal origin. A number of acute-phase proteins and indices of liver function and cholestasis were also assayed. The three antigens increased only in patients with pancreatic cancer. Higher CA 19-9 and CEA, but not ferritin, levels were found only in patients with hepatic metastases. Acute-phase proteins and synthetic functional indices were found to be higher and lower, respectively, in patients with pancreatic malignancy when compared with controls. Multiple regression analysis documented the dependence of circulating ferritin, but not of CA 19-9 and CEA, on the systemic indices. Canonical correlation showed a similar trend for CA 19-9 and CEA, which differed from that of ferritin. Ferritin was found to depend on the presence of systemic and hepatic alterations, especially of cholestasis. We can conclude that the variations of serum glycoprotein markers in patients with pancreatic cancer depend on various regional and systemic factors. CA 19-9 and CEA are related mainly to the extent of the neoplasia. The influence of a decreased liver function capacity associated or not to cholestasis and the interrelation with the acute-phase response may also be suggested. Ferritin, on the other hand, is related to a higher degree than CA 19-9 and CEA to hepatic dysfunction and also behaves similar to an acute-phase protein.

Adult↗
PubMed1990

Effect of nifedipine on urinary excretion of calcium and calcium-controlling hormones in essential hypercalciuria.

Nifedipine has been shown to lower urinary calcium in "essential" hypercalciuria. However, the mechanism(s) by which this action takes place is completely unknown. This study describes the effect of nifedipine on some calcium-controlling hormones in essential hypercalciuria. Nifedipine (20 mg/day) was administered to ten essential hypercalciuric patients, and urinary PgE2, plasma bicyclic PgE2, 1,25 vitamin D3, and PTH were assayed before and after drug administration. Nifedipine promoted a significant fall in urinary calcium (352.1 +/- 87.67 SD vs. 231.2 +/- 74.62 mg/hr; t = 7.35, p less than .0001) and PgE2 (343.92 +/- 42.71 vs. 245.03 +/- 35.41 SD ng/24 hr; t = 6.18, p less than .0002), as well as in plasma bicyclic PgE2 (310.00 +/- 30.91 vs. 200.00 +/- 31.62 SD pg/ml; t = 9.86, p less than .0001) and 1,25 (OH)2 vitamin D3 (32.77 +/- 3.23 vs. 26.94 +/- 2.94 SD pg/ml; t = 6.53, p less than .0001), while PTH remained unaltered (18.50 +/- 3.63 vs. 19.50 +/- 4.09 SD ng/ml; t = 0.85, p, ns). Urinary calcium and PgE2 correlated positively before (r = 0.81, p less than .005) but not after treatment. The fall in urinary PgE2 brought about by nifedipine seems to be due to an inhibition of PgE2 synthesis, since the absolute decrements in both urinary PgE2 and plasma PgE2 metabolites were positively correlated (r = 0.79, p less than .007). No correlation was found between the absolute decrements of plasma bicyclic PgE2 and 1,25 (OH)2 vitamin D3. These data seem to suggest that the fall in urinary calcium brought about by nifedipine is in some way related to PgE2 synthesis inhibition and to uncoupling of 1,25 (OH)2 vitamin D3 and PTH action.

Adult↗
PubMed1990

Renal handling of amylase and immunoreactive trypsin in pancreatic cancer and chronic pancreatitis.

In order to evaluate the renal metabolism of amylase and immunoreactive trypsin (IRT) in chronic pancreatic disease, we assayed amylase, IRT and creatinine in serum and urine and gamma-glutamyl transferase (GGT) in dialyzed urine as well as alpha-glucosidase (AGL) and ribonuclease (RNase) in 24 control subjects, 34 patients with pancreatic cancer, 52 with chronic pancreatitis and 32 with extra-pancreatic diseases. Urinary amylase and IRT outputs were found to be more elevated in chronic pancreatitis than in control subjects. The levels of serum amylase, its renal inputs and outputs were correlated with the corresponding IRT values. Multiple regression analyses (dependent on amylase or IRT urinary outputs, circulating levels of the two enzymes, creatinine clearance and the excretion of GGT, AGL and RNase predictor variables) showed significant correlations. The standardized partial regression coefficients found to be significant were: GGT, RNase and serum amylase for amylase, and GGT and RNase for IRT. No difference was found between amylase and IRT outputs in patients with chronic pancreatitis, taking the presence or the absence of alcohol abuse, exocrine insufficiency and pancreatic pseudocysts into consideration. Urinary GGT excretion correlated with serum amylase and IRT levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

How does liver dysfunction influence serum CA 19-9 in pancreatic cancer?

Serum CA 19-9 was determined in 83 control subjects, 99 patients with pancreatic cancer, 104 with chronic pancreatitis and 137 with extra-pancreatic diseases mainly of gastrointestinal origin in order to evaluate whether hepatic factors can influence circulating CA 19-9 in pancreatic cancer. Sensitivity, specificity and accuracy of this test in determining pancreatic malignancy were: 74%, 83% and 57%. We divided patients into two groups: group A (159 cases) and group B (181 cases) with and without anatomical liver damage (presence of primary or metastatic cancer, cirrhosis, hepatitis, steatofibrosis, cholangitis). Group A presented higher CA 19-9 values as compared to group B. Significant correlations were found in group B but not in group A between CA 19-9 and ALT, ALP and total bilirubin. Multiple regression analysis (CA 19-9 dependent and ALT, ALP and total bilirubin predictor variables) was significant only in group B. The standardized partial regression coefficients found to be significant were those of ALP and total bilirubin. We can conclude that CA 19-9 is an index of pancreatic cancer with satisfactory sensitivity and specificity. The presence of anatomical liver damage seems to increase the value of this index, probably releasing CA 19-9 into the bloodstream. Extra-hepatic cholestasis may also be an important factor in elevating CA 19-9 probably by reducing the hepatic catabolism of this glycoprotein.

Adult↗
PubMed1990

The serum tissue polypeptide antigen in the detection of hepatocellular carcinoma in cirrhotic patients.

The aim of our work was to assess the performance of tissue polypeptide antigen in detecting hepatocellular carcinoma in cirrhotic patients, while also checking for any influence of liver dysfunction on the serum level of the marker. One hundred and twenty-five consecutive cirrhotic patients, 35 with and 90 without, hepatocellular carcinoma were studied. Tissue polypeptide antigen had a different distribution in the two groups and the best diagnostic accuracy with 48.6% sensitivity and 85.6% specificity was found at the cut-off value of 240 UL-1. In cirrhotic patients significant linear correlations were found between tissue polypeptide antigen and alanine-transaminase, aspartate-transaminase, G-glutamyl-transpeptidase and alkaline phosphatase; there was no correlation with bilirubin or pseudo-cholinesterase. In patients with hepatocellular carcinoma a significant linear correlation was found only with alanine and aspartate transaminase and G-glutamyl-transpeptidase. The analysis of covariance still showed a significant difference between mean tissue polypeptide antigen levels in the two groups also accounting for covariates. These results suggest that: a) the liver dysfunction may be involved in increasing tissue polypeptide antigen values; b) tissue polypeptide antigen has a different distribution in cirrhotic patients with and without hepatocellular carcinoma also accounting for covariates; these findings further support the specificity of tissue polypeptide antigen.

Biomarkers, Tumor↗
PubMed1989

Does bile play a fundamental role in inducing and influencing acute reflux pancreatitis in rat?

Acute pancreatitis by closed duodenal loop in two groups of rats, with or without biliary diversion, was induced to ascertain any role that bile might have in codetermining and influencing the disease. Both the histological findings and the serum amylase levels showed the presence of mild acute pancreatitis in both groups. The histological and/or biochemical findings and the survival rates were similar for rats with and rats without biliary diversion. We may therefore conclude that the closed duodenal loop causes acute pancreatitis of a mild degree in the rat; bile did not appear to play a fundamental role in inducing or in influencing the outcome of the acute pancreatic inflammation in this experimental model.

Acute Disease↗
PubMed1989

Renal tubular dysfunction in pancreatic cancer and chronic pancreatitis.

Urinary excretion of alpha-glucosidase (AGL), gamma-glutamyltransferase (GGT) and ribonuclease (RNase), and serum amylase and immunoreactive trypsin (IRT) were determined in 38 control subjects, 48 patients with pancreatic cancer, 77 with chronic pancreatitis and 47 with extrapancreatic diseases in order to ascertain the presence of a renal tubular damage and to investigate its etiology. A significantly increased frequency of pathological results for all urinary enzymes was documented in the various groups of patients as compared to controls. Significant correlations were detected among AGL, GGT and RNase. Considering the subjects as a whole, GGT and RNase excretions correlated with serum IRT and amylase; the two urinary enzymes were found to be higher when jaundice was present. In chronic pancreatic disease enzymuria was related to increased serum pancreatic enzymes; in extrapancreatic diseases it was associated to hyperbilirubinemia. The vast majority of patients with pancreatic cancer and elevated urinary enzymes presented hepatic metastases and/or jaundice. We can conclude that an anatomical and functional tubular impairment is detectable in some patients with chronic pancreatic and extrapancreatic diseases. Tubular damage seems to least in part to be related to pancreatic inflammation and necrosis in chronic pancreatic disease, while jaundice may be found to play an important role in diseases of the hepatobiliary tract. In pancreatic cancer, liver dysfunction (presence of liver metastases and/or extrahepatic cholestasis) also appears to be involved in altering tubular cells.

Adult↗