[Combined method for enzymatic determination of glucose and urea of blood].
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Biomedical subjects
Publications and source records attributed to A Burlina.
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Sera from 64 patients with HBsAg-negative chronic liver disease with or without cirrhosis were investigated for aminoterminal peptide of type III procollagen (sP-III-P) as a suitable marker of hepatic fibrosis; 244 healthy control subjects were included in the study. A close correlation (p less than 0.01) between sP-III-P levels and histological activity was observed; on the contrary, no correlation was found between the same serum marker of liver fibroplasia and biochemical activity or clinical severity of the disease. We conclude that sP-III-P as a suitable marker of liver overload of collagen fibers is strongly correlated with the histological activity of the disease. Local immune reactions produce soluble substances that might stimulate fibroblastic activity. The test has a significant sensitivity and a very high specificity as a marker of chronic liver disease with histological activity.
We studied the behavior of some biochemical markers of fibrosis, the aminoterminal propeptide of type III procollagen (P-III-P), laminin, hyaluronate and fibronectin, in the sera of patients with primary biliary cirrhosis (PBC). Significant increases were found in serum laminin, hyaluronate and P-III-P and, more important, a significant correlation was found between the histological stage of the disease and serum hyaluronate. This parameter seems to distinguish between early PBC (I and II stages) and advanced disease with fibrosis. Moreover, a correlation between the histological stage and serum levels of both laminin and P-III-P was observed. Serum laminin, however, increases particularly in advanced disease, whereas high levels of sP-III-P are already present in the early stage. Finally, no significant differences were found between the plasma fibronectin levels of patients with primary biliary cirrhosis and those of controls.
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The behavior of trypsin/creatinine clearance ratio (Ctr/Ccr) and serum immunoreactive trypsin (IRT) was evaluated in a total of 168 subjects with pancreatic cancer, chronic pancreatitis and non-pancreatic digestive diseases. Amylase/creatinine clearance ratio (Cam/Ccr) and serum amylase levels were also evaluated in order to establish their possible relationship with Ctr/Ccr and IRT values. Elevated Ctr/Ccr and IRT values were observed in several patients with pancreatic cancer and chronic pancreatitis. Abnormal IRT and Ctr/Ccr values were found in 28.2 and 4% of non-pancreatic digestive diseases, respectively. IRT and amylase serum levels showed consensual modifications, while Ctr/Ccr showed a behavior different from that of Cam/Ccr. Liver damage seems to play a role in increasing serum IRT levels of patients without pancreatic involvement, while the increased Ctr/Ccr seems to depend on other factors, for instance renal tubular dysfunction.
UNLABELLED: The aims of this study were to (1) evaluate the diagnostic utility of a new tumor marker, TPS, with respect to TPA and CA 19-9 in patients with pancreatic cancer; (2) ascertain the reliability of the markers in predicting survival, and (3) evaluate the effect of liver dysfunction on the results. CA 19-9, TPA and TPS were measured in the serum of 19 control subjects, 42 patients with pancreatic cancer, 29 with chronic pancreatitis, and 52 with extrapancreatic diseases. CA 19-9 was confirmed to be the best serological indicator of pancreatic cancer, while TPA and TPS lacked both sensitivity and specificity. Pancreatic cancer patients with liver metastases had higher mean CA 19-9 and TPA, but not TPS, values than pancreatic cancer patients without metastases. A shorter survival time was associated with the presence of liver metastases and with higher serum tumor marker levels. CA 19-9, TPA and TPS were found to be correlated with liver function test results (ALT, ALP and bilirubin). IN CONCLUSION: (1) TPS adds no significant information to that obtained using CA 19-9 in the diagnosis of pancreatic cancer; (2) CA 19-9 and TPA, but not TPS, are influenced by the presence of liver metastases; (3) the main factor to influence survival is advanced disease, which is in turn associated with higher tumor marker levels, and (4) liver dysfunction can influence not only CA 19-9 and TPA, as already described, but also TPS.
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Several studies are present in the literature about the efficacy of medical treatment with biliary acid, orally administered, on the symptomatic gallstone patients. Both this drugs act, with different mechanisms, on the same pathophysiological pathway, represented by the supersaturated bile in cholesterol. Aim of the present investigation was to study the possible modifications of serum bile acids pattern and of lipoproteins in a large sample of gallstone patients under long-term treatment with biliary acids. One hundred and twelve patients with radiolucent gallstones entered the study; 54 received chenodeoxycholic acid (CDCA) and 58 ursodeoxycholic (UDCA) at dosage of 15 mg/kg/daily. Blood samples for determination of serum cholesterol, triglycerides, phospholipids, lipoproteins, total and fractionated biliary acids were collected from each subjects every three months for a mean "follow-up" of 24 months. The levels of serum cholesterol, triglycerides and phospholipids showed a mild decrease only in the patients under therapy with CDCA, while no modifications were detected using UDCA. The same was found for two other parameters, HDL-cholesterol and lipoproteins, with both treatments during the overall period of follow-up. The biliary acids levels showed a significant increase only in the patients treated with CDCA, but no differences were found between "responders" and "non responders" to the therapy.
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In order to verify the role of CEA in the differential diagnosis of pancreatic cancer and to evaluate some influencing factors like age, tumor spread and liver dysfunction, this antigen was measured in the sera of 60 control subjects, 45 patients with pancreatic cancer, 37 with chronic pancreatitis, 67 with benign, and 28 with malignant extra-pancreatic diseases. CEA was found to be elevated in 23/45 pancreatic cancers, in 8/37 chronic pancreatitis, in 17/67 benign and in 9/28 malignant extra-pancreatic diseases. Significant correlations were documented between CEA and age in all the subjects; between CEA and immunoglobulins G in liver cirrhosis and between CEA and alkaline phosphatase in gastrointestinal extra-pancreatic malignancies. In pancreatic cancer higher CEA levels were detected in patients with metastases. We can conclude that CEA is of limited value in the differential diagnosis of pancreatic cancer; it does not seem to be able to detect early pancreatic tumors. Age and liver dysfunction may contribute towards elevating this marker in serum.
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