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Biomedical subjects

M Plebani

Publications and source records attributed to M Plebani.

At least 325 records · Page 18Linked to original sources
PubMed1988

Renal involvement in chronic pancreatic disease: effects on trypsin and amylase plasma-urine transfer.

This study was undertaken in order to ascertain the behaviour of amylase and trypsin fractional clearances in chronic pancreatic disease and to speculate on the factors involved. Renal tubular function was also assessed in these patients. An increase of both clearances was found in a number of patients with pancreatic cancer and chronic pancreatitis. Amylase urinary output seems to be mainly related to the circulating enzyme levels; urinary IRT is principally accounted for by a functional tubular impairment. Tubular damage was observed in a number of patients with chronic pancreatic disease. This was related to pancreatic inflammation in chronic pancreatitis and to several factors, among which jaundice and pancreatic damage, in pancreatic cancer.

Amylases↗
PubMed1988

Tissue polypeptide antigen, galactosyltransferase isoenzyme II and pancreatic oncofetal antigen serum determination: role in pancreatic cancer diagnosis.

The clinical usefulness of tissue polypeptide antigen, galactosyltransferase II and pancreatic oncofetal antigen was evaluated in detecting pancreatic cancer and in differentiating this malignancy from chronic pancreatitis and other diseases (mainly of the liver and biliary tract) which may enter in differential diagnosis. TPA seems to be the most sensitive among these indices in detecting pancreatic cancer and appears to discriminate this malignancy quite satisfactorily from chronic pancreatitis. It is also frequently pathological in a number of other diseases and is influenced by the presence of liver dysfunction. GT II and POA do not grossly differ from TPA in specificity, but they appear to be less sensitive. Both are frequently pathological in hepato-biliary diseases. All these markers seem, therefore, to be of limited value in the diagnosis of pancreatic cancer.

Antigens, Neoplasm↗
PubMed1988

Serum markers and clinical data in diagnosing pancreatic cancer: a contrastive approach.

In order to assess the value of serum markers and simple clinical data in the differential diagnosis of pancreatic cancer, we studied 32 control subjects and 28 patients with pancreatic cancer, 26 with chronic pancreatitis, and 37 with extra-pancreatic diseases. CA 19-9 was found to be the best marker in detecting pancreatic cancer. Among the clinical data, presence and onset of pain attacks, age, and weight loss were selected as the most informative in assessing chronic pancreatic disease. Clinical data correctly classified 88.5% of chronic pancreatitis and 75.0% of pancreatic cancer; serum markers identified pancreatic tumor in 67.9% of the patients. The adjunct of serum markers to clinical data did not improve accuracy in diagnosing chronic pancreatic disease. Since clinical data and serum markers generally become positive at an advanced stage of the disease, early diagnosis of pancreatic cancer is a goal still to be attained.

Adult↗
PubMed1988

Importance of control materials in quality assessment of cyclosporine determination.

The importance of control materials in intralaboratory quality assessment of cyclosporine A determination was analyzed. Two types of control materials and a human pool serum were evaluated. The first material was a two-level lyophilized cyclosporine human whole blood control (TLCC); the other was a tri-level therapeutic drug monitoring control (TDMC). The drug was determined in all specimens by both tritiated and iodinated radioimmunoassay. The coefficients of variation obtained in TLCC samples were significantly lower in comparison with the TDMC samples and similar to that of the human pool.

Cyclosporins↗
PubMed1988

Limits of CEA and ferritin in the diagnosis of pancreatic cancer.

In this paper the clinical usefulness of CEA and ferritin in the diagnosis of pancreatic cancer was pointed out. CEA was found to be increased in 51% of patients with pancreatic cancer; it was also abnormal in 22% of chronic pancreatitis and 31% of extra-pancreatic diseases. In patients with metastatic pancreatic cancer CEA was found to be more elevated than in those with localized tumor. CEA correlated with the age of the subjects in all material; in liver cirrhosis with IgG and in extra-pancreatic gastro-intestinal malignancies with alkaline-phosphatase. Ferritin was found to be increased in 73% of pancreatic cancer patients; it was also abnormal in 40% of chronic pancreatitis and in 38% of extra-pancreatic diseases. Patients with chronic pancreatitis studied during a relapsing phase all had elevated serum ferritin. We can conclude that neither CEA nor ferritin are useful indices of pancreatic malignancy, due to the lack of sensitivity or specificity. Both are influenced by several factors: CEA mainly by age and liver dysfunction, ferritin by the presence of an acute inflammation with cell necrosis.

Biomarkers, Tumor↗
PubMed1988

[Pepsinogen].

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Clinical Enzyme Tests↗
PubMed1988

[Creatinine].

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Adenosine Triphosphate↗
PubMed1988

[Ferritin].

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Ferritins↗
PubMed1987

Prednisone inhibits late asthmatic reactions and airway inflammation induced by toluene diisocyanate in sensitized subjects.

To determine the importance of airway inflammation for late asthmatic reactions induced by toluene diisocyanate (TDI), we investigated whether prednisone prevented them [corrected] by modifying the associated airway inflammatory reaction. We measured FEV1 before and at regular intervals after exposure to TDI and performed bronchoalveolar lavage at 8 hours after TDI in two groups of subjects with previously documented late asthmatic reactions, in one group, after no treatment, and in the other group, after treatment with prednisone (50 mg/day for 4 days). After no treatment, each subject developed a late asthmatic reaction, an increase in airway responsiveness, polymorphonuclear leukocytosis, and increased albumin in bronchoalveolar lavage. By contrast, after treatment with prednisone, no subject developed a late asthmatic reaction or an increase in airway responsiveness, and the number of leukocytes and the concentration of albumin were normal in bronchoalveolar lavage. These results suggest that late asthmatic reactions induced by TDI may be caused by airway inflammation and that prednisone may block them [corrected] by inhibiting the inflammatory reaction of the airway induced by TDI in sensitized subjects.

Adult↗
PubMed1987

Effect of 3-hydroxy-3-methylglutarate treatment on plasma ketone bodies, triglycerides, and HDL-cholesterol in streptozotocin-diabetic rats.

3-Hydroxy-3-methylglutaric acid administration to streptozotocin-diabetic rats produced a net decrease of plasma ketone bodies and triglycerides together with a slight decrease of total cholesterol. A nonsignificant enhancement of HDL-cholesterol and a negligible change in HDL-phospholipid was also observed. The effect of 3-hydroxy-3-methylglutarate was dose dependent and was more evident with the compound intraperitoneally injected than orally administered with drinking water. [14C]-3-hydroxy-3-methylglutarate was administered either orally or intraperitoneally both to diabetic and control groups of animals, and a higher radioactivity accumulated in liver and kidneys of diabetic rats compared to the controls. The possible mechanism of action of 3-hydroxy-3-methylglutarate is briefly discussed.

Animals↗
PubMed1987

Bronchoalveolar neutrophilia during late asthmatic reactions induced by toluene diisocyanate.

The mechanism by which late asthmatic reactions are induced by toluene diisocyanate (TDI), a low molecular weight chemical that causes occupational asthma in exposed subjects, is unknown. We investigated whether early and late asthmatic reactions induced by TDI are associated with changes in airway responsiveness to methacholine and airway inflammation as determined by bronchoalveolar lavage. We measured FEV1 before and at regular intervals after exposure to TDI, and performed dose-response curves to methacholine and bronchoalveolar lavage at 8 h after TDI in a group of 6 subjects with late asthmatic reactions and in 6 subjects with only early asthmatic reactions. The same procedure was followed 2 h after TDI in a group of 6 subjects with previously documented late asthmatic reactions and in a group of 6 subjects without any previously documented asthmatic reaction after TDI. In subjects with late asthmatic reactions, neutrophils were increased at both 2 and 8 h, and eosinophils and airway responsiveness were increased only at 8 h. By contrast, neutrophils, eosinophils and airway responsiveness were not increased at 8 h after TDI in subjects with an early asthmatic reaction or at 2 h after TDI in normal control subjects. These results suggest that late asthmatic reactions to TDI, and the associated increase in airway responsiveness, may be caused by airway inflammation.

Asthma↗
PubMed1987

Immunoglobulin A (lambda chains) conjugated with lactate dehydrogenase in serum.

An atypical pattern for lactate dehydrogenase (EC 1.1.1.27) isoenzymes in a patient with sclerosis of the bladder neck was ascribable to complexing between lactate dehydrogenase and IgA. This complex formation was also replicable "in vitro." We determined that the IgA bound to lactate dehydrogenase was of the lambda type, a very unusual occurrence.

Humans↗
PubMed1987

[Thyrotropin].

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Aging↗