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Biomedical subjects

Lucio Gullo

Publications and source records attributed to Lucio Gullo.

At least 19 recordsLinked to original sources
PubMed2006

Day-to-day variations of serum pancreatic enzymes in benign pancreatic hyperenzymemia.

BACKGROUND & AIMS: Benign pancreatic hyperenzymemia is a newly identified syndrome that is characterized by a chronic increase of serum pancreatic enzymes in the absence of pancreatic disease. When checked at intervals of months or years, the enzyme levels show considerable variation from one test to another, and enzyme normalization is sometimes seen. The purpose of this study was to determine whether these variations can occur on a day-to-day basis. METHODS: Forty-two subjects with benign pancreatic hyperenzymemia, 28 men and 14 women, mean age 50 years, range 16-68 years, were studied. In each subject serum amylase, pancreatic isoamylase, and lipase levels were determined once daily on each of 5 consecutive days; in 15 of the 42 subjects studied, serum trypsin level was also measured. RESULTS: In 8 (19%) of the 42 subjects, the serum enzyme levels were abnormally elevated for all 5 days of the study but showed wide fluctuations. In 33 (78.6%) subjects, the hyperenzymemia showed considerable day-to-day variations that included normalizations. In the remaining subject (2.4%), all enzymes were normal. In most of the subjects with hyperenzymemia, 37 of 41, all enzyme levels were elevated, with lipase, and trypsin when performed, showing the highest values. Of the remaining 4 subjects, in 3 only amylase and pancreatic isoamylase were increased and in 1 only lipase. CONCLUSIONS: The results show that there are marked day-to-day variations, with frequent normalizations, of serum enzyme levels in subjects with benign pancreatic hyperenzymemia. The reason for these wide day-to-day fluctuations is not known.

Adolescent↗
PubMed2006

Benign pancreatic hyperenzymemia in children.

One of us recently described chronic pancreatic hyperenzymemia in the absence of pancreatic or other disease in adult subjects. The aim of the present study was to describe this form of pancreatic hyperenzymemia in children. The study involved 15 children with this condition seen from September 1996 to December 2004. After initial evaluation, each child was seen by us once annually until the end of the study. Each check-up included serum amylase (normal values 20-220 IU/L), pancreatic isoamylase (17-115 IU/L) and lipase (24-270 IU/L) determinations as well as abdominal ultrasound. In six children, fecal elastase was also determined. At the initial assessment, 13 of the 15 children had abnormal serum increases in all three enzymes, one showed an increase only in lipase, and in the remaining child all three enzymes were present in normal concentrations. These latter two children had had abnormally elevated levels of all enzymes at the examination performed before this study began. During follow-up, enzyme concentrations remained abnormally elevated, although with wide fluctuations and transient normalizations. Considering the highest values of enzymes found in the various examinations performed during this study, the increase over the upper normal limit was in the range of 1.5- to 5.2-fold for amylase, 2.2-to 8.0-fold for pancreatic isoamylase, and 2.0- to 15.4-fold for lipase. Fecal elastase was normal in the six children in whom it was measured. No child had evidence of pancreatic or other disease, either at initial evaluation or during follow-up. The results of this study describe benign pancreatic hyperenzymemia in children. Although it is a benign condition, awareness of it is important to avoid unnecessary concern and multiple diagnostic procedures.

Amylases↗
PubMed2006

Can pancreatic steatosis explain the finding of pancreatic hyperenzymemia in subjects with dyslipidemia?

OBJECTIVE: It has been proposed by some investigators that benign pancreatic hyperenzymemia could result from pancreatic steatosis that they believe would have been caused by dyslipidemia; their diagnosis of steatosis was based on the finding of a hyperechogenic pancreas at ultrasound. The aim of this study was to assess the validity of this proposed model. METHODS: The study group was composed of 18 subjects with benign pancreatic hyperenzymemia, 12 men and 6 women; mean age, 55 years; range, 38 to 68 years. All 18 had dyslipidemia and 9 had hyperechogenic pancreas at ultrasound. In addition, 6 subjects with benign pancreatic hyperenzymemia but who did not have dyslipidemia or hyperechogenic pancreas and 10 healthy subjects with none of these conditions were also studied as controls. In each of these subjects, magnetic resonance imaging of the pancreas was performed to assess the presence of pancreatic steatosis. RESULTS: Magnetic resonance imaging showed normal pancreas with no signs of fatty infiltration in all 18 subjects with dyslipidemia, including those with both dyslipidemia and hyperechogenic pancreas at ultrasound. A similar result was found in all control subjects. CONCLUSION: The finding of a completely normal pancreas at magnetic resonance imaging does not support the proposed model in which pancreatic hyperenzymemia in subjects with dyslipidemia is attributed to pancreatic steatosis.

Adult↗
PubMed2005

Alcoholic pancreatitis: new insights into an old disease.

Alcoholic pancreatitis is an old disease that continues to present controversial issues. One of the most hotly debated issues is whether alcoholic pancreatitis is a chronic disease from the beginning or if instead it becomes chronic after repeated episodes of acute pancreatitis. Histologic studies, including very large series of patients with alcoholic pancreatitis, have clearly shown that this disease is chronic from the beginning and that, if acute necrotic pancreatitis occurs, it is associated with chronic lesions. The possibility that acute alcoholic pancreatitis can occur in the absence of chronic lesions cannot be excluded, but, if this occurs, it is rare. In addition to alcohol, genetic factors certainly play a determining role. Until now many genetic studies have been made on chronic pancreatitis; the first dealt with hereditary pancreatitis. In this disease it has been shown that mutations of the cationic trypsinogen gene and of SPINK1 are implicated in its pathogenesis. Concerning alcoholic pancreatitis, several studies have been made, but the results so far are disappointing.

Carrier Proteins↗
PubMed2005

Obesity and the risk of pancreatic cancer: an italian multicenter study.

OBJECTIVE: The purpose of this work was to determine whether obesity is a risk factor for pancreatic cancer. METHODS: We studied 400 patients with this tumor and 400 controls matched for sex and age from various Italian cities. We used a standardized questionnaire that was compiled at personal interview, with particular attention to body weight at the time of the interview, and for those with the tumor, their weight before onset of the disease. Body mass index (BMI) was calculated as the patient's weight in kilograms divided by their height in meters squared. RESULTS: The risk of pancreatic cancer adjusted for smoking was 5-fold higher (P < 0.001) in patients with a BMI less than 23 kg/m2 after diagnosis compared with patients with a BMI ranging from 23 to 29.9 kg/m2, whereas the risk in patients with BMI of at least 30 kg/m2 was not significant (P = 0.689). Taking into account BMI before diagnosis, smoking was confirmed as a significant risk factor (odds ratio = 1.68; P = 0.001) for pancreatic cancer, whereas no significant relationship was found between BMI classes and the risk of pancreatic cancer (P = 0.984). CONCLUSIONS: These findings indicate that obesity is not a risk factor for pancreatic cancer.

Adult↗
PubMed2005

Mutations of the CFTR gene in idiopathic pancreatic hyperenzymemia.

OBJECTIVES: Idiopathic pancreatic hyperenzymemia is a new syndrome that is characterized by a chronic increase of serum pancreatic enzymes in the absence of pancreatic disease. The aim of this study was to assess whether mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene may have a role in the etiology of this hyperenzymemia. METHODS: Seventy subjects with idiopathic pancreatic hyperenzymemia, 44 men and 26 women (mean age, 48 years; range, 8-74 years), were studied. Thirteen of these 70 subjects had the familial form of the syndrome. The mutation analysis of the CFTR gene was carried out using diagnostic commercial kits for the simultaneous detection of 29 mutations and Tn polymorphism. RESULTS: Among the 70 subjects studied, 7 (10.0%) had CFTR gene mutations. None of these 7 subjects had the familial form of pancreatic hyperenzymemia. These mutations were DeltaF 508 in 1 subject, 2789 + 5 G > A in another subject, and T5 allele in the remaining 5. All these mutations were heterozygous, with the exception of 1 T5 allele that was homozygous in 1 subject. CONCLUSIONS: The frequencies of the mutations of the CFTR gene found in these subjects are similar to the carrier frequencies in the general Italian population. This finding does not support a role for CFTR gene mutations in the etiology of idiopathic pancreatic hyperenzymemia.

Adolescent↗
PubMed2004

Tumor M2-pyruvate kinase, a new metabolic marker for pancreatic cancer.

An isoenzyme of pyruvate kinase (Tu M2-PK) is overexpressed by tumor cells and can be measured in blood by a specific immunoenzymatic assay. Our objective was to investigate the diagnostic value of Tu M2-PK in comparison with that of CA 19-9 in pancreatic cancer. We studied 265 subjects: 60 with histologically confirmed pancreatic cancer, 43 with benign pancreatic diseases (acute and chronic pancreatitis), 5 with benign cystic neoplasms of the pancreas, 9 with neuroendocrine tumors, 77 with other abdominal malignancies, 47 with benign digestive diseases, and 24 healthy controls. Levels of plasma Tu M2-PK and serum CA 19-9 were determined by commercially available specific immunoassays. The diagnostic sensitivity and specificity of Tu M2-PK for pancreatic cancer were 85 and 41%, respectively, while those of CA 19-9 were 75 and 81%. The combination of the two tests significantly increased sensitivity (97%) but lowered specificity (38%). In discriminating between pancreatic cancer and acute or chronic pancreatitis, Tu M2-PK turned out to be less accurate than CA 19-9. In patients without pancreatic tumor, cholestasis appeared not to affect the values of Tu M2-PK, while CA 19-9 was found to be significantly higher. Tu M2-PK was also abnormally high in the majority of patients with other digestive malignancies or neuroendocrine tumors. The results demonstrate that Tu M2-PK has a satisfactory sensitivity but a poor specificity in the diagnosis of pancreatic cancer. Used together with CA 19-9, the sensitivity increases considerably.

Acute Disease↗
PubMed2004

Does acute alcoholic pancreatitis precede the chronic form or is the opposite true? A histological study.

OBJECTIVES: Whether acute alcoholic pancreatitis occurs in a normal pancreas or in a pancreas that has already been altered by chronic pancreatitis is unclear. Our objective is to clarify the relation between acute and chronic alcoholic pancreatitis by histologic study of the pancreas in a group of patients having a first attack of acute alcoholic pancreatitis. METHODS: From January 1989 to December 1999, 138 patients with acute pancreatitis, of whom 28 had alcoholic pancreatitis, were seen by us; in 21 of the latter 28 patients, it was the first attack. Of these 21, 6 underwent surgery for acute necrotic pancreatitis. In all 6 patients, adequate pancreatic biopsies were obtained during surgery. Tissue samples were prepared for histologic examination according to standard procedures. RESULTS: In all 6 patients, both acute necrotic and chronic lesions were found. The chronic lesions had characteristics of chronic calcifying pancreatitis and consisted of perilobular and intralobular fibrosis. loss of exocrine parenchyma, dilated interlobular ducts, and protein plugs within dilated ducts. CONCLUSIONS: This study suggests that acute alcoholic pancreatitis develops in a pancreas already affected by chronic pancreatitis. The hypothesis that in alcoholics chronic pancreatitis derives from acute pancreatitis is not supported by the present data.

Acute Disease↗
PubMed2004

Exocrine pancreatic function after alcoholic or biliary acute pancreatitis.

OBJECTIVES: There have been various studies of exocrine pancreatic function after acute pancreatitis, but few have examined the relationship between this function and the etiology of the pancreatitis. The aim of this work was to study pancreatic function in patients who had had acute alcoholic or acute biliary pancreatitis. METHODS: Seventy-five patients who had had a single attack of acute pancreatitis were studied. The etiology was alcohol in 36 and cholelithiasis in 39. Pancreatic function was studied between 4 and 18 months after pancreatitis by duodenal intubation in 18 patients (8 alcohol, 10 lithiasis) and by the amino acid consumption test (AACT) in the remaining 57 (28 alcohol, 29 lithiasis). For those who underwent AACT, the test was repeated 1 year after the first examination. RESULTS: Among the 36 patients with alcoholic pancreatitis, most had impaired pancreatic function at both duodenal intubation (8/8, 100%) and at AACT (22/28, 78.6%); at the second test, the AACT remained pathological (18/23, 82.1%). Of the 39 patients with biliary pancreatitis, only 4 of the 10 (40%) who underwent duodenal intubation and only 5 of the 29 (17.2%) who performed AACT had pancreatic insufficiency; at the second test, only 4 of the 26 (15.4%) who repeated the AACT were pathological. The differences in the frequency and degree of pancreatic insufficiency between patients with alcoholic and those with biliary pancreatitis were statistically significant. CONCLUSIONS: The results show that after alcoholic acute pancreatitis, the pancreatic insufficiency was significantly more frequent and more severe than after biliary pancreatitis. These findings together with the fact that the insufficiency was also more persistent suggest that acute alcoholic pancreatitis may occur in a pancreas that already has chronic lesions.

Acute Disease↗
PubMed2003

Coagulative disorders in human acute pancreatitis: role for the D-dimer.

INTRODUCTION AND AIMS: We investigated coagulative disorders, particularly the role of the D-dimer, in acute pancreatitis where coagulation abnormalities related to disease severity are known to occur. METHODOLOGY: D-dimer levels in 30 patients with acute pancreatitis were evaluated; pancreatitis was mild and uncomplicated in 11 patients, accompanied by complications in 15, and severe in 4. We attempted to find a relationship between the D-dimer level and the antithrombin III level, prothrombin time, partial thromboplastin time, the C-reactive protein level, and results of routine laboratory tests. RESULTS: In the 11 patients with uncomplicated pancreatitis, the D-dimer level increased about 1.5 times over the limit, while in the 15 patients with complications and the four patients with severe pancreatitis, the D-dimer level increased about seven times above the normal limit; this difference was highly significant (p < 0.0001). The rise in the D-dimer level was inversely related to albumin and calcium levels (p = 0.0001) and directly related to the C-reactive protein level, fibrinogen level and leukocyte count (p = 0.0001), prothrombin time (p = 0.006), partial thromboplastin time (p = 0.03), and acute abdominal collections and lung involvement (p = 0.0001). The increase appeared early on, lasting for the entire study and peaking on days 3-6. CONCLUSIONS: The D-dimer is the expression of pancreatitis and the extension of systemic involvement; it may be considered a prominent link in the chain of events leading to severe disease.

Aged↗
PubMed2003

Mutations of the CFTR gene in pancreatic disease.

INTRODUCTION: An association has been found between CFTR gene mutations and chronic pancreatitis; however, there is a lack of information about the frequency of CFTR gene mutations in acute pancreatitis and in pancreatic cancer. AIM: To prospectively evaluate the prevalence of CFTR gene mutations in acute pancreatitis, chronic pancreatitis, and pancreatic cancer. METHODOLOGY: Ninety-eight consecutive patients were studied and divided into 3 groups: 34 patients with acute pancreatitis, 46 patients with chronic pancreatitis, and 18 patients with pancreatic cancer. The mutation analysis of the CFTR gene was carried out using diagnostic commercial kits for the simultaneous detection of 29 mutations and Tn polymorphism. RESULTS: Among the 98 patients studied, 12 (12.2%) had CFTR gene mutations: 2 of the 34 patients (5.9%) with acute pancreatitis, 9 of the 46 (19.6%) with chronic pancreatitis, and 1 of the 18 (5.6%) with pancreatic cancer. All the mutations were found in heterozygosis (2 DeltaF508, 1 W1282X, and 9 T5 allele). CONCLUSION: Our prospective study adds further information about the frequency of CFTR mutations in patients with a single episode of acute pancreatitis. Furthermore, our results suggest an association of CFTR gene mutations with chronic alcoholic pancreatitis and emphasize the need for a multicenter study, possibly multinational, to conclusively establish the role of CFTR mutations as a genetic susceptibility factor for this disease.

Acute Disease↗
PubMed2003

Nonfunctioning pancreatic endocrine tumors: a multicenter clinical study.

OBJECTIVES: Nonfunctioning pancreatic endocrine tumors (NFPTs) are rare neoplasms that have been the object of few studies that have involved only small numbers of patients. This study was carried out to obtain a comprehensive and up-to-date clinical picture of these tumors. METHODS: A total of 184 patients with NFPT admitted to three Italian hospitals in the last 15 yr were studied. The diagnosis of NFPT was confirmed histologically using conventional and immunohistochemical techniques. Data were obtained from the medical charts or directly from the patients. RESULTS: There were 85 men (46.2%) and 99 women (53.8%). The mean age at diagnosis was 55.2 yr (range 17-82 yr). The percentage of smokers and alcohol drinkers was similar to that in the general population. Seven patients (3.9%) had a family history of exocrine pancreatic carcinoma. In 120 cases (65.2%), the diagnosis was made after workup for pain or other symptoms, in the remaining 64 cases (34.8%), the tumor was discovered incidentally by ultrasound; in this group survival was significantly greater than it was for the symptomatic patients (p=0.0043). Survival was also found to be improved by tumor resection (p<0.0001), absence of metastases (p<0.0001), and small tumor size (< or =3 cm) (p<0.0007). CONCLUSIONS: NFPTs were slightly more frequent in women and were diagnosed most often in middle-aged individuals. No risk factors other than a family history of exocrine pancreatic carcinoma were found. Tumor discovery while patients were still asymptomatic, tumor resection, absence of metastases, and tumor size < or =3 cm significantly prolonged survival.

Adenoma, Islet Cell↗
PubMed2003

Effect of secretin on serum pancreatic enzymes and on the Wirsung duct in chronic nonpathological pancreatic hyperenzymemia.

AIM: Chronic nonpathological pancreatic hyperenzymemia (CNPH) is a new syndrome characterized by an increase in serum pancreatic enzymes in the absence of pancreatic disease. The aim of this study was to increase our understanding of this condition by determining the serum pancreatic enzyme response as well as changes in the caliber of the Wirsung duct after secretin stimulation. METHODS: Twenty subjects with CNPH and 9 healthy subjects without CNPH were studied. Blood samples were drawn 5 and 0 min before and 5, 10, 15, 30, 45, and 60 min after intravenous injection of secretin (1 U/kg). Amylase, pancreatic isoamylase, and lipase concentrations were determined. The caliber of the Wirsung duct was measured by ultrasonography. RESULTS: The injection of secretin caused a marked and statistically significant (p < 0.05) increase in serum pancreatic enzymes in the subjects with CNPH that persisted for the duration of the study. The increase over the basal value was in the range of 1.2- to 1.6-fold for amylase, 1.4- to 2.1-fold for pancreatic isoamylase, and 2.6- to 4.2-fold for lipase. In the control subjects the increase was mild, but statistically significant (p < 0.05), ranging from 1.1- to 1.2-fold for amylase, 1.2- to 1.4-fold for pancreatic isoamylase, and 1.5- to 2.2-fold for lipase. The injection of secretin caused a slight increase in the diameter of the Wirsung duct in both groups of subjects, but this was statistically significant only during the first 30 min of the study. CONCLUSIONS: The serum pancreatic enzyme response to secretin was more marked in CNPH than in controls. The Wirsung duct showed no alterations after secretin injection that would help to explain the hyperenzymemia.

Adult↗
PubMed2002

Impaired alveolar gas exchange in acute pancreatitis.

We evaluated the alveolar-arterial oxygen difference (deltaA-a) and the ratio between PaO2 and the fractional concentration of inspired oxygen (P/F) in acute pancreatitis. Eleven patients had mild uncomplicated disease, six showed acute abdominal fluid collections, six had acute abdominal collections and asymptomatic x-ray lung involvement, three presented transient dyspneic episodes, and four had severe acute pancreatitis requiring prolonged oxygen therapy. In the uncomplicated disease, respiratory function was normal; in the six patients with abdominal collections only, deltaA-a increased by 50% and P/F decreased by 20-30%; in the six patients with abdominal collections and asymptomatic x-ray lung involvement, deltaA-a increased by 50-70% and P/F decreased by 40%; the three patients with dyspneic episodes showed a twofold increase in deltaA-a and a 40% decrease in P/F; the four patients with severe pancreatitis had a two- to threefold increase in deltaA-a and a 40-50% decrease in P/F. Hence respiratory function is normal only in uncomplicated pancreatitis; in the presence of complications, disturbance of gas exchange always occurs, requiring careful control and treatment.

Abdominal Pain↗