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R de Franchis

Publications and source records attributed to R de Franchis.

At least 19 recordsLinked to original sources
PubMed1992

Changes of IgG-bearing cell populations in the portal tracts of patients with chronic liver disease of viral etiology: an evaluation by immunoperoxidase method and computerized image analysis.

Little is known about the distribution of IgG-bearing cell subpopulations in normal liver and their possible changes in disease conditions. We developed an immunohistochemical method that proved suitable and accurate for the identification and characterization of IgG-bearing cells and their subpopulations in liver specimens. The method uses specific monoclonal antibodies on serial mirror liver sections. We applied this method to four normal liver tissue specimens and 25 liver biopsy samples of chronic hepatitis of viral etiology. Only rare IgG-bearing cells could be observed in the portal tracts of normal liver specimens. In contrast, a dense infiltrate of such cells was seen in liver specimens from patients with chronic viral hepatitis. The density of IgG-bearing cells in such patients ranged from 6 to 20 cells x 10(-4) micron2 in the different specimens (mean = 11 x 10(-4) micron2). The increase in IgG-bearing cells did not appear to be related to the histological diagnosis, to the degree of histological inflammatory activity or to the type of viral infection. The major population of IgG-bearing cells consisted of IgG1-positive cells (68%); IgG2- (17%), IgG3- (8%) and IgG4 (7%)-bearing cells represented only minor fractions. The increased prevalence of IgG1-bearing cells observed in chronic hepatitis but not in normal liver specimens suggests that these findings may reflect an activation of antibody production directed toward viral antigens or antigenic structures of self. The identification of the antigenic specificities of the antibodies produced by IgG-bearing cells might provide important clues in understanding the pathogenesis of chronic viral hepatitis.

Biopsy, Needle↗
PubMed1992

Detection of liver involvement in inflammatory bowel disease by abdominal ultrasound scan.

Fifty patients with ulcerative colitis, 24 with Crohn's disease, and 50 controls were studied by liver function tests and abdominal ultrasound scan. Twenty-two percent of ulcerative colitis patients, 29% of Crohn's disease patients, and none of the controls showed abnormal liver function tests. All subjects with abnormal liver function tests also had changes in ultrasound liver scan, consisting of hepatomegaly and/or a dysechoic liver echo pattern. Furthermore, the same ultrasound changes were observed, in the absence of any liver function test abnormalities, in 58% of ulcerative colitis patients, 50% of Crohn's disease patients and 6% of controls (P less than 0.0005, inflammatory bowel disease versus controls). Overall, some evidence of liver involvement, as judged by abnormal liver tests and/or abnormal ultrasound liver scan, was detected in about 80% of inflammatory bowel disease patients. Six patients with minor abnormalities of liver function tests underwent liver biopsy and 5 of them had pericholangitis. Ultrasound liver scan may provide a useful tool to evaluate the occurrence of liver involvement in inflammatory bowel disease patients.

Adolescent↗
PubMed1992

Familial aggregation of inflammatory bowel disease in northern Italy: a multicenter study. The Gruppo di Studio per le Malattie Infiammatorie Intestinali (IBD Study Group).

To assess the familial aggregation of inflammatory bowel disease (IBD) in Italy, the family pedigrees of 411 patients with ulcerative colitis (UC) and 241 patients with Crohn's disease (CD) seen at 14 participating hospitals were studied. Sufficient information was obtained on 97% of 3752 first-degree relatives, 80% of 8869 second-degree relatives, and 74% of 5791 cousins. Thirty-six propositi (5.52%) had a total of 44 affected relatives (16 CD, 28 UC). The prevalence of IBD was higher in first- than in second-degree relatives and cousins (791, 112, and 163 in 100,000, respectively). A strong intrafamilial disease concordance was observed, with 26 cases of UC and 6 of CD among relatives of UC patients and 10 cases of CD and 2 of UC among relatives of CD patients. The prevalence of UC among first-degree relatives of UC patients and that of CD among first-degree relatives of CD patients was 680 and 531 in 100,000, respectively. In conclusion, there is a high degree of familial aggregation for IBD in Italy, with a strong intrafamilial disease concordance.

Adolescent↗
PubMed1992

Clinical variability of cardio-facio-cutaneous syndrome: report of two additional cases.

We describe two new cases of cardio-facio-cutaneous (CFC) syndrome, and underline the clinical variability of the CFC phenotype in our two patients presenting with border-line psychomotor development. The first patient showed some additional clinical manifestations, such as cryptorchidism and scoliosis, and the second one had atypical skin lesions.

Cryptorchidism↗
PubMed1992

Why do varices bleed?

About one third of cirrhotic patients with esophageal varices eventually bleed from ruptured varices. The incidence of rebleeding is extremely high during the first 6 weeks after the initial bleeding but declines gradually thereafter. Later, the rebleeding risk returns to baseline levels, i.e., equals that of patients who have never bled. The size of varices and the presence of red color signs on the variceal wall are recognized by most investigators as important in assessing the risk of variceal hemorrhage. Prognostic indexes such as the NIEC index, which incorporate the endoscopic signs with clinical data such as the Child-Pugh score, have been shown to predict the probability of first variceal hemorrhage of individual patients reliably. Other important parameters are the presence of ascites and, in alcoholic cirrhotics, the lack of abstinence from alcohol. The presence of endoscopic signs of bleeding or of stigmata of recent bleeding, of large varices, or of liver failure at the time of first bleeding are risk factors for early rebleeding. The most important risk factors for late rebleeding are the presence of large varices, overt signs of hepatic decompensation, the development of hepatocellular carcinoma, and lack of alcohol abstinence.

Endoscopy, Gastrointestinal↗
PubMed1991

Hepatocellular carcinoma in Italian patients with cirrhosis.

BACKGROUND AND METHODS: Patients with cirrhosis of the liver are recognized as being at risk for hepatocellular carcinoma. The magnitude of the risk, the natural history of this disease, and the possibilities for detecting potentially curable tumors in patients in the Western world are unknown. To address these questions, we examined 447 Italian patients with well-compensated cirrhosis (which was of viral origin in 62 percent of them) from 1985 through 1990, performing serum alpha-fetoprotein assays and real-time ultrasonography every 3 to 12 months. RESULTS: Hepatocellular carcinoma was found in 30 patients (7 percent) at base line and in another 29 patients (7 percent of 417 patients free of tumor at base line) during follow-up periods averaging 33 months (range, 1 to 48). The cumulative hazard of the development of hepatocellular carcinoma during follow-up was higher among patients with persistently elevated serum alpha-fetoprotein levels (12 with tumors among 42 with such levels) than among those with fluctuating levels (11 among 82) or those with consistently normal levels (6 among 255). Only 17 patients had potentially operable tumors. The proportion of potentially operable tumors among those detected during follow-up was significantly lower than the proportion at enrollment (4 of 29 vs. 13 of 30, P = 0.027). The survival at one year of the 12 patients who underwent surgery was 67 percent, and the tumor-recurrence rate was 60 percent. Outcome was not appreciably different for the five patients who refused surgery. CONCLUSIONS: In the West, as in Asia, patients with cirrhosis of the liver are at substantial risk for hepatocellular carcinoma, with a yearly incidence rate of 3 percent. Our screening program did not appreciably increase the rate of detection of potentially curable tumors.

Adult↗
PubMed1991

Risk of thromboembolic complications in patients with inflammatory bowel disease. Study of hemostasis measurements.

A large number of hemostasis measurements complications were performed in 20 patients with inflammatory bowel disease; whose changes have been associated with an increased risk of thromboembolic. Of the 20 patients, 9 (45%) had one or more changes suggestive of activation of the hemostatic system. Such changes were more frequently observed in patients with active disease. Two patients had changes in the fibrinolytic system (high plasminogen activator inhibitor-1 levels) and 2 in the natural anticoagulants (low antithrombin III activity). Nine patients had increased plasma fibrinogen levels and 6 patients had slightly increased levels of anticardiolipin antibodies. Most of the changes observed were not related to the type, location or activity of the disease. These data show that various biochemical abnormalities may be found in patients with inflammatory bowel disease, which may account for their increased risk of thrombosis, and suggest that multiple mechanisms may interact in determining such complications.

Adult↗
PubMed1991

Aldolase B mutations in Italian families affected by hereditary fructose intolerance.

Hereditary fructose intolerance (HFI) is an inborn error of metabolism caused by aldolase B deficiency. The aldolase B gene has been cloned and the following mutations causing HFI have been identified: A149P (a G----C transversion in exon 5), A174D (a C----A transversion in exon 5), L288 delta C (a base pair deletion in exon 8), and N334K (a G----C transversion in exon 9). We have investigated the occurrence of these mutations in 11 Italian patients affected by HFI using PCR and hybridisation to specific oligomers. We found that four patients were homozygous for the A149P mutation, two patients were homozygous for the A174D mutation, three patients were compound heterozygotes for both the A149P and A174D mutations, one patient was homozygous for the N334K mutation, and one patient did not show any of the reported mutations (HFI diagnosis carried out by aldolase B assay). The L288 delta C mutation has not been found in this survey.

Base Sequence↗
PubMed1990

Molecular analysis of aldolase B genes in hereditary fructose intolerance.

The molecular basis of hereditary fructose intolerance (HFI) was studied in 50 subjects (41 pedigrees, 82 apparently independent mutant alleles of aldolase B) by direct analysis of aldolase B genes amplified by means of the polymerase chain reaction. The mutation A149P (ala 149----pro) was found in 67% of alleles but was significantly more common in patients from northern than from southern Europe. Two other point mutations of aldolase B were identified. A174D (C----A; ala 174----asp) was found in subjects from Italy, Switzerland, and Yugoslavia (overall frequency 16%) but not in those from the United Kingdom, France, or the United States. L288 delta C carried a single base-pair deletion causing frameshift at codon 288 and was restricted to Sicilian subjects. By testing for these mutations in amplified DNA with a limited panel of allele-specific oligonucleotides, more than 95% of HFI patients will be susceptible to genetic diagnosis.

Alleles↗
PubMed1990

Gastric histology and function tests in Italian patients with dermatitis herpetiformis.

Gastric mucosal histology and function were evaluated in 57 Italian subjects with dermatitis herpetiformis (DH), by means of multiple endoscopic biopsies, gastrin and pepsinogen I (Pg I) serum levels, and parietal cell antibodies (PCA). One hundred and forty-nine patients with nonulcer dyspepsia served as reference population for the prevalence of atrophic gastritis of the body. Seventeen DH patients (30%) and 23 controls (15.4%) showed atrophic gastritis of the body mucosa (p less than 0.05). Nine of the DH patients with atrophic gastritis of the body also had atrophic changes in the antrum. Six patients, all with severe atrophic gastritis, had high gastrin levels and PCA; five of these six also had low Pg I levels. We found an increased prevalence of abnormal indirect function tests among patients with atrophic gastritis is due to the younger age of the patients in our series. Thus, atrophic gastritis can be detected early on a histologic basis, but functional impairment occurs later, as the mucosal damage increases in severity.

Adolescent↗
PubMed1989

Beta-blockade prevents recurrent gastrointestinal bleeding in well-compensated patients with alcoholic cirrhosis: a multicenter randomized controlled trial.

To assess the efficacy of beta-blockers in preventing rebleeding in selected cirrhotic patients and to compare the tolerance, safety and patient compliance of a selective and a nonselective beta-blocker, 94 patients were randomly assigned to propranolol (32 patients), atenolol (32 patients) or placebo (30 patients). Randomization was made at least 15 days after the bleeding episode. Propranolol was given orally at increasing doses until the resting pulse rate was reduced by approximately 25%. Atenolol was given at a fixed dose of 100 mg per day. Patients were followed up for a mean of 357 days. Rebleeding occurred in 14 patients in the placebo group, 10 in the atenolol group and eight in the propranolol group. The incidence of rebleeding was significantly lower in patients receiving propranolol than in those on placebo (propranolol vs. placebo: p = 0.01, logrank test). Atenolol was less effective than propranolol (atenolol vs. placebo: p = 0.065, logrank test). Bleeding-free survival was better for patients on active drugs than for those on placebo (propranolol vs. placebo = p = 0.01, atenolol vs. placebo: p = 0.05, logrank test). Retrospective analysis revealed that, whatever the type of treatment, abstinence from alcohol was crucial in preventing rebleeding. We conclude that beta-blocker treatment is effective in preventing rebleeding from esophageal varices in carefully selected alcoholic cirrhotic patients who survive at least 2 weeks after acute variceal hemorrhage and stop drinking.

Actuarial Analysis↗
PubMed1989

Evidence of altered structural and secretory glycoconjugates in the jejunal mucosa of patients with gluten sensitive enteropathy and subtotal villous atrophy.

The pattern of lectin histochemistry in formalin fixed, paraffin embedded normal jejunal and subtotal villous atrophy specimens from patients with gluten sensitive enteropathy were compared. There was no significant difference in the binding pattern of five lectins (Arachis hypogaea, Canavalia ensiformis, Lens culinaris, Phaseolus vulgaris and Triticum vulgaris) between normal and abnormal specimens. There were significant changes in the binding pattern of three lectins (Dolichos biflorus, Ulex europaeus, Ricinus communis), with special reference to goblet cells staining. These changes were present in all the specimens studied, regardless of the clinical diagnosis of dermatitis herpetiformis or coeliac disease. Dolichos biflorus reactive goblet cells were significantly decreased (p less than 0.001) in abnormal tissue and confined to the luminal edge of the mucosa. Strong reactivity of goblet cells in abnormal tissue was recorded with Ricinus communis and Ulex europaeus, lectins that bind to few or no goblet cells in normal tissue. These findings show that modifications of structural and secretory glycoconjugates occur in the jejunal mucosa of patients with gluten sensitive enteropathy.

Atrophy↗
PubMed1989

Beta-blockers in the secondary prevention of gastrointestinal haemorrhage in well-compensated cirrhotics. A multicentre randomised controlled study.

To assess the efficacy of beta-blockers in the prevention of rebleeding in selected cirrhotics and to compare the tolerability, safety of, and patient compliance with, a selective and a non-selective beta-blocker, 94 patients were randomly assigned to propranolol (32), atenolol (32), or placebo (30). Randomisation was made at least 15 days after the bleeding episode. Propranolol was given orally in increasing doses until the resting pulse rate was reduced by approximately 25%. Atenolol was given at a fixed dose of 100 mg/day. Patients were followed up for a mean of 357 days. Rebleeding occurred in 14 patients in the placebo group, 10 in the atenolol group and 8 in the propranolol group. The incidence of rebleeding was significantly lower in patients receiving propranolol than in those on placebo (PR vs PL: p less than 0.01, log-rank test). Atenolol was less effective than propranolol (AT vs PL: p = 0.065, log-rank test) but bleeding-free survival was improved for patients on active drugs compared with those patients on placebo (PR vs PL: p = 0.01; AT vs PL: p = 0.05, log-rank test). Retrospective analysis revealed that, whatever the type of treatment, abstinence from alcohol was crucial in preventing rebleeding. It was concluded that beta-blocker treatment is effective in preventing rebleeding from oesophageal varices in carefully selected alcoholic cirrhotics who survive at least 2 weeks after acute variceal haemorrhage and who cease drinking.

Adrenergic beta-Antagonists↗
PubMed1989

Esophageal motility in cirrhotics with and without esophageal varices.

Esophageal manometry was performed in 45 cirrhotics with varices, in 15 cirrhotics without varices, and in 20 normal subjects, to define the effect of varices on esophageal motility. Cirrhotics with varices showed a decreased amplitude of motor waves in the lower half of the esophagus (p less than 0.01), an increased duration of primary peristaltic waves along the entire length of the esophagus (upper esophagus, p less than 0.05; lower esophagus, p less than 0.01), and an increased peak-to-peak speed of primary peristaltic waves (p less than 0.01). Resting lower esophageal sphincter pressure and duration of sphincter relaxation were similar in patients and controls. The above-mentioned abnormalities might be due to the mechanical effect of the presence of varices.

Adolescent↗
PubMed1988

Ultrasound-assisted percutaneous liver biopsy: superiority of the Tru-Cut over the Menghini needle for diagnosis of cirrhosis.

A total of 1192 consecutive patients with diffuse liver disease were randomized to have percutaneous liver biopsy specimens taken with the Menghini or the Tru-Cut needle, to compare tissue yield, safety, and accuracy of the two needles for diagnosing cirrhosis. The sites of puncture were determined by prebiopsy ultrasound scans. Adequate samples were obtained from 94% with the Tru-Cut needle and from 79.2% with the Menghini needle (p less than 0.001). Accuracy in diagnosing cirrhosis was 89.5% for the Tru-Cut needle and 65.5% for the Menghini needle (p less than 0.05). Complication rates were very low and similar for both needles. Under these conditions, the Tru-Cut needle is superior to the Menghini needle for diagnosing cirrhosis.

Biopsy, Needle↗
PubMed1987

Evaluation of structural and secretory glycoconjugates in normal human jejunum by means of lectin histochemistry.

The labelling pattern of eight lectins was studied in jejunal samples from ten normal subjects, in order to define the normal distribution of structural and secretory glycoconjugates in the small bowel. The following lectins were studied by means of a peroxidase technique on formalin-fixed samples: Arachis hypogaea, Ricinus communis, Canavalia ensiformis, Lens culinaris, Phaseolus vulgaris, Triticum vulgaris, Ulex europaeus, Dolichos biflorus. Phaseolus vulgaris reacted with goblet cell mucus throughout the villus-crypt axis. Conversely Ulex europaeus, Dolichos biflorus and Triticum vulgaris lectin labelling of goblet cells appeared to be confined to the upper part of the villi. This finding suggests that during cell migration from crypt to villus tip, the continuing maturation of goblet cells is associated with the differentiation of secretory carbohydrates, which probably parallels the cell maturation cycle. Lectin histochemistry appears to be a reliable tool for the study of structural and secretory glycoconjugates in the jejunal mucosa, and might be of value in the study of diseases in which the cell-maturation cycle in the small bowel is altered.

Concanavalin A↗