Gerardo Nardone

Prof. Dr. Gerardo Nardone

orcid

Research Focus & Metrics

Academic Career Length

44Years (1983-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
1 June 2012 in Nutrition, Metabolism and Cardiovascular Diseases
Verified
Journal Article
Closed access
DCDebora Compare
Debora Compare
PCP. Coccoli
P. Coccoli
ARAlba Rocco
Alba Rocco
ONO.M. Nardone
O.M. Nardone
SMS. De Maria
S. De Maria
GNGerardo Nardone
Gerardo Nardone

1 June 2015 in United European Gastroenterology Journal
Verified
Journal Article
Open access
GNGerardo Nardone
Gerardo Nardone
DCDebora Compare
Debora Compare
Introduction: Although long thought to be a sterile organ, due to its acid production, the human stomach holds a core microbiome.Aim: To provide an update of findings related to gastric microbiota and its link with gastric diseases.Methods: We conducted a systematic review of the literature.Results: The development of culture‐independent methods facilitated the identification of many bacteria. Five major phyla have been detected in the stomach: Firmicutes, Bacteroidites, Actinobacteria, Fusobacteria and Proteobacteria. At the genera level, the healthy human stomach is dominated by Prevotella, Streptococcus, Veillonella, Rothia and Haemophilus; however, the composition of the gastric microbiota is dynamic and affected by such factors as diet, drugs and diseases. The interaction between the pre‐existing gastric microbiota and Helicobacter pylori infection might influence an individual's risk of gastric disease, including gastric cancer.Conclusions: The maintenance of bacterial homeostasis could be essential for the stomach's health and highlights the chance for therapeutic interventions targeting the gastric microbiota, even if gastric pH, peristalsis and the mucus layer may prevent bacteria colonization; and the definition of gastric microbiota of the healthy stomach is still an ongoing challenging task.

1 January 2014 in World Journal of Gastroenterology
Verified
Journal Article
Open access
ARAlba Rocco
Alba Rocco
DCDebora Compare
Debora Compare
DADebora Angrisani
Debora Angrisani
MZMarco Sanduzzi Zamparelli
Marco Sanduzzi Zamparelli
GNGerardo Nardone
Gerardo Nardone
The harmful use of alcohol is a worldwide problem. It has been estimated that alcohol abuse represents the world’s third largest risk factor for disease and disability; it is a causal factor of 60 types of diseases and injuries and a concurrent cause of at least 200 others. Liver is the main organ responsible for metabolizing ethanol, thus it has been considered for long time the major victim of the harmful use of alcohol. Ethanol and its bioactive products, acetaldehyde-acetate, fatty acid ethanol esters, ethanol-protein adducts, have been regarded as hepatotoxins that directly and indirectly exert their toxic effect on the liver. A similar mechanism has been postulated for the alcohol-related pancreatic damage. Alcohol and its metabolites directly injure acinar cells and elicit stellate cells to produce and deposit extracellular matrix thus triggering the “necrosis-fibrosis” sequence that finally leads to atrophy and fibrosis, morphological hallmarks of alcoholic chronic pancreatitis. Even if less attention has been paid to the upper and lower gastrointestinal tract, ethanol produces harmful effects by inducing: (1) direct damaging of the mucosa of the esophagus and stomach; (2) modification of the sphincterial pressure and impairment of motility; and (3) alteration of gastric acid output. In the intestine, ethanol can damage the intestinal mucosa directly or indirectly by altering the resident microflora and impairing the mucosal immune system. Notably, disruption of the intestinal mucosal barrier of the small and large intestine contribute to liver damage. This review summarizes the most clinically relevant alcohol-related diseases of the digestive tract focusing on the pathogenic mechanisms by which ethanol damages liver, pancreas and gastrointestinal tract.

7 December 2021 in Gut
Verified
Journal Article
Closed access
PDF file
AVAlessandro Vitale
Alessandro Vitale
Gianluca Svegliati-BaroniGianluca Svegliati-Baroni
Gianluca Svegliati-Baroni
AOAlessio Ortolani
Alessio Ortolani
MCMonica Cucco
Monica Cucco
GRGiulio V Dalla Riva
Giulio V Dalla Riva
FFFabio Farinati
Fabio Farinati
Background Metabolic dysfunction-associated fatty liver disease (MAFLD) represents a new inclusive definition of the whole spectrum of liver diseases associated to metabolic disorders. The main objective of this study was to compare patients with MAFLD and non-MAFLD with hepatocellular carcinoma (HCC) included in a nationally representative cohort. Methods We analysed 6882 consecutive patients with HCC enrolled from 2002 to 2019 by 23 Italian Liver Cancer centres to compare epidemiological and future trends in three subgroups: pure, single aetiology MAFLD (S-MAFLD); mixed aetiology MAFLD (metabolic and others, M-MAFLD); and non-MAFLD HCC. Results MAFLD was diagnosed in the majority of patients with HCC (68.4%). The proportion of both total MAFLD and S-MAFLD HCC significantly increased over time (from 50.4% and 3.6% in 2002–2003, to 77.3% and 28.9% in 2018–2019, respectively, p<0.001). In Italy S-MAFLD HCC is expected to overcome M-MAFLD HCC in about 6 years. Patients with S-MAFLD HCC were older, more frequently men and less frequently cirrhotic with clinically relevant portal hypertension and a surveillance-related diagnosis. They had more frequently large tumours and extrahepatic metastases. After weighting, and compared with patients with non-MAFLD, S-MAFLD and M-MAFLD HCC showed a significantly lower overall (p=0.026, p=0.004) and HCC-related (p<0.001, for both) risk of death. Patients with S-MAFLD HCC showed a significantly higher risk of non-HCC-related death (p=0.006). Conclusions The prevalence of MAFLD HCC in Italy is rapidly increasing to cover the majority of patients with HCC. Despite a less favourable cancer stage at diagnosis, patients with MAFLD HCC have a lower risk of HCC-related death, suggesting reduced cancer aggressiveness.

1 March 2000 in Gut
Verified
Journal Article
Open access
PDF file
PMP Martinelli
P Martinelli
RTR Troncone
R Troncone
FPF Paparo
F Paparo
PTP Torre
P Torre
ETE Trapanese
E Trapanese
LGL Greco
L Greco
BACKGROUND Up to 50% of women with untreated coeliac disease experience miscarriage or an unfavourable outcome of pregnancy. In most cases, after 6–12 months of a gluten free diet, no excess of unfavourable outcome of pregnancy is observed. The prevalence of undiagnosed coeliac disease among pregnant women is not known. AIM To determine the prevalence of untreated coeliac disease among women attending the obstetrics-gynaecological department. METHODS Endomysial antibodies, which are specific and sensitive for coeliac disease, were evaluated in all women attending the obstetrics-gynaecology department of a large city hospital over a 90 day period. RESULTS Of 845 pregnant women screened, 12 were identified as having coeliac disease. Three had previously been diagnosed but were not following a gluten free diet. The remaining nine underwent a small intestinal biopsy, which confirmed the diagnosis. The outcome of pregnancy was unfavourable in seven of these 12 women. Six healthy babies were born with no problems after the women had been on a gluten free diet for one year. CONCLUSIONS Overall, 1 in 70 women was affected by coeliac disease, either not diagnosed (nine cases) or not treated (three cases). Their history of miscarriages, anaemia, low birth weight babies, and unfavourable outcome of pregnancy suggests that testing for coeliac disease should be included in the battery of tests prescribed for pregnant women. Coeliac disease is considerably more common than most of the diseases for which pregnant women are routinely screened. Unfavourable events associated with coeliac disease may be prevented by a gluten free diet.

1 November 1999 in Alimentary Pharmacology & Therapeutics
Verified
Journal Article
Open access
PDF file
GNGerardo Nardone
Gerardo Nardone
ARAlba Rocco
Alba Rocco
TBT Balzano
T Balzano
GBG Budillon
G Budillon
Background: : The treatment of angiodysplasia and watermelon stomach, vascular abnormalities implicated in gastrointestinal bleeding of obscure origin, is a major clinical problem.Aim: : To determine the efficacy of octreotide in patients with long‐standing gastrointestinal bleeding due to acquired angiodysplasia and watermelon stomach, resistant to previous treatments and not suitable for surgery because of old age and/or concomitant disorders.Patients and methods: : We treated 17 patients (seven had isolated angiodysplasia, seven had multiple upper and lower gastrointestinal angiodysplasia, and three had watermelon stomach) with octreotide (0.1 mg subcutaneous t.d.s. for 6 months). Six of the patients had liver cirrhosis, one had Glanzmann‐type platelet derangement, two had cardiovascular diseases and one had chronic uraemia.Results: : Octreotide treatment stopped bleeding in 10 patients. A transient improvement was observed in four, who needed subsequent cyclical retreatment to correct low haemoglobin levels. No effect was observed in three, probably due to the severity of the concomitant disorders.Conclusions: : Octreotide is a safe drug that may be useful to control the recurrent gastrointestinal bleeding due to acquired angiodysplasia and watermelon stomach, especially in patients who are not candidates for surgery due to old age and/or concomitant disorders.