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| 1 | Understanding and treating refractory constipation显示文摘Chronic constipation is a frequently encountered disorder in clinical practice. Most constipated patients benefit from standard medical approaches. However, current therapies may fail in a proportion of patients. These patients deserve better evaluation and thorough investigations before their labeling as refractory to treatment. Indeed, several cases of apparent refractoriness are actually due to misconceptions about constipation, poor basal evaluation (inability to recognize secondary causes of constipation, use of constipating drugs) or inadequate therapeutic regimens. After a careful reevaluation that takes into account the above factors, a certain percentage of patients can be defined as being actually resistant to first-line medical treatments. These subjects should firstly undergo specific diagnostic examination to ascertain the subtype of constipation. The subsequent therapeutic approach should be then tailored according to their underlying dysfunction. Slow transit patients could benefit from a more robust medical treatment, based on stimulant laxatives (or their combination with osmotic laxatives, particularly over the short-term), enterokinetics (such as prucalopride) or secretagogues (such as lubiprostone or linaclotide). Patients complaining of obstructed defecation are less likely to show a response to medical treatment and might benefit from biofeedback, when available. When all medical treatments prove to be unsatisfactory, other approaches may be attempted in selected patients (sacral neuromodulation, local injection of botulinum toxin, anterograde continence enemas), although with largely unpredictable outcomes. A further although irreversible step is surgery (subtotal colectomy with ileorectal anastomosis or stapled transanal rectal resection), which may confer some benefit to a few patients with refractoriness to medical treatments. | Gabrio Bassotti Corrado Blandizzi | 2014 | World Journal of Gastrointestinal Pharmacology and Therapeutics2014，5，2： | 23 |
| 2 | Lansoprazole prevents experimental gastric injury induced by non-steroidal anti-inflammatory drugs through a reduction of mucosal oxidative damage显示文摘AIM: This study investigated the mechanisms of protection afforded by the proton pump inhibitor lansoprazole against gastric injury induced by different non-steroidal antiinflammatory drugs (NSAIDs) in rats.METHODS: Male Sprague-Dawley rats were orally treated with indomethacin (100 μmol/kg), diclofenac (60 μmol/kg),piroxicam (150 μmol/kg) or ketoprofen (150 μmol/kg).Thirty minutes before NSAIDs, animals were orally treated with lansoprazole 18 or 90 μmol/kg. Four hours after the end of treatments, the following parameters were assessed: gastric mucosal PGE2, malondialdehyde (MDA), myeloperoxidase (MPO) or non-proteic sulfhydryl compounds (GSH) levels; reverse transcription-polymerase chain reaction (RT-PCR) of mucosal COX-2 mRNA; gastric acid secretion in pylorus-ligated animals; in vitro effects of lansoprazole (1-300 μmol/L) on the oxidation of low density lipoproteins (LDLs) induced by copper sulphate.RESULTS: All NSAIDs elicited mucosal necrotic lesions which were associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels were detected in the gastric mucosa of indomethacin- or piroxicam-treated animals. Indomethacin enhanced mucosal cyclooxygenase-2 expression, while not affecting cyclooxygenase-1. At the oral dose of 18 μmol/kg lansoprazole partly counteracted diclofenac-induced mucosal damage, whereas at 90 μmol/kg it markedly prevented injuries evoked by all test NSAIDs. Lansoprazole at 90 μmol/kg reversed also the effects of NSAIDs on MPO, MDA and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced cyclooxygenase-2 expression. However, both lansoprazole doses markedly inhibited acid secretion in pylorus-ligated rats. Lansoprazole concentration-dependently reduced the oxidation of LDLs in vitro.CONCLUSION: These results suggest that, besides the inhibition of acid secretion, lansoprazole protection against NSAID-induced gastric damage depends on a reduction in mucosal oxidative injury, which is also responsible for an increment of sulfhydryl radical bioavailability. It is also suggested that lansoprazole does not influence the downregulation of gastric prostaglandin production associated with NSAID treatment. | Corrado Blandizzi Matteo Fornai Rocchina Colucci Gianfranco Natale Valter Lubrano Cristina Vassalle Luca Antonioli Gloria Lazzeri Mario Del Tacca | 2005 | World Journal of Gastroenterology2005，11，26： | 9 |
| 3 | Overlap of functional heartburn and gastroesophageal reflux disease with irritable bowel syndrome显示文摘Several studies indicate a significant degree of overlap between irritable bowel syndrome(IBS)and gastroesophageal reflux disease(GERD).Likewise,both functional heartburn(FH)and IBS are functional digestive disorders that may occur in the same patients.However,data establishing a solid link between FH and IBS are lacking,mainly because the clinical definition of FH has undergone substantial changes over the years.The available literature on the overlap between GERD or FH and IBS highlights considerable heterogeneity in terms of the criteria and diagnostic procedures used to assess heartburn and IBS.In particular,several epidemiological studies included patients with concomitant IBS and GERD without any attempt to distinguish FH(as defined by the RomeⅢcriteria)from GERD via pathophysiological investigations.Independent of these critical issues,there is preliminary evidence supporting a significantdegree of FH-IBS overlap.This underscores the need for studies based on updated diagnostic criteria and accurate pathophysiological classifications,particularly to distinguish FH from GERD.This distinction would represent an essential starting point to achieving a better understanding of pathophysiology in the subclasses of patients with GERD and FH and properly assessing the different degrees of overlap between IBS and the subcategories of heartburn.The present review article intends to appraise and critically discuss current evidence supporting a possible concomitance of GERD or FH with IBS in the same patients and to highlight the pathophysiological relationships between these disorders. | Nicola de Bortoli Irene Martinucci Massimo Bellini Edoardo Savarino Vincenzo Savarino Corrado Blandizzi Santino Marchi | 2013 | World Journal of Gastroenterology2013，19，35： | 9 |
| 4 | Intestinal epithelial barrier and neuromuscular compartment in health and disease显示文摘A number of digestive and extra-digestive disorders,including inflammatory bowel diseases,irritable bowel syndrome,intestinal infections,metabolic syndrome and neuropsychiatric disorders,share a set of clinical features at gastrointestinal level,such as infrequent bowel movements,abdominal distension,constipation and secretory dysfunctions.Several lines of evidence indicate that morphological and molecular changes in intestinal epithelial barrier and enteric neuromuscular compartment contribute to alterations of both bowel motor and secretory functions in digestive and extra-digestive diseases.The present review has been conceived to provide a comprehensive and critical overview of the available knowledge on the morphological and molecular changes occurring in intestinal epithelial barrier and enteric neuromuscular compartment in both digestive and extra-digestive diseases.In addition,our intent was to highlight whether these morphological and molecular alterations could represent a common path(or share some common features)driving the pathophysiology of bowel motor dysfunctions and related symptoms associated with digestive and extra-digestive disorders.This assessment might help to identify novel targets of potential usefulness to develop original pharmacological approaches for the therapeutic management of such disturbances. | Vanessa D’Antongiovanni Carolina Pellegrini Matteo Fornai Rocchina Colucci Corrado Blandizzi Luca Antonioli Nunzia Bernardini | 2020 | World Journal of Gastroenterology2020，26，14： | 6 |
| 5 | Constipation,deficit in colon contractions and alpha-synuclein inclusions within the colon precede motor abnormalities and neurodegeneration in the central nervous system in a mouse model of alphasynucleinopathy显示文摘Background:Gastrointestinal dysfunction can affect Parkinson’s disease(PD)patients long before the onset of motor symptoms.However,little is known about the relationship between gastrointestinal abnormalities and the development of PD.Contrary to other animal models,the human A53T alpha-synuclein(αS)transgenic mice,Line G2–3,developsαS-driven neurological and motor impairments after 9 months of age,displaying a long presymptomatic phase free of central nervous system(CNS)dysfunction.Methods:To determine whether this line can be suitable to study constipation as it occurs in prodromal PD,gastrointestinal functionality was assessed in young mice through a multidisciplinary approach,based on behavioral and biochemical analysis combined with electrophysiological recordings of mouse intestinal preparations.Results:We found that the A53TαS mice display remarkable signs of gastrointestinal dysfunction that precede motor abnormalities andαS pathology in the CNS by at least 6 months.YoungαS mice show a drastic delay in food transit along the gastrointestinal tract,of almost 2 h in 3 months old mice that increased to more than 3 h at 6 months.Such impairment was associated with abnormal formation of stools that resulted in less abundant but longer pellets excreted,suggesting a deficit in the intestinal peristalsis.In agreement with this,electrically evoked contractions of the colon,but not of the ileum,showed a reduced motor response in both longitudinal and circular muscle layers inαS mice already at 3 months of age,that was mainly due to an impaired cholinergic transmission of the underlying enteric nervous system.Interestingly,the presence of insoluble and aggregatedαS was found in enteric neurons in both myenteric and submucosal plexi only in the colon of 3 months oldαS mice,but not in the small intestine,and exacerbated with age,mimicking the increase in transit delay and the contraction deficit showed by behavioral and electrical recordings data.Conclusions:Gastrointestinal dysfunction in A53TαS mice represents an early sign ofαS-driven pathology without concomitant CNS involvement.We believe that this model can be very useful to study disease-modifying strategies that could extend the prodromal phase of PD and haltαS pathology from reaching the brain. | Lucia Rota Carolina Pellegrini Laura Benvenuti Luca Antonioli Matteo Fornai Corrado Blandizzi Antonino Cattaneo Emanuela Colla | 2019 | Translational Neurodegeneration2019，8，1： | 5 |
| 6 | NKG2A and COVID-19: another brick in the wall显示文摘Coronavirus disease 2019(COVID-19)is a viral infection caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2;formerly designated as 2019-nCoV),a novel betacoronavirus firstly identified during a burst of respiratory illness cases in Wuhan City,Hubei Province,China.1 Unfortunately,within a few weeks,the SARS-COV2 virus started to spread globally,producing a pandemic of an extremely spreadable and potentially fatal disease,becoming a cause of great concern for global public health.1 Despite the current estimates of COVID-19 case fatality rate suggest that this coronavirus is less deadly than other pathogens driving other large-scale outbreaks,such as SARS,Middle East respiratory syndrome,or Ebola,the main concern is that this infection is able to spread more easily than other diseases,including seasonal influenza. | Luca Antonioli Matteo Fornai Carolina Pellegrini Corrado Blandizzi | 2020 | Cellular & Molecular Immunology2020，17，6： | 3 |
| 7 | Serotonin receptors and their role in the pathophysiology and therapy of irritable bowel syndrome显示文摘 | C. Stasi M. Bellini G. Bassotti C. Blandizzi S. Milani | 2014 | Techniques in Coloproctology2014，，7： | 2 |
| 8 | Protective action of omeprazole against gastric mucusal injury induced by hemorrhagic shock in rats显示文摘 | Blandizzi C Gherardi G Natale G | 1996 | Dig Dis Sci1996，39，10： | 1 |
| 9 | Safe prescribing of non-steroidal anti-inflammatory drugs in patients with osteoarthritis-an expert consensus addressing benefits as well as gastrointestinaland cardiovascular risks显示文摘 | Scarpignato C Lanas A Blandizzi C | 2015 | BMC Med2015，13，1： | 1 |
| 10 | Anti-TNF agents as therapeutic choice in immune-mediated inflammatory diseases: focus on adalimumab 显示文摘 | Armuzzi A Lionetti P Blandizzi C | 2014 | Int J Immunopathol Pharmacol2014，27，1： | 1 |
| 11 | Macrolide antibiotics as anti - inflammatory agents : roxithromycin in an unexpected role 显示文摘 | Agen C Danesi R Blandizzi C | 1993 | Agents Actions1993，30，1： | 1 |
| 12 | Anti-TNF agents as therapeutic choice in immune-mediated inflammatory diseases: focus on adalimumab 显示文摘 | Armuzzi A Lionetti P Blandizzi C | 2014 | J Immunopathol Pharmacol2014，27，1： | 1 |
| 13 | Gastrin promotes humancolon cancer cell growth via CCK-2 receptor-mediated cyclooxygen-ase-2 induction and prostaglandin E2 production 显示文摘 | Colucci R Blandizzi C Tanini M | 2005 | Br J Pharma-col2005，144，3： | 1 |
| 14 | Clinical efficacy of esome- prazole in the prevention and healing of gastrointestinal toxicity as- sociated with NSAIDs in elderly patients 显示文摘 | Blandizzi C Tuccori M Colucci R | 2008 | Drugs Aging2008，25，3： | 1 |
| 15 | Clinical efficacy of esomeprazole in the prevention and healing of gastrointestinal toxicity associated with NSAIDs in elderly patients显示文摘 | Blandizzi C Tuccori M Colucci R | 2008 | Drugs Aging2008，25，3： | 1 |
| 16 | Role of coxibs in the strategies for gastrointestinal protection in patients requiring chronic non-steroidal anti-inflammatory therapy显示文摘 | Corrado Blandizzi Marco Tuccori Rocchina Colucci Matteo Fornai Luca Antonioli Narcisa Ghisu Mario Del Tacca | 2008 | Pharmacological Research2008，，2： | 1 |
| 17 | Macrolide antibiotics as anti-inflammatory agents:roxithromycin in an unexpected role显示文摘 | AGEN C DANESI R BLANDIZZI C | 1993 | Agents Actions1993，30，1： | 1 |
| 18 | Platelet sero- tonint transporter in patients with diarrhea predomi- nant irritable bowel syndrome both before and after treatment with alosetron 显示文摘 | Bellini M Rappelli L Blandizzi C | 2003 | Am J Gastroenterol2003，98，12： | 1 |
| 19 | Emerging role of cyclooxygenase isoforms in the control of gastrointestinal neuromuscular functions显示文摘 | Matteo Fornai Luca Antonioli Rocchina Colucci Nunzia Bernardini Narcisa Ghisu Marco Tuccori Roberto De Giorgio Mario Del Tacca Corrado Blandizzi | 2009 | Pharmacology and Therapeutics2009，，1： | 1 |
| 20 | The pharmacokinetics of ilaprazole for gastro-esophageal reflux treatment显示文摘 | Nicola de Bortoli Irene Martinucci Maria Giacchino Corrado Blandizzi Santino Marchi Vincenzo Savarino Edoardo Savarino | 2013 | Expert Opinion on Drug Metabolism & Toxicology2013，，10： | 1 |
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