piperidines and Ulcer

piperidines has been researched along with Ulcer* in 10 studies

Reviews

3 review(s) available for piperidines and Ulcer

ArticleYear
Gastrointestinal: Refractory parastomal ulcers of Behcet's disease responsive to tofacitinib.
    Journal of gastroenterology and hepatology, 2023, Volume: 38, Issue:4

    Topics: Behcet Syndrome; Humans; Piperidines; Pyrimidines; Ulcer

2023
Case report: Refractory intestinal Behçet's syndrome successfully treated with tofacitinib: A report of four cases.
    Frontiers in immunology, 2022, Volume: 13

    Behçet's syndrome (BS) is a chronic form of relapsing multisystem vasculitis, characterized by recurrent oral and genital ulcers. Intestinal BS is a special type of BS. Volcano-shaped ulcers in the ileocecum are a typical finding of intestinal BS, and punched-out ulcers can be observed in the intestine or esophagus. At present, there is no recognized radical treatment for intestinal BS. Glucocorticoids and immunosuppressants are currently the main drugs used to improve the condition. Although it has been reported that monoclonal anti-TNF antibodies may be effective for some refractory intestinal BS, further randomized, prospective trials are necessary to confirm these findings. Some patients are restricted from using biological agents because of serious allergic reactions of drugs, inconvenient drug injections or the impact of the novel coronavirus epidemic. If endoscopic remission (endoscopic healing) is not achieved for a prolonged period of time, serious complications, such as perforation, fistula formation, and gastrointestinal bleeding can be induced. Therefore, it is necessary to develop new treatment methods for controlling disease progression. We reviewed the relevant literature, combined with the analysis of the correlation between the pathogenesis of BS and the mechanism of Janus kinase (JAK) inhibition, and considered that tofacitinib (TOF) may be effective for managing refractory intestinal BS. We report for the first time that four patients with severe refractory intestinal BS were successfully treated with TOF. We hope to provide valuable information on JAK inhibitors as potential therapeutic targets for the treatment of severe refractory intestinal BS.

    Topics: Antibodies, Monoclonal; Behcet Syndrome; Biological Factors; COVID-19; Humans; Immunosuppressive Agents; Intestines; Janus Kinase Inhibitors; Janus Kinases; Piperidines; Prospective Studies; Pyrimidines; Tumor Necrosis Factor Inhibitors; Ulcer

2022
Influence of pathophysiology, severity, and cost on the medical management of gastroesophageal reflux disease.
    American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists, 1996, Nov-15, Volume: 53, Issue:22 Suppl 3

    This article summarizes the pathophysiology of gastroesophageal reflux disease (GERD) and the wide spectrum in disease and symptom severity as they influence the selection of cost-effective treatment strategies. The vast majority of patients with GERD have mild symptoms, no gross endoscopic evidence of esophagitis, and little risk of developing complications. More than 85% of patients with GERD symptoms have uncomplicated disease. Diffuse ulcerations or complications (grade III or IV esophagitis) occur in only 3.5% of patients < 65 years of age. However, some patients with GERD can develop severe complications, including esophageal obstruction, significant blood loss, and, in rare circumstances, perforation. Furthermore, adenocarcinoma of the esophagus, which is increasing in incidence faster than any other cancer, is caused by GERD. Although severe ulcerations are uncommon in young patients, they occur in 20-30% of patients over age 65. Patients with ulcerative esophagitis are not only more prone to develop complications, they are also more resistant to treatment. Cost-effective medical management of GERD must take into account the wide spectrum of symptom and disease severity. Therapy consists of both nonpharmacologic treatment and the appropriate use of medications from several classes of drugs, either alone or in combination. Traditionally, prokinetic agents or histamine receptor antagonists have been used as primary therapy; proton-pump inhibitors are reserved for more resistant cases. The rationale for this and for alternative approaches is discussed.

    Topics: Aged; Anti-Ulcer Agents; Cisapride; Drug Interactions; Drug Therapy, Combination; Esophagitis, Peptic; Gastroesophageal Reflux; Histamine H2 Antagonists; Humans; Metoclopramide; Omeprazole; Piperidines; Serotonin Antagonists; Ulcer

1996

Other Studies

7 other study(ies) available for piperidines and Ulcer

ArticleYear
Multiple esophageal ulcers due to tofacitinib 10 mg twice daily for ulcerative colitis.
    Clinical journal of gastroenterology, 2020, Volume: 13, Issue:3

    A 26-year-old man was admitted to our institution for ulcerative colitis treatment. He used mesalamine, steroid, immunomodulators, and anti-TNFα anti-body, but it was difficult to maintain remission. We started induction therapy with tofacitinib (TOF) 10 mg twice daily. He maintained clinical remission but had chest pain 44 days after the start of TOF. Esophagogastroduodenoscopy showed multiple ulcers from middle to lower esophagus. Although rare, TOF induced esophageal ulcers were considered based on his clinical course and endoscopic findings.

    Topics: Adult; Colitis, Ulcerative; Esophageal Diseases; Esophagoscopy; Esophagus; Humans; Male; Piperidines; Protein Kinase Inhibitors; Pyrimidines; Ulcer

2020
Anti-Ulcer Efficacy of Soluble Epoxide Hydrolase Inhibitor TPPU on Diclofenac-Induced Intestinal Ulcers.
    The Journal of pharmacology and experimental therapeutics, 2016, Volume: 357, Issue:3

    Proton pump inhibitors such as omeprazole (OME) reduce the severity of gastrointestinal (GI) ulcers induced by nonsteroidal anti-inflammatory drugs (NSAIDs) but can also increase the chance of dysbiosis. The aim of this study was to test the hypothesis that preventive use of a soluble epoxide hydrolase inhibitor (sEHI) such as TPPU can decrease NSAID-induced ulcers by increasing anti-inflammatory epoxyeicosatrienoic acids (EETs). Dose- [10, 30, and 100 mg/kg, by mouth (PO)] and time-dependent (6 and 18 hours) ulcerative effects of diclofenac sodium (DCF, an NSAID) were studied in the small intestine of Swiss Webster mice. Dose-dependent effects of TPPU (0.001-0.1 mg/kg per day for 7 days, in drinking water) were evaluated in DCF-induced intestinal toxicity and compared with OME (20 mg/kg, PO). In addition, the effect of treatment was studied on levels of Hb in blood, EETs in plasma, inflammatory markers such as myeloperoxidase (MPO) in intestinal tissue homogenates, and tissue necrosis factor-α (TNF-α) in serum. DCF dose dependently induced ulcers that were associated with both a significant (P < 0.05) loss of Hb and an increase in the level of MPO and TNF-α, with severity of ulceration highest at 18 hours. Pretreatment with TPPU dose dependently prevented ulcer formation by DCF, increased the levels of epoxy fatty acids, including EETs, and TPPU's efficacy was comparable to OME. TPPU significantly (P < 0.05) reversed the effect of DCF on the level of Hb, MPO, and TNF-α Thus sEHI might be useful in the management of NSAID-induced ulcers.

    Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Cytoprotection; Diclofenac; Enzyme Inhibitors; Epoxide Hydrolases; Gene Knockout Techniques; Intestinal Mucosa; Intestines; Male; Mice; Peroxidase; Phenylurea Compounds; Piperidines; Solubility; Tumor Necrosis Factor-alpha; Ulcer

2016
Successful treatment with alectinib after crizotinib-induced esophageal ulceration.
    Lung cancer (Amsterdam, Netherlands), 2015, Volume: 88, Issue:3

    Crizotinib was the first clinically available inhibitor of the tyrosine kinase ALK, and next-generation ALK inhibitors, such as alectinib, are now under development. Although crizotinib is generally well tolerated, severe esophageal injury has been reported as a rare but serious adverse event of crizotinib therapy. We now describe the successful treatment with alectinib of a patient who developed crizotinib-induced esophageal ulceration.

    Topics: Carbazoles; Carcinoma, Non-Small-Cell Lung; Crizotinib; Endoscopes; Esophageal Diseases; Female; Humans; Lung Neoplasms; Middle Aged; Piperidines; Protein Kinase Inhibitors; Pyrazoles; Pyridines; Tomography, X-Ray Computed; Treatment Outcome; Ulcer

2015
Antagonism of protease-activated receptor 2 protects against experimental colitis.
    The Journal of pharmacology and experimental therapeutics, 2012, Volume: 340, Issue:2

    Many trypsin-like serine proteases such as β-tryptase are involved in the pathogenesis of colitis and inflammatory bowel diseases. Inhibitors of individual proteases show limited efficacy in treating such conditions, but also probably disrupt digestive and defensive functions of proteases. Here, we investigate whether masking their common target, protease-activated receptor 2 (PAR2), is an effective therapeutic strategy for treating acute and chronic experimental colitis in rats. A novel PAR2 antagonist (5-isoxazoyl-Cha-Ile-spiro[indene-1,4'-piperidine]; GB88) was evaluated for the blockade of intracellular calcium release in colonocytes and anti-inflammatory activity in acute (PAR2 agonist-induced) versus chronic [2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced] models of colitis in Wistar rats. Disease progression (disease activity index, weight loss, and mortality) and postmortem colonic histopathology (inflammation, bowel wall thickness, and myeloperoxidase) were measured. PAR2 and tryptase colocalization were investigated by using immunohistochemistry. GB88 was a more potent antagonist of PAR2 activation in colonocytes than another reported compound, N¹-3-methylbutyryl-N⁴-6-aminohexanoyl-piperazine (ENMD-1068) (IC₅₀ 8 μM versus 5 mM). Acute colonic inflammation induced in rats by the PAR2 agonist SLIGRL-NH₂ was inhibited by oral administration of GB88 (10 mg/kg) with markedly reduced edema, mucin depletion, PAR2 receptor internalization, and mastocytosis. Chronic TNBS-induced colitis in rats was ameliorated by GB88 (10 mg/kg/day p.o.), which reduced mortality and pathology (including colon obstruction, ulceration, wall thickness, and myeloperoxidase release) more effectively than the clinically used drug sulfasalazine (100 mg/kg/day p.o.). These disease-modifying properties for the PAR2 antagonist in both acute and chronic experimental colitis strongly support a pathogenic role for PAR2 and PAR2-activating proteases and therapeutic potential for PAR2 antagonism in inflammatory diseases of the colon.

    Topics: Animals; Body Weight; Calcium Signaling; Colitis; Colon; Cytokines; Edema; HT29 Cells; Humans; Indenes; Intestinal Mucosa; Male; Oligopeptides; Piperazines; Piperidines; Rats; Rats, Wistar; Receptor, PAR-2; Sulfasalazine; Survival Rate; Transendothelial and Transepithelial Migration; Trinitrobenzenesulfonic Acid; Tryptases; Ulcer

2012
[Pharmacologic and toxicologic studies on benzilic acid-(N,N-dimethyl-2-hydroxymethylpiperidinium)estermethylsulfate--a new spasmolytic].
    Arzneimittel-Forschung, 1966, Volume: 16, Issue:8

    Topics: Animals; Asthma; Benzilates; Cardiovascular System; Cats; Dogs; Embryo, Mammalian; Gastric Juice; Gastrointestinal Motility; Guinea Pigs; Intestines; Mice; Muscle, Smooth; Muscles; Nervous System; Piperidines; Pupil; Rabbits; Rats; Respiration; Salivation; Trachea; Ulcer

1966
DIOXATRINE, A POTENT AND SPECIFIC RUMENAL ULCER-PREVENTING AGENT IN RATS.
    The Journal of pharmacy and pharmacology, 1964, Volume: 16

    Topics: Atropine; Glucose; Mydriatics; Parasympatholytics; Peptic Ulcer; Pharmacology; Piperidines; Rats; Research; Ulcer

1964
An evaluation of prantal in ulcer management: follow-up of preliminary report.
    The American journal of gastroenterology, 1953, Volume: 20, Issue:11

    Topics: Follow-Up Studies; Parasympatholytics; Peptic Ulcer; Piperidines; Ulcer

1953