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Clinical Interventions in Aging 2007The prevalence of gastroesophageal reflux disease (GERD) increases with age and elderly are more likely to develop severe disease. Older patients often complain of less... (Review)
Review
The prevalence of gastroesophageal reflux disease (GERD) increases with age and elderly are more likely to develop severe disease. Older patients often complain of less severe or frequent heartburn than younger patients and they may present with atypical symptoms such as dysphagia, weight loss, or extraesophageal symptoms. Proton pump inhibitors (PPIs) are central in the management of GERD and are unchallenged with regards to their efficacy. They are considered safe and more effective than histamine receptor antagonists for healing esophagitis and for preventing its recurrence using a long term maintenance treatment. PPI have minimal side effects and few slight drug interactions and are considered safe for long term treatment. Pantoprazole is significantly effective both for acute and long-term treatment with excellent control of relapse and symptoms. It is well tolerated even for long-term therapy and its tolerability is optimal. Pantoprazole shows to have minimal interactions with other drugs because of a lower affinity for cytocrome P450 than older PPIs. Although the majority of elderly has concomitant illnesses and receive other drugs, this does not adversely effect the efficacy of pantoprazole because of its pharmacokinetics, which are independent of patient age. Clinical practice suggests that a low dose maintenance of PPIs should be used in older patients with GERD.
Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Aged; Anti-Ulcer Agents; Gastroesophageal Reflux; Humans; Pantoprazole; Patient Satisfaction; Quality of Life; Time Factors
PubMed: 18044079
DOI: 10.2147/ciia.2007.2.1.85 -
Gastroenterology Jan 2020
Topics: Aspirin; Double-Blind Method; Factor Xa Inhibitors; Humans; Pantoprazole; Platelet Aggregation Inhibitors; Rivaroxaban
PubMed: 31704304
DOI: 10.1053/j.gastro.2019.08.063 -
Acta Pharmacologica Sinica Nov 2021Liver fibrosis is one of the most severe pathologic consequences of chronic liver diseases, and effective therapeutic strategies are urgently needed. Proton pump...
Liver fibrosis is one of the most severe pathologic consequences of chronic liver diseases, and effective therapeutic strategies are urgently needed. Proton pump inhibitors (PPIs) are H/K-ATPase inhibitors and currently used to treat acid-related diseases such as gastric ulcers, which have shown other therapeutic effects in addition to inhibiting acid secretion. However, few studies have focused on PPIs from the perspective of inhibiting hepatic fibrosis. In the present study, we investigated the effects of pantoprazole (PPZ), a PPI, against liver fibrosis in a bile duct ligation (BDL) rat model, human hepatic stellate cell (HSC) line LX-2 and mouse primary HSCs (pHSCs), and explored the potential mechanisms underlying the effects of PPZ in vitro and in vivo. In BDL rats, administration of PPZ (150 mg· kg· d, i.p. for 14 d) significantly attenuated liver histopathological injury, collagen accumulation, and inflammatory responses, and suppressed fibrogenesis-associated gene expression including Col1a1, Acta2, Tgfβ1, and Mmp-2. In LX-2 cells and mouse pHSCs, PPZ (100-300 μM) dose-dependently suppressed the levels of fibrogenic markers. We conducted transcriptome analysis and subsequent validation in PPZ-treated LX-2 cells, and revealed that PPZ inhibited the expression of Yes-associated protein (YAP) and its downstream targets such as CTGF, ID1, survivin, CYR61, and GLI2. Using YAP overexpression and silencing, we demonstrated that PPZ downregulated hepatic fibrogenic gene expression via YAP. Furthermore, we showed that PPZ promoted the proteasome-dependent degradation and ubiquitination of YAP, thus inhibiting HSC activation. Additionally, we showed that PPZ destabilized YAP by disrupting the interaction between a deubiquitinating enzyme OTUB2 and YAP, and subsequently blocked the progression of hepatic fibrosis.
Topics: Animals; Bile Ducts; Gene Expression Profiling; HEK293 Cells; Hepatic Stellate Cells; Humans; Ligation; Liver Cirrhosis; Male; Pantoprazole; Proteolysis; Proton Pump Inhibitors; Rats; Rats, Sprague-Dawley; YAP-Signaling Proteins
PubMed: 34465912
DOI: 10.1038/s41401-021-00754-w -
American Journal of Critical Care : An... Jul 2008
Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Critical Illness; Famotidine; Histamine H2 Antagonists; Humans; Pantoprazole; Peptic Ulcer Hemorrhage; Proton Pump Inhibitors; Respiration, Artificial
PubMed: 18593828
DOI: No ID Found -
The Journal of the American Osteopathic... Dec 2019
Topics: Abdominal Pain; Anti-Bacterial Agents; Anti-Ulcer Agents; Emphysema; Foreign Bodies; Gastritis; Humans; Male; Melena; Middle Aged; Pantoprazole; Piperacillin, Tazobactam Drug Combination; Tomography, X-Ray Computed
PubMed: 31790130
DOI: 10.7556/jaoa.2019.140 -
Drug Development Research Jun 2024Hepatocellular carcinoma (HCC) is one of the deadliest cancers. The prevention and therapy for this deadly disease remain a global medical challenge. In this study, we...
Hepatocellular carcinoma (HCC) is one of the deadliest cancers. The prevention and therapy for this deadly disease remain a global medical challenge. In this study, we investigated the effect of pantoprazole (PPZ) on the carcinogenesis and growth of HCC. Both diethylnitrosamine (DEN) plus CCl4-induced and DEN plus high fat diet (HFD)-induced HCC models in mice were established. Cytokines and cell proliferation-associated gene in the liver tissues of mice and HCC cells were analyzed. Cellular glycolysis and Na/H exchange activity were measured. The preventive administration of pantoprazole (PPZ) at a clinically relevant low dose markedly suppressed HCC carcinogenesis in both DEN plus CCl4-induced and HFD-induced murine HCC models, whereas the therapeutic administration of PPZ at the dose suppressed the growth of HCC. In the liver tissues of PPZ-treated mice, inflammatory cytokines, IL1, CXCL1, CXCL5, CXCL9, CXCL10, CCL2, CCL5, CCL6, CCL7, CCL20, and CCL22, were reduced. The administration of CXCL1, CXCL5, CCL2, or CCL20 all reversed PPZ-suppressed DEN plus CCL4-induced HCC carcinogenesis in mice. PPZ inhibited the expressions of CCNA2, CCNB2, CCNE2, CDC25C, CDCA5, CDK1, CDK2, TOP2A, TTK, AURKA, and BIRC5 in HCC cells. Further results showed that PPZ reduced the production of these inflammatory cytokines and the expression of these cell proliferation-associated genes through the inhibition of glycolysis and Na/H exchange. In conclusion, PPZ suppresses the carcinogenesis and growth of HCC, which is related to inhibiting the production of inflammatory cytokines and the expression of cell proliferation-associated genes in the liver through the inhibition of glycolysis and Na/H exchange.
Topics: Animals; Carcinoma, Hepatocellular; Glycolysis; Liver Neoplasms; Mice; Pantoprazole; Male; Cell Proliferation; Humans; Mice, Inbred C57BL; Carcinogenesis; Diethylnitrosamine; Cytokines; Cell Line, Tumor; Diet, High-Fat
PubMed: 38764200
DOI: 10.1002/ddr.22198 -
Current Drug Safety 2022Pantoprazole is a Proton Pump Inhibitor, commonly used by clinicians all over the world as a gastric acid synthesis inhibitor for a wide variety of gastrointestinal...
BACKGROUND
Pantoprazole is a Proton Pump Inhibitor, commonly used by clinicians all over the world as a gastric acid synthesis inhibitor for a wide variety of gastrointestinal disorders. The efficacy and the safety of the drug are unsurmountable. PPIs are being prescribed nowadays for unapproved indications. It is one of the widely used medications in the world. Consequently, adverse events are commonly reported nowadays with proton pump inhibitors, and it is essential to improve physician awareness regarding judicious prescribing practice.
OBJECTIVE
To report a case of anaphylaxis to pantoprazole, that occurred in a patient admitted with gastrointestinal complaints.
CASE SUMMARY
Within few minutes of intravenous infusion of pantoprazole, a 75-year-old female developed anaphylaxis. The adverse drug reaction was promptly diagnosed, and the patient was resuscitated.
CONCLUSION
It is imperative that clinicians should be aware of this adverse effect that might occur with pantoprazole and hence be more cautious while prescribing the drug, especially in the elderly.
Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Aged; Anaphylaxis; Female; Humans; Omeprazole; Pantoprazole; Proton Pump Inhibitors
PubMed: 34323194
DOI: 10.2174/1574886316666210728115356 -
Annals of Internal Medicine Oct 2019
Topics: Aspirin; Double-Blind Method; Humans; Pantoprazole; Proton Pump Inhibitors; Rivaroxaban
PubMed: 31610558
DOI: 10.7326/ACPJ201910150-045 -
Journal of Medical Case Reports Jun 2020Hyponatremia is the most common electrolyte disorder. Thiazides, antidepressants, antipsychotic drugs, and antiepileptic drugs are well-known causes of hyponatremia....
BACKGROUND
Hyponatremia is the most common electrolyte disorder. Thiazides, antidepressants, antipsychotic drugs, and antiepileptic drugs are well-known causes of hyponatremia. Proton pump inhibitor use is a rare cause of hyponatremia and, when reported, it is due to one specific proton pump inhibitor, mostly omeprazole.
CASE PRESENTATION
A 67-year-old Caucasian male was referred to our out-patient clinic because of hyponatremia (127 mmol/L) found at routine laboratory examination. He had consulted his general practitioner because of abdominal pains. No other symptoms were present. At physical examination, he appeared euvolemic and had no abdominal tenderness. Besides omeprazole for reflux esophagitis he used no medication. Additional laboratory results included: serum osmolarity 274 mOsmol/kg, urinary osmolarity 570 mOsmol/kg, and urinary sodium 35 mmol/L. Other causes of hyponatremia were excluded and we diagnosed hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion secondary to use of omeprazole. Omeprazole was replaced by ranitidine after which his serum sodium levels normalized to 135 mmol/L. During follow-up, because of persistent reflux complaints despite ranitidine use, ranitidine was switched to another proton pump inhibitor: pantoprazole. After this intervention, his serum sodium level declined again to 133 mmol/L. We concluded that both omeprazole and pantoprazole induced syndrome of inappropriate antidiuretic hormone secretion in this patient.
CONCLUSION
Hyponatremia is worrisome and awareness of medication-induced hyponatremia, especially due to proton pump inhibitors, is needed. In our case, sequential hyponatremia occurred with two different proton pump inhibitors, suggesting a class effect. Therefore, when syndrome of inappropriate antidiuretic hormone secretion due to a proton pump inhibitor is diagnosed, preferably no other medication from the same class is prescribed. When after consideration another proton pump inhibitor is prescribed, serum sodium concentrations should be monitored.
Topics: Aged; Asymptomatic Diseases; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Omeprazole; Pantoprazole; Proton Pump Inhibitors
PubMed: 32594911
DOI: 10.1186/s13256-020-02423-8 -
Alimentary Pharmacology & Therapeutics Feb 1993
Clinical Trial Comparative Study Randomized Controlled Trial
Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adenosine Triphosphatases; Benzimidazoles; Circadian Rhythm; Dose-Response Relationship, Drug; Double-Blind Method; Gastric Acid; Gastric Mucosa; Humans; Hydrogen-Ion Concentration; Omeprazole; Pantoprazole; Sulfoxides
PubMed: 8439633
DOI: 10.1111/j.1365-2036.1993.tb00077.x