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American Journal of Therapeutics 2018
Topics: Aged; Gastroesophageal Reflux; Humans; Male; Pancreas; Pancreatitis, Chronic; Pantoprazole; Proton Pump Inhibitors; Tomography, X-Ray Computed
PubMed: 28282309
DOI: 10.1097/MJT.0000000000000567 -
Current Drug Safety 2024Pantoprazole is a proton pump inhibitor mainly used to treat conditions causing excess stomach acid. Stevens-Johnson syndrome (SJS) is a rare bullous disease. The main...
INTRODUCTION
Pantoprazole is a proton pump inhibitor mainly used to treat conditions causing excess stomach acid. Stevens-Johnson syndrome (SJS) is a rare bullous disease. The main etiologic factors are drugs, especially antibiotics, anticonvulsants, oxicam and allopurinol. Proton pump inhibitors have been rarely reported as a causative agent in SJS, and only sporadic cases secondary to pantoprazole have just been mentioned in the literature.
CASE REPORT
A 49-year-old woman was referred to the dermatology department for a pruritic generalized eruption, associated with erosive cheilitis. The patient reported self-medication by pantoprazole for two weeks. Physical examination revealed target-like lesions with bullous center in some areas. A skin detachment on the left breast and the neck affecting 10% of the total body surface area was observed. Mucosal examination revealed erosive, painful cheilitis covered by large hemorrhagic crusts and erosions of the nasal cavity. The lesions cleared completely few days after pantoprazole withdrawal and local corticosteroids. Further investigations ruled out infectious etiologies.
CONCLUSION
This case highlights the possible occurrence of hypersensitivity reactions due to the use of a PPI, which is a widely used medication and a generally well-tolerated drug.
Topics: Female; Humans; Middle Aged; Stevens-Johnson Syndrome; Pantoprazole; Cheilitis; Anti-Bacterial Agents; Anticonvulsants
PubMed: 36823997
DOI: 10.2174/1574886318666230224092818 -
International Journal of Molecular... Sep 2022Proton pump inhibitors (PPIs) are an antacid drug often used in acid-related disorders. They decrease acid secretion in the stomach by blocking an enzyme called H+/K+... (Review)
Review
Proton pump inhibitors (PPIs) are an antacid drug often used in acid-related disorders. They decrease acid secretion in the stomach by blocking an enzyme called H+/K+ ATPase which controls acid production. Introduced to the market in 1989, their use has increased rapidly worldwide and they are now among the top 10 most prescribed drugs in the United States. As of 2015, the FDA has already approved six drugs of this class (omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole and rabeprazole). Recently, the risks and benefits of long-term PPI use were questioned and many studies indicated that their use should be carefully considered, especially in young patients, whose treatment with these drugs could last many years. Even greater concerns have been raised about a potential positive association between PPIs and osteoporotic fracture risk including the hip, spine and wrist. Although based on observational studies, there is substantial evidence associating the long-term use of PPIs and fracture. This relationship is only partially admitted due to the lack of consistent effects of PPIs on bone mineral density loss. Therefore, this narrative review aimed to discuss the recent findings pertaining to the risk of osteoporotic fracture associated with PPIs, in particular prolonged use, and to call for further research to elucidate the mechanisms associated with this bone fragility.
Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adenosine Triphosphatases; Antacids; Bone Density; Dexlansoprazole; Esomeprazole; Humans; Lansoprazole; Omeprazole; Osteoporotic Fractures; Pantoprazole; Proton Pump Inhibitors; Rabeprazole; United States
PubMed: 36142643
DOI: 10.3390/ijms231810733 -
Indian Journal of Pediatrics Dec 2009
Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Female; Humans; Infant, Newborn; Pantoprazole; Proton Pump Inhibitors; Thrombocytopenia
PubMed: 20012806
DOI: 10.1007/s12098-009-0224-9 -
The New England Journal of Medicine Mar 2019
Topics: Gastrointestinal Hemorrhage; Humans; Intensive Care Units; Pantoprazole; Proton Pump Inhibitors
PubMed: 30855753
DOI: 10.1056/NEJMc1900206 -
Journal of Pharmacy Practice Jun 2023Pantoprazole is a proton pump inhibitor (PPI) class drug that is widely used in the treatment of SRMD (stress-related mucosal disease in critical ill patients. PPI are...
Pantoprazole is a proton pump inhibitor (PPI) class drug that is widely used in the treatment of SRMD (stress-related mucosal disease in critical ill patients. PPI are one class of drugs used commonly both for treatment and prophylactic therapy for stress ulcers in intensive care unit (ICU). We report a case of a 51-year old male who was referred to PKU Hospital. He was admitted to ICU with diagnosis of Hyperosmolar Hyperglymic State and bronchopneumonia. Thrombocytopenia was noted in admission. There was more than 70% decrease in platelet count after initiation of pantoprazole. Patient received Thrombocyte Concentrate (TC) transfusion and corticosteroid iv for several days, but only had minor increase in platelet count. The platelets recovered after stopping pantoprazole. In the present case report, another exposures to parenteral pantoprazole in a dose of 40 mg once daily reproduced the same adverse drug reaction. In comparison to lansoprazole, thrombocytopenia from pantoprazole is more severe that necessitate TC transfusion and corticosteroid trial. However, in the present case, TC transfusion and corticosteroid fail to escalate platelet count. This finding suggests probability of non-immune mechanism of pantoprazole-induced thrombocytopenia. Pantoprazole may induce thrombocytopenia with new features that were immediately developed, resulting a decrease in platelet count >70%. The mechanism found in this case may be non-immune. Drug-induced thrombocytopenia is one of the rare complications that has to be kept in mind with the use of pantoprazole.
Topics: Male; Humans; Middle Aged; Pantoprazole; Blood Platelets; Thrombocytopenia; Proton Pump Inhibitors; Lansoprazole
PubMed: 34965162
DOI: 10.1177/08971900211064715 -
The New England Journal of Medicine Mar 2019
Topics: Gastrointestinal Hemorrhage; Humans; Intensive Care Units; Pantoprazole; Proton Pump Inhibitors
PubMed: 30855752
DOI: 10.1056/NEJMc1900206 -
BioMed Research International 2023Recent researches have failed to uncover a clear explanation for proton pump inhibitors' bone-loss effects. In light of pantoprazole's effects on gastrin secretion, the...
BACKGROUND
Recent researches have failed to uncover a clear explanation for proton pump inhibitors' bone-loss effects. In light of pantoprazole's effects on gastrin secretion, the goal of this study was to see if it caused bone loss through gastrin secretion.
METHODS
Forty male rats were divided into control, octreotide (Oct), pantoprazole (Pan), and pantoprazole plus octreotide (Pan+Oct) groups. Serum calcium, phosphorous, alkaline phosphatase, parathyroid hormone, and gastrin were measured before and three months after the treatment, and bone densitometry was examined. The rats' femoral bones were examined stereologically at the end of the investigation.
RESULTS
The Pan group had considerably greater levels of serum alkaline phosphatase, parathyroid hormone (PTH), and gastrin, but this was prevented in the presence of Oct, a gastrin secretion inhibitor. All parameters of femoral bone densitometry in the Pan group were significantly lower than the control after treatment which was considerably inhibited in the presence of Oct. Furthermore, when compared to the control and Oct groups, the rats in the Pan group had a lower trabecular volume, femur bone weight, and volume, as well lower number of osteocytes. The amount of osteoclasts, on the other hand, was much higher in the Pan group than in the other groups.
CONCLUSION
Overall findings revealed that pantoprazole caused bone loss, which could be prevented by adding octreotide. Because these detrimental effects were not detected in rats given both Oct and Pan, it was suggested that the effect of Pan on bone was produced by a hypergastrinemic condition.
Topics: Male; Animals; Rats; Pantoprazole; Gastrins; Alkaline Phosphatase; Octreotide; Bone Diseases, Metabolic; Parathyroid Hormone
PubMed: 37711876
DOI: 10.1155/2023/2594664 -
Liver International : Official Journal... Jun 2018Although very rare, pantoprazole can result in acute hepatitis. It has yet to be reported, however, that it can also cause chronic autoimmune hepatitis.
BACKGROUND
Although very rare, pantoprazole can result in acute hepatitis. It has yet to be reported, however, that it can also cause chronic autoimmune hepatitis.
AIM, METHOD AND RESULTS
We report the case of a patient in whom pantoprazole administration for 2 months was followed by acute liver injury with severe jaundice and features of autoimmunity. A liver biopsy revealed acute hepatocellular lesions associated with cholestasis, acute cholangitis and polymorphous inflammatory infiltration suggestive of drug-induced liver injury. The jaundice disappeared following discontinuation of the pantoprazole. There was, however, chronic autoimmune liver injury, with the occurrence of extensive liver fibrosis within a few months. This led to the administration of immunosuppressive agents, which led to progressive and complete recovery associated with the disappearance of autoantibodies.
CONCLUSION
This observation further supports the notion that pantoprazole can induce acute hepatocellular hepatitis, and it strongly suggests that it may trigger acute cholangitis and autoimmune liver injury. This case also helps document that some drugs can induce chronic autoimmune hepatitis that can resolve with immunosuppressive treatment.
Topics: Chemical and Drug Induced Liver Injury; Cholangitis; Cholestasis; Female; Hepatitis, Autoimmune; Humans; Immunosuppressive Agents; Jaundice; Liver; Liver Cirrhosis; Liver Function Tests; Middle Aged; Pantoprazole; Proton Pump Inhibitors
PubMed: 29532602
DOI: 10.1111/liv.13737 -
International Journal of Clinical... Jun 1996This review summarizes the results of pharmacokinetic and pharmacodynamic drug interaction studies in man with pantoprazole, a new, selective proton pump inhibitor.... (Review)
Review
This review summarizes the results of pharmacokinetic and pharmacodynamic drug interaction studies in man with pantoprazole, a new, selective proton pump inhibitor. Various mechanisms have to be considered as causes for potential drug-drug interactions. Proton pump inhibitors (PPIs) in general may alter the absorption of drugs by increasing the intragastric pH. Due to the presence of an imidazole ring, the PPIs of the class of substituted benzimidazole sulfoxides may interfere with the metabolism of other drugs by altering the activity of drug metabolizing enzymes of the cytochrome P450 system, via either induction or inhibition. With the increasing use of PPIs, their interaction potential gains therapeutic importance as was the case with the first and second generation of H2-blockers (cimetidine and ranitidine, respectively). The enhanced selectivity of pantoprazole to the gastric H+/K(+)-ATPase characterizes the new PPI generation. In contrast to omeprazole, pantoprazole has a low potential to interact with the cytochrome P450 system in man. In the drug interaction studies conducted so far, substrates for all relevant cytochrome P450 families involved in the metabolism of drugs in man were investigated. Pantoprazole did not affect the pharmacokinetics or pharmacodynamics of antipyrine, caffeine, carbamazepine, diazepam, diclofenac, digoxin, ethanol, glibenclamide, a hormonal contraceptive (combination of levonorgestrel and ethinylestradiol), metoprolol, nifedipine, phenprocoumon, phenytoin, theophylline and warfarin in man. Pantoprazole also neither induced the metabolism of antipyrine or caffeine, nor increased urinary excretion of the induction markers D-glucaric acid and 6 beta-hydroxycortisol. Vice versa, the investigated drugs had no relevant influence on the pharmacokinetics of pantoprazole.
Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Benzimidazoles; Drug Interactions; Enzyme Inhibitors; Humans; Omeprazole; Pantoprazole; Proton Pump Inhibitors; Sulfoxides
PubMed: 8793611
DOI: No ID Found