78-453: Pantoprazole , sold under the brand name Protonix , among others, is a medication used for the treatment of stomach ulcers , short-term treatment of erosive esophagitis due to gastroesophageal reflux disease (GERD), maintenance of healing of erosive esophagitis , and pathological hypersecretory conditions including Zollinger–Ellison syndrome . It may also be used along with other medications to eliminate Helicobacter pylori . Pantoprazole
156-484: A burning or dull ache. Other symptoms include belching , vomiting, weight loss, or poor appetite . About a third of older people with peptic ulcers have no symptoms. Complications may include bleeding , perforation , and blockage of the stomach . Bleeding occurs in as many as 15% of cases. Common causes include infection with Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Other, less common causes include tobacco smoking , stress as
234-542: A superfamily of enzymes containing heme as a cofactor that mostly, but not exclusively, function as monooxygenases . However, they are not omnipresent; for example, they have not been found in Escherichia coli . In mammals, these enzymes oxidize steroids , fatty acids , xenobiotics , and participate in many biosyntheses. By hydroxylation, CYP450 enzymes convert xenobiotics into hydrophilic derivatives, which are more readily excreted. P450s are, in general,
312-519: A urea breath test , testing the stool for signs of the bacteria, or a biopsy of the stomach. Other conditions that produce similar symptoms include stomach cancer , coronary heart disease , and inflammation of the stomach lining or gallbladder inflammation . Diet does not play an important role in either causing or preventing ulcers. Treatment includes stopping smoking, stopping use of NSAIDs, stopping alcohol , and taking medications to decrease stomach acid. The medication used to decrease acid
390-495: A "reverse type I" spectrum, by processes that are as yet unclear. Inhibitors and certain substrates that bind directly to the heme iron give rise to the type II difference spectrum, with a maximum at 430 nm and a minimum at 390 nm (see inset graph in figure). If no reducing equivalents are available, this complex may remain stable, allowing the degree of binding to be determined from absorbance measurements in vitro C: If carbon monoxide (CO) binds to reduced P450,
468-404: A chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease. Peptic ulcers are a form of acid–peptic disorder . Peptic ulcers can be classified according to their location and other factors. Gastric ulcers are most often localized on
546-424: A consequence of the parietal scarring. A gastric peptic ulcer is a mucosal perforation that penetrates the muscularis mucosae and lamina propria, usually produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows four zones: fibrinoid necrosis, inflammatory exudate, granulation tissue and fibrous tissue. The fibrous base of
624-418: A different chemical that had been chosen as a development candidate. Byk Gulden partnered with Smith Kline & French in 1984. The compound's development names were BY1029 and SK&F96022. By 1986 the companies had created the sodium salt, pantoprazole sodium sesquihydrate, and decided to develop it as it was more soluble and stable, and was more compatible with other ingredients used in the formulation. It
702-451: A heme-iron center. The iron is tethered to the protein via a cysteine thiolate ligand . This cysteine and several flanking residues are highly conserved in known P450s, and have the formal PROSITE signature consensus pattern [FW] - [SGNH] - x - [GD] - {F} - [RKHPT] - {P} - C - [LIVMFAP] - [GAD]. In general, the P450 catalytic cycle proceeds as follows: Mechanistic details, including
780-458: A molecular biology lab at UWA in Perth, Western Australia. A 1998 New England Medical Journal study found that mastic gum , a tree resin extract, actively eliminated the H. pylori bacteria. However, multiple subsequent studies (in mice and in vivo) have found no effect of using mastic gum on reducing H. pylori levels. Cytochrome P450 Cytochromes P450 ( P450s or CYPs ) are
858-426: A peptic ulcer is two times for aspirin users. Risk of bleeding increases if NSAIDs are combined with selective serotonin reuptake inhibitor (SSRI), corticosteroids , antimineralocorticoids , and anticoagulants . The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins . NSAIDs block the function of cyclooxygenase 1 ( COX-1 ), which
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#1732788005425936-409: A result of other serious health conditions, Behçet's disease , Zollinger–Ellison syndrome , Crohn's disease , and liver cirrhosis . Older people are more sensitive to the ulcer-causing effects of NSAIDs. The diagnosis is typically suspected due to the presenting symptoms with confirmation by either endoscopy or barium swallow . H. pylori can be diagnosed by testing the blood for antibodies ,
1014-452: Is oxidation by CYP3A4 . Pantoprazole metabolites are not thought to have any pharmacological significance. It is usually given with a prokinetic drug because of inactivity in the acidic environment of the stomach. Pantoprazole binds irreversibly to H+K+ATPase ( proton pumps ) to suppress the secretion of acid. Due to irreversible binding of the pumps, new pumps have to be made before acid production can be resumed. The drug's plasma half-life
1092-547: Is a proton-pump inhibitor (PPI) and its effectiveness is similar to that of other PPIs. It is available by mouth and by injection into a vein . Common side effects include headaches, diarrhea, abdominal pain, and joint pain . More serious side effects may include severe allergic reactions , a type of chronic inflammation known as atrophic gastritis , Clostridioides difficile colitis , low magnesium , and vitamin B12 deficiency . Use in pregnancy appears to be safe. Pantoprazole
1170-461: Is a higher rate of complication for those who underwent surgery to patch the stomach bleeding site when compared to repeated endoscopy. Angiographic embolisation has a higher rebleeding rate but a similar rate of death to surgery. According to expert opinion, for those who are already on anticoagulants, the international normalized ratio (INR) should be kept at 1.5. For aspirin users who required endoscopic treatment for bleeding peptic ulcer, there
1248-540: Is a proton pump inhibitor that decreases gastric acid secretion. It works by inactivating (H+/K+)-ATPase function in the stomach. The study of pantoprazole began in 1985, and it came into medical use in Germany in 1994. It is available as a generic medication . In 2022, it was the sixteenth most commonly prescribed medication in the United States, with more than 30 million prescriptions. In Australia, it
1326-402: Is about two hours. After administration, the time for the drug to reach peak plasma concentrations is 2 to 3 hours. The percentage of the drug that is protein bound is 98%. Pantoprazole was discovered by scientists at Byk Gulden, a subsidiary of Altana ; the drug discovery program started in 1980, producing pantoprazole in 1985. The compound was actually created by chemists working to scale up
1404-529: Is defined as a bolus dose of 80 mg followed by an infusion of 8 mg per hour for 72 hours—in other words, the continuous infusion of PPI of greater than 192 mg per day. Intravenous PPI can be changed to oral once there is no high risk of rebleeding from peptic ulcer. For those with hypovolemic shock and ulcer size of greater than 2 cm, there is a high chance that the endoscopic treatment would fail. Therefore, surgery and angiographic embolism are reserved for these complicated cases. However, there
1482-405: Is especially true in ulcers of the greater curvature of the stomach ; most are also a consequence of chronic H. pylori infection. If a peptic ulcer perforates, air will leak from inside the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the person stands, as when having
1560-422: Is essential for the production of these prostaglandins. Besides this, NSAIDs also inhibit stomach mucosa cells proliferation and mucosal blood flow, reducing bicarbonate and mucus secretion, which reduces the integrity of the mucosa. Another type of NSAIDs, called COX-2 selective anti-inflammatory drugs (such as celecoxib ), preferentially inhibit COX-2 , which is less essential in the gastric mucosa. This reduces
1638-410: Is estimated at 70% of the population, whereas developed countries show a maximum of a 40% ratio. Overall, H. pylori infections show a worldwide decrease, more so in developed countries. Transmission occurs via food, contaminated groundwater, or human saliva (such as from kissing or sharing food utensils). Peptic ulcer disease had a tremendous effect on morbidity and mortality until the last decades of
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#17327880054251716-414: Is increased as food enters the stomach. Pain in duodenal ulcers would be aggravated by hunger and relieved by a meal and is associated with night pain. Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the person's age. Furthermore, typical ulcers tend to heal and recur, and as a result the pain may occur for few days and weeks and then wane or disappear. Usually, children and
1794-421: Is indicated if there is active bleeding in the stomach, visible vessels, or an adherent clot. Endoscopy is also helpful in identifying people who are suitable for hospital discharge. Prokinetic agents such as erythromycin and metoclopramide can be given before endoscopy to improve endoscopic view. Either high- or low-dose PPIs are equally effective in reducing bleeding after endoscopy. High-dose intravenous PPI
1872-489: Is not successful. Peptic ulcers are present in around 4% of the population. New ulcers were found in around 87.4 million people worldwide during 2015. About 10% of people develop a peptic ulcer at some point in their life. Peptic ulcers resulted in 267,500 deaths in 2015, down from 327,000 in 1990. The first description of a perforated peptic ulcer was in 1670, in Princess Henrietta of England . H. pylori
1950-583: Is present, EGD can often provide an alternative diagnosis. One of the reasons that blood tests are not reliable for accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection. Additionally, a false negative result is possible with a blood test if the person has recently been taking certain drugs, such as antibiotics or proton-pump inhibitors . The diagnosis of Helicobacter pylori can be made by: The breath test uses radioactive carbon to detect H. pylori. To perform this exam,
2028-605: Is suitable for its survival. It expresses blood group antigen-binding adhesin (BabA) and outer inflammatory protein adhesin (OipA), which enables it to attach to the gastric epithelium. The bacterium also expresses virulence factors such as CagA and PicB , which cause stomach mucosal inflammation. The VacA gene encodes for vacuolating cytotoxin, but its mechanism of causing peptic ulcers is unclear. Such stomach mucosal inflammation can be associated with hyperchlorhydria (increased stomach acid secretion) or hypochlorhydria (reduced stomach acid secretion). Inflammatory cytokines inhibit
2106-436: Is the antidote of choice. The lifetime risk for developing a peptic ulcer is approximately 5% to 10% with the rate of 0.1% to 0.3% per year. Peptic ulcers resulted in 301,000 deaths in 2013, down from 327,000 in 1990. In Western countries, the percentage of people with H. pylori infections roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80, etc.). Prevalence is higher in third world countries, where it
2184-515: Is the gene that encodes the enzyme CYP2E1 —one of the enzymes involved in paracetamol (acetaminophen) metabolism. The CYP nomenclature is the official naming convention, although occasionally CYP450 or CYP 450 is used synonymously. These names should never be used as according to the nomenclature convention (as they denote a P450 in family number 450). However, some gene or enzyme names for P450s are also referred to by historical names (e.g. P450 BM3 for CYP102A1) or functional names, denoting
2262-470: Is the most popular agent in peptic ulcer prevention. However, there is no evidence that H2 antagonists can prevent stomach bleeding for those taking NSAIDs. Although misoprostol is effective in preventing peptic ulcer, its properties of promoting abortion and causing gastrointestinal distress limit its use. For those with high cardiovascular risk, naproxen with PPI can be a useful choice. Otherwise, low-dose aspirin, celecoxib, and PPI can also be used. Once
2340-522: Is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer. Pantoprazole is metabolized in the liver by the cytochrome P450 system. Metabolism mainly consists of demethylation by CYP2C19 followed by sulfation . Another metabolic pathway
2418-491: Is two times increased risk of rebleeding but with ten times reduced risk of death at eight weeks following the resumption of aspirin. For those who were on double antiplatelet agents for indwelling stent in blood vessels, both antiplatelet agents should not be stopped because there is a high risk of stent thrombosis. For those who were under warfarin treatment, fresh frozen plasma (FFP), vitamin K, prothrombin complex concentrates, or recombinant factor VIIa can be given to reverse
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2496-477: Is used to determine whether a person should be treated inside a hospital or as an outpatient. Intravenous PPIs can suppress stomach bleeding more quickly than oral ones. A neutral stomach pH is required to keep platelets in place and prevent clot lysis. Tranexamic acid and antifibrinolytic agents are not useful in treating peptic ulcer disease. Early endoscopic therapy can help to stop bleeding by using cautery , endoclip , or epinephrine injection. Treatment
2574-441: Is usually either a proton pump inhibitor (PPI) or an H2 blocker , with four weeks of treatment initially recommended. Ulcers due to H. pylori are treated with a combination of medications, such as amoxicillin , clarithromycin , and a PPI. Antibiotic resistance is increasing and thus treatment may not always be effective. Bleeding ulcers may be treated by endoscopy , with open surgery typically only used in cases in which it
2652-509: Is well described as a cause of peptic ulcers, which are also known as stress ulcers . While chronic life stress was once believed to be the main cause of ulcers, this is no longer the case. It is, however, still occasionally believed to play a role. This may be due to the well-documented effects of stress on gastric physiology, increasing the risk in those with other causes, such as H. pylori or NSAID use. Dietary factors, such as spice consumption, were hypothesized to cause ulcers until
2730-852: The Wayback Machine ) and allele names ( CYP Allele Nomenclature Committee ). Based on the nature of the electron transfer proteins, P450s can be classified into several groups: The most common reaction catalyzed by cytochromes P450 is a monooxygenase reaction, e.g., insertion of one atom of oxygen into the aliphatic position of an organic substrate (RH), while the other oxygen atom is reduced to water: Many hydroxylation reactions (insertion of hydroxyl groups) use CYP enzymes, but many other hydroxylases exist. Alpha-ketoglutarate-dependent hydroxylases also rely on an Fe=O intermediate but lack hemes. Methane monooxygenase, which converts methane to methanol, are non-heme iron-and iron-copper-based enzymes. The active site of cytochrome P450 contains
2808-475: The elderly do not develop any symptoms unless complications have arisen. A burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers. This pain can be misinterpreted as hunger , indigestion , or heartburn . Pain is usually caused by the ulcer, but it may be aggravated by the stomach acid when it comes into contact with the ulcerated area. The pain caused by peptic ulcers can be felt anywhere from
2886-407: The iron (and eventually molecular oxygen ). Genes encoding P450 enzymes, and the enzymes themselves, are designated with the root symbol CYP for the superfamily , followed by a number indicating the gene family , a capital letter indicating the subfamily, and another numeral for the individual gene. The convention is to italicize the name when referring to the gene. For example, CYP2E1
2964-480: The oxygen rebound mechanism , have been investigated with synthetic analogues, consisting of iron oxo heme complexes. Binding of substrate is reflected in the spectral properties of the enzyme, with an increase in absorbance at 390 nm and a decrease at 420 nm. This can be measured by difference spectroscopies and is referred to as the "type I" difference spectrum (see inset graph in figure). Some substrates cause an opposite change in spectral properties,
3042-406: The parietal cell acid secretion. H. pylori also secretes certain products that inhibit hydrogen potassium ATPase ; activate calcitonin gene-related peptide sensory neurons, which increases somatostatin secretion to inhibit acid production by parietal cells; and inhibit gastrin secretion. This reduction in acid production causes gastric ulcers. On the other hand, increased acid production at
3120-434: The pyloric antrum is associated with duodenal ulcers in 10% to 15% of H. pylori infection cases. In this case, somatostatin production is reduced and gastrin production is increased, leading to increased histamine secretion from the enterochromaffin cells, thus increasing acid production. An acidic environment at the antrum causes metaplasia of the duodenal cells, causing duodenal ulcers. Human immune response toward
3198-419: The small intestine , or sometimes the lower esophagus . An ulcer in the stomach is called a gastric ulcer , while one in the first part of the intestines is a duodenal ulcer . The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain , and upper abdominal pain that improves with eating. With a gastric ulcer, the pain may worsen with eating. The pain is often described as
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3276-520: The 20th century when epidemiological trends started to point to an impressive fall in its incidence. The reason that the rates of peptic ulcer disease decreased is thought to be the development of new effective medication and acid suppressants and the rational use of nonsteroidal anti-inflammatory drugs (NSAIDs). John Lykoudis , a general practitioner in Greece , treated people for peptic ulcer disease with antibiotics beginning in 1958, long before it
3354-400: The 3rd compartment pH in alpacas . It has been shown to be generally safe to use in cattle, sheep and goats. The subcutaneous bioavailability is greater than 100% in calves. In calves intravenous and subcutaneous administration has been shown to significantly elevate abomasal pH. Stomach ulcer Peptic ulcer disease is a break in the inner lining of the stomach , the first part of
3432-405: The age of 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by esophagogastroduodenoscopy . The timing of symptoms in relation to the meal may differentiate between gastric and duodenal ulcers. A gastric ulcer would give epigastric pain during the meal, associated with nausea and vomiting, as gastric acid production
3510-430: The bacteria also determines the emergence of peptic ulcer disease. The human IL1B gene encodes for Interleukin 1 beta , and other genes that encode for tumour necrosis factor (TNF) and Lymphotoxin alpha also play a role in gastric inflammation. Taking nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin can increase the risk of peptic ulcer disease by four times compared to non-users. The risk of getting
3588-670: The catalytic activity and the name of the compound used as substrate. Examples include CYP5A1 , thromboxane A 2 synthase, abbreviated to TBXAS1 ( T hrom B o X ane A 2 S ynthase 1 ), and CYP51A1 , lanosterol 14-α-demethylase, sometimes unofficially abbreviated to LDM according to its substrate ( L anosterol) and activity ( D e M ethylation). The current nomenclature guidelines suggest that members of new CYP families share at least 40% amino-acid identity, while members of subfamilies must share at least 55% amino-acid identity. Nomenclature committees assign and track both base gene names ( Cytochrome P450 Homepage Archived 2010-06-27 at
3666-399: The diagnosis of H. pylori is confirmed, the first-line treatment would be a triple regimen in which pantoprazole and clarithromycin are combined with either amoxicillin or metronidazole . This treatment regimen can be given for 7–14 days. However, its effectiveness in eradicating H. pylori has been reducing from 90% to 70%. However, the rate of eradication can be increased by doubling
3744-605: The dosage of pantoprazole or increasing the duration of treatment to 14 days. Quadruple therapy (pantoprazole, clarithromycin, amoxicillin, and metronidazole) can also be used. The quadruple therapy can achieve an eradication rate of 90%. If the clarithromycin resistance rate is higher than 15% in an area, the usage of clarithromycin should be abandoned. Instead, bismuth -containing quadruple therapy can be used (pantoprazole, bismuth citrate, tetracycline , and metronidazole) for 14 days. The bismuth therapy can also achieve an eradication rate of 90% and can be used as second-line therapy when
3822-613: The drug was set to expire in 2010, but Teva Pharmaceuticals filed an Abbreviated New Drug Application (ANDA) in 2007, and Wyeth and Nycomed sued Teva for patent infringement, but Teva decided to launch its generic drug "at risk" that year, before the patent had been invalidated. Wyeth launched an authorized generic in 2008. Pfizer and Takeda's patent exclusivity expired in 2010, and an administrative exclusivity they had for pediatric use expired in January 2011, and full generic competition began. The litigation between Teva and Pfizer/Takeda
3900-530: The effect of warfarin. High doses of vitamin K should be avoided to reduce the time for rewarfarinisation once the stomach bleeding has stopped. Prothrombin complex concentrates are preferred for severe bleeding. Recombinant factor VIIa is reserved for life-threatening bleeding because of its high risk of thromboembolism. Direct oral anticoagulants (DOAC) are recommended instead of warfarin as they are more effective in preventing thromboembolism. In case of bleeding caused by DOAC, activated charcoal within four hours
3978-648: The finding is unknown, but risks and benefits are recommended for consideration in determining the use of therapy for the mother and child. In people taking PPIs for longer than six months, a dose taper is recommended prior to discontinuation. Due to its effect of reducing stomach acidity, use of pantoprazole can affect absorption of drugs that are pH-sensitive, such as ampicillin esters, ketoconazole , atazanavir , iron salts , amphetamine and mycophenolate mofetil . Additional medications that are affected include bisphosphonate derivatives, fluconazole, clopidogrel, and methotrexate. The mechanism of action of pantoprazole
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#17327880054254056-556: The first-line triple-regimen therapy has failed. NSAID-associated ulcers heal in six to eight weeks provided the NSAIDs are withdrawn with the introduction of proton pump inhibitors (PPI). For those with bleeding peptic ulcers, fluid replacement with crystalloids is sometimes given to maintain volume in the blood vessels. Maintaining haemoglobin at greater than 7 g/dL (70 g/L) through restrictive blood transfusion has been associated with reduced rate of death. Glasgow-Blatchford score
4134-410: The help of tests such as endoscopies or barium contrast x-rays . The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment, or when they first appear in a person who is over age 45 or who has other symptoms such as weight loss , because stomach cancer can cause similar symptoms. Also, when severe ulcers resist treatment, particularly if a person has several ulcers or
4212-440: The hospital, intravenous administration is indicated when patients are unable to take the medication by mouth. Pantoprazole is only indicated for the short-term treatment of erosive esophagitis in children ages seven and older; and the safety and effectiveness of pantoprazole have only been established in the treatment of erosive esophagitis in children. The incidence of adverse effects occurring in people aged 65 years and older
4290-447: The hydrophobic state of the mucus, the permeability of the lining epithelium and mitochondrial machinery of the cell itself. In this way NSAID's ulcers tend to complicate faster and dig deeper in the tissue causing more complications, often asymptomatically until a great portion of the tissue is involved. Physiological (not psychological) stress due to serious health problems, such as those requiring treatment in an intensive care unit,
4368-438: The increase is modest in comparison to the primary risk factor. Other causes of peptic ulcer disease include gastric ischaemia , drugs, metabolic disturbances, cytomegalovirus (CMV), upper abdominal radiotherapy, Crohn's disease , and vasculitis . Gastrinomas ( Zollinger–Ellison syndrome ), or rare gastrin-secreting tumors, also cause multiple and difficult-to-heal ulcers. It is still unclear whether smoking increases
4446-402: The late 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with H. pylori infection, it does not seem to independently increase risk. Even when coupled with H. pylori infection,
4524-443: The lesser curvature of the stomach. The ulcer is a round to oval parietal defect ("hole"), 2–4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irregular in the acute form of peptic ulcer, and regular but with elevated borders and inflammatory surrounding in the chronic form. In the ulcerative form of gastric cancer, the borders are irregular. Surrounding mucosa may present radial folds, as
4602-512: The navel up to the sternum , it may last from few minutes to several hours, and it may be worse when the stomach is empty. Also, sometimes the pain may flare at night, and it can commonly be temporarily relieved by eating foods that buffer stomach acid or by taking anti-acid medication. However, peptic ulcer disease symptoms may be different for everyone. Helicobacter pylori is one of the major causative factors of peptic ulcer disease. It secretes urease to create an alkaline environment, which
4680-723: The news that ulcers are a curable infection and that health can be greatly improved and money saved by disseminating information about H. pylori . In 2005, the Karolinska Institute in Stockholm awarded the Nobel Prize in Physiology or Medicine to Marshall and his long-time collaborator Warren "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease." Marshall continues research related to H. pylori and runs
4758-523: The person is asked to drink a tasteless liquid that contains the carbon as part of the substance that the bacteria breaks down. After an hour, the person is asked to blow into a sealed bag. If the person is infected with H. pylori , the breath sample will contain radioactive carbon dioxide . This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria. The possibility of other causes of ulcers, notably malignancy ( gastric cancer ), needs to be kept in mind. This
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#17327880054254836-474: The probability of getting peptic ulcers; however, it can still delay ulcer healing for those who already have a peptic ulcer. Peptic ulcers caused by NSAIDs differ from those caused by H. pylori as the latter's appear as a consequence of inflammation of the mucosa (presence of neutrophil and submucosal edema), the former instead as a consequence of a direct damage of the NSAID molecule against COX enzymes, altering
4914-402: The risk of getting peptic ulcers. The diagnosis is mainly established based on the characteristic symptoms. Stomach pain is the most common sign of a peptic ulcer. More specifically, peptic ulcers erode the muscularis mucosae , at minimum reaching to the level of the submucosa (contrast with erosions, which do not involve the muscularis mucosae). Confirmation of the diagnosis is made with
4992-403: The terminal oxidase enzymes in electron transfer chains, broadly categorized as P450-containing systems . The term "P450" is derived from the spectrophotometric peak at the wavelength of the absorption maximum of the enzyme (450 nm ) when it is in the reduced state and complexed with carbon monoxide . Most P450s require a protein partner to deliver one or more electrons to reduce
5070-476: The ulcer may contain vessels with thickened wall or with thrombosis. Conditions that may appear similar include: Prevention of peptic ulcer disease for those who are taking NSAIDs (with low cardiovascular risk) can be achieved by adding a proton pump inhibitor (PPI), an H2 antagonist , or misoprostol . NSAIDs of the COX-2 inhibitors type may reduce the rate of ulcers when compared to non-selective NSAIDs. PPI
5148-463: The ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid . An esophagogastroduodenoscopy (EGD), a form of endoscopy , also known as a gastroscopy , is carried out on people in whom a peptic ulcer is suspected. It is also the gold standard of diagnosis for peptic ulcer disease. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer
5226-432: The use of pantoprazole past a duration of 12 months. Pantoprazole may also be used in combination with antibiotics to treat ulcers caused by Helicobacter pylori . It can also be used for long-term treatment of Zollinger-Ellison syndrome . It may be used to prevent gastric ulcers in those taking NSAIDs . For improved efficacy of pantoprazole, the oral tablet formulation is taken half an hour prior to ingestion of food. In
5304-520: Was commonly recognized that bacteria were a dominant cause for the disease. Helicobacter pylori was identified in 1982 by two Australian scientists, Robin Warren and Barry J. Marshall , as a causative factor for ulcers. In their original paper, Warren and Marshall contended that most gastric ulcers and gastritis were caused by colonization with this bacterium, not by stress or spicy food , as had been assumed before. The H. pylori hypothesis
5382-616: Was first identified as causing peptic ulcers by Barry Marshall and Robin Warren in the late 20th century, a discovery for which they received the Nobel Prize in 2005. Signs and symptoms of a peptic ulcer can include one or more of the following: A history of heartburn or gastroesophageal reflux disease (GERD) and use of certain medications can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAIDs (non-steroidal anti-inflammatory drugs) that inhibit cyclooxygenase and most glucocorticoids (e.g., dexamethasone and prednisolone ). In people over
5460-543: Was first marketed in Germany in 1994. Wyeth licensed the US patent from Altana, and obtained marketing approval from the US FDA in 2000 under the trade name Protonix. In 2004, worldwide sales of the drug were $ 3.65 billion, about half of which were in the US. In 2007, Altana's drug business was acquired by Nycomed. Nycomed was in turn acquired by Takeda in 2011 and Wyeth was acquired by Pfizer in 2009. The patent protecting
5538-1154: Was marketed as a combination drug with domperidone under the brand names Aciban-DSR, Acillect-DSR, Asoprazole-D, Buffet-DXR, Depam, Domelong P, Dycizol, Eracid-D, F-Pan DSR, Fulpan-D, Fulpan-DSR, Gerdom, Gi-Fri, Gopan-D, Gopan-DSR, GR8-OD, Kurepane-DSR, Latop-D, Monpan-D, Monpan-DSR, Nupenta-DSR, Odipan-DSR, Oritop-D, Oritop-DSR, P-Bit-D, P-Bit-DSR, P-Zole DSR, P-Zole-D, PAA-DSR, Palio-D, Pamtrazol-D, Pan-D, Pancrazio-DSR, Pandiff, Pandostal, Pandostal-OD, Panfast-DSR, Panopaz-D, Panor-D, Panpot-DSR, Pansa-D, Pantact-D, Pantin-D, Pantin-RD, Pantocar-D, Pantocom-D, Pantoflux, Pantojoy-DXR, Pantokool-D, Pantolex-DS, Pantopacid-D, Pantopacid-SR, Pantorica-D, Pantozol-D, Pantozol-DSR, Pantra-D, Pantune-D, Panveda-D, Panzo-D, Panzol Plus, Panzol-D, Paz-DN, Peblo-D, Peblo-DSR, Penkool-DSR, Penlip-D, Pentalink-D, Pentastar-D, Pentozed-D, Peptac D, Peptac DSR, Pepticool-DXR, Pintel-DSR, Pop-DSR, Praize-D, Praize-D Forte, Prazole Plus, Prazosan-DSR, Predom, Predom-OD, Prolex-DSR, Prolus-DSR, Protocent-DSR, Protopan-D, Protopan-H, Ripane-D, Ripane-DSR, Trazol-DSR, PTA-D, Ulcicap-PD, Ultop DSR, Ultoz-D, Wonon-D, Wonon-DSR, and Zovanta-D. It
5616-886: Was marketed in combination with itopride under the brand names Ganaton Total, Kurepan-IT, Nupenta-ITR, P-Bit-ISR, Pepnil-ITO, Prolus-ISR, and Protopan-I. It was marketed in combination with clarithromycin and amoxicillin as Gastrocomb, Klacid Hp7, Panclamox, and ZacPac. It was marketed in combination with levosulpiride as Panlife-LS and in combination with naproxen as Arthopan. In veterinary medicine, pantoprazole appears to be safe to use in several large animal species. The pharmacokinetics of pantoprazole have been explored in several veterinary species, including calves, alpacas and foals with half lives reported as 2.81, 0.47, and 1.43 hours, respectively. Pantoprazole appears to be eliminated more quickly in goats when compared to calves, with goats having an elimination half-life of less than one hour. Pantoprazole has been demonstrated to increase
5694-3815: Was marketed under many brands worldwide, including: Acernix, Aciban, Acida, Acido-X, Acidrol, Acidwell, Acilib, Acilibre, Acillect, Acipan, Acrid, Alapanzol, Amphoter, Anagastra, Anesteloc, Antaxid, Antopral, Anulacid, Anxel, Apazol, Appryo, Aptizole, Apton, Armcid, Asoprazole, Aspan, Aurizol-P, Awamed, Azatol, Biotop V, Brandocare, Branzol, Buffet, Buscopan Reflusso, Caprol, Ciprazol, Citrel, Clessol, Comenazol, Conoran, Contix, Contracid, Contraflux, Contro-Cap, Controloc, Cool Pan, Delpanto EC, Digene Total, Digespan, Dosanloc, Empaflun, Eracid, Erprazol, Esopan, Eupantol, Exopan, Extream, Extreme, F-Pan, Farmazol, Fenix, Fexmor, Fu Shi Tan, Fulpan, Fupan, Gastblok, Gastenz, Gastrazol-L, Gastriwin, Gastrolan, Gastroloc, Gastromax, Gastronorm, Gastroprozal, Gastrostad, Gastrowell, Gastrozol, Gerdamegh, Gerprazol, Gesoflux, Gondea, Gopan, Hansazol, Hasanloc, Helix, Iboprot, Inipant, Inipepsia, Inipomp, IPP, Ippracid, Ipraalox, Kaiji, Kairol, Letopra, Loxanto, Luoxu, Lupipan, Maalox, Mag, Manez, Marozel, Monpan, Nelgast, Nexpan, Noacid, Noacid, Nolpaza, Normogastrol, Noxadif, Ntap, Nuosen, Nupenta, Oritop, Osipan, Ozepran, Ozpan, Ozzion, P-20, P-40, P-Bit, P-OD, P-PPI, P-Zole, Pacid, Paciddia, Palio, Palmy, Pamel, Pamtrazol, Pamyl, Pan, Panbloc, Pancleus, Pancrazio, Pandev, Pane, Panfast, Pangest, Panglen, Panlan, Panlisu, Panloc, Panloz, Panmeilu, Panocer, Panogastin, Panopaz, Panor, Panoral, Panore, Panpot, Panpra, Panprabene, Panprax, Panprazol, Panprazox, Panpro, Panproton, Panpure, Panrazol, Panrazole, Panrbe, Panref, Pansa, Pansec, Panso, Pantac, Pantacid, Pantact, Pantagi, Pantakind, Pantaltius, Pantap, Pantasur, Pantaz, Pantazol, Pantecta, Pantex, Pantexel, Pantezol, Panthec, Panthron, Pantid, Pantin, Pantip, Pantium, Panto, Panto-Denk, Panto-Gas, Pantobex, Pantoc, Pantocal, Pantocar, Pantocare, Pantocas, Pantocer, Pantocid, Pantocim, Pantocom, Pantocure, Pantodac, Pantodar, Pantofin, Pantofir, Pantogastrix, Pantogen, Pantogerolan, PantoJenson, Pantokem, Pantokool, Pantolax, Pantoline, Pantoloc, Pantolok, Pantolup, Pantomax, Pantomed, Pantometylentina, Pantomyl, Pantonis, Pantonix, Pantop, Pantopacid, Pantopan, Pantopaz, Pantopep, Pantopi, Pantopra-Q, Pantopraz, Pantoprazal, Pantoprazol, Pantoprazole, Pantoprazolo, Pantoprazolum, Pantoprem, Pantoprix, Pantoprol, Pantopump, Pantor, Pantorc, Pantoren, Pantorica, Pantosal, Pantosan, Pantosec, Pantosid, Pantostad, Pantotab, Pantotis, Pantover, Pantoz, Pantozim, Pantozol, Pantozole, Pantpas, Pantra, Pantrol, Pantroz, Pantul, Pantune, Pantus, Panveda, Panvell, Panz, Panzat, Panzel, Panzilan, Panzilan, Panzol, Panzole, Panzor, Parastamic, Paz, Peblo, Penkool, Penlip, Pentalink, Pentastar, Pentowin, Pentoz, Pentozed, Peploc, Peptac, Peptazol, Peptazole, Pepticaid, Pepticool, Peptix, Peptoloc, Pepzol, Perloc, Pipanzin, Pozola, Praize, Pranza, Praz-Up, Prazobloc, Prazocid, Prazolacid, Prazolan, Prazole, Prazolpan, Prazopant, Pregel, Prevacid, Previfect, Previfect, Progen, Prolex, Promtec, Propanz, Protech, Protinum, Protium, Protocent, Protocid, Protofix, Protoloc, Proton, Proton-P, Protonex, Protonil, Protonix, Protopan, PTA, Pulcet, Pumpisel, Ranloc, Razon, Rcpan, Redacib, Refluxine, Refluxopan, rifun, Ripane, Roxitrol, Sedipanto, Segregam, Seltraz, Sipar, Sodac, Somac, Sozol, Stamic, Stomafor, Stripole, Sumipral, Supacid, Super OM, Suppi, Supracam, Supracid, Surmera, Tai Mei Ni Ke, Tecta, Tonval, Topazol, Topra, Topraz, Topzole, Toraflux, Tropaz, Trupan, Ulceron, Ulcoreks, Ulcotenal, Ulprix, Ulsepan, Ulstop, Ultop, Ultoz, Unigastrozol, Vencid, Ventro-Pant, Vomizole, Wei Di, Wei Ke An, Wonon, Xotepic, Yoevid, Zamotil, Zaprol, Zencopan, Zgaton, Zimpax, Zipant, Zipantol, Zipantola, Ziprol, Zolan, Zolemer, Zolpan, Zolpanz, Zolpra, Zoltex, Zoltum, Zontop, Zoprax, Zovanta, Zurcal, and Zurcazol. It
5772-407: Was one of the top 10 most prescribed medications between 2017 and 2023. Pantoprazole is used for short-term treatment of erosion and ulceration of the esophagus for adults and children five years of age and older caused by gastroesophageal reflux disease . It can be used as a maintenance therapy for long-term use after initial response is obtained, but there have not been any controlled studies about
5850-533: Was published in 1984 in the Australian Medical Journal and is among the most cited articles from the journal. In 1997, the Centers for Disease Control and Prevention , with other government agencies, academic institutions, and industry, launched a national education campaign to inform health care providers and consumers about the link between H. pylori and ulcers. This campaign reinforced
5928-410: Was settled in 2013, with Teva paying the patent holders $ 2.15 billion in damages for its early launch. As of 2017, the drug was marketed under many brands worldwide, including as a combination drug with domperidone , a combination with itopride , in combination with both clarithromycin and amoxicillin , in combination with levosulpiride , and in combination with naproxen . As of 2017, it
6006-415: Was similar to that in people aged 65 years and less. In reproductive studies using doses largely greater than the recommended doses performed on rats and rabbits, there was no evident harm on the development of the baby. Pantoprazole has been found to pass through the breast milk. Additionally, in rodent cancer studies, pantoprazole has been shown to potentially cause tumor growth. The clinical relevance of
6084-405: Was still poorly received, so in an act of self-experimentation Marshall drank a Petri dish containing a culture of organisms extracted from a person with an ulcer and five days later developed gastritis. His symptoms disappeared after two weeks, but he took antibiotics to kill the remaining bacteria at the urging of his wife, since halitosis is one of the symptoms of infection. This experiment
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