Pantoprazole

383.37

383.37

1312995-182-4

759257

DTXSID4023416

Off-white solid

A02BC02|A - Alimentary tract and metabolism

106

2.4

Solid

1.51±0.1 g/cm3(Predicted)

139-140 °C (decomp)

586.9±60.0 °C(Predicted)

308.7±32.9 °C

1.643

Freely soluble in water.In water, 48 mg/L at 25 deg C /Estimated/

1.25X10-12 mm Hg at 25 deg C /Estimated/

3.92and 8.19

Henry's Law constant = 5.84X10-20 atm-cu m/mol at 25 °C /Estimated/

3.92 and 8.19|pKa1 = 3.92, pKa2 = 8.19

183.4 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]|188.02 Ų [M-H]-

Freely soluble in water, very slightly soluble in phosphate buffer at pH 7.4, and practically insoluble in hexane. /Sodium/|White to off-white crystalline powder and is racemic /Sodium sesquihydrate/|Hydroxyl radical reaction rate constant = 1.0X10-14 cu cm/molc-sec at 25 °C /Estimated/

III

8

UN 3265 8/PG 2

3

20/21/22-37/38-41-48

22-26-36/37/39-45

Xn

P201, P202, P260, P261, P263, P264, P270, P271, P273, P280, P281, P301+P312, P302+P352, P304+P312, P304+P340, P305+P351+P338, P308+P313, P312, P321, P322, P330, P332+P313, P337+P313, P362, P363, P391, P403+P233, P405, P501

H302+H312+H332

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl pantoprazole sodium, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Pantoprazole Sodium/

Der G; An Overview of Proton Pump Inhibitors; Gastroenterol Nurs 26 (5): 182-90 (2003)|Poole P; Pantoprazole; Am J Health Syst Pharm 58 (11): 999-1008 (2001). The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of pantoprazole are reviewed.

|Warning|H302+H312+H332 (20%): Harmful if swallowed, in contact with skin or if inhaled [Warning Acute toxicity, oral; acute toxicity, dermal; acute toxicity, inhalation]|P261, P264, P270, P271, P280, P301+P312, P302+P352, P304+P312, P304+P340, P305+P351+P338, P312, P321, P322, P330, P332+P313, P337+P313, P362, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 10 companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

**Rat Oral LD 50** 747 mg/kg **Tumorigenicity** Because of the chronic nature of GERD, there may be a potential for long-term administration of pantoprazole. In long-term rodent studies, pantoprazole was carcinogenic and its administration lead to rare types of gastrointestinal tumors. The relevance of these findings to tumor development in humans is unknown at this time. **Teratogenic Effects** This drug falls under pregnancy category B category. Reproduction studies have been performed in rats at oral doses up to 88 times the recommended human dose (RHD), as well as in rabbits at oral doses up to 16 times the RHD, and have shown no evidence of impaired fertility or harm to the fetus caused by pantoprazole. No adequate and well-controlled studies in pregnant women have been completed. Because animal reproduction studies are not always predictive of human response, this drug should only be used during pregnancy if clearly required. **Nursing Mothers** Pantoprazole and its metabolites have been found to be excreted in the milk of rats. Pantoprazole excretion in human milk has been found in a study performed with a single nursing mother after one 40 mg oral dose. The clinical relevance of this finding is not known, however, it is advisable to take note of this finding when considering pantoprazole use during nursing. Many drugs excreted in human breastmilk have a risk for serious adverse effects in nursing infants.

Despite its wide use, pantoprazole has only rarely been associated with hepatic injury. In large scale, long term trials of pantoprazole, serum ALT elevations have occurred in less than 1% of patients and at rates similar to those that occur with placebo or comparator drugs. Only a small number of cases of clinically apparent liver disease attributed to pantoprazole have been published, but the clinical pattern of injury has resembled acute hepatic necrosis which has been described with other proton pump inhibitors. Clinically apparent liver injury due to proton pump inhibitors generally arises within the first 4 weeks of therapy and is characterized by an acute hepatocellular pattern of injury with rapid recovery upon withdrawal. Rash, fever and eosinophilia are rare, as is autoantibody formation. In large case series of drug induced liver injury, pantoprazole has accounted for few instances of symptomatic acute liver injury.

Pantoprazole causes prolonged inhibition of gastric acid secretion, and thereby may interfere with the absorption of these medications /ampicillin or iron salts or ketoconazole/ and others for which bioavailability is determined by gastric pH. /Pantoprazole sodium/|Pantoprazole, although metabolized by hepatic cytochrome p450 systems, does not appear to either inhibit or induce cytochrome p450 enzyme activity. To date, no clinically significant interactions have been noted from such commonly used drugs as diazepam, phenytoin, nifedipine, theophylline, digoxin, warfarin, or oral contraceptives. /Pantoprazole sodium/|Pantoprazole, by increasing gastric pH, has the potential to affect the bioavailability of any medication for which absorption is pH-dependent. Also, pantoprazole may prevent the degradation of acid-labile drugs. /Pantoprazole sodium/|In other in vivo studies, ethanol, glyburide, caffeine, antipyrine, metronidazole, and amoxicillin, had no clinically relevant interactions with pantoprazole. /Pantoprazole sodium/

Approximately 98%

Pantoprazole's production and use as a antiulcerative(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 13,000(SRC), determined from a structure estimation method(2), indicates that pantoprazole is expected to be immobile in soil(SRC). The pKa1 and pKa2 of pantoprazole are 3.92 and 8.19(3), respectively, indicating that this compound will primarily exist in the protonated form in the environment and cations generally adsorb to organic carbon and clay more strongly than their neutral counterparts(4). Volatilization of pantoprazole from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.84X10-20 atm-cu m/mole(SRC), using a fragment constant estimation method(5). Pantoprazole is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.25X10-12 mm Hg(SRC), determined from a fragment constant method(6). Biodegradation of pantoprazole in soil is unknown(SRC).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 13,000(SRC), determined from a structure estimation method(2), indicates that pantoprazole is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 5.84X10-20 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). The pKa1 and pKa2 of pantoprazole are 3.92 and 8.19(5), respectively, indicating that this compound will primarily exist in the protonated form in the environment; cations generally adsorb more strongly to suspended solids and sediment than their neutral counterparts(6). According to a classification scheme(7), an estimated BCF of 10.3(SRC), from an estimated log Kow of 2.22(8) and a regression-derived equation(9), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Biodegradation of pantoprazole in water is unknown(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), pantoprazole, which has a an estimated vapor pressure of 1.25X10-12 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase pantoprazole may be removed from the air by wet and dry deposition(SRC).

Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Pantoprazole may be susceptible to direct photolysis in aqueous solution or on soil(SRC), since the sodium salt has a maximum absorption at 289 nm(1).

An estimated BCF of 10.3 was calculated for pantoprazole(SRC), using an estimated log Kow of 2.22(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc for pantoprazole can be estimated to be 13,000(SRC). According to a classification scheme(2), this estimated Koc value suggests that pantoprazole is expected to be immobile in soil. The pKa1 and pKa2 of pantoprazole are 3.92 and 8.19(3), respectively, indicating that this compound will primarily exist in the protonated form in the environment. Cations generally adsorb more strongly to organic carbon and clay than their neutral counterparts(4).

The Henry's Law constant for pantoprazole is estimated as 5.84X10-20 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that pantoprazole is expected to be essentially nonvolatile from water surfaces(2). The pKa1 and pKa2 of pantoprazole are 3.92 and 8.19(3), respectively, indicating that this compound will primarily exist in the protonated form in the environment therefore volatilization from moist soil and water surfaces are not expected to be an important fate process. Pantoprazole is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure 1.25X10-12 mm Hg(SRC), determined from a fragment constant method(4).

Pantoprazole and its metabolites are excreted in the milk of rats. It is not known whether pantoprazole is excreted in human milk. ...

Occupational exposure to pantoprazole may occur through inhalation and dermal contact with this compound at workplaces where pantoprazole is produced or used. The general population may be exposed to pantoprazole via ingestion of pharmaceutical products containing pantoprazole. (SRC)

**Pantoprazole Injection**: **Treatment of gastroesophageal reflux disease associated with a history of erosive esophagitis** Pantoprazole for injection is indicated for short-term treatment (7-10 days) of patients having gastroesophageal reflux disease (GERD) with a history of erosive esophagitis, as an alternative to oral medication in patients who are unable to continue taking pantoprazole delayed-release tablets. _Safety and efficacy of pantoprazole injection as the initial treatment of patients having GERD with a history of erosive esophagitis have not been demonstrated at this time_. **Pathological Hypersecretion Associated with Zollinger-Ellison Syndrome** Pantoprazole for injection is indicated for the treatment of pathological hypersecretory conditions associated with Zollinger-Ellison Syndrome or other neoplastic conditions. **Pantoprazole delayed-release oral suspension**: **Short-Term Treatment of erosive esophagitis associated with gastroesophageal reflux disease (GERD)** Indicated in adults and pediatric patients five years of age and above for the short-term treatment (up to 8 weeks) in the healing and symptomatic relief of erosive esophagitis. For adult patients who have not healed after 8 weeks of treatment, an additional 8-week course of pantoprazole may be considered. Safety of treatment beyond 8 weeks in pediatric patients has not been determined. **Maintenance of healing of erosive esophagitis** Indicated for maintenance of healing of erosive esophagitis and reduction in relapse rates of daytime and nighttime heartburn symptoms in adult patients with GERD. **Pathological hypersecretory conditions including Zollinger-Ellison syndrome** Indicated for the long-term treatment of the above conditions.|FDA Label|Short-term treatment of reflux symptoms (e.g. heartburn, acid regurgitation) in adults.|Short-term treatment of reflux symptoms (e.g. heartburn, acid regurgitation) in adults.,|Treatment of Helicobacter spp. infections

Pantoprazole is a proton pump inhibitor (PPI) and a potent inhibitor of gastric acidity which is widely used in the therapy of gastroesophageal reflux and peptic ulcer disease. Pantoprazole therapy is associated with a low rate of transient and asymptomatic serum aminotransferase elevations and is a rare cause of clinically apparent liver injury.

Antiulcer Agents

Pantoprazole delayed-release tablets are indicated for the short-term (up to 8 weeks) treatment of heartburn and other symptoms associated with gastroesophageal reflux disease (GERD). Pantoprazole for injection is indicated for the short-term (7 to 10 days) treatment of GERD in patients who are unable to continue taking pantoprazole delayed-release tablets. Pantoprazole for injection is not indicated for initial treatment of GERD. /Included in US product labeling/ /Pantoprazole sodium/|Pantoprazole is indicated for the prevention of relapse in patients with reflux esophagitis. /NOT included in US product labeling/ /Pantoprazole sodium/|Pantoprazole is indicated for short-term (up to 4 weeks) treatment for symptom relief and healing in patients with active duodenal ulcer. /NOT included in US product labeling/ /Pantoprazole sodium/|Pantoprazole, in combination with clarithromycin and either amoxicillin or metronidazole, is indicated for treatment of patients with an active duodenal ulcer who are Helicobacter pylori positive. /NOT included in US product labeling/ /Pantoprazole sodium/|For more Therapeutic Uses (Complete) data for PANTOPRAZOLE (6 total), please visit the HSDB record page.

Anaphylaxis has been reported with the use of IV pantoprazole sodium. Immediate medical intervention and drug discontinuance are required if anaphylaxis or other severe hypersensitivity reactions occurs. /Pantoprazole sodium/|Adverse effects occurring in more than 1% of patients receiving oral pantoprazole for up to 8 weeks and more frequently than in those receiving placebo include diarrhea and hyperglycemia. Adverse effects occurring in 1% or more of patients receiving oral pantoprazole for up to 12 months and more frequently than in those receiving ranitidine include headache, abdominal pain, and abnormal liver function test results. Adverse effects occurring in 4% or more of patients receiving IV pantoprazole and that were possibly, probably, or definitely related to treatment include abdominal pain, chest pain, rash, and pruritus. Adverse effects occurring in more than 1% of patients receiving IV pantoprazole and that generally had an unclear relationship to the drug include headache, injection site reaction, dyspepsia, diarrhea, vomiting, dizziness, and rhinitis. /Pantoprazole sodium/|There have been spontaneous reports of adverse events; angioedema (Quincke's edema); anterior ischemic optic neuropathy; severe dermatologic reactions, including erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis (TEN, some fatal); hepatocellular damage leading to jantice and and hepatic failure; pancreatitis; pancytopenia; and rhabdomyolysis. In addition, also observed have been confusion, hypokinesia, speech disorder, increased salivation, vertigo, nausea, tinnitus, and blurred vision. /Pantoprazole sodium/|FDA Pregnancy Risk Category: B /NO EVIDENCE OF RISK IN HUMANS. Adequate, well controlled studies in pregnant women have not shown increased risk of fetal abnormalities despite adverse findings in animals, or, in the absence of adequate human studies, animal studies show no fetal risk. The chance of fetal harm is remote but remains a possibility./ /Pantoprazole sodium/|For more Drug Warnings (Complete) data for PANTOPRAZOLE (8 total), please visit the HSDB record page.

This drug acts to decrease gastric acid secretion, which reduces stomach acidity. Pantoprazole administration leads to long-lasting inhibition of gastric acid secretion. **General Effects** Pantoprazole has been shown to reduce acid reflux-related symptoms, heal inflammation of the esophagus, and improve patient quality of life more effectively than histamine-2 receptor antagonists (H2 blockers). This drug has an excellent safety profile and a low incidence of drug interactions. It can be used safely in various high-risk patient populations, including the elderly and those with renal failure or moderate hepatic dysfunction. Due to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as pantoprazole have been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal _C. difficile_), reduced absorption of micronutrients including iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life. PPIs such as pantoprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginie (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary syndromes. **A note on laboratory testing abnormalities** During treatment with antisecretory medicinal products such as pantoprazole, serum gastrin (a peptide hormone that stimulates secretion of gastric acid) increases in response to the decreased acid secretion caused by proton pump inhibition. The increased gastrin level may interfere with investigations for neuroendocrine tumors. Published evidence suggests that proton pump inhibitors should be stopped 14 days before chromogranin A (CgA) measurements. This permits chromogranin A levels, that might be falsely elevated after proton pump inhibitor treatment, to return to the normal reference range. Reports have been made of false-positive results in urine screening tests for tetrahydrocannabinol (THC) in patients receiving the majority of proton pump inhibitors, including pantoprazole. A confirmatory method should be used.

Compounds that inhibit H(+)-K(+)-EXCHANGING ATPASE. They are used as ANTI-ULCER AGENTS and sometimes in place of HISTAMINE H2 ANTAGONISTS for GASTROESOPHAGEAL REFLUX. (See all compounds classified as Proton Pump Inhibitors.)|Various agents with different action mechanisms used to treat or ameliorate PEPTIC ULCER or irritation of the gastrointestinal tract. This has included ANTIBIOTICS to treat HELICOBACTER INFECTIONS; HISTAMINE H2 ANTAGONISTS to reduce GASTRIC ACID secretion; and ANTACIDS for symptomatic relief. (See all compounds classified as Anti-Ulcer Agents.)

Pantoprazole is absorbed after oral administration as an enteric-coated tablet with maximum plasma concentrations attained within 2 – 3 hours and a bioavailability of 77% that does not change with multiple dosing. Following an oral dose of 40mg, the Cmax is approximately 2.5 μg/mL with a tmax of 2 to 3 hours. The AUC is approximately 5 μg.h/mL. There is no food effect on AUC (bioavailability) and Cmax. Delayed-release tablets are prepared as enteric-coated tablets so that absorption of pantoprazole begins only after the tablet leaves the stomach.|After a single oral or intravenous (IV) dose of 14C-labeled pantoprazole to healthy, normal metabolizing subjects, about 71% of the dose was excreted in the urine, with 18% excreted in the feces by biliary excretion. There was no kidney excretion of unchanged pantoprazole.|The apparent volume of distribution of pantoprazole is approximately 11.0-23.6 L, distributing mainly in the extracellular fluid.|**Adults**: With intravenous administration of pantoprazole to extensive metabolizers, total clearance is 7.6-14.0 L/h. In a population pharmacokinetic analysis, the total clearance increased with increasing body weight in a non-linear fashion. **Children**: clearance values in the children 1 to 5 years old with endoscopically proven GERD had a median value of 2.4 L/h.|Time to peak concentration: Following an oral dose of 40 mg in extensive metabolizers with normal hepatic function: 2.4 hours. When pantoprazole is taken with food, the time to peak concentration is variable and may be significantly increased. /Pantoprazole sodium/|Peak serum concentration: Following an oral dose of 40 mg in extensive metabolizers with normal hepatic function: 2.4 ug/mL. Following an intravenous dose of 40 mg administered over 15 minutes to extensive metabolizers with normal hepatic function: 5.51 ug/mL. /Pantoprazole sodium/|Elimination: Renal: 71%. Fecal: 18% (biliary excretion). Dialysis removes insignificant amounts of pantoprazole. /Pantoprazole sodium/|Rapidly absorbed. However, absorption maybe delayed up to 2 hours or more if pantoprazole is taken with food. Bioavailability (oral): 77%. /Pantoprazole sodium/|For more Absorption, Distribution and Excretion (Complete) data for PANTOPRAZOLE (6 total), please visit the HSDB record page.

Pantoprazole is heavily metabolized in the liver by the cytochrome P450 (CYP) system. Pantoprazole metabolism is independent of the route of administration (intravenous or oral). The main metabolic pathway is _demethylation_, by _CYP2C19_ hepatic cytochrome enzyme, followed by sulfation; other metabolic pathways include oxidation by CYP3A4. There is no evidence that any of the pantoprazole metabolites are pharmacologically active. After hepatic metabolism, almost 80% of an oral or intravenous dose is excreted as metabolites in urine; the remainder is found in feces and originates from biliary secretion.|Pantoprazole is extensively metabolized in the liver through the cytochrome P450 (CYP) system. Pantoprazole metabolism is independant of route of administration (intravenous or oral). The main metabolic pathway is demethylation,by CYP2C19, with subsequent sulfation; other metabolic pathways include oxidation by CYP3A4. ... CYP2C19 displays a known genetic polymorphism due to its deficiency in some sub-populations (eg 3% of Caucasians and African-Americans and 17 to 23% of Asians). /Pantoprazole sodium/

About 1 hour|Elimination: Following oral or intravenous administration: 1 hour. The half-life of pantoprazole is prolonged (7 to 9 hours) in patients with cirrhosis of the liver and in genetically determined slow metabolizers (3.5 to 10 hours). /Pantoprazole sodium/

Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump, expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid). Proton pump inhibitors such as pantoprazole are substituted _benzimidazole_ derivatives, weak bases, which accumulate in the acidic space of the parietal cell before being converted in the _canaliculi_ (small canal) of the gastric parietal cell, an acidic environment, to active _sulfenamide_ derivatives. This active form then makes disulfide bonds with important cysteines on the gastric acid pump, inhibiting its function. Specifically, pantoprazole binds to the _sulfhydryl group_ of H+, K+-ATPase, which is an enzyme implicated in accelerating the final step in the acid secretion pathway. The enzyme is inactivated, inhibiting gastric acid secretion. The inhibition of gastric acid secretion is stronger with proton pump inhibitors such as pantoprazole and lasts longer than with the H(2) antagonists.|Pantoprazole is a proton pump inhibitor. It accumulates in the acidic compartment of parietal cells and is converted to the active form, a sulfanilamide, which binds to hydrogen-potassium-ATP-ase at the secretory surface of gastric parietal cells. Inhibition of hydrogen-potassium-ATPase blocks the final step of gastric acid production, leading to inhibition of both basal and stimulated acid secretion. The duration of inhibition of acid secretion does not correlate with the much shorter elimination half-life of pantoprazole. /Pantoprazole sodium/

Pantoprazole is not removed by hemodialysis. In cases of overdosage, treatment should be symptomatic and supportive

/SIGNS AND SYMPTOMS/ Anaphylaxis has been reported with the use of IV pantoprazole sodium. Immediate medical intervention and drug discontinuance are required if anaphylaxis or other severe hypersensitivity reactions occurs. /Pantoprazole sodium/|/CASE REPORTS/ There have been spontaneous reports of overdosage with pantoprazole, including a suicide in which pantoprazole 560 mg and undetermined amounts of chloroquine and zopiclone were also ingested. There have also been spontaneous reports of patients taking similar amounts of pantoprazole (400 and 600 mg) with no adverse effects. /Pantoprazole sodium/|/CASE REPORTS/ A 61 -year-old man took one tablet of pantoprazole 40 mg one year after first being treated with the drug. Within hours after ingestion, he developed malaise, generalized pruritus and urticaria, a swollen tongue and eyes, and diffuse sweating; his blood pressure decreased to 75/50 mm Hg. Because of the acute onset of symptoms and close temporal association with exposure to the drug, as well as previous exposure to it, the reactions can be classified as anaphylactic shock to PPIs. /Pantoprazole sodium/|/CASE REPORTS/ A case of acute interstitial nephritis, which developed after 6 weeks of treatment with pantoprazole /was reported/. A 23-year-old man presented with acute renal failure requiring renal replacement therapy. Acute interstitial nephritis was diagnosed by renal biopsy and was successfully treated with corticosteroids and withdrawal of pantoprazole. /Pantoprazole sodium/|/CASE REPORTS/ A 46-year-old woman presented for an emergency admission because of colic-like upper abdominal pain and markedly impaired general condition. Eight days before admission she had started and continued to take pantoprazole because of symptoms of gastroesophageal reflux. Clinical examination and laboratory tests indicated abnormal liver functions suggesting hepatitis. Serology largely excluded an infectious, autoimmunological or metabolic cause. Duplex sonography gave no evidence of bile obstruction or Budd-Chiari syndrome. The patient's condition and laboratory tests after the drug had been discontinued gradually improved on symptomatic treatment, indicating pantoprazole-induced hepatitis. Intake of proton pump inhibitors is a rare cause but should be considered in the differential diagnosis of hepatitis of uncertain etiology. /Pantoprazole sodium/

BY 1023

Pantoprazole is available as enteric coated tablets containing 45.1 mg of the sodium salt sesquihydrate equivalent to 40 mg ... of the free anhydrous acid, and as a lyophylisate for iv infusion.|Trade name: Protonix

Preparation: B. Kohl et al, EP 166287; eidem, US 4758579 (1986, 1988 both to Byk Gluden)|Information available in 2004 indicated that Pantoprazole was used in the manufacture of pharmaceutical preparations in the following countries: Algeria, Argentina, Bahrain, Brazil, Costa Rica, Dominican Republic, El Salvador, Guatemala, Honduras, India, Iraq, Israel, Jordan, Lebanon, Libyan Arab Jamahiriya, Luxembourg, Malaysia, Mexico, Nicaragua, Nigeria, Oman, Panama, Poland, Portugal, Romania, Saudi Arabia, Singapore, Somalia, South Africa, Sudan, Thailand, Tunisia, United Arab Emirates, Yemen (1,2)|Information available in 2004 indicated that Pantoprazole sodium was used in the manufacture of pharmaceutical preparations in the following countries: Argentina, Australia, Austria, Belgium, Brazil, Canada, Chile, Colombia, Croatia, Czech Republic, Denmark, Ecuador, Finland, France, Germany, Greece, Hong Kong, Hungary, India, Indonesia, Ireland, Italy, Luxembourg, Mexico, Netherlands, New Zealand, Norway, Poland, Portugal, Romania, Slovenia, South Africa, Spain, Sweden, Switzerland, Turkey, United Kingdom, USA, Yugoslavia (1,2) /Pantoprazole sodium/

HPLC determination in plasma and serum

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