Determination of Lansoprazole by Direct Injection of Plasma and High Performance Liquid Chromatography with Column Switching

High performance liquid chromatography with column switching has been developed for the determination of lansoprazole in plasma. The plasma samples were injected onto a pretreatment column packed with LiChromprep RP2 (25～40 mm) after simple dilution with distilled water. Distilled water was used to wash out protein and other polar components in plasma. After switching, the concentrated lansoprazole was eluted in the backflush mode onto a Shimpack CLC ODS column with methanol 0 2 mol·L 1 ammonium acetate (65:35) as mobile phase. Purge solutions were used for clean up and for regenerating the pretreatment column. The method showed good precision and recovery. The detection limit was 0 005 mg·L -1 plasma. The RSD’s (intra and interday) were less than 2 5% and 5 3% respectively. The method has been successfully used to determine pharmacokinetics of lansoprazole in Chinese volunteers.

Proton pump inhibitor treatment of patients with gastroesophageal reflux-related chronic cough:A comparison between two different daily doses of lansoprazole

AIM： To compare two different daily doses of lansoprazole given for 12 weeks and to assess the role of gastrointestinal （GI） investigations as criteria for selecting patients. METHODS： Out of 45 patients referred for unexplained chronic persistent cough, 36 had at least one of the GI investigations （endoscopy, 24-h esophageal pH- metry and a 4-week trial of proton pump inhibitor （PPI） therapy） positive and were randomly assigned to receive either 30 mg lansoprazole o.d. or 30 mg lansoprazole b.i.d, for 12 weeks. Symptoms were evaluated at baseline （visit 1） after the PPI test （visit 2） and after the 12-week lansoprazole treatment period （visit 3）. RESULTS： Thirty-five patients completed the study protocol. Twenty-one patients （60.0%） reported complete relief from their cough with no difference between the two treatment groups （58.8% and 61.1% had no cough in 30 mg lansoprazole and 60 mg lansoprazole groups, respectively）. More than 80% of the patients who had complete relief from their cough at the end of the treatment showed a positive response to the PPI test. CONCLUSION： Twelve weeks of lansoprazole treatment even at a standard daily dose, is effective in patients with chronic persistent cough. A positive response to an initial PPI test seems to be the best criterion for selecting patients who respond to therapy.

Maintenance for healed erosive esophagitis:PhaseⅢcomparison of vonoprazan with lansoprazole

AIM To compare vonoprazan 10 and 20 mg vs lansoprazole 15 mg as maintenance therapy in healed erosive esophagitis(EE).METHODS A total of 607 patients aged ≥ 20 years, with endoscopically-confirmed healed EE following 8 wk of treatment with vonoprazan 20 mg once daily, were randomized 1:1:1 to receive lansoprazole 15 mg(n = 201), vonoprazan 10 mg(n = 202), or vonoprazan 20 mg(n = 204), once daily. The primary endpoint of the study was the rate of endoscopically-confirmed EE recurrence during a 24-wk maintenance period. The secondary endpoint was the EE recurrence rate at Week 12 during maintenance treatment. Additional efficacy endpoints included the incidence of heartburn and acid reflux, and the EE healing rate 4 wk after the initiation of maintenance treatment. Safety endpoints comprised adverse events(AEs), vital signs, electrocardiogram findings, clinical laboratory results, serum gastrin and pepsinogen Ⅰ/Ⅱ levels, and gastric mucosa histopathology results.RESULTS Rates of EE recurrence during the 24-wk maintenance period were 16.8%, 5.1%, and 2.0% with lansoprazole 15 mg, vonoprazan 10 mg, and vonoprazan 20 mg, respectively. Vonoprazan was shown to be non-inferior to lansoprazole 15 mg(P < 0.0001 for both doses). In a post-hoc analysis, EE recurrence at Week 24 was significantly reduced with vonoprazan at both the 10 mg and the 20 mg dose vs lansoprazole 15 mg(5.1% vs 16.8%, P = 0.0002, and 2.0% vs 16.8%, P < 0.0001, respectively); by contrast, the EE recurrence rate did not differ significantly between the two doses of vonoprazan(P = 0.1090). The safety profiles of vonoprazan 10 and 20 mg were similar to that of lansoprazole 15 mg in patients with healed EE. Treatment-related AEs were reported in 11.4%, 10.4%, and 10.3% of patients in the lansoprazole 15 mg, vonoprazan 10 mg, and vonoprazan 20 mg arms, respectively.CONCLUSION Our findings confirm the non-inferiority of vonoprazan 10 and 20 mg to lansoprazole 15 mg as maintenance therapy for patients with healed EE.

Comparative study of omeprazole, lansoprazole, pantoprazole and esomeprazole for symptom relief in patients with reflux esophagitis

AIM: To clarify whether there is any difference in the symptom relief in patients with reflux esophagitis following the administration of four Proton pump inhibitors (PPIs). METHODS: Two hundred and seventy-four patients with erosive reflux esophagitis were randomized to receive 8 wk of 20 mg omeprazole (n = 68), 30 mg of lansoprazole (n = 69), 40 mg of pantoprazole (n = 69), 40 mg of esomeprazole (n = 68) once a day in the morning. Daily changes in heartburn and acid reflux symptoms in the first 7 d of administration were assessed using a six-point scale (0: none; 1: mild; 2: mild-moderate; 3: moderate; 4: moderate-severe; 5: severe). RESULTS: The mean heartburn score in patients treated with esomeprazole more rapidly decreased than those receiving other PPI. Complete resolution of heartburn was also more rapid in patients treated with esomeprazole for 5 d compared with omeprazole (P = 0.0018, P = 0.0098, P = 0.0027, P = 0.0137, P = 0.0069, respectively), lansoprazole (P = 0.0020, P = 0.0046, P = 0.0037, P = 0.0016, P = 0.0076, respectively), and pantoprazole (P = 0.0006, P = 0.0005, P = 0.0009, P = 0.0031, P = 0.0119, respectively). There were no significant differences between the four groups in the rate of endoscopic healing of reflux esophagitis at week 8. CONCLUSION: Esomeprazole may be more effective than omeprazole, lansoprazole, and pantoprazole for the rapid relief of heartburn symptoms and acid reflux symptoms in patients with reflux esophagitis.

Comparative study of esomeprazole and lansoprazole in triple therapy for eradication of Helicobacter pylori in Japan

AIM: To evaluate the efficacy and safety of esomeprazole-based triple therapy compared with lansoprazole therapy as first-line eradication therapy for patients with Helicobacter pylori (H. pylori) in usual post-marketing use in Japan, where the clarithromycin (CAM) resistance rate is 30%.

Molecular mechanism and functional consequences of lansoprazole-mediated heme oxygenase-1 induction

AIM： To investigate the molecular mechanism and functional consequences of heme oxygenase-1 （HO-1） activation by lansoprazole in endothelial cells and macrophages. METHODS： Expression of HO-1 mRNA was analyzed by Northern blotting. Western blotting was used to determine the HO-1 and ferritin protein levels. NADPH-dependent reactive oxygen species （ROS） formation was measured with lucigenin-enhanced chemiluminescence. HO-1 promoter activity in mouse fibroblasts, stably transfected with a 15-kb HO-1 gene that drives expression of the reporter gene luciferase, was assessed usingin vivo bioluminescence imaging. RESULTS： Lansoprazole levels in endothelial cells increased HO-1 mRNA and HO-1 protein levels in macrophages. In addition, lansoprazole-induced ferritin protein levels in both cell systems. Moreover, induction of the antioxidant proteins HO-1 and ferritin by lansoprazole was followed by a decrease in NADPH- mediated ROS formation. The radical scavenging properties of lansoprazole were diminished in the presence of the HO inhibitor, chromium mesoporphyrin IX. Induction of HO-1 gene expression by lansoprazole was not related to oxidative stress or to the activation of the mitogen-activated protein kinase pathway. However, the phosphatidylinositol 3-kinase inhibitor LY294002 showed a concentration-dependent inhibition of HO-1 mRNA and promoter activity.CONCLUSION： Activation of HO-1 and ferritin may account for the gastric protection of lansoprazole and is dependent on a pathway blocked by LY294002.

Lansoprazole prevents experimental gastric injury induced by non-steroidal anti-inflammatory drugs through a reduction of mucosal oxidative damage

AIM:This study investigated the mechanisms of protection afforded by the proton pump inhibitor lansoprazole against gastric injury induced by different non-steroidal anti-inflammatory drugs (NSAIDs) in rats. METHODS: Male Sprague-Dawley rats were orally treated with indomethacin (100 μmol/kg), diclofenac (60 μmol/kg), piroxicam (150 μmol/kg) or ketoprofen (150 μmol/kg). Thirty minutes before NSAIDs, animals were orally treated with lansoprazole 18 or 90 umol/kg. Four hours after the end of treatments, the following parameters were assessed: gastric mucosal PGE2, malondialdehyde (MDA), myeloperoxidase (MPO) or non-proteic sulfhydryl compounds (GSH) levels; reverse transcription-polymerase chain reaction (RT-PCR) of mucosal COX-2 mRNA; gastric acid secretion in pylorus-ligated animals; in vitro effects of lansoprazole (1-300 μmol/L) on the oxidation of low density lipoproteins (LDLs) induced by copper sulphate. RESULTS: All NSAIDs elicited mucosal necrotic lesions which were associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels were detected in the gastric mucosa of indomethacin- or piroxicam-treated animals. Indomethacin enhanced mucosal cyclooxygenase-2 expression, while not affecting cyclooxygenase-1. At the oral dose of 18 μmol/kg lansoprazole partly counteracted diclofenac-induced mucosal damage, whereas at 90 μmol/kg it markedly prevented injuries evoked by all test NSAIDs. Lansoprazole at 90 μmol/kg reversed also the effects of NSAIDs on MPO, MDA and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced cyclooxygenase-2 expression. However, both lansoprazole doses markedly inhibited acid secretion in pylorus-ligated rats. Lansoprazole concentration-dependently reduced the oxidation of LDLs in vitro. CONCLUSION: These results suggest that, besides the inhibition of acid secretion, lansoprazole protection against NSAID-induced gastric damage depends on a reduction in mucosal oxidative injury, which is also responsible for an increment of sulfhydryl radical bioavailability. It is also suggested that lansoprazole does not influence the down-regulation of gastric prostaglandin production associated with NSAID treatment.

Lansoprazole-associated collagenous colitis:Diffuse mucosal cloudiness mimicking ulcerative colitis

There have only been a few reports on lansoprazole-associated collagenous colitis. Colonic mucosa of collagenous colitis is known to be endoscopically normal. We present a case of collagenous colitis where the mucosa showed diffuse cloudiness mimicking ulcerative colitis. A 70-year-old woman developed watery diarrhea four to nine times a day. She had interstitial pneumonia at 67 and reflux esophagitis at 70 years. Lansoprazole 30 mg/d had been prescribed for reflux esophagitis for nearly 6 mo. Lansoprazole was withdrawn due to its possible side effect of diarrhea. Colonoscopy disclosed diffuse cloudiness of the mucosa which suggested ulcerative colitis. Consequently sulfasalazine 2 g/d was started. The patient's diarrhea dramatically disappeared on the following day. However, biopsy specimens showed subepithelial collagenous thickening and infi ltration of inflammatory cells in the lamina propria, confirming the diagnosis of collagenous colitis. One month after sulfasalazine therapy was initiated, colonoscopic and histological abnormalities resolved completely. Five months later the diarrhea recurred. The findings on colonoscopy and histology were the same as before, confirming a diagnosis of collagenous colitis relapse. We found that the patient had begun to take lansoprazole again 3 mo ahead of the recent diarrhea. Withdrawal of lansoprazole promptly resolved the diarrhea. Endoscopic and histological abnormalities were also completely resolved, similar to the first episode. Retrospectively, the date of commencement of sulfasalazine and discontinuation of lansoprazole in the first episode was found to be the same. We conclude that this patient had lansoprazole-associated collagenous colitis.

Vonoprazan 20 mg vs lansoprazole 30 mg for endoscopic submucosal dissection-induced gastric ulcers

AIM To compare the healing effects of vonoprazan and lansoprazole on gastric ulcers induced by endoscopic submucosal dissection(ESD).METHODS Data were obtained from a total of 26 patients.Fourteen patients were randomized to the vonoprazan group and 12 were randomized to the lansoprazole group.Patients were administered either 20 mg vonoprazan or 30 mg lansoprazole per day after ESD.Endoscopic images just after ESD,on day 8,and on day 28 were used for the evaluation of the shrinking rate of ESD ulcers.The shrinking rates and the incidence of delayed bleeding were compared between the 2 groups.RESULTS The shrinking rates of ESD ulcers on day 8 [vonoprazangroup: 61.8%(range: 24.0%-91.1%),lansoprazole group: 71.3%(range: 25.2%-88.6%)] and on day 28 [vonoprazan group: 95.3%(range: 76.2%-100%),lansoprazole group: 97.2%(range: 81.1%-99.8%)] were not statistically different between the 2 groups.On day 28,most of the ulcers in both groups healed to more than 90%,whereas 3 of 14(21.4%) in the vonoprazan group and 1 of 12(8.3%) in the lansoprazole group had delayed ulcer healing,which was not statistically different(P = 0.356).The frequency of delayed bleeding was 0 in the both groups.Taken together,there were no significant differences between the two drug groups.CONCLUSION Our study indicates that vonoprazan is potent for the management of ESD ulcers although lansoprazole is also sufficient and cost-effective.

Stronger inhibition of gastric acid secretion by lafutidine, a novel H_2 receptor antagonist, than by the proton pump inhibitor lansoprazole

AIM: To compare the antisecretory activity and plasma drug concentrations of a single oral dose of 10 mg lafutidine, a novel H2 receptor antagonist, with those of the proton pump inhibitor lansoprazole (LPZ) 30 mg. METHODS: Ten volunteers without H pylori infection participated in this crossover study comparing lafutidine 10 mg with LPZ 30 mg. Intragastric pH was monitored for 6 h in all participants, and blood samples were collected from four randomly selected individuals after single-dose administration of each drug. RESULTS: The median intragastric pH was significantly higher in individuals who received lafutidine 10 mg than in those who received LPZ 30 mg 2, 3, 4, 5, and 6 h after administration. Maximal plasma drug concentration was reached more promptly with lafutidine 10 mg than with LPZ 30 mg. CONCLUSION: In H pylori-negative individuals, gastric acid secretion is more markedly inhibited by lafutidinethan by LPZ.

Identification of Oxidative Degradation Products of Lansoprazole by Using High Resolution Mass Spectrometry Spectral Data

The study focused on the application of high-resolution mass spectrometry for the identification of impurities in pharmaceutical small molecules. A high-performance liquid chromatography (HPLC) coupled high resolution mass spectrometer (HRMS) was used for identification of oxidative degradation impurities (DIs) of lansoprazole. The utilization of HRMS facilitates to determine the accurate mass of impurities and their fragment/product ions. A fast mass spectrometer (MS) compatible reverse phase chromatography method was used to investigate the oxidative stressed impurities. HPLC column;C18 (50 × 4.6 mm, 3.5 μm) was used with gradient elution. Spectral data acquired using information dependent acquisition (IDA) with real time dynamic background subtraction algorithm (DBS). Three oxidative impurities: DI-I (m/z 386.0781), DI-II (m/z 402.0734) and DI-III (m/z 386.0785), was observed during this study;interpretation of high resolution spectral data of all three impurities was carried out;elemental composition and molecular structure was proposed for major fragments. In this study mass error was found ≤7.7 parts per million (ppm).

Hydrolytic Degradation Study of Lansoprazole, Identification, Isolation and Characterisation of Base Degradation Product

Lansoprazole degradation is accelerated in both acidic and basic medium in water. The present investigation deals with the hydrolytic degradation of Lansoprazole. Acidic medium degradation show all known impurities and degradation products whereas basic degradation studies show new impurity which has higher molecular weight than Lansoprazole. New impurity was identified, isolated using mass based auto purification system and characterised by 1H NMR, 13C NMR, HMBC, HSQC, NOE, COSY and HRMS experiments. Isolated impurity was showing molecular weight of 467.10, molecular formula of C23H16F3N5OS and its name is 7-(3-Methyl-4-(2,2,2-trifluoroethoxy) pyridin-2-yl)-7H-benzo[4,5]imidazo[2,1-b]benzo[4,5]imidazo[2,1-d][1,3,5]thiadiazine.

Validation of HPLC and FIA Spectrophotometric Methods for the Determination of Lansoprazole in Pharmaceutical Dosage Forms and Human Plasma

A chromatographic and aspectrophotometric methods for the quantitative determination of lansoprazole in pharmaceutical combinations and human plasma were developed. The analytical parameters were studied according to International Conference on Harmonization guidelines. The Flow Injection Analysis (FIA) method is based on the oxidation of lansoprazole by a known excess of N-bromosuccinimide (NBS) in an acidic medium, followed by a reaction of excess oxidant with chloranilic acid (CAA) to bleach its purple color. The separation was carried out using RP-C18 column with a mobile phase composed of ACN: TEA: phosphate buffer (60: 0.2: 39.8 v/v) adjusted to pH = 4.

质子泵抑制剂Lansoprazole和Pantoprazole的药理与临床

第一代质子泵抑制剂奥美拉唑(omepra-zole)以具有抑制H^+/K^+-ATP酶的独特作用,完全阻断任何刺激引起的胃酸分泌,强烈持久地抑制胃酸分泌,对常规疗法不能奏效的消化性溃疡和严重食管反流病的疗效明显优于数年来高居世界最畅销药物之首的雷尼替丁。自奥美拉唑1988年2月在瑞典上市以来,法、美等40多个国家已销售应用,1990年已跃为世界畅销的第35位药物。质子泵抑制剂已引起人们极大的关注。

Formulation Optimization Utilizing D-Optimal Experimental Design of Oral Capsules Containing Enteric-Coated Pellets of Lansoprazole and<i>in vivo </i>Bioequivalence

An optimized formulation of capsules containing Lansoprazole enteric-coated pellets using D-Optimal design with a polynomial statistical model were prepared by using Eudragit?L100 as an enteric coated polymer to provide resistance to simulated gastric acid dissolution in buffer media. D-Optimal experimental design was used to determine the optimal level for three coating layers that were applied to formulate the enteric-coated pellets including a drug loading layer, a sub-coating, and an outer enteric coating. Dissolution studies were performed on the prepared Lansoprazole capsules. Less than 5 percent of Lansoprazole was released in 60 minutes in an acidic dissolution medium (pH 1.2) and greater than 90 percent of active ingredient was released in the next 60 minutes in a buffer dissolution medium (pH 6.8). The Lansoprazole capsules were stable with no observable change in physico-chemical properties in accelerated and normal storage conditions for 6 and 18 months, respectively. The pharmacokinetic parameters Cmax, Tmax, AUC0-t, and AUC0-∞ were determined after administration of the D-Optimal design optimized capsules of LPZ to healthy beagle dogs and were statistically compared to Gastevin? capsules as a reference (KRKA, Slovenia) using the non-compartmental method with the aid of WinNonlin 5.2 software. The analysis of variance showed that the two formulations did not demonstrate bioequivalence using a 90% confidence interval range (80% - 120%) of Cmax, AUC0-t, and AUC0-∞. No significant difference in Tmax was found at the 0.95 significance level using the Wilcoxon signed-rank test. D-Optimal Experimental Design provided definitive direction for an optimal formulation of capsules containing enteric-coated pellets of lansoprazole loaded within the coating of pellets that provided similar bioequivalence to Gastevin.

Evaluation of the Influence of Hyoscine Butylbromide on the Oral Bioavailability of Lansoprazole in Healthy Adult Volunteers

The gastroesophageal reflux and/or peptic ulcer diseases are clinical conditions that occur usually accompanied of symptomatic pain. Lansoprazole, a proton pump inhibitor class drug is widely used in clinical practice for treatment of these diseases. However, its efficacy can be improved by combining with spasmolytic and/or visceral analgesic such as hyoscine butylbromide. Since hyoscine butylbromide is barely absorbed and exerts some local effects at gastrointestinal tract which may modify the absorption of lansoprazole, it is important to establish if there is a pharmacokinetic interaction after the oral concomitant administration of both drugs. For this objective, twenty-five subjects received under a crossover design an oral administration of lansoprazole (15 mg) plus placebo or a fixed-dose combination with hyoscine butiylbromide (15 mg + 10 mg, respectively). Plasma samples were obtained at different times during 10 hours. Lansoprazole plasma concentrations were determined by a high performance liquid chromatography method coupled to tandem mass spectrometry. Fixed-dose combination was well tolerated. Lansoprazole pharmacokinetic parameters were: Cmax 621.81 ± 212.79 and 450.38 ± 192.14 ng/mL;AUC0-t 1941.36 ± 845.57 and 1454.66 ± 757.28 ng·h/mL;tmax 2.83 ± 0.99 and 3.40 ± 1.82h;t1/2 1.35 ± 0.39 and 1.45 ± 0.51 h, for alone and combined fixed-dose formulation, respectively. Pharmacokinetic parameters were compared by analysis of variance and ratios of AUC0-t, Cmax and 90% confidence intervals obtained. Since confidence intervals exceed the 80% - 125% limits for these parameters, we conclude that there is a significantly pharmacokinetic interaction of lansoprazole when it is administered concomitantly with hyoscine butylbromide.

Repurposing lansoprazole to alleviate metabolic syndrome via PHOSPHO1 inhibition

Drug repurposing offers an efficient approach to therapeutic development.In this study,our bioinformatic analysis first predicted an association between obesity and lansoprazole(LPZ),a commonly prescribed drug for gastrointestinal ulcers.We went on to show that LPZ treatment increased energy expenditure and alleviated the high-fat diet-induced obesity,insulin resistance,and hepatic stea-tosis in mice.Treatment with LPZ elicited thermogenic gene expression and mitochondrial respiration in primary adipocytes,and induced cold tolerance in cold-exposed mice,suggesting the activity of LPZ in promoting adipose thermogenesis and energy metabolism.Mechanistically,LPZ is an efficient inhibitor of adipose phosphocholine phosphatase 1(PHOSPHOI)and produces metabolic benefits in a PHOS-PHO1-dependent manner.Our results suggested that LPZ may stimulate adipose thermogenesis by inhi-biting the conversion of 2-arachidonoylglycerol-lysophosphatidic acid(2-AG-LPA)to 2-arachidonoylglycerol(2-AG)and reduce the activity of the thermogenic-suppressive cannabinoid recep-tor signaling.In summary,we have uncovered a novel therapeutic indication and mechanism of LPZ in managing obesity and its related metabolic syndrome,and identified a potential metabolic basis by which LPZ improves energy metabolism.

Vonoprazan 10 mg or 20 mg vs.lansoprazole 15 mg as maintenance therapy in Asian patients with healed erosive esophagitis:A randomized controlled trial

Background:Erosive esophagitis(EE)is a gastroesophageal reflux disease characterized by mucosal breaks in the esophagus.Proton pump inhibitors are widely used as maintenance therapy for EE,but many patients still relapse.In this trial,we evaluated the noninferiority of vonoprazan vs.lansoprazole as maintenance therapy in patients with healed EE.Methods:We performed a double-blind,double-dummy,multicenter,phase 3 clinical trial among non-Japanese Asian adults with endoscopically confirmed healed EE from April 2015 to February 2019.Patients from China,South Korea,and Malaysia were randomized to vonoprazan 10 mg or 20 mg once daily or lansoprazole 15 mg once daily for 24 weeks.The primary endpoint was endoscopically confirmed EE recurrence rate over 24 weeks with a noninferiority margin of 10%using a two-sided 95%confidence interval(CI).Treatment-emergent adverse events(TEAEs)were recorded.Results:Among 703 patients,EE recurrence was observed in 24/181(13.3%)and 21/171(12.3%)patients receiving vonoprazan 10 mg or 20 mg,respectively,and 47/184(25.5%)patients receiving lansoprazole(differences:-12.3%[95%CI,-20.3%to-4.3%]and-13.3%[95%CI,-21.3%to-5.3%],respectively),meeting the primary endpoint of noninferiority to lansoprazole in preventing EE recurrence at 24 weeks.Evidence of superiority(upper bound of 95%CI<0%)was also observed.At 12 weeks,endoscopically confirmed EE recurrence was observed in 5/18,2/20,and 7/20 of patients receiving vonoprazan 10 mg,vonoprazan 20 mg,and lansoprazole,respectively.TEAEs were experienced by 66.8%(157/235),69.0%(156/226),and 65.3%(158/242)of patients receiving vonoprazan 10 mg,vonoprazan 20 mg,and lansoprazole,respectively.The most common TEAE was upper respiratory tract infection in 12.8%(30/235)and 12.8%(29/226)patients in vonoprazan 10 mg and 20 mg groups,respectively and 8.7%(21/242)patients in lansoprazole group.Conclusion:Vonoprazan maintenance therapy was well-tolerated and noninferior to lansoprazole for preventing EE recurrence in Asian patients with healed EE.Trial Registration:https://clinicaltrials.gov;NCT02388737.

Analysis and monitoring of drug therapy in a patient with peptic ulcer complicated by infection:A case report

BACKGROUND The role of primary-level medical pharmacists in medical institutions in China is limited;therefore,it is necessary to explore the role of pharmacists in the process of drug treatment.CASE SUMMARY A Chinese pharmacist participated in the complete treatment of a patient with a duodenal ulcer.The rationale for drug treatment was evaluated,and adjustments were made to the antacid and anti-infective regimen,as well as the dose and frequency of administration.Body temperature,routine blood examination,and adverse drug reactions were strictly monitored.During treatment,the pharmacist recommended anti-infective therapy with ampicillin-sulbactam,which effectively controlled the infection.Additionally,the pharmacist suggested changing famotidine to lansoprazole for acid suppression and gastroprotective treatment,combined with Chinese patent medicine such as Kangfuxin Liquid.This is the first case report of a pharmacist in primary-level medical institutions adjusting drug use for patients with duodenal ulcer and pulmonary infection.CONCLUSION A pharmacist participated in the treatment process,provided individualized medication adjustment,and achieved good clinical results.

Simultaneous Determination of Amoxicillin, Lansoprazole, and Levofloxacin in Pharmaceuticals by HPLC with UV-Vis Detector

In this study,a specific and rapid high-performance liquid chromatography(HPLC)method has been developed and validated for the simultaneous determination of amoxicillin,lansoprazole,and levofloxacin in pharmaceuticals.Paracetamol was used as internal standard(IS)in the measurements.UV-Vis absorption spectra of the analytes and the IS were taken for the determination of suitable absorption wavelength of UV-Vis detector(diode array detector,DAD)in the HPLC instrument.A reverse-phase C18 column was used in the separation and determination of amoxicillin,lansoprazole,and levofloxacin together with the IS.The pharmaceutical analytes were quantified by the UV-Vis diode array detector in the HPLC using MeOH-0.01 M CH_(3)COONH_(4)(70:30)as the mobile phase.The linear calibration curves of them were measured in the ranges of 15-40 mg/L,2.5-15.0 mg/L,and 7.5-20.0 mg/L for amoxicillin,lansoprazole,and levofloxacin,respectively.Excellent calibration correlations(R^(2):0.9942,0.9997,and 0.9974)were obtained.The percentage recoveries of the amoxicillin,lan-soprazole,and levofloxacin in commercial pharmaceuticals were obtained as 105.5%,98.57%,and 102.5%,respectively.The results showed that amoxicillin,lansoprazole,and levofloxacin together with paracetamol IS could be separated and determined simultaneously with low LOD and LOQ values using the proposed HPLC method.