Novel Nonsurgical Treatment Modality For Gastroduodenal Outlet Obstruction: A Randomized Controlled Trial

Abstract

Objectives

Gastric outlet obstruction (GOO) includes obstruction in the antropyloric area or in the bulbar or post-bulbar duodenum. Endoscopic balloon dilatation therapy combined with proton-pump inhibitors (PPIs) has been the standard of care. This study evaluates the efficacy of addition of misoprostol along with standard treatment versus standard treatment only in the treatment of GOO.

Materials and Methods

In this prospective, single-center, randomized controlled trial, consecutive patients of benign GOO were randomized into misoprostol + standard treatment (intervention arm) versus standard treatment only (control arm) into 1:1 ratio.

Statistical Analysis

Continuous variables were compared using t-tests, and categorical variables using chi-square tests. Note that p-values of < 0.05 were considered significant. Intention-to-treat analysis was performed.

Results

Forty patients of benign GOO were evaluated (mean age 36.05 ± 1.843, 57.5% males). Subjects in the intervention arm achieved significantly more procedural and clinical success (p 0.006 and 0.010), respectively. Improvement in nutritional status was significantly more in the intervention group (hemoglobin [p 0.015]; Δ albumin [p 0.032]), while the number of mean dilations required in them were significantly lower (p 0.004). The need for bypass surgery/reconstructive surgery was significantly lower in the control group (p 0.010). The side effect profile was similar in both the groups.

Conclusion

This study concludes that addition of misoprostol along with PPI and standard endoscopic therapy significantly improves the procedural success along with clinical outcome and nutritional status while obviating the need of surgical interventions of the patient with GOO.

 

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Keywords

gastric outlet obstruction - misoprostol - endoscopic balloon dilatation - esophageal stricture - corrosive

Introduction

Gastric outlet obstruction (GOO), characterized by blockage in the antropyloric area or duodenum, can stem from both malignant and benign causes. While malignancy is more common in adults, benign GOO, often caused by peptic ulcer disease (PUD), caustic ingestion, opioid use, and nonsteroidal anti-inflammatory drug (NSAID) use, remains a significant clinical challenge.[1] [2] The incidence of GOO due to PUD has decreased since the discovery of Helicobacter pylori and its association with PUD.[3] [4] [5] Complications of GOO include malnutrition, aspiration, pain, and respiratory failure.[6] [7] [8] In India, caustic ingestion, both accidental and suicidal, is a major cause, with studies showing a high percentage of patients developing GOO after such ingestion. The chances of developing GOO is directly proportional to mucosal injury.[9] [10] [11] Opioid use, particularly in India, has also emerged as a frequent cause of benign GOO, possibly due to prolonged mucosal contact with acidic contents and inhibition of enteric reflexes.[12] [13] [14] Chronic NSAID use contribute to ulceration by inhibiting prostaglandin production, necessitating concomitant use of H2 receptor antagonists or proton-pump inhibitors (PPIs).[15] Misoprostol, a synthetic prostaglandin E1 analog, protects the gastric lining by stimulating mucus and bicarbonate secretion, mucosal blood flow, and cellular repair.[16] [17] Studies have shown its efficacy in healing peptic ulcers and reducing complications like GOO in chronic NSAID users. For maintenance phase PPIs are more effective.[18] [19] [20] [21] Endoscopic balloon dilatation (EBD) is the preferred treatment for benign GOO, with surgery reserved for refractory cases.[22] We hypothesized that the addition of misoprostol therapy along with standard endoscopic therapy and concomitant PPI may result in higher and rapid ulcer healing rates and, therefore, may lead to better outcomes; moreover, misoprostol is more useful in acute healing phase, hence, we used concomitant misoprostol therapy with PPIs for a duration of 2 weeks after cessation of etiological agents, and PPI therapy was continued for 14 weeks versus PPI alone and standard endoscopic therapy (EBD) and conducted this pilot study.

 

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Materials and Methods

This randomized controlled trial was conducted at SMS Medical College and Associated Hospital, Jaipur, Rajasthan, India, from August 2020 to December 2023 (CTRI/2020/07/026501). The study included patients over 18 years old with benign GOO caused by NSAIDs, opioids, caustics, or PUD. Chronic NSAID use was defined as use > 3 times/week for ≥ 3 months, and chronic opioid use as daily consumption for ≥ 4 months.[23] [24]

Exclusion Criteria

• Contraindications to misoprostol (pregnancy, history of cerebrovascular accident, coronary artery disease, uncontrolled hypertension, atypical uterine bleeding),

• GOO associated with chronic pancreatitis, Crohn's disease, tuberculosis, or fibrotic/healed/nonactive strictures,

• continued use of NSAIDs/opioids/smoking,

• H. pylori infection,

• malignant etiology, and

• refusal to consent.

Diagnosis of GOO was based on clinical, radiological, and endoscopic findings. Four-quadrant biopsies were taken to rule out malignancy, tuberculosis, Crohn's disease, and H. pylori, and rapid urease tests was performed in all. Patients were randomized to either sequential EBD plus PPI (pantoprazole 40 mg twice a day) for 14 weeks (control group) or misoprostol (400 mcg three times a day for 2 weeks) plus EBD plus PPI (pantoprazole 40 mg twice a day) for 14 weeks (intervention group). H. pylori-positive patients received standard triple therapy and were excluded. Randomization was done using a computer-generated random numbers done by Research Randomizer app. Patients were followed for 1 year. The sample size of 40 patients was empirically determined due to limited existing data.

EBD was performed by a single endoscopist (P.A.) using controlled radial expansion (CRE) balloon dilators (6–20 mm) Boston Scientific. Patients were kept in fasting for 8 to 12 hours, and gastric decompression was performed if needed. Pharyngeal anesthesia and conscious sedation were administered. The stricture was visualized endoscopically and a guidewire was advanced through it. The balloon was positioned across the stricture under fluoroscopy and inflated to a predetermined pressure for 60 seconds (up to 2 minutes if needed) as shown in [Fig. 1]. Dilation was repeated every 2 to 3 weeks until a 15-mm lumen was achieved. Gastric residue assessment was also used to guide dilatation.[25] Esophageal strictures, when present, were also dilated using CRE balloons to 15 mm. The endpoint of esophageal stricture dilatation was 15 mm and once the diameter of more than 12 mm was achieved, then GOO was addressed endoscopically.[26] [27] Adjunctive therapies like corticosteroids, sucralfate, triamcinolone, antacids, and stenting were not used. Use of sucralfate in the acute or subacute phase of corrosive ingestion is recommended.[28] Since all the patients of caustic GOO presented after 3 weeks of ingestion, hence it was not used. PPIs were used per institutional practice for 14 weeks and throughout the study for idiopathic PUD-related GOO.

Severity and nutritional status was addressed using the Zargar classification for caustic injury and GOO score.[9] [29] Patients with corrosive GOO (Zargar IIB/IIIA) underwent feeding jejunostomy (FJ) for nutritional support. Dilatation was started after 3 weeks postingestion. In noncorrosive GOO, patients with a GOO score < 2 underwent FJ. Prior to endoscopic intervention, oral intake was gradually introduced as luminal diameter increased as per protocol.[25] Misoprostol was administered sublingually or rectally if oral intake was not possible. Parenteral nutrition was used for patients with dehydration or poor nutritional status until FJ became functional. There is some evidence that patients with caustic esophageal/pyloric stricture should be dilated at least after a period of 3 weeks of conservative management.[30] In our study, all patients presented to us after 3 weeks of ingestion, hence we started dilatation as soon as technically feasible.

 

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Outcome Analysis

The primary outcome was obviation of need of surgery.

The secondary outcomes included:

• symptom resolution (heartburn, vomiting, abdominal pain, postprandial fullness),

• number of EBD sessions, and

• improvement in nutritional status (hemoglobin, serum albumin).

Procedural success was defined as achieving 15 mm dilation and no gastric residue.[25] Clinical success was defined as sustained symptom resolution (GOO score of 3), sustained till the study's end. Primary failure was the inability to achieve procedural success, secondary failure was the failure to achieve clinical success despite procedural success, and recurrence was symptom relapse and stricture redevelopment after achieving clinical success.

Follow-up visits were conducted every 2 to 3 weeks or as needed for 1 year after achievement of procedural success. Patients' telephone number and contact address were recorded and contact number of corresponding author (P.A.) and coauthors (M.S., G.D.) were also provided so that patients may contact in case of any actual or perceived emergency. Standing instructions were provided to emergency medical officers to admit them if they presented with any significant problem, which may be related or unrelated to the primary disease.

 

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Statistical Analysis

It was performed using PSPP 2.0.1. Continuous variables were compared using t-tests, and categorical variables using Fisher's exact tests. p-Values of < 0.05 were considered significant. Per protocol analysis was performed.

Due to the coronavirus disease 2019 pandemic-induced travel restrictions and limitation of endoscopic access, 28 patients (33.3%) were lost to follow-up and 16 patients were excluded due to malignancy or other causes.

 

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Ethical Approval

Approval was obtained from the institute review board and ethics committee prior to the study. CTRI No. CTRI/ 2020/07/026501.

 

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Results

Eighty-four patients were initially evaluated, and 40 completed the study (20 per arm). Males comprised 57.5% of the study population. The most common etiology was corrosive ingestion (50%), followed by NSAIDs (25%), peptic stricture (17.5%), and opioid use (7.5%). The most common symptoms were abdominal pain (85%) and vomiting (80%), and dysphagia in patients with esophageal involvement. Esophageal stricture prevalence was similar in both groups. Most of the patients had middle esophageal strictures (4/7 in the intervention arm and 5/8 in the control arm). One in each group had upper esophageal stricture and two patients in both groups had multiple strictures involving both mid and upper esophagus ([Table 1]).

Table 1 Baseline characteristics in subjects with gastroduodenal obstruction enrolled in our study (n = 40)

Characteristics	Intervention arm (misoprostol + PPI)	Control arm (PPI)	p-Value
Age (y)	34.35 ± 10.649	37.75 ± 12.624	0.363
Sex – Male	11	12	1.000
Female	9	8
BMI (kg/m2)	20.78 ± 3.83	20.48 ± 2.81	0.780
Smoker – Male	6	4	0.41
Female	0	0
Native
Rajasthan	5	7	0.731
Other states	15	13
Hemoglobin (g/dL)	9.78 ± 2.17	10.55 ± 1.57	0.206
Serum albumin (g/dL)	2.99 ± 0.595	3.23 ± 0.525	0.185
Etiology
Corrosive	10	10	0.515
NSAIDs	4	6
Peptic	5	2
Opium/Opioids	1	2
Symptoms
Dysphagia	7	8	1.000
Abdominal pain	17	17	1.000
Vomiting	16	16	1.000
Loss of weight (≥ 5% in last 1 month)	15	11	0.320
Associated esophageal stricture	7	8	1.000
GOO score	1.35 ± 0.745	1.15 ± 0.813	0.422
Duration between insult and presentation as GOO (in weeks) corrosives	7.30 ± 2.058	6.90 ± 2.132	0.674
Symptomatic period before inclusion into study of noncorrosives (In weeks)	5.60 ± 1.174	5.30 ± 1.059	0.556

Abbreviations: GOO, gastric outlet obstruction; NSAID, nonsteroidal anti-inflammatory drug; PPI, proton-pump inhibitor.

Clinical success was significantly higher in the intervention group (80%) compared to the control group (35%) (p = 0.010). Procedural success was also significantly higher in the intervention group (90%) compared to the control group (45%) (p = 0.006). Primary failure was significantly lower in the intervention group (10%) compared to the control group (55%) (p = 0.006). Secondary failure was not significantly different between the groups ([Tables 2] and [3]).

Table 2 Final clinical success in subjects of gastroduodenal obstruction in the intervention and control arm at the end of study period

	Clinical success	Requirement of surgery
Control arm (PPI)	7	12 + 1	20
Intervention arm (misoprostol + PPI)	16	3 + 1	20
	20	20	p < 0.010

Abbreviation: PPI, proton-pump inhibitor.

Table 3 Procedural success in subjects of gastroduodenal obstruction in the intervention and control arm

Procedural success
	Yes	No
Control arm (PPI)	9	11	20
Intervention arm (misoprostol + PPI)	18	2	20
	20	20	p = 0.005

Abbreviation: PPI, proton-pump inhibitor.

Gastrojejunostomy was performed in majority of patients but stricturoplasty/pyloroplasty was performed in 2 patients (1 in each arm) who did not achieve clinical/procedural success. The number of dilations required was significantly lower in the intervention group (3.35 ± 0.813) compared to the control group (4.35 ± 1.040) (p = 0.004). Hemoglobin and albumin levels also significantly improved in the intervention group (p = 0.015 and p = 0.032, respectively). Diarrhea was the most common adverse reaction, with no significant difference between the groups ([Tables 4] and [5]).

Table 4 Improvement in nutritional status and number of dilatation sessions in both arms

	Control arm (PPI)	Intervention arm (misoprostol + PPI)	p-Value
ΔHb (absolute increment in hemoglobin levels in g/dL)	0.870 ± 0.801	1.540 ± 0.859	0.015
ΔAlbumin (absolute increment in albumin levels in g/dL)	0.400 ± 0.229	0.675 ± 0.493	0.032
Number of dilatations	4.35 ± 1.040	3.35 ± 0.813	0.004

Abbreviations: Hb, hemoglobin; PPI, proton-pump inhibitor.

Table 5 Adverse reactions in both the groups

	Intervention arm (misoprostol + PPI)	Control arm (PPI)	p-Value
Diarrhea	9	5	0.320
Abdominal pain	5	4	1.000
Bloating	3	4	1.000
Headache	2	1	1.000
Menstrual irregularity	0	0	–

Abbreviation: PPI, proton-pump inhibitor.

 

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Discussion

The basis of conducting this study and including misoprostol as an add-on therapy in all etiologies of GOO was based on evidence that misoprostol increases bicarbonate secretion, promotes mucosal barrier and integrity, and possibly also enhances motility, thus decreasing acid contact with mucosa and promote mucosal healing, but in the maintenance phase of ulcer healing PPIs are supposed to be superior.[16] [18] These properties can benefit any etiology of ulcerative GOO.

The optimum duration and timing of misoprostol therapy in patients with corrosive intake or with a history of chronic opioid/NSAID use is unclear. So, we empirically gave misoprostol for 2 weeks after exposure cessation, previous studies used misoprostol therapy concomitant with long-term justified NSAIDs use.[19] [20] [21] Since we included only patients in whom the exposure to etiological agent has ceased like NSAID/opium/smoking, we gave misoprostol only in the healing phase and continued PPI for the healing phase of 14 weeks.

In our study, the most common etiology of benign GOO was corrosive injury (50%). There is heterogeneity in various studies from India, as Kochhar et al[25] reported caustic ingestion (53.8%) as the most common etiology, while Maharshi et al[31] reported opioid abuse (29%), whereas Sharma et al[32] reported PUD (42.6%). This contrast could represent either a true epidemiological difference or reflect skewed access to health care or referral bias.

The main corrosive found in our study was hydrochloric acid (11/20) used as a toilet cleaner and followed by sodium hydroxide (6/20) used in various industries. Corrosive ingestion can lead to esophageal strictures, complicating GOO management. The prevalence of opioid use in our country is 2.06% with heterogeneous distribution and is more prevalent in our adjoining states like Haryana and Punjab.[33] In our study, 7.5% of patients used opioids (mostly tramadol) and 25% used NSAIDs (mostly ibuprofen/paracetamol). Including excluded patients with opioid addiction, the total opioid user breakdown was tramadol (5/9), heroin (3/9), and opium (1/9). Opioid-induced GOO is primarily reported in India, often linked to recreational use. NSAID users typically took them for musculoskeletal pain for over a year, but only experienced GOO symptoms for 5 to 6 weeks before presentation. These patients were referred to our deaddiction center for counseling and management.

Idiopathic peptic strictures (no significant NSAID use/H. pylori infection) constituted 17.5%, whereas in other countries it is believed that PUD still constitutes around 90% of GOO.[34]

Most studies have used 15 mm endpoint for esophageal dilation, others have dilated up to 16 to 18 mm, similarly the endpoint of pyloric dilation has been 15 mm in majority.[25] Therefore, this was defined as procedural success as dilatation of more than 15 mm can increase the risk of perforation.[34] [35]

We started with low diameter for balloon dilatation (usually 8 mm), dilated only till 15 mm, and as all patients of corrosive ingestion presented after the acute phase was over (> 3 weeks), fortunately we did not encounter any postprocedure perforation.

Two patients in each study arm had multiple strictures and all these strictures were dilated with the same diameter in the same session, sometimes colonoscope was required in negotiating these strictures as due to gastric dilatation the upper gastrointestinal endoscope was totally consumed and could not reach the distal stricture, especially if the stricture was beyond the first part of the duodenum. Four patients in the control arm while three patients in the intervention arm had complex pyloric stricture (length > 2.5 cm/tortuous/severely angulated or edematous) [36] [37] Difference between the two groups was not significant (p = 1.000).

We defined clinical success as symptom resolution without surgical intervention till the completion of follow-up (1 year), which is a more relevant endpoint, as many patients even after procedural success achieved either partial or no clinical success (vide [Tables 2] and [3]). The possible explanation for this could be altered anatomy, persistent enteric nervous dysfunction, and cicatrization/fibrosis. Clinical success at the end of study in the intervention arm and control arm was 16/20 (80%) and 7/20 (35%), respectively (p = 0.010). Moreover, the mean number of dilations required were significantly less (p = 0.004) in the intervention group versus control (3.35 ± 0.813 vs. 4.35 ± 1.040). In all the patients in whom we achieved stable clinical success, routine esophagogastroduodenoscopy, which was done after the study, did not show any appreciable stricture. Primary failure was seen in 2/20 (10%) in the intervention arm and in 11/20 (55%) in the control arm, which was significant (p = 0.006). Secondary failure was seen in 2/18(11.11%) in the intervention arm and in 2/9 (22.22%) in the control arm (p = 0.578).

A significant proportion of patients in the intervention arm versus the control arm did not require surgery (p = 0.010) and this is relevant, because the majority of our patients were severely anemic and nutritionally deprived ([Table 4]), making them high-risk candidates for surgery and for various postoperative complications. Nutritional recovery (improvement in hemoglobin and serum albumin) was also more significant in the intervention arm (p = 0.015 and p = 0.032, respectively), hence, effective endoscopic therapy and medical therapy is of great value to such patients as it prevents surgery with possible high risk of complications and poor outcomes.

Since in our study population, corrosive stricture constituted around 50%, therefore comparison with previously published data would be more useful if we compare it with studies that have included a sizeable proportion of corrosive strictures, as it is obvious that a corrosive stricture would pose different set of problems as compared to an opioid stricture or a benign PUD-related stricture and long-term prognosis is dependent upon the etiology of the stricture as well.[38]

A few high-quality studies have been done on benign GOO from a single center from India by Kochhar et al. In a study on 264 patients of benign GOO (> 50% corrosives), procedural success and clinical success was 75.7 and 92.04%, respectively, requiring a mean number of dilations of 2.55 and 5.37, respectively. While in the same study, procedural success and clinical success in 142 patients of corrosive-induced GOO were 66.2 and 90.1% requiring a mean number of dilatations of 3.45 and 7.25, respectively, of the 264 patients, 9 (3.4%) had perforations during EBD.[25] In another study from the same center, 31 patients of caustic GOO underwent EBD, 30 patients achieved procedural success (96.7%); with mean number of dilatations around 9, one patient developed perforation (3.2%),[39] while in another study 111 patients of caustic-induced GOO underwent EBD and procedural and clinical success was achieved in 85.6 and 97.3%, respectively, requiring a mean number of dilatation sessions of 5.3 and 7.21. The initial balloon diameter at the start of dilatation and the last balloon diameter were 9.6 ± 2.06 and 14.5 ± 1.6 mm, respectively. Perforation was encountered in 2 (1.80%) patients. There were no recurrences in a follow-up period of 98 months.[36]

In a study by Chiu et al,[40] out of 18 patients of caustic-induced GOO, clinical success was achieved in 44.4% only, requiring a mean number of dilations of 5.5 in the GOO-only group and 13.7 in the esophageal stricture and GOO group. Whereas Solt at al[41] achieved a success rate of 35% in 17 patients of corrosive-induced GOO after EBD.

In another study by Rana et al,[27] 25 patients of benign GOO underwent EBD, and it was successful in 21/25 (84%). Patients required one to six sessions of endoscopic dilatation (mean = 2.2 ± 1.2). Corrosive-induced GOO required more dilatation sessions (3.83 ± 0.75) compared to peptic GOO (2.1 ± 0.56), whereas in a study by Hamzaoui et al[42] that included 45 patients of only PUD-related GOO for EBD, 13 (29%) patients had to undergo surgery despite EBD.

These studies demonstrate disparate and divergent results of EBD in pyloric strictures, we could only achieve a procedural response rate of 45% in the control arm, which agrees with the finding of Solt et al and Chiu et al,[40] [41] whereas Kochhar et al[25] [36] [39] reported a procedural and clinical success varying from 75.7 to 96.7% and 92.04 to 97.3%, respectively; however, in misoprostol procedural and clinical success rates were 90% (18/20) and 80% (16/20), respectively. The difference was highly significant across the two study arms (p = 0.006 and 0.010), highlighting the efficacy of misoprostol as an adjunctive therapy.

Probable explanations for divergent result from our study (particularly the control arm) include the fact that Kochhar et al[25] have used adjunctive therapy in the form of intralesional triamcinolone injection in a subset of patients, besides in some studies, the mean number of dilations in corrosives was much more (5.3–9).[25] [36] [39] While we have not dilated beyond five sessions, moreover in our study, most of the patients had GOO score of < 2, which cannot be compared to other study populations as they have not utilized this score, a low GOO score would imply a more severe stricturing disease; furthermore, all patients of caustic ingestion had a Zargar score of IIB/IIIA, whereas no such data is available from their study, so the comparability of study population is uncertain, additionally as both the studies were conducted at different tertiary care centers, there is a strong possibility of referral bias. In our study, there are sizeable number of patients who have complex strictures (3 in the intervention arm and 4 in the control arm) and two patients in each arm had multiple strictures, but complex strictures were excluded by Kochhar et al,[25] [36] hence their findings may not be comparable with us as complex strictures are usually refractory to EBD.[37]

The number of dilatation sessions alone may not be the sole determinant of the outcome as Chiu et al[40] reported a low clinical success rate of 44.4% despite greater number of dilatation sessions (mean 13.7 in esophageal + pyloric stricture), closely correlating with our observations, this reiterates that other factors such as severity of disease process, concomitant esophageal involvement, and presence of complex/multiple stricture may also influence outcome and these variables may be a poor prognostic marker for successful EBD.[37] [43] [44] [45] It is of interest to note that in the misoprostol treatment arm, patients with complex and/or multiple strictures also showed markedly improved response to therapy highlighting its efficacy as an adjunctive therapy to EBD.

We restricted our dilatation sessions to five per patients at the most, as this is the criteria for refractory stricture.[25] Additionally, there were other reasons, a large number of patients were referral patients from adjoining states, belonged to resource-constrained socioeconomic strata with low education level, this in turn reflected in inadequate dietary management through FJ in some and these patients also needed to go back to work as soon as possible, moreover, multiple/prolonged follow-up visits were also difficult, hence, after five sessions we opted for surgical management as there is evidence that timely surgery leads to better quality of life and recovery.[46] [47] [48]

Misoprostol is well tolerated as the adverse effect profile was not significantly different across the study arms ([Table 5]). The intervention group, which received misoprostol in addition to EBD and PPI, exhibited significantly higher rates of clinical and procedural success and required fewer dilations with improvement in nutritional status versus the control group.

There are some limitations of our study. First, the effective dosage, timing, and duration of misoprostol therapy is unknown. Second, the study population had heterogeneous etiology, so effectiveness of misoprostol might vary based on the etiology, which is unexplored, as subgroup analysis was not performed. Moreover, it was a single-center pilot study with a small sample size and with significant dropout rate.

 

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Conclusion

From this study, we can safely conclude that the addition of misoprostol along with PPI and standard endoscopic therapy (EBD) significantly improves the procedural success along with clinical outcome and nutritional status of the patient with GOO while reducing dilatation sessions. Moreover, it also decreased requirement of surgery in malnourished patients, as surgery in such settings has a poor outcome. Limitations include the fact that this was a small single-center study, so further research may need to be carried out to establish the exact role of misoprostol, duration of its therapy, and its clinical impact in endoscopic management of GOO and its complications. The role of misoprostol in varying etiology of GOO is also unclear as subgroup analysis was not possible due to small sample size, further timing of misoprostol therapy in corrosive injury is presently ambiguous and its utility in the acute phase and possible role in the prevention of stricture development per se is obscure. For generalizability of these findings to the general population would require more data and research.

Fig. 1 (A) Barium meal showing multifocal stricture in the duodenum, post-bulbar (chronic synthetic opioid intake). (B) Barium meal depicting duodenal stricture (chronic nonsteroidal anti-inflammatory drugs [NSAIDs] use). (C) Endoscopic view of benign pyloric stenosis before dilatation. (patient “X”). (D) Endoscopic view of pyloric stricture dilatation with controlled radial expansion (CRE) balloon (patient “X”). (E) Final endoscopic image showing nonappreciable pyloric stricture after end of study (patient “X”). (F) Endoscopic view of concomitant esophageal stricture (patient “X”). (G) Endoscopic view of esophageal stricture dilatation with CRE balloon (patient “X”).

 

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Conflict of Interest

None declared.

Authors' Contributions

Conceptualization: P.A.,M.S.,G.D., and S.N. Data curation: M.S.,G.D., and V.S.N. Formal analysis: All authors. Investigation: All authors. Methodology: P.A., G.S., G.D., and A.J. Project administration: P.A., A.J., and G.S. Resources: G.D., V.S.N., G.S., and S.N. Software: M.S., P.A., and G.S. Supervision: P.A., A.J., and S.N. Validation: P.A. and G.S. Visualization: P.A., M.S., and G.D. Writing-original draft: P.A., M.S., and V.S.N. Writing-review and editing: M.S., P.A., and G.S. All authors approved the final version of the article, including the authorship list.

Patients' Consent

Informed consent was taken from the patients.

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Artikel online veröffentlicht:
01. Juli 2025