Bulbit of the stomach and duodenum: symptoms and treatment

"Bulbit" is a common term for inflammation of the duodenal bulb (bulbar duodenitis). In modern gastroenterology, it is considered part of a spectrum of duodenitis and peptic disease: it is most often associated with Helicobacter pylori, nonsteroidal anti-inflammatory drugs (NSAIDs), and acid-peptic hypersensitivity. The term is found in endoscopic reports, but is becoming less common; the diagnosis is formulated as "duodenitis/ulcer of the duodenal bulb" with an indication of the cause. [1]

The main complaints are hunger or nocturnal pain in the epigastrium, heartburn, early satiety, nausea, and sometimes pain 2-3 hours after eating (peptic profile). With H. pylori, symptoms often fluctuate over years: periods of remission are followed by exacerbations due to stress, dietary errors, and smoking. When taking NSAIDs, the pain can be "silent" or even bleeding. [2]

Today, the key strategy is to establish the underlying cause. If H. pylori is the cause, eradication is required according to modern protocols; if NSAIDs are the cause, therapy should be reviewed and gastroprotective measures implemented; if celiac disease/chronic inflammatory diseases are suspected, morphological verification and specialized treatment should be performed. Blind symptomatic "acid suppression" without etiotropy provides short-term results and misses risks. [3]

It is important to remember that bulbar duodenitis often coexists with duodenal ulcers. In most patients, the ulcer is caused by H. pylori and/or NSAIDs; as the prevalence of H. pylori declines, the proportion of NSAID-associated and "rare" causes increases. This determines the diagnostic checklist and treatment priorities. [4]

Code according to ICD-10 and ICD-11

In ICD-10, duodenitis is coded in block K29 "Gastritis and duodenitis": K29.80 - "Duodenitis without bleeding," K29.81 - "Duodenitis with bleeding." If a bulbal ulcer is detected, codes K26.x "Duodenal ulcer" are used for complications. The word "bulbitis" itself is not included in the classifier; it fits under "duodenitis"/"duodenal ulcer." [5]

In ICD-11, duodenitis is classified under the "Diseases of the Duodenum" section and is coded as DA51.Z "Duodenitis, Unspecified" with the possibility of post-coordination (specification of etiology, activity, bleeding). For ulcers, codes from the "Peptic Ulcer" section are used. [6]

The choice of code depends on the final diagnosis: “bulbar duodenitis H. pylori-associated”, “NSAID-induced duodenitis”, “duodenal ulcer without complications”, “duodenal ulcer with bleeding”, etc. This is important for routing, payment and monitoring. [7]

If duodenitis is a manifestation of celiac disease or Crohn's disease, the main disease code is indicated plus duodenitis as a manifestation/localization. [8]

Epidemiology

Duodenitis is common and often concentrated in the bulbar region, the area where duodenal ulcers typically form; historical data show a frequent combination of duodenitis and ulcers in the bulbar region. At the population level, H. pylori and NSAIDs/aspirin predominate as causes of inflammation and ulceration. [9]

The prevalence of H. pylori is declining in economically developed countries but remains high in some regions, so the infection's contribution to duodenitis/ulcers remains significant. At the same time, the relative proportion of NSAID-associated lesions is increasing due to the widespread availability of analgesics and an aging population. [10]

Celiac disease is a less common but important cause of chronic duodenitis (by histology). Diagnosis is confirmed by serology and biopsy with the Marsh/Oberhuber/Corrazza-Villanacci assessment; this influences long-term nutritional and monitoring strategies. [11]

The role of bile (alkaline) reflux as a cause of duodenogastric/duodenal inflammation varies; the influence of motility and microbiota is actively studied. Sucralfate can reduce morphological inflammation in reflux gastritis, but may not produce a significant symptomatic effect. [12]

Table 1. Where bulbitis/duodenitis “lives” and why this is important

Fact	Comment
Inflammation most often occurs in the bulbar area.	Coincides with the typical localization of duodenal ulcers. [13]
Main reasons	H. pylori and NSAIDs/aspirin. [14]
The prevalence of celiac disease	Less common, but requires different tactics (diet, morphology). [15]
Role of reflux/motility	Possible; mucoprotectors reduce inflammation, but not always with clinical benefit. [16]

Reasons

1. Helicobacter pylori is the leading etiology of duodenitis/ulcers of the duodenal bulb: bacterial inflammation, hypergastrinemia, and impaired mucosal defenses increase the acid load on the duodenal bulb. Eradication treats the cause and reduces the risk of recurrence. [17]
2. NSAIDs and aspirin inhibit the synthesis of prostaglandins, impair blood flow and mucosal protection, and increase the risk of erosions/ulcers and bleeding, especially in the elderly and when combined with antiplatelet agents/anticoagulants/steroids. [18]
3. Acid-peptic aggression and duodenogastric/bile reflux are additional contributors to bulbar inflammation; some patients respond to mucoprotectors (sucralfate), but symptomatic benefit is inconsistent. [19]
4. Other causes: celiac disease (immune enteropathy), Crohn's disease, infections (rare), hypersecretory conditions (gastrinoma). These are rare, but important – they cannot be missed if the clinical picture is atypical or the course is refractory. [20]

Risk factors

Classic modifiable factors include H. pylori, NSAIDs/aspirin, smoking, and alcohol: all of which impair mucosal protection and healing. Additional risks include older age, concomitant anticoagulants/antiplatelet agents/steroids, and severe comorbidities. [21]

A history of ulcers, complications (bleeding), family history, chronic stress, and irregular eating patterns increase the likelihood of relapses and symptomatic flare-ups. In such cases, the threshold for endoscopy and eradication is lower. [22]

If celiac disease/Crohn's disease is suspected, a family history of autoimmune diseases, dermatitis herpetiformis, iron deficiency, and weight loss are noted. These clues are a reason for a duodenal biopsy even with a scant endoscopic picture. [23]

After extensive gastric/GB surgery, bile reflux and chronic inflammation may occur; measures to protect the mucosa and correct motility/diet are helpful. [24]

Pathogenesis

With H. pylori, inflammation of the antrum → ↑gastrin → ↑acid production → duodenal chyme hyperacidification and bulb damage. Against this background, foci of "gastric metaplasia" form in the duodenum, which are colonized by H. pylori and maintain the inflammatory cycle. Eradication breaks this cycle. [25]

NSAIDs inhibit prostaglandins E2/I2, which reduces mucosal protection and microcirculation, increasing acid-peptic damage. Combinations of NSAIDs and aspirin/anticoagulants significantly increase the risk of bleeding. [26]

In "alkaline" (bile) reflux, aggressive bile salts and lysolecithin damage the mucosa; models show disturbances in migrating motor complexes and discoordinated evacuation. In some patients, morphology improves with sucralfate, but symptoms are not always the same. [27]

Celiac disease causes immune inflammation of the villi: permeability increases, and the motility of the upper gastrointestinal tract changes; in this group, “duodenitis” is only the visible tip of the iceberg, and the pathogenetic treatment is a gluten-free diet. [28]

Symptoms

Most common symptoms include dull or burning epigastric pain on an empty stomach/at night, heartburn, bitterness, nausea, and a feeling of fullness after a small amount of food. The classic "peptic" variant is pain 2-3 hours after eating, with relief after a snack or antacids. [29]

NSAID-related symptoms may be silent until bleeding occurs: weakness, dizziness, melena, and coffee-ground vomiting. These are reasons for immediate medical attention. [30]

In celiac disease, abdominal symptoms are accompanied by weight loss, iron deficiency, osteopenia, and dermatitis herpetiformis; in adults, extraintestinal manifestations often predominate. [31]

Any “red flags” (dysphagia, hematemesis/melena, progressive weight loss, anemia, age >60 years, family history of cancer) are an argument for primary endoscopy without delay. [32]

Table 2. “Portrait” of pain in bulbar duodenitis/ulcer

Sign	Typical	What does it suggest?
"Hunger" pains at night, relief from food	Yes	Peptic mechanism
Pain after NSAIDs, minimal dyspepsia	Often	NSAID-lesion/risk of bleeding
Pain + weight loss, anemia	Alarming	Endoscopy and biopsy are needed
Dyspepsia + deficiencies (iron/vitamins)	Possible	Rule out celiac disease

Forms and stages

Clinically, the following are distinguished: (1) superficial/catarrhal duodenitis (endoscopically - edema, hyperemia, erosions); (2) erosive; (3) ulcerative (formed ulcer of the bulb). Regardless of the etiology, morphology does not determine the tactics - the cause is more important. [33]

By course: acute (due to H. pylori/NSAIDs/stress), chronic recurrent, refractory (despite correct therapy). Refractory disease requires checking adherence, H. pylori eradication, hidden NSAID use, and rare causes (gastrinoma, Crohn's disease). [34]

By complications: no complications, with bleeding, with penetration/perforation (rare), with strictures of the outlet (in chronic ulcers). The severity determines the route (outpatient vs. inpatient). [35]

Separately - H. pylori-associated, NSAID-induced, reflux-associated, celiac duodenitis: the wording indicates the mechanics of treatment and secondary prevention. [36]

Complications and consequences

Upper gastrointestinal bleeding is the main acute complication; the risk is higher with NSAIDs/antiplatelet agents/anticoagulants and in the elderly. Relapses are possible with undetected/untreated H. pylori and continued NSAID use. [37]

Perforation and penetration are less common but require emergency surgery. A "rigid" gastric outlet is a consequence of large ulcers healing with scar tissue; it manifests as vomiting, weight loss, and alkalosis. [38]

Chronic inflammation maintains pain, reduces quality of life, impairs sleep/nutrition, and performance. In the celiac disease group, nutritional deficiencies and systemic complications develop without treatment. [39]

Long-term asymptomatic NSAID therapy without gastroprotection increases mortality precisely due to complications of peptic ulcer disease - an important argument for reconsidering pain relief. [40]

Diagnostics

Basic algorithm: assessment of “red flags”, H. pylori test (breath test ¹³C or stool antigen) followed by eradication if positive, and in case of flags/age/warning signs - esophagogastroduodenoscopy (EGD) with antrum/body biopsy according to the Sydney system and duodenal biopsy if celiac disease is suspected. [41]

Endoscopic findings in duodenitis include hyperemia, edema, and erosions/ulcers of the duodenal bulb. In cases of ulceration, tests for H. pylori (urease/histology/immunohistochemistry) are performed, taking into account the effect of PPIs/antibiotics. In cases of refractory duodenal ulceration, eradication monitoring is performed without PPIs and a search for hidden NSAIDs is performed. [42]

Laboratory tests include a complete blood count (anemia), ferritin/iron, and hemoglobin levels in case of bleeding, as well as tests for occult blood. Suspected celiac disease is confirmed by tTG-IgA (with total IgA) and a biopsy with grading according to Marsh/Oberhuber/Corrazza-Villanacci. [43]

There are no definitive "screening" tests for bile reflux; diagnosis is clinical and endoscopic. In some cases, pH impedance, motility assessment, and trial courses of mucoprotectors/prokinetics are used. [44]

Table 3. When and what to examine if bulbitis is suspected

Situation	First line examination	For what
No "flags", <60 years	Non-invasive test for H. pylori	Etiotropy without invasion
"Flags", ≥60 years, ASP/NSAIDs	EGDS + biopsy (stomach ± 12 PC)	Rule out ulcer/bleeding/unusual etiology
Refractory	Eradication monitoring, NSAID revision, search for rare causes	Change tactics
Suspicion of celiac disease	tTG-IgA + biopsy 12PCS	Confirm immune enteropathy

Differential diagnosis

Peptic duodenal ulcer is a "relative" of bulbitis: it shares the same causes (H. pylori/NSAIDs), but there is a mucosal defect of >5 mm. It is distinguished from duodenitis by endoscopy; clinically, it has more pronounced "peptic" pain and a risk of complications. [45]

Functional dyspepsia mimics the pain of bulbitis, but endoscopy is normal. A short course of PPIs is helpful, followed by low-dose neuromodulators and behavioral approaches as needed. It is important not to "overtreat" with PPIs if EGD is normal. (Review sources.)

Celiac disease is the cause of "chronic duodenitis" according to histology: pain is accompanied by deficiencies and extraintestinal manifestations. It is treated not with PPIs, but with a gluten-free diet. [46]

Bile/alkaline reflux gastritis/duodenitis - associated with surgery/dyskinesia; enterogastric reflux, bitterness, nausea. Mucoprotectors/motility correction help some patients; the evidence base is moderate. [47]

Table 4. Quick differences in common scenarios

Scenario	Endoscopy	The key to diagnosis	First line
Bulbit (H. pylori)	Hyperemia/erosion/ulcer of the bulb	Positive test for H. pylori	Eradication + PPI
NSAID-duodenitis	Erosions/ulcers, often "silent"	History of NSAIDs/Aspirin	Cancellation/replacement + PPI/gastroprotection
Celiac duodenitis	Villous atrophy	tTG-IgA serology + biopsy	Gluten-free diet
Reflux duodenitis	Endoscopy is variable	Connection with operations/bitterness	Mucoprotectors ± prokinetics

Treatment

1) H. pylori eradication is the central point. According to the current ACG position (2024) and specialized reviews: a 14-day bismuth-quadruple regimen is preferred; triple PPI-clarithromycin therapy is not used empirically without susceptibility data. Alternatives: rifabutin-triple or dual regimen with a potassium-competing acid blocker (vonoprazan) with amoxicillin - 14 days. Success is confirmed by a breath test/stool antigen ≥4 weeks after treatment (and ≥2 weeks without PPIs). [48]

2) PPIs/secretion inhibitors and mucoprotection. A 4-8 week course of PPIs is the standard for healing erosions/ulcers of the bulb. For NSAID-treated ulcers, analgesia should be reviewed and gastroprotection (PPIs or misoprostol) should be continued if therapy is unavoidable. Sucralfate is acceptable as a local mucosal protector, especially for reflux, but the clinical effect is variable. [49]

3) Tactics for NSAID-induced injury. If possible, discontinue NSAIDs, switch to selective COX-2 inhibitors with gastroprotection in risk groups, use the minimum effective dose, and monitor combinations with antiplatelet/anticoagulants/steroids. This effectively reduces the risk of recurrent bleeding. [50]

4) Celiac disease/other rare causes. If confirmed, a gluten-free diet should be monitored with correction of deficiencies; in Crohn's disease, standard IBD therapy should be administered based on activity and localization. Sporadic hypersecretory conditions (e.g., gastrinoma) require specialized management. [51]

Table 5. H. pylori eradication: what to prescribe today

Situation	Mode	Duration	Notes
First line (sensitivity unknown)	Bismuth-quadruple: PPI + bismuth + tetracycline + metronidazole	14 days	ACG 2024 Preferred Choice
Alternative (without penicillin allergy)	Dual on vonoprazan + amoxicillin	14 days	"Potassium-competing blocker" + AMOX
Reserve/after failures	Rifabutin-triple	14 days	In case of relapse/resistance
Cure control	Breath test/stool antigen	≥4 weeks after the course	Discontinue PPI ≥2 weeks before testing [52]

Table 6. NSAIDs and the risk of ulcers: how to reduce

Risk factor	What to do
High doses/long term	Minimize dose/duration
Combinations (aspirin, anticoagulants, steroids)	Avoid combinations; if unavoidable - PPI/misoprostol
History of ulcers/bleeding	Gastroprotection by default
Old age/comorbidity	Low threshold for EGD/therapy reassessment [53]

Table 7. Nutrition and lifestyle for bulbitis (evidence-based and myth-free)

Direction	Practice	For what
Smoking/alcohol	Denial/minimization	Improving mucosal healing
Nutrition	Eat small meals, avoid overeating, and avoid individual triggers	Pain/reflux relief
NSAIDs	Only for strict indications; alternative/gastroprotection	Reducing complications
Commitment	Complete eradication, confirm cure	Reduction of relapses [54]

Prevention

Primary. Careful use of NSAIDs/aspirin: use as indicated, in minimal doses, with gastroprotection in risk groups. Smoking cessation and moderation in alcohol consumption improve healing and reduce the frequency of exacerbations. Sanitary practices and screening for H. pylori (according to local protocols) reduce the peptic ulcer burden. [55]

Secondary. After confirmed eradication, conduct a control test of cure, teach the "rules of PPIs," manage triggers (smoking, late heavy dinners), and promptly perform endoscopy if any "flags" appear. If NSAIDs are unavoidable, maintain ongoing gastroprotection and regularly reassess medication requirements. [56]

Forecast

In H. pylori-associated bulbitis, the prognosis is favorable with eradication: inflammation subsides, and the risk of relapse and ulcerative complications is sharply reduced. In NSAID-induced lesions, the key to outcome is a review of pain management and gastroprotection: without these, relapses and bleeding are frequent. [57]

Reflux-associated and celiac forms require targeted treatment (mucoprotection/motility correction/diet), otherwise symptoms recur. Overall, with the right approach, most patients achieve sustained remission and return to normal activity. [58]

FAQ

• Is "bulbit" a separate disease or a type of duodenitis/ulcer?

Today, this is considered bulbar duodenitis in the spectrum of duodenitis/peptic ulcer. Treatment is determined by the cause: H. pylori, NSAIDs, reflux, celiac disease, etc. [59]

• What is the current main treatment regimen for H. pylori?

A 14-day bismuth quadruple therapy is the default regimen for unknown susceptibility. Alternatives include rifabutin triple therapy or dual therapy with vonoprazole and amoxicillin (14 days). Effectiveness must be confirmed by testing. [60]

• If I take NSAIDs, how can I reduce the risk of bulbitis and ulcers?

Use the lowest effective dose, avoid combinations with aspirin/anticoagulants/steroids, discuss gastroprotection (PPI or misoprostol), regularly reassess the need for NSAIDs. [61]

• Is a strict "table number 1" diet necessary?

There's no evidence to support strict diets. Individualized trigger approaches work: frequent meals, moderate fat intake, avoiding large late dinners, and limiting coffee and spicy foods as tolerated. The most important thing is to eliminate the underlying cause and complete eradication. (Overview recommendations.)