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Giới thiệu
Peptic ulcer disease (PUD) is characterized by mucosal damage secondary
to pepsin and gastric acid secretion. It is the principal cause of upper
gastrointestinal (GI) hemorrhage. This most commonly occurs in the stomach and
proximal duodenum, infrequently in the lower esophagus, distal duodenum or
jejunum.
PUD is suspected in patients with dyspepsia, a history of nonsteroidal
anti-inflammatory drug (NSAID) use or Helicobacter pylori (H pylori)
infection. Dyspepsia is a non-specific term indicating discomfort in the upper
abdomen. Refractory PUD is considered in patients with ulcers that fail to heal
after 8-12 weeks of therapy. A giant ulcer with a size of >2 cm is an
atypical type of PUD that is now rarely encountered; a biopsy may be needed to
rule out gastric cancer.
Dịch tễ học
The incidence of uncomplicated PUD is approximately 1 case per 1,000 person-years, while the incidence of ulcer complications is approximately 0.7 cases per 1,000 person-years. The prevalence of PUD is higher in areas endemic for H pylori and with low socioeconomic status. Familial clustering is now attributed to person-to-person transmission of H pylori or a genetic susceptibility to H pylori infection rather than a genetic predisposition to gastric ulcers. Gastric ulcers are more prevalent in Asia, particularly in Japan, while duodenal ulcers are more commonly diagnosed in Western countries. Both duodenal and gastric ulcers have increased incidence with age. Males are more likely to be affected than females.
Sinh lý bệnh
Ulceration in peptic ulcer disease occurs when a disruption in the
integrity and normal processes of the gastric mucosa leads to an imbalance
between the stomach's acid production and its protective barrier. H pylori
infection causes pangastritis, which increases basal and stimulated gastric
acid secretion by inhibiting somatostatin release and stimulating gastrin
release.
NSAIDs damage the gastric mucosa mainly through inhibition of
prostaglandin synthesis and its cytoprotective effects. The gastric acid
secretion is increased. Mucus and bicarbonate secretion is inhibited. The blood
flow to the gastric mucosa is significantly reduced.
Stress-related mucosal disease caused by a critical illness results
from a reduction in splanchnic and mucosal perfusion, which reduces bicarbonate
secretion and mucosal blood flow, decreases gastrointestinal motility, and causes
acid back diffusion. The damage to surface epithelial cells decreases
bicarbonate production leading to further damage to the protective gastric
lining. Once the superficial mucosa is breached, deeper layers are exposed to
acid damage, causing subsequent inflammation and potential ulceration.

Yếu tố nguy cơ
Seventy
percent (70%) of PUD cases occur in patients aged 25-64 years old. The incidence
of complicated PUD increases with age. Most cases are secondary to H pylori
infection and use of NSAIDs. Some evidence states that H pylori
infection may be food- or waterborne and may spread from person to person. In
patients with a bleeding ulcer, it is recommended to test for and treat H
pylori. Patients who are on long-term NSAIDs have an annual risk of
life-threatening ulcer-related complications of 1-4%. In patients on NSAIDs,
PUD bleeding may be caused by older age and use of concomitant steroid or high NSAID
doses. H pylori infection and NSAID use increase the risk and intensity
of NSAID-related mucosal damage. Both are the primary causes of PUD
complications (eg bleeding and perforation).
Other risk factors may include drugs (eg low-dose Aspirin,
corticosteroids, bisphosphonates, anticoagulants), potassium chloride,
chemotherapeutic agents, radiation therapy, the presence of acid-hypersecretory
states (eg Zollinger-Ellison syndrome), cancer, chronic disease, severe
physiologic stress (eg multiorgan failure, ventilator support >48 hours,
extensive burns [Curling’s ulcer] or head injury [Cushing’s ulcer]), viral
infection, lifestyle factors (eg diet, alcohol use, smoking), and genetic
factors.