Duodenitis is defined as a condition of inflammation in the lining of the duodenum, the first section of the small intestine.
Causes and Risk factors
A. Causes
1. Medication
Prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as
ibuprofen (Advil, Motrin), naproxen (Aleve), or aspirin, in some people,
it can lead to irritation causes of inflammation in the lining of the
duodenum. There is a report of a 40-year-old previously healthy white
man presented to the emergency
department at American University of Beirut Medical Center, Beirut,
Lebanon, with developed symptomatic severe transmural duodenitis
and periduodenal mesenteric streaking, consistent with a complicated
ulcer, probably associated with very short-term exposure to tiaprofenic
acid(3a).
2. Bacteria infections (Helicobacter pylor)
In the study of 138 (92 males, 46 females) patients aged 4.5-85 years [mean (7) =
45+/-SD 17.8 years] who had upper gastrointestinal endoscopy were
analyzed for presence of H. pylori, found that eighty-three had histopathology
alone, while 55 others had both histology and culture. Endoscopic
diagnosis included duodenal ulcer (DU) (n=35, 23%); gastric ulcer (n=4,
3%); gastric cancer (n=14, 9%); NUD, including gastritis (n=49, 32%); duodenitis
(n=47, 31%); and normal (n=16, 11%). Overall, H. pylori was positive in
107 of 138 (77.5%) patients. There was a significant association of H.
pylori with DU and NUD (p<0.000). Three-quarters of cases of normal
endoscopy harbored H. pylori. The finding of 80% and 85% H. pylori in
gastritis and duodenitis, respectively, was of interest(4).
3. Gastroesophageal reflux disease
In the study to determine the relationship between symptoms and H.
pylori eradication
and to determine whether H. pylori eradication results in symptoms or
endoscopic findings of GERD, researchers at the University of Wisconsin
Medical School, Milwaukee, showed that he presence of epigastric pain
was significantly associated with
persistent H. pylori infection 1 month after therapy (odds ratio 2.3,
95% CI: 1.02-5.2; P=0.041), as was nausea (OR 7.1, 95% CI: 0.93-55.6;
P=0.029). The presence of epigastric pain was significantly associated
with ulcer relapse at 6 months (OR 7.5, 95% CI: 3.6-15.7; P < 0.001)
as was nausea (OR 5.1, 95% CI: 1.7-16.0; P=0.002). Heartburn was not
associated with eradication of H. pylori or ulcer relapse. New onset reflux
symptoms were reported by 17% (17 of 101 patients) at 6 months and were
not significantly different in patients with (15%) and without (22%)
persistent H. pylori infection (P=0.47)(5).
4. Parasitic infection
There is a report of a case of a 24-year-old male patient admitted for recent
ascites and splenomegaly of unknown origin. The patient was referred to
our institution with complaints of diarrhea, epigastric pain, abdominal
cramping and weight loss over the past three weeks, Upper gastrointestinal system endoscopy performed a few days later
revealed diffuse severe erythematous pangastritis and gastroduodenal
gastric reflux. Duodenal biopsies showed chronic nonspecific duodenitis. Antrum and corpus biopsies showed chronic gastritis. The final diagnosis was consistent with parasitic infection while the clinical, sonographic and histological findings suggested an eosinophilic ascites(6).
5. Nucleic acids by phases of cavitary secretion
In the study of the concentration of nucleic acids in the cavitary secretion
phase reflects the state of the gastroduodenal mucosa and
physicochemical properties of the mucus of Sixty patients with
gastroduodenal diseases (chronic gastritis, chronic duodenitis from surface to atrophic and during exacerbation), sgowed that changes in the distribution of nucleic acids by phases of cavitary secretion were revealed. A decrease in the total content of nucleic acids in cavitary contents was paralleled by decreased activity of chronic gastritis and duodenitis and normalization of colloid and gel-forming properties of the mucus(7)
6. Viral infection
In the study to investigate endoscopic and histopathological findings in the duodenum of
patients with Strongyloides stercoralis (S. stercoralis)
hyperinfection, reseachers at the indicated that twenty-four (96%) of the patients investigated were under
immunocompromised condition which was mainly due to a human T
lymphotropic virus type 1 (HTLV-1) infection.
The abnormal endoscopic findings, mainly edematous mucosa, white villi
and erythematous mucosa, were observed in 23 (92%) patients. The degree
of duodenitis
including villous atrophy/destruction and inflammatory cell infiltration
corresponded to the severity of the endoscopic findings(8).
7. Celiac disease, Whipple's disease and Crohn's disease
In studied the count and identification of inflammatory cells in duodenal biopsies of specific duodenitis. In celiac disease
there is an increase of lymphocytes in the epithelial layer, and rich
population of plasmacells in the lamina propria of duodenal mucosa. In
Whipple's disease
the reticulum cell component of lamina propria is increased, while
total inflammatory cells are within normal limits, and both lymphocytes
and plasmacells are decreased. The comparison between duodenal and
jejunal findings shows similar data in celiac and Whipple's disease. In Crohn's disease
the inflammatory cell count differs from controls only in presence of
radiological or endoscopical features of duodenal involvement(9).
8. Toothpick ingestion
There is a report of two patients with duodenal inflammation secondary to toothpick ingestion. In the first patient, there was acute onset of severe abdominal pain, with findings on computed tomography consistent with marked duodenal inflammation. Endoscopy revealed a toothpick embedded in the wall of the duodenum with associated ulceration. In the second patient, 4 months of chronic abdominal
pain was evaluated by upper endoscopy which revealed a toothpick
embedded in a 1-cm ulcer found in the third portion of the duodenum(9a).
9. Etc.
B. Risk Factors
1. Smoking and gender
In the study of the extent of duodenitis
on the site opposite the ulcer determined by histological
examination, showed that Sixty per cent of the duodenal ulcers were healed after
three weeks. By univariate analysis, the following factors affect the
healing; pain radiation
to back and pain duration during treatment (p less than 0.001),
multiple or deep ulcers, narrowing of duodenal bulb (p less than 0.01),
number of pain attacks and poor appetite (p less than 0.05). By the
stepwise logistic regression model, the following factors were selected
as predictors for healing of duodenal ulcer with 76% correct
classification: pain radiation
to back (p = 0.002), deep ulcer (p = 0.013), multiple ulcers (p =
0.028). Number of cigarettes/day (p less than 0.007) and male sex (p =
0.036). By this model, the prediction of healing could be accurately
assessed in 78% in a new sample. Individual treatment should be carried
out on the basis of these factors(10).
2. Alcohol abuse
Even though, there is no any relation existing between the percentage
of cases with atrophic inflammation and the kind of drinks or the
content of ethanol
in them, but examinations concerning the secretory function of the stomach
showed lower values of hydrochloric acid secretion, both in basic
conditions and after pentagastrin stimulation, in patients addicted to alcohol as compared to the control. Continuous abuse of alcohol
predisposes to atrophic inflammation of the gastric mucosa, and the
appearance of this type of inflammatory changes is related to the
duration of addiction. The longer the addiction, the lower the secretion
of hydrochloric acid is(11).
3. Stress
GDD in the young is a very frequent pathology, which may be triggered
off by abrupt changes in life style, especially in those patients who
are unable to react positively to changes in the outer world. GD
pathology arises most frequently during the first five months of
military service, especially within the third and the fourth month(12).
4. Etc.
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Sources
(3a) http://www.ncbi.nlm.nih.gov/pubmed/18158085
(4) http://www.ncbi.nlm.nih.gov/pubmed/17304966
(5) http://www.ncbi.nlm.nih.gov/pubmed/10632644
(6) http://www.ncbi.nlm.nih.gov/pubmed/21552435
(7) http://www.ncbi.nlm.nih.gov/pubmed/12132379
(8) http://www.ncbi.nlm.nih.gov/pubmed/18350608
(9) http://www.ncbi.nlm.nih.gov/pubmed/71989
(9a) http://www.ncbi.nlm.nih.gov/pubmed/8792719
(10) http://www.ncbi.nlm.nih.gov/pubmed/3356359
(11) http://www.ncbi.nlm.nih.gov/pubmed/12898897
(12) http://www.ncbi.nlm.nih.gov/pubmed/9479996
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