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Tuesday, 3 December 2013

Duodenitis - The Causes and Risk Factors

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