A 34-year-old man was admitted to hospital complaining of epigastric pain and chronic
diarrhea without blood or mucus. He had no weight loss. His hematologic, biochemical,
and serologic tests and stool examination showed normal results, but his levels of
immunoglobulin A (IgA) were under the lower limit. Endoscopic examination revealed
multiple millimetric polypoid lesions throughout the duodenum and terminal ileum ([Fig. 1]). Histologic examination showed findings of chronic Helicobacter pylori gastritis and lymphoid follicular hyperplasia in the small bowel. A small-bowel series
revealed rapid small-bowel transit and numerous small nodular filling defects throughout
the small bowel ([Fig. 2]).
Fig. 1 a, b Endoscopic appearance of second part of the duodenum: a multiple polypoid lesions 3 – 5 mm in size throughout the duodenum; b terminal ileum.
Fig. 2 Small-bowel series revealed numerous nodular filling defects throughout the small
bowel.
The patient was treated for H. pylori gastritis with a regimen containing levofloxacin, a proton pump inhibitor, and amoxicillin
for 14 days. At 2 months after the end of the eradication therapy, C14 urea breath test gave a negative result. At follow-up endoscopy, the duodenal nodules
had regressed ([Fig. 3]). The patient was referred to an immunologist for further investigation.
Fig. 3 Duodenum in posttreatment period: nodules have decreased in size and number.
Nodular lymphoid hyperplasia (NLH) of the gastrointestinal tract is a rare pathology
in adults. It is characterized by the presence of numerous visible mucosal nodules
measuring up to 5 mm in diameter. Histologically, hyperplastic lymphoid follicles
with large germinal centers are seen in the lamina propria and superficial submucosa.
The etiology is unknown. Viral agents, giardiasis, and common variable immunodeficiency
have been suggested to be associated with NLH [1]. The association of NLH with H. pylori and IgA deficiency has been rarely described in the literature [2]
[3]. Treatment of the H. pylori infection can provide regression of nodules. However, treatment of all infections
is very difficult, and infections tend to be more persistent in patients with immune
deficiencies. Endoscopists should consider the possibility of IgA deficiency in patients
who present with diffuse nodular lesions in the small bowel, and H. pylori infection should be tested for and, if found, treated with an appropriate drug regimen.
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