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Nonspecific Duodenitis: An Unusual Presentation

Naveh, Yehezkel; Kleinhaus, Uriel*; Kerner, Edwiga; Berant, Moshe

Journal of Pediatric Gastroenterology & Nutrition: April 1997 - Volume 24 - Issue 4 - p 434-438
Case Reports
Free

From the Departments of Pediatrics,*Diagnostic Radiology and Pathology, Rambam Medical Center, and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel

Received February 11, 1991; revised October 10, 1995; accepted June 10, 1996.

Address correspondence and reprint requests to Dr. Y. Naveh, Department of Pediatrics, Rambam Medical Center, POB 9602, Haifa 31096. Israel.

Fiberoptic endoscopy of the upper gastrointestinal tract in children is a relatively recent development, which has enabled a better definition of some diseases of the gastrointestinal tract in children. Over the last 20 years, the diagnostic and therapeutic capabilities of the procedure have often obviated the need for abdominal surgery and have reduced the number of exploratory laparotomies. Subtle changes of the stomach and duodenum overlooked by radiologists may be diagnosed by complementary endoscopy. Hsu et al. (1) described 31 infants and children with endoscopically proven acute duodenal ulcers; multiple ulcers were found in 17 patients and were present in the bulb as well as in the second part of the duodenum in six patients. These patients remained symptom-free 2-6 years after the initial diagnosis. Duodenal inflammatory changes with no ulceration, namely, duodenitis or nonspecific duodenitis, have been described in adults (2,3) who suffered from variable dyspeptic symptoms mimicking peptic ulcer disease (4). However, review of the literature revealed only scant clinical descriptions of nonspecific duodenitis in children (5). The present study describes two adolescents who suffered from duodenitis and presented with dramatic symptoms related to the digestive system.

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CASE HISTORIES

Patient 1

An 11-year-old boy was admitted because of cramping periumbilical pain and persistent vomiting of 5 days' duration. There was no history of his taking acetylsalicylic acid (aspirin), nonsteroidal antiinflammatory drugs, antibiotics, or any other medication prior to the present illness.

Physical examination revealed a well-developed, mildly dehydrated child. Blood pressure was 130/70 mm Hg (17.3/9.3 kPa), heart rate 92 beats/min and regular, and temperature 37.4°C. The upper abdomen was moderately tender. Otherwise, the results of physical examination were normal.

Laboratory studies showed a hemoglobin level of 13.5 g/dl and a white blood cell (WBC) count of 4,800/μl with 30% segmented neutrophils, 15% banded neutrophils, 39% lymphocytes, and 16% monocytes. Platelet count was 277,000/μl. The erythrocyte sedimentation rate (ESR) was 14 mm/h. The results of urinalysis and urine culture were normal. Repeated stool cultures and examinations for parasites were negative. A simultaneous multiple analysis computerized (SMAC) test shows normal results. Serum gastrin was 43.6 pg/ml (43.6 ng/L). A serology test and blood cultures for salmonella and brucellae were negative. Imaging examinations showed the following: Ultrasonography and computerized tomography of the abdomen were normal. A single-contrast upper gastrointestinal barium examination demonstrated an atonic duodenal sweep with very thick mucosal folds (Fig. 1A). A shaggy border was thought to represent mucosal erosions at the beginning of the third part of the duodenum (Fig. 1A).

Upper gastrointestinal tract endoscopy showed normal esophagus, stomach, and duodenal bulb. The mucosa of the second part of the duodenum was erythematous and edematous and showed superficial erosions. The third part of the duodenum was normal. Biopsies of the second part of the duodenum revealed chronic, diffuse inflammation and distortion of the normal villous structure (Fig. 2). The inflammatory infiltrate was mostly mononuclear, with areas of plasma cell infiltration. No trophozoites of Giardia lamblia were demonstrated by hematoxylin and eosin stain, nor Helicobacter pylori by Giesma and Gram stains.

Following endoscopy, the patient was treated twice daily with 200 mg cimetidine given intravenously. Abdominal pain ceased on the third day, and the temperature dropped gradually to normal on the 6th day of cimetidine administration. After 7 days of intravenous therapy, oral cimetidine, 400 mg daily, was given for another 5 weeks. The patient was sent home on the 12th hospital day and was followed up in our outpatient clinic. A repeated barium meal study after 6 months was normal (Fig. 1B), and a repeated upper gastrointestinal endoscopy after 15 months showed normal esophagus, stomach, duodenal bulb, and second and third parts of the duodenum. Biopsies of the second part of the duodenum revealed normal duodenal mucosa without inflammatory changes (Fig. 3). Follow-up over 6 years was uneventful, and no clinical recurrence was noted.

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Patient 2

A 14-year-old boy was referred from another hospital because of persistent abdominal pain and weight loss. Past history was noncontributory. No medication had been taken. His illness had started 3 weeks prior to admission to our hospital with vomiting, diarrhea, and abdominal pain. Vomiting and diarrhea stopped during his hospitalization in the other hospital, while diffuse, cramping abdominal pain associated with flatulence persisted. The pain was most marked in the epigastrium and periumbilical area and worsened after drinking or eating. The patient had lost 5 kg in weight during the preceding 3 weeks.

Laboratory examinations performed at the referring hospital revealed a hemoglobin level of 15 gm/dl, a WBC count of 14,000/μl, and a platelet count of 380,000/μl. Agglutination tests for salmonellae and brucella were negative. The ESR was 50 mm/h. The brucella result of urinalysis was normal. Repeated stool cultures and examinations for ova and parasites were negative. A blood culture was sterile. The SMAC showed normal results except for fibrinogen levels of 600 and 720 mg/dl (6.0 and 7.2 gm/L). A single-contrast upper gastrointestinal barium examination showed a normal-appearing esophagus and stomach, but thickened mucosal folds were observed along the whole duodenal sweep (Fig. 4). A mildly shaggy border as attributed to hypersecretion, but the possibility of erosions could not be ruled out. All these changes extended into the proximal small bowel.

After 16 days of hospitalization, the patient was referred to our department with the suspicion of lymphoma, Crohn's disease, or familial Mediterranean fever. Physical examination on admission revealed a thin (weight 34 kg), sick child. His blood pressure was 105/60 mm Hg, heart rate 92 beats/min, and temperature 36°C. A systolic murmur, grade 2/6, was heard on the left sternal border. The abdomen was soft and quite tender in the epigastric and periumbilical areas. Otherwise, the physical examination showed no abnormalities.

Laboratory studies revealed a hemoglobin level of 15.6 gm/dl and a leukocyte count of 13,200/μl with 71% segmented neutrophils, 7% banded neutrophils, 14% lymphocytes, and 8% monocytes. The platelet count was 321,000/μl. The ESR was 25 mm/h. The results of urinalysis and urine culture were normal. Stool culture and examination for ova and parasites were negative. The SMAC showed normal results. A Watson capsule was used in the referring hospital to obtain biopsy specimens from the distal duodenal mucosa, just proximal to the ligment of Treitz. The histopathologic examination showed mucosa with a well-preserved villous structure. The lamina propria was diffusely infiltrated by chronic and subacute inflammatory cells. Trophozoites of Giardia lamblia were not demonstrated, and no evidence of amyloidosis, lymphoma, or granuloma formation was found (Fig. 5).

Upper gastrointestinal endoscopy demonstrated a normal esophagus and stomach. The first and second parts of the duodenum showed an erythematous, edematous and friable mucosa with superficial erosions.

The patient was treated with cimetidine, 800 mg once daily, for 6 weeks. Within a few days, the abdominal pain ceased and the patient regained his appetite. Six weeks after discharge, the boy was seen in our outpatient clinic. He was entirely healthy and had gained 7 kg in weight. Repeat upper gastrointestinal endoscopy 2 years later revealed normal esophagus, stomach, duodenal bulb, and second and third parts of the duodenum.

Biopsies of the second part of the duodenum showed a normal duodenal mucosa (Fig. 6). There was no recurrence of clinical symptoms over a 7-year period of follow-up.

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DISCUSSION

The few cases of nonspecific duodenitis reported so far in children have not indicated any typical clinical symptom complex (5). Therefore, fiberoptic endoscopy, radiologic examinations, and pathologic findings of the duodenal mucosa become important in the evaluation of patients suspected of having duodenitis. Gelfand et al. (6) reviewed 157 adult patients with endoscopically diagnosed duodenitis. They evaluated the sensitivity and specificity of four radiologic signs: thickened folds, mucosal nodules, bulbar deformity, and erosions. They concluded that the overall sensitivity and specificity of these signs were 77.7 and 76.5%, respectively. In our patients, the radiologic signs noted on barium examination consisted mainly of thickened mucosal folds, which are the most sensitive but least specific radiologic sign of duodenitis (6). The possibility of erosions, which are considered as a very specific sign of the condition, was raised in patient 1.

During the last two decades, upper gastrointestinal endoscopy has become one of the most frequently employed investigations in pediatric gastroenterology. Until fiberoptic instruments were developed for children, more than half of all the complaints of hematemesis, melena, and abdominal pain went undiagnosed (7). Upper gastrointestinal endoscopy has improved diagnosis and/or treatment of many gastrointestinal diseases. It is indicated in patients with upper and lower gastrointestinal bleeding, recurrent abdominal pain localized to the midepigastric area (especially when associated with nausea, vomiting or diarrhea, and weight loss), persistent vomiting, caustic or foreign body ingestion, esophageal strictures, sclerotherapy of esophageal varices, placement of gastrostomy and jejunostomy feeding tubes, electro- or photocoagulation of bleeding gastric or duodenal ulcers and angiomas, and electrocautery of antral webs or as a complementary investigation for inconclusive radiographic studies (7). Therefore, the superiority of endoscopy over radiography is well established and should indeed constitute the initial investigative procedure whenever indicated and wherever a skilled pediatric gastroenterologist is available. The sequence of the investigations as performed in our patients was dictated by the prompt availability of radiographic examinations for the emergency room pediatrician over the weekend in patient 1, whereas patient 2 underwent an upper gastrointestinal radiographic examination prior to referral to our unit.

Oderda et al. (5) modified and tabulated the pathologic criteria of Hasan et al. (8) and Whitehead et al. (9) for the diagnosis of duodenitis. Out of their 32 children with duodenal disease, only four fulfilled the accepted pathologic criteria for a diagnosis of duodenitis. In our cases, the histologic picture conformed with the diagnostic criteria of Hasan et al. (8) and Whitehead et al. (9).

The positive response of our patients to cimetidine may lend support to the suggestion that their disease was peptic in nature (10,11), although a viral etiology cannot be ruled out. Hsu et al. (1) suggested that young children may develop acute duodenal ulcers after viral illnesses and that those ulcers usually heal quickly irrespective of their morphology, site, and number. The similarities between their patients and ours are the male preponderance; presentation with vomiting, fever, and diarrhea; and positive endoscopic findings. On the other hand, their patients had a high incidence of gastrointestinal bleeding and had acute duodenal ulcerations, which were self-limiting in most cases. The fact that our patients remained totally asymptomatic during 6 and 7 years, respectively, without having received anti-Helicobacter pylori treatment, supports a viral etiology rather than Helicobacter pylori-induced peptic disease. Unfortunately, gastric antral biopsies and serologic tests for diagnosing Helicobacter pylori infection were not routine in our medical center at the time these patients were hospitalized (1988 and 1989).

The endoscopic, radiologic, and pathologic findings, and the clinical course over a prolonged follow-up, leave no doubt about the diagnosis of nonspecific duodenitis in our patients. Their presentation of acute unrelenting abdominal pain and vomiting, without any history of peptic disease, could have led to an unwarranted decision to perform an exploratory laparotomy. Awareness of pediatricians and surgeons of the possibility that duodenitis may present with dramatic symptoms simulating abdominal catastrophe can spare affected children extended suffering and unnecessary invasive procedures.

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REFERENCES

1. Hsu HY, Chang MH, Wang TH, et al. Acute duodenal ulcer. Arch Dis Child 1989;64:774-9.
2. Cotton PB, Price AB, Tighe JR, Beales JSM. Preliminary evaluation of “duodenitis” by endoscopy and biopsy. Br Med J 1973;3:430-3.
3. Gelzayd EA, Gelfand DW, Rinaldo JA Jr. Nonspecific duodenitis: a distinct clinical entity. Gastrointest Endosc 1973;19:131-8.
4. Thomson WO, Joffe SN, Robertson AG, Lee FD, Imrie CW, Blumgart LH. Is duodenitis a dyspeptic myth? Lancet 1977;1:1197-8.
5. Oderda G, Forni M, Farina L, Dell'Olio D, Ansaldi N. Duodenitis in children: clinical, endoscopic, and pathological aspects. Gastrointest Endosc 1987;33:366-9.
6. Galfand DW, Dale WJ, Ott DJ, et al. Duodenitis: endoscopicradiologic correlation in 272 patients. Radiology 1985;157:577-81.
7. Ament ME, Vargas J. Fiberoptic upper intestinal endoscopy. In: Walker WA, Durie PR, Hamilton JR, Walker-Smith JA, Watkins JB, eds. Pediatric gastrointestinal disease. Philadelphia: B.C. Decker, 1991:1247-56.
8. Hasan M, Frances HAY, Sircus W, Ferguson A. Nature of the inflammatory cell infiltrate in duodenitis. J Clin Pathol 1983;36:280-8.
9. Whitehead R, Roca M, Meikle DD, Skinner J, Truelove SC. The histological classification of duodenitis in fiberoptic biopsy specimens. Digestion 1975;13:129-36.
10. Bayeli PF, Bargagli D, Benelli R, Abate L. Studio clinico su 33 quadri istologici di duodenite cronica non specifica. G Ital End Dig 1983;6:133-40.
11. Anonymous. Duodenitis-any progress? [Editorial]. Lancet 1985;2:1222-3.
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