|Year : 2021 | Volume
| Issue : 1 | Page : 37-39
S Palaniappan, Manoj Munirathinam, A Murali
MIOT Advanced Center for GI and Liver Diseases, Chennai, Tamil Nadu, India
|Date of Submission||12-Aug-2020|
|Date of Decision||25-Aug-2020|
|Date of Acceptance||25-Aug-2020|
|Date of Web Publication||04-Dec-2020|
No. 14, 2nd Cross Street, Nolambur Phase 2, Mogappair West, Chennai - 600 037, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Tuberculosis (TB) of the gastrointestinal tract is common in India. The most common site is the ileocecal region. TB involving the duodenum is rare. It can present as duodenal ulcer, gastric outlet obstruction, and rarely with periduodenal lymph nodal involvement and bile duct erosion. Here, we report a patient who presented with pain abdomen and significant weight loss. Evaluation revealed a duodenal ulcer with paraduodenal nodal mass with probable contained perforation. Endoscopic ultrasound with fine-needle aspiration cytology of the nodal mass revealed the diagnosis of TB. She was started on anti-TB therapy and responded well with complete resolution. This case report emphasizes the need for having TB as a differential diagnosis for duodenal ulcer in an endemic country like India.
Keywords: Duodenal ulcer, endoscopic ultrasound, paraduodenal node
|How to cite this article:|
Palaniappan S, Munirathinam M, Murali A. Duodenal tuberculosis. Gastroenterol Hepatol Endosc Pract 2021;1:37-9
| Introduction|| |
The ileocecal region is the most common site of abdominal tuberculosis (TB) (almost 85%). TB of the stomach and duodenum are uncommon and accounts for <2% of all cases of abdominal TB. Duodenal TB is an uncommon disease most often presenting with gastric outlet obstruction resulting in malnutrition. TB causing duodenal ulceration with periduodenal lymphadenopathy is quite rare and we present a similar case scenario here.
| Case Report|| |
A 53-year-old female was admitted to our hospital with complaints of upper abdominal pain of 4 days duration. The pain was burning type, intermittent, lasting for few minutes, increased after food intake with no radiation, or postural variation. She had significant weight loss of 15 kg in 2 months. Her appetite was also reduced. She did not have vomiting, hematemesis, melena, abdominal distension, fever, or jaundice. She was not a diabetic or a hypertensive and was not on any chronic drug intake. There was no past history of TB or contact with TB.
On examination, she was anemic with epigastric tenderness. No other clinical lead noted. Evaluation showed hemoglobin of 9 g% with normal total count and platelets. Erythrocyte sedimentation rate was 40 mm/h. Ultrasound of the abdomen revealed contracted gall bladder with wall thickening of 4 mm with mild pericholecystic fluid collection. The renal and liver function tests were normal. Serum amylase and lipase were normal. Hemoglobin A1c was elevated - 7.2.
An upper gastrointestinal (GI) endoscopy revealed an excavated ulcer of about 1.5 cm × 1.5 cm covered with slough at the D1–D2 junction in the anterosuperior wall [Figure 1]. Rapid urease test was positive. Since the patient had significant weight loss, contrast computed tomography of the abdomen was done, which showed focal mucosal defect in the duodenum with adjacent fluid, and multiple heterogeneously enhancing lesion with areas of necrosis and air pockets in peripancreatic and periportal region – possibly enlarged necrotic lymph nodes-probable contained perforation [Figure 2]. Despite all these findings on imaging, the patient was very stable clinically, tolerating oral feeds with normal bowel movements. Surgical opinion was obtained, and they suggested conservative management.
She was started on intravenous proton-pump inhibitors and anti-Helicobacter pylori therapy. She responded symptomatically to conservative management and was pain-free at discharge. Her abdomen examination was unremarkable throughout the hospital stay, and she was tolerating oral diet adequately. After 1 week of anti-H. pylori therapy, she developed rashes in her hands with itching, and hence, the anti-H. pylori therapy was discontinued, and she was put on tablet ranitidine.
After 4 weeks, a relook upper GI endoscopy was done to reassess the duodenal lesion. It showed a bulky, edematous, nodular mucosal lesion with ulceration at the base in D1–D2 junction-biopsies were taken [Figure 3]. Histopathology showed extensive ulceration with neutrophilic and lymphocytic infiltration.
Endoscopic ultrasonography showed duodenal wall edema with multiple peripancreatic and periportal (2.2 cm × 1.4 cm largest) lymph nodes. Nodes were heterogeneous and lobulated with calcific foci, and the architecture was lost. Endoscopic ultrasound (EUS)-fine-needle aspiration cytology of node-3 passes done [Figure 4]. The cell block analysis showed caseous necrosis with granulomas composed of multinucleated epithelioid histiocytes and Langerhans giant cells most consistent with TB. GenXpert MTB/RIF was positive. Hence, a diagnosis of duodenal TB with periduodenal lymphadenopathy was made. The patient was started on anti-TB drugs. She gained weight adequately and became asymptomatic. Repeat endoscopy after 8 months revealed healed duodenal mucosa.
Review of literature
Duodenal TB may primarily affect the duodenum or produce compression due to the enlarged lymph nodes. It can present like peptic ulcer disease or can present with gastric outlet obstruction secondary to duodenal stricture. Abdominal pain and vomiting may occur, and some patients may even present with upper GI bleed. Active pulmonary TB can be seen in 10%–50% of patients with duodenal TB. Few cases of choledochoduodenal fistulas secondary to TB lymphadenitis have been reported in the literature.,
High index of suspicion is necessary to diagnose duodenal TB usually aided by radiological investigation, exploratory laparotomy, and histopathological examination of the tissue. The pathology is characterized by transverse ulcers, fibrosis, thickening and stricturing of the bowel wall, enlarged and matted mesenteric lymph nodes, omental thickening, and peritoneal tubercle.,
The disease may present at any age but commonly seen in young adults. Pathologically, there are two principal types of intestinal TB-ulcerative and hyperplastic TB. Ulcerative type is secondary to pulmonary TB and arises as a result of swallowing tubercle bacilli. There are multiple ulcers in the affected segments lying transversely, and the overlying serosa is thickened, reddened, and covered in tubercles. Hyperplastic type is caused by the ingestion of Mycobacterium tuberculosis by patients with a high resistance to organism. The infection establishes itself in lymphoid follicles, and the resulting chronic inflammation causes thickening of the intestinal wall and narrowing of the lumen. There is early involvement of regional lymph nodes which may caseate., Endoscopy may not be diagnostic and biopsies obtained show only nonspecific inflammatory changes; hence, explorative laparotomy was required in most of the cases. Nowadays, EUS-guided tissue sampling from the involved nodes can help in establishing the diagnosis.
Choledochoduodenal fistula is a relatively rare form of biliary-intestinal fistula, and it contributes to 3.5%–20% of all internal biliary fistulas., The most common etiology of choledochoduodenal fistula is penetrating duodenal ulcers, observed in 80% of cases. Duodenal involvement contributes to only 2.5% of TB enteritis. This exceedingly rare incidence is attributable to the high acidity and paucity of lymphoid tissue in the duodenum as well as rapid transit of food in the gastroduodenal area which is hostile to the tubercle bacilli. There is usually extensive lymph node involvement in the surrounding regions.
TB of the duodenum is more often confused with peptic ulcer disease and establishing an etiology of tuberculous for duodenal ulcer is challenging. Diagnosis of TB requires demonstration of acid-fast bacilli or caseous granulomas on biopsy. However, these biopsies are positive only in a 30% of cases, and sometimes, the diagnosis is made only at laparoscopy. Endoultrasonography of the abdomen can be beneficial if lymph nodes are visualized and image-guided fine-needle aspiration from these nodes may help in establishing the diagnosis of TB preoperatively. Anti - Tubercular treatment (ATT) is the mainstay of treatment with gastroduodenal TB. As per the standard guidelines of the treatment of TB four drugs should be used for a minimum of 2 months, followed by two drugs (isoniazid and rifampicin) for the next 4 months. Patients with gastroduodenal TB who present with the features of gastric outlet obstruction, endoscopy-based techniques should be considered as the standard operating procedure in the diagnosis and management. Surgical intervention is required only in the relatively small proportion who do not respond to the combination of ATT and endoscopic balloon dilatation.
Although TB is a rare cause of duodenal ulcer, it should always be considered as a differential diagnosis in countries like India, where TB is common. If the diagnosis of TB can be established preoperatively, by means of endoscopic biopsy from the duodenal ulcer or EUS-guided fine-needle aspiration of abdominal lymph nodes as illustrated in our case, anti-tubercular treatment can be curative, eliminating the need for surgery. Hence, early suspicion and diagnosis are imperative in the management of duodenal TB.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Alvares JF, Devarbhavi H, Makhija P, Rao S, Kottoor R. Clinical, colonoscopic, and histological profile of colonic tuberculosis in a tertiary hospital. Endoscopy 2005;37:351-6.
Padma V, Anand NN, Rajendran SM, Gurukal S, Primary tuberculosis of stomach. J Indian Med Assoc 2012;110:187-8.
Misra D, Rai RR, Nundy S, Tandon RK. Duodenal tuberculosis presenting as bleeding peptic ulcer. Am J Gastroenterol 1988;83:203-4.
Tishler JM. Duodenal tuberculosis. Radiology 1979;130:593-5.
Desta TT, Man KM, Bouvier D, Leung JW. Choledocho-enteric fistula due to Mycobacterium tuberculosis in a patient with acquired immunodeficiency syndrome. Gastrointest Endosc 1998;48:623-6.
Chaudhary A, Bhan A, Malik N, Dilawari JB, Khanna SK. Choledocho-duodenal fistula due to tuberculosis. Indian J Gastroenterol 1989;8:293-4.
Baloch NA, Baloch MA, Baloch FA. A study of 86 cases of abdominal tuberculosis. J Surg Pak Int 2008;13:30-2.
Bakhshi GD, Ansari WA, Chavan PR, Sarangi S. Duodenal tuberculosis mimicking superior mesenteric artery syndrome. Bombay Hosp J 2005;47:286-8.
Mirza MR, Sarwar M. Duodenal tuberculosis. Pak J Med Sci 2004;20:253-5.
Sharma MP, Bhatia V. Abdominal tuberculosis. Indian J Med Res 2004;120:305-15.
Raul SK, Das NA, Vakil R, Palijor YD, Joseph SC. Duodenal tuberculosis presenting as gastric outlet obstruction. Indian J Surg 2003;65:277-9.
Michowitz M, Farago C, Lazarovici I, Solowiejczyk M. Choledochoduodenal fistula: A rare complication of duodenal ulcer. Am J Gastroenterol 1984;79:416-20.
Hoppenstein JM, Medoza CB Jr., Watne AL. Choledochoduodenal fistula due to perforating duodenal ulcer disease. Ann Surg 1971;173:145-7.
Miyamoto S, Furuse J, Maru Y, Tajiri H, Muto M, Yoshino M. Duodenal tuberculosis with a choledocho-duodenal fistula. J Gastroenterol Hepatol 2001;16:235-8.
Rao YG, Pande GK, Sahni P, Chattopadhyay TK. Gastroduodenal tuberculosis management guidelines, based on a large experience and a review of the literature. Can J Surg 2004;47:364-8.
Agrawal S, Shetty SV, Bakshi G. Primary hypertrophic tuberculosis of the pyloroduodenal area: report of 2 cases. J Postgrad Med 1999;45:10-2.
] [Full text]
[Figure 1], [Figure 2], [Figure 3], [Figure 4]