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ABDOMINAL TUBERCULOSIS

Presenter : Dr.Aravinda P.S


Moderator : Dr. Vivek Gautam

DEFINITION
Abdominal tuberculosis includes TB of gastro-intestinal tract, peritoneum, omentum,
mesentery, lymph nodes and other solid intra-abdominal organs like liver, pancreas and
spleen.
EPIDEMIOLOGY
Abdominal tuberculosis is one of the most common forms of extra-pulmonary TB (1). TB
peritonitis constitutes 4-10% of all patients with extra pulmonary TB (1). Incidences of
isolated intestinal Tb in unselected autopsy series from India has been reported to vary from
0.02-5.1% (2). In Delhi 0.8% of all hospital admissions were reported to be due to intestinal
TB (3). In India, Tb has been reported to be the cause in 3-5% of patients with intestinal
obstruction (4). About 5-7% of all gastro-intestinal perforations (excluding appendix
perforations) have been reported to be due to TB (5).
CLASSIFICATION OF ABDOMINAL TUBERCULOSIS
1. Gastro-intestinal
Ulcerative
Hypertrophic or hyperplastic
Sclerotic or fibrous
Diffuse colitis
2. Peritoneal
Acute TB peritonitis
Chronic peritoneal tuberculosis
Ascitic form
Encysted or loculated form
Fibrous form (adhesive/ plastic type)
3. Mesentery and its contents
Mesenteric adenitis
Mesenteric cyst
Mesenteric abscess
Bowel adhesions
Rolled-up omentum
4. Solid viscera
Liver, biliary tract & gall bladder, pancreas and spleen
5. Retroperitoneal lymph node TB etc.
MICROBIOLOGY

Mycobacterium tuberculosis, Mycobacterium bovis and non tuberculous mycobacteria


(atypical mycobacteria) can cause extra pulmonary TB. M.tuberculosis is the most
frequently isolated organism. With wide spread pasteurization of milk and strict control of
TB in dairy herds, abdominal TB caused by M. bovis is rarely seen in the present era.
PATHOGENESIS AND ROUTES OF INFECTION
Peritoneal TB - haematogenous spread of infection from an active pulmonary tuberculosis
or activation of long-standing latent foci of TB infection of peritoneum can result in TB
peritonitis. Contiguous spread of infection from an intestinal lesion or fallopian tube is
relatively infrequent mechanism. Very rarely, TB peritoneum has been described as a
complication of peritoneal dialysis.
Gastro-intestinal TB it can be primary due to ingestion of milk or food materials
contaminated with M. Bovis, which is rare in the present era, or secondary to M.
Tuberculosis infection elsewhere in the body. Infection more often reaches the abdomen by
a) swallowing of infected sputum containing the bacilli; b) haematogenous spread from a
focus of active pulmonary TB, military TB or silent bacteraemic phase of primary TB; c)
spread from the infected adjacent viscera. The organism may also disseminate in the bile
from a hepatic granuloma.
HISTOPATHOLOGY
The typical feature of tuberculosis is the caseating granuloma (Tubercles). These are seen in
all diseased areas including bowel, mesenteric lymph nodes and peritoneum etc. The
granulomas have a peripheral zone of lymphocytes, plasma cells and langhans giant cells
with central area of caseating necrosis. Healing of grauloma may lead to fibrosis and
calcification.
PATHOLOGY
1) Peritoneal TB
Acute TB peritonitis it is extremely rare and may be seen in the following
circumstances : miliary phase of the disease, perforation of intestinal TB and local
dissemination from a ruptured, caseating mesenteric lymph node. This condition may
resemble acute abdomen and such patients may often be subjected to emergency
surgery. On opening the abdomen, straw coloured fluid may be present with tubercles
scattered over the peritoneum and greater omentum.
Chronic TB peritonitis this type is more common and typically presents as ascites.
The fluid is usually clear and straw coloured, but may be sanguinous. Peritoneal
adhesions that range from thin and flimsy to thick and dense may occur. Presence of
adhesions may lead to loculated ascites. The characteristic lesions are miliary nodules
that may increase in size and coalesce to form a plastic type of adhesion, which may
completely obliterate the peritoneal cavity forming an abdominal cocoon. The

omentum may be thickened to form a transversely placed mass called rolled-up


omentum
2) Intestinal tuberculosis
Any region from mouth to anus can be affected by tuberculosis. Ileocaecal area is the most
commonly affected site (6). The striking predilection for this site is thought to be due to
abundance of lymphoid tissue (Peyers patches). Increased physiological stasis, increased rate
of fluid and electrolyte absorption and minimal digestive activity permitting greater contact
time between the organism and mucosal surface in the ileocaecal area render this region more
vulnerable to the development of intestinal TB.
The vulnerability of ileocaecl region has also been attributed directly to Peyers patches and
the associated microfold cells (M-cells). The Bacilli Calmette-Guerin (BCG) vaccine has
been shown to be phagocytosed by the M-cells and transported to the antigen presenting cells
in the Peyers patches without any evidence epithelial inflammation (7).
Often, intestinal lesions start as crypt abscess, followed by infection of Peyers patches. As
the disease progresses, the lymphoid follicles become infiltrated and inflammation extends
throughout the submucosa. Eventually the epithelial layers above the Peyers patches ulcerate
giving rise to characteristic histopathologic appearance of ulcerative TB enteritis.
Gastro-intestinal TB can be of ulcerative, hypertrophic, sclerotic and diffuse colitis form.
Ulcerative form - The ulcerative form of intestinal TB usually occurs in adult
patients who are malnourished. There is induration and oedema of the diseased
segment of the intestine with an increase in serosal fat. Tuberculous ulcers can be
solitary or multiple and usually lie transverse to the long axis of the gut girdle ulcers.
Longitudinal or irregularly shaped ulcers may occasionally be seen. Areas of normal
appearing mucosa may be found amidst the diseased segment (skip lesions).
The ulcers are of varying depth extending from the submucosa to muscularis propria
or even serosa. As TB ulcers are most often horizontally located, healing and fibrosis
result in stricture formation (napkin ring strictures) and lead to obstructive symptoms.
Adhesions between the bowel loops prevent free perforation but promote formation of
intestinal fistula. Severe haemorrhage due to endarteritis is rare. The related
mesenteric lymph nodes enlarge and may caseate to form mesenteric abscesses.
Hypertrophic or hyperplastic form - Unlike ulcerative form, hypertrophic intestinal
TB commonly occurs in young patients who are relatively well nourished. Caecum is
the most commonly affected site. Hypertrophic intestinal TB occurs due to a low
volume infection by a less virulent organism in a host with good resistance and wound
healing capacity. This form is characterized by extensive inflammation and fibrosis
that often results in the adherence of bowel, mesentery and lymph nodes into a mass.
This mass may occasionally appear to be an exophytic neoplasm arisisng from the
mucosal surface. On histopathological examination, lymphoid follicular overgrowth

and hyperplastic germinal centre with infiltration by plasma cells, lymphocytes,


eosinophils and giant cells are present.
Caseation though not always present in the gut, is often seen in the mesenteric lymph
nodes. Caseation may occasionally be absent in tuberculosis granulomas. These non
caseating granulomas may be difficult to distinguish from those seen in Chrons
disease. Confluence of granulomas, relative absence of cracks and fissures and
submucosal oedema are important findings that favour the diagnosis of TB (8).
Diffuse colitis form - Another much less common form of TB is diffuse colitis, which
is endoscopically very simiar to ulcerative colitis. Diffuse colitis cannot be easily
distinguished from ulcerative colitis on the basis of mucosal appearance alone.
Sclerotic form - Sclerotic variety is associated with stricture that can be solitary or
multiple (8).
In gastro-intestinal tuberculosis, luminal narrowing is often caused by adjacent TB
lymphadenitis that results in traction, diverticula formation, narrowing, fixation and sinus
tract formation.
Entero-enteric, entero-vesical and entero-cutaneous fistulae can also occur in GI tuberculosis.
3) TB of mesentery and its contents
Enlarged mesenteric lymph nodes may be felt as lump in the abdomen, usually in the right
iliac fossa. Uncommonly, the presentation may mimic acute appendicitis. Tuberculosis
pseudomesenteric cyst has also been described.
CLINICAL FEATURES
Abdominal tuberculosis is most frequently seen in the age group between 20-40 years and
females outnumber the males by 2:1. The onset is usually insidious and the initial symptoms
are often vague and non-specific, which is particularly true for peritoneal tuberculosis. As the
disease progresses the individual may develop fever, which is present in two-third of patients,
night sweats, malaise, weakness, anorexia and weight loss. The appearance of specific
symptoms depends upon the predominant site of involvement.
Peritoneal tuberculosis Patients usually present with ascites. Less frequently, there may be
adhesions and loculated fluid collection resulting in the classic doughy abdomen. Patients
with peritoneal tuberculosis, especially females, often have coexisting tuberculosis of the
pelvic organs. Hence, good pelvic examination and endometrial biopsy may provide the
simplest method of confirming the diagnosis.
Gastro-intestinal tuberculosis the most common symptom in patients with GI tuberculosis
is abdominal pain and is present in almost all the patients (1,6). The pain is most commonly
located in right lower quadrant of abdomen, though a significant proportion of patients may
complain of diffuse, central, epigastric or left lower quadrant pain. The pain may be diffuse or

dull aching, especially when the peritoneum and mesenteric lymph nodes are involved and
colicky in case of intestinal obstruction.
Diarrhoea occurs in 11-20% of the patients (1,6). Liquid to semisolid stools are passed 6-8
times a day. Mucus is usually present. Blood or frank pus may be passed rarely. Diarrhoea is
almost always associated with intestinal ulceration, although it can sometimes occur in the
absence of any mucosal disease and is thought to occur due to generalized inflammatory
response. In primary small bowel disease the stools are large in amount, foul smelling and
resemble those seen in malabsorption. Diarrhoea alternating with constipation has been
described in 8.8-20% of patients (1,6).
Other symptoms include flatulence, nausea, altered bowel habit and borbrygmi. Abdominal
distension suggests ascites or persistent subacute intestinal obstruction. Typical duodenal
ulcer like pain may occur when the duodenum is involved.
Physical examination
Patients with chronic abdominal tuberculosis are often malnourished and anaemic. In some
the abdomen may be completely normal on examination, but most demonstrate some
abnormal findings. There may be visible peristalsis and the distended bowel loops can be
palpated. The abdomen may be distended or the signs may be more localized, usually in the
right lower quadrant. An ileocaecal mass may be felt in the right ileac fossa or higher up in
the right lumbar region. A doughy abdomen suggesting peritoneal disease has become less
common in recent years. A rolled up omentum when present, is felt as transversely placed
mass in the epigastric region. Loculated ascites, mesenteric cysts and mesenteric abscesses
present as cystic masses.
Patients with ascites may have shifting dullness and a fluid thrill. In patients with large bowel
disease a diffusely thickened and tender colon may be felt. Other findings include
hepatosplenomegaly, pelvic abnormalities mimicking gynaecological tumours and the
features of gastric outlet obstruction due to direct involvement of stomach or extrinsic
compression of duodenum by enlarged mesenteric lymph nodes. Rectal examination may
reveal any fistulae, fissures or stricture.

COMPLICATIONS

Mal absorption
Intestinal obstruction
Perforation peritonitis
Acute bleeding from rectum or hemetemesis
Fistulas ( entero-enteric, entero-vesical, enero-cutaneous) etc.

DIAGNOSIS

Since the discovery of tubercle bacilli it has been possible to make a precise diagnosis of
tuberculosis. However, in patients with abdominal tuberculosis the causative organism often
difficult to identify and the diagnosis is generally made by the indirect methods.
1) Haematology and serum biochemistry
Laboratory investigations are nonspecific and do not contribute to the diagnosis. There is a
varying degree of anaemia, leucopenia with relative lymphocytosis. Raised erythrocyte
sedimentation rate (ESR) is reported in 50-100% of patients (1,6). However, ESR was found
to be normal in many histologically proven patients with abdominal TB (1,6). Serum albumin
levels tend to be depressed. Serum alkaline phosphatase may be raised (1,6).
2) Tuberculin skin test
A positive skin test has been reported in 55-100% of patients of abdominal TB (1,6).
However, positive skin test neither confirms nor excludes abdominal TB in areas where TB is
highly endemic and in those who have received BCG vaccine because of high rates of
positivity in healthy individuals.
3) Ascitic fluid analysis
Ascitic fluid leucocytes count is usually 150 4000 cells / mm 3 and consists of lymphocytes
predominantly. For unknown reasons, neutrophilic response has been observed in patients
with TB peritonitis associated with peritoneal dialysis (9). Red blood cells may be found
often in the ascitic fluid.
The serum-ascitic fluid albumin gradient is less than 1.1 in more than 90% of patients (1).
Ascitic fluid reveals AFB in less than 3% of cases and culture for Mycobacterium
tuberculosis is positive in less than 20% of cases (1).
4) Adenosine deaminase ( ADA)
Adenosine deaminase (also known as ADA) is an enzyme involved in purine metabolism. It
is needed for the breakdown of adenosine from food and for the turnover of nucleic acids in
tissues. There are 2 isoforms of ADA: ADA1 and ADA2. ADA1 is found in most body cells,
particularly lymphocytes and macrophages, ADA2 was first identified in human spleen. It
was subsequently found in other tissues including the macrophage where it co-exists with
ADA1. ADA is involved in the proliferation and differentiation of lymphocytes, especially T
lymphocytes; hence, it is a marker of cell mediated immunity (type 4 hypersensitivity
reaction).
When a cut-off value of 32 IU / litre is chosen, the sensitivity and specificity of ascitic fluid
ADA are found to be 98% and 95% respectively ( 10). False negative results are seen in
cirrhosis of liver and HIV infection and false positive results are seen in malignant ascitis.
Interferon ( IFN- ) which is significantly higher in TB ascitis can be used to differentiate
TB ascitis from non-TB ascits.

5) Serodiagnosis
The serum CA-125 level that is normally elevated in ovarian malignancy is also raised in
some patients with abdominal TB. The level falls with anti-tuberculous treatment.
6) Polymerase chain reaction
The technique has been used in a variety of clinical specimens including sputum, CSF,
pleural and peritoneal fluids and biopsy tissues with sensitivity, specificity and positive
predictive value of 85%, 99% and 95% respectively.
7) Imaging studies
Chest x-ray
Associated pulmonary TB has been described in 24-28% of patients with abdominal TB.
X ray abdomen
Features like calcified lymph nodes, calcified granuloma in solid organs, dilated bowel loops,
air-fluid levels and free gas under diaphragm may be found in abdominal TB.
Barium studies
Barium studies have been the most useful investigation for the diagnosis of intestinal TB till
recently. Although the radiological features of intestinal TB are non-specific, several findings
are highly suggestive of disease. Enteroclysis (small bowel enema) followed by barium
enema is useful for evaluation of intestinal TB.
Features of intestinal TB in barium meal follow through (BMFT)
Hyper segmentation ( Stierlins sign) & flocculation of barium because of extreme
irritability due to mucosal ulceration there will be a rapid transit and lack of barium
retention in the inflamed segment of the small bowel one of the earliest signs.
Contractecd and pulled-up caecum
Mucosal ulceration ulcers may be linear or stellate and are situated along the
circumference of the wall.
Irregular thickened mucosal folds
Inverted umbrella sign (Fleischners sign) thickening of ileoceacal valve which
gives a broad triangular appearance with the base towards the caecum.
Stenosis or string sign
Dilated bowel loops
Both Stierlins sign and string sign are also seen in Crohns disease and hence not specific for
intestinal TB.
Oesophageal TB Barium swallow
Ulcers

Stricture
Pseudo tumour
Sinus / fistulae
Traction diverticulae

Duodenal TB Barium meal


Segmental narrowing
Pseudo tumour
Widening of C loop

Abdominal ultrasonography
Abdominal ultrasound often reveals a mass made up of matted loops of small bowel with
thickened walls, diseased omentum, mesentery and loculated ascitis (11). Ultrasound is very
sensitive in detecting small quantities of ascitic fluid. Fine septae may be seen in ascitic
fluid, which are considered to be diagnostic of abdominal Tb (11). These strands are usually
arise from the serosa of small bowel and may be observed in malignant ascitis also (12).
Loculated ascitis probably represents walled-off peritoneal inflammation. Interloop ascitis
gives rise to characteristic club sandwich appearance of alternating echogenic and echo-free
layers of bowel wall and inter loop fluid (13).
Mesenteric thickening is better detected in presence of ascitis and is often seen as the stellate
sign of bowel loops radiating out from its root. Enteritis with bowel wall thickening which is
usually uniform and concentric as opposed to eccentric thickening at the mesenteric border
seen in the Crohns disease and the variegated appearance seen in malignancy. This may be
difficult to appreciate on ultrasonography. Lymphoma of the bowel remains an important
differential diagnosis. Lymphadenopathy which may be discrete or matted particularly in
periportal, peripancreatic and mesenteric region is seen. Calcification, heterogenous
echotexture and necrosis may also be identified in lymphadenopathy.
CECT abdomen
Similar findings as noted on ultrasound, but with better resolution and definition are seen
with the CT scan. The ascitic fluid , thickening and nodularity of peritoneum and mesentery
can be more easily identified on CT scan. Other findings include - lymphadenopathy,
thickened bowel loops, granulomas or abscess in the liver, pancreas and spleen may be seen.
8) Endoscopy
Fibre optic endoscopes have made it possible to visualize directly the gastrointestinal tract.
Colonoscopy is the easiest and most direct method of establishing the diagnosis of TB colitis.
On colonoscopy, the ileocaecal valve may be oedematous or deformed. Other findings may
be, mucosal ulceration, nodules, pseudopolyps, narrowing and stricture of the bowel. Rarely,

there may be diffuse disease of the colon with hyperaemia and friability of mucosa
mimicking ulcerative colitis.
However, as with most diagnostic procedures in intestinal TB, endoscopic findings are not
pathognomonic. The endoscopic findings can be mistaken for Crohns disease. In TB
intestine, ulcers are usually transverse, have sharply defined margins with erythema of
surrounding mucosa. Fibrosis is common with short stricture (<3cms). In Crohns disease
ulcers are serpiginous, often longitudinal, with relatively normal surrounding mucosa.
Endoscopic biopsy specimens show granulomas and epitheloid cells in 40-74% of patients,
caseous necrosis in 8-21% cases and positive cultures in 6-40% of patients with intestinal TB.
A combination of histology and culture of the biopsy specimen can establish the diagnosis in
80% of cases (14). Endoscopy is also useful in excluding other conditions such as carcinoma,
lymphoma and caecal amoeboma.
9) Fine needle aspiration cytology ( FNAC)
In patients with palpable masses, FNAC has been shown to have a high diagnostic accuracy
(15). In patients with lymphadenopathy, abscesses and focal lesions of viscera, FNAC
confirms the diagnosis (16). Lowenstein-Jensen culture of the FNAC material increases the
yield further. The FNAC during colonoscopy s likely to add to the diagnostic yield in patients
with ileocaecal or clonoic TB (15).
10) Laparoscopy
Direct inspection and biopsy of the peritoneum are perhaps the most effective method of
diagnosing TB peritonitis. Characteristic laparoscopic findings include multiple, yellowishwhite military nodules over visceral and parietal peritoneum; erythematous, thickened and
hyperaemic peritoneum; turbid ascitis and adhesions. Laparoscopy alone will facilitate an
accurate presumptive diagnosis in 80-95% of patients (1). Laparoscopic biopsy may reveal
AFB in 75% and caseating granulomas in 85-90% 0f patients (1)

TREATMENT
The treatment of abdominal tuberculosis is primarily medical. Since acid-fast bacilli and
caseation necrosis are seen in minority of patients and culture takes several weeks, empirical
anti tuberculous therapy should be initiated in every patient with suspected tuberculosis.
Earlier, patients with abdominal TB have been treated with antituberculous drug regimens of
8-12 months duration (17). However, recent evidence suggest that six months short course
chemotherapy regimens are effective in all forms of abdominal TB (18). In India, majority of
patients with abdominal TB get treated with DOTS using standardized intermittent treatment
regimens under RNTCP of Govt.of India.
Drug dosage

Daily dosage

Intermittent dosage
( thrice weekly)

Drugs

mg /
kg

Dosage (mg)

mg / kg

Dosage (mg)

Rifampicin (R)

10

600 (450)

10

600 (450)

Isoniazid (H)

300

10

600

Pyrazinamide (Z)

20-30

1.5-2.0 g
(1.0-1.5 g)

30-40

2.0-2.5 g
(1.5-2.0 g)

Ethambutol (E)

15

Streptomycin (S)

12-15

30
750 ( 500750)

12-15

750 (500-750)

Figures in paracentesis indicate drug dosage in patients with weight < 50 kgs.
Dosage schedule
Total duration is 6 months
Initial 2 months is intensive phase followed by 4 months of continuation phase
Rifampicin, isoniazid and pyrazinamide are used in the intensive phase. A fourth drug
ethambutol or streptomycin is added if drug resistance rate is more than 4%
Rifampicin and isoniazid are used in the continuation phase
It is advisable to administer pyridoxine hydrochloride (5-10 mg) to all patients to
prevent isoniazid induced peripheral neuropathy.

Response to treatment
The clinical response to treatment is excellent. Systemic symptoms such as fever, malaise and
weight loss subside in a few weeks. Mucosal abnormalities take longer and barium studies
and endoscopy demonstrate regression of the lesions in most individuals. The majority of
patients (approx. 70%) with subacute intestinal obstruction and evidence of intestinal stricture
show complete resolution of radiological abnormality.

ROLE OF SURGERY
Indications

Intestinal obstruction due to stricture, bowel adhesions etc.


Perforation peritonitis
Intra abdominal or mesesnteric abscess
Internal or external fistula
In doubtful cases where malignancy cannot be ruled out with reasonable accuracy

Surgical options
Stricturoplasty
Resection of the diseased segment with end to end anstomosis
Limited ileocaecal resection with a five cms margin from visibly abnormal tissue or
limited right hemicolectomy and endto-end a anastomosis for hypertrophic
ileocaecal TB (19).

Bypass surgery, such as entero-enterostomy, ileotransverse colostomy is not


recommended for obstructive lesions as these procedures may facilitate the formation
of blind loops leading to obstruction, malabsorption or both (20).

REFERENCES
1.Marshall JB. Tuberculosis of gastro-intestinal tract and peritoneum. Am J Gastroenterol
1993;88:989-99
2.Tribedi BD, Gupta DM. Intestinal tuberculosis in Bengal. J Indian med Assoc 1941;11:41
3.Chuttani HK. Intestinal Tuberculosis. In: Card WI, Creamer B, editors. Modern trends in
gastroenterology. London: Butterworth; 1970. P.309-27
4.Bhansali SK,Sethna JR.Intestinal obstruction:A clinical analtsis of 348 cases.Indian JSurg
1970;32:57-70
5.Bhansali SK.Gastrointestinal perforations;Clinical study of 96 cases.J postgrad
Med1967;13:1-12
6. Pimparker B D Donde U M. Intestinal tuberculosis.I.clinical and radiological studies.J
Assoc physicians india 1974;22:205-18.
7. Fujimura Y.Functional morphology of microfold cells[M cells] in peyers patchesphagocytosis and transport of BCG by M cells into rabbit peyers patches. Gastroenterol
Jpn1986;21:325-35
8.Tandon HD,Prakash A. Pathology of intestinal tuberculosis and its distension from crohns
disease. Gut 1972:13:260-9

9. Malik GH,Al-Harbi AS,Al-Mohaya S,Kechrid M,Sheita MS,Azhari O. Tuberculous


peritonitis in patients on chronic peritoneal dialysis:case reports .Saudi J kidney Dis Transpl
2003;14:65-9
10. Sharma SK, Tahir M, Mohan A, Smith-Rohrberg D, Mishra HK, Pandey RM. Diagnostic
accuracy of acsitic fluid IFN-gamma and adenosine deaminase assays in the diagnosis of
tuberclous acsitis. J Interferon cytokines Res2006;26:484-8
11. Denton T, Hossain J. A radiological study of abdominal tuberculosis in Saudi
population,with special reference to ultrasound and computed tomography. Clin radiol
1993;47:409-14
12. Gompels BM, Darlington LG. Ultrasonic diagnosis of tuberculous peritonitis. BR J
Radiol 1978;51:1018-9
13. Kedar RP, Shah PP, Shivde RS, Malde HM. Sonographic findings in gastrointestinal and
peritoneal tuberculosis. Clin Radiol 1994;49:24-9
14. Singh V,Kumar P,Kamal J,Prakash V,Vaiphei K,Singh KW.Clinicocolonoscopic profile of
colonic tuberculosis.Am J Gastroenterol 1996;91:565-8
15. Radhika S,Gupta SK,ChakrabartiA,Rajwanshi A,Joshi K.Role of culture for
microbacteria in fine-needle aspiration diagnosis of tuberculous lymphadenitis.iagn
Cytopathol 1989;5:260-2
16. Malik A,Saxena NC. Ultrasound in abdominal tuberculosis.Abdom Imaging 2003;28:5879
17. Anand BS,Nanda R,Sachdev GK.Response of tuberculous stricture to antituberculous
treatment.Gut 1988;29:62-9
18. Balasubramanian R,Narayan M,Balambal R,Tripaty SP,Sudararaman R,venkatesan
P.Randamised and controlled trial of short-course chemotherapy in abdominal tuberculosis a
five-year report.Int J Tuberg Lung Dis 1997;1:44-51
19. Pujari BD,Modified surgical procedures in intestinal tuberculosis .Br J Surg 1979;66:1801
20. Bennani A,Ouazzani H,Fadli F,Dafiri N,Ouazzani L.Diagnostic and therapeutic aspects of
peritoneal tuberculosis in morocco.Apropos of 300 cases.Ann Gastroenterol Hepatol
1988;24:347-54